Академический Документы
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V Voice:
79- Alaryngeal Speech…………………………………………………………………………………………….443
80- Laryngitis……………………………………………………………………………………………………………446
81- Hoarseness & VC Paralysis………………………………………………………………………………..451
82- Benign Lesion of the Larynx……………………………………………………………………………...458
83- Controversies in Laryngology……………………………………………………………………………462
84- Cumming's- Larynx Anatomy……………………………………………………………………………..465
85- Cumming's- Electromyogaraphy of Latyngeal & Pharyngeal Muscles……………….470
86- Cumming's- Laryngeal & Pharyngeal Function…………………………………………………..472
87- Cumming's- Neurological Evaluation of Larynx & Pharynx………………………………..478
88- Cumming's- Phonosurgical Procedures……………………………………………………………..483
89- Cumming's- Benign Vocal Fold Disorders…………………………………………………………..488
90- Cumming's- Laser Surgery in Larynx……………………………………………………………………496
91- Voice Rehabilitation after Laryngectomy………………………………………………………….…499
92- Glottic & Subglottic Stenosis……………………………………………………………………………….502
93- Laryngeal Development………………………………………………………………………………………504
94- Larynx…………………………………………………………………………………………………………………..509
VI Trauma:
95- Auricular Trauma Salvage……………………………………………………………………………………512
96- Facial Trauma………………………………………………………………………………………………………514
97- Auricular Trauma…………………………………………………………………………………………………519
98- Laryngeal Trauma…………………………………………………………………………………………………521
99- Management of Soft Tissue Trauma……………………………………………………………………525
100- Mandibular Fractures……………………………………………………………………………..528
101- Maxillary & Periorbital Fractures……………………………………………………………534
102- Fractures of Nasal & Frontal Sinuses………………………………………………………541
103- Penetrating Face & Neck Trauma…………………………………………………………….548
104- Complex Facial Trauma with Plating…………………………………………………………552
105- POS- Trauma……………………………………………………………………………………………..554
IX Otology:
173- Audiological Tests………………………………………………………………………………………958
174- Cumming's – Tympanostomy Tubes…………………………………………………………..962
175- Development of Ear …………………………………………………………………………………..965
176- Anatomy & Physiology of Hearing………………………………………………………………971
177- Vestibular Function & Anatomy…………………………………………………………………977
178- Balance Function Tests……………………………………………………………………………….981
179- Audiotary Assesment………………………………………………………………………………….986
180- Cumming's – Temporal Bone Anatomy………………………………………………………994
181- Neurophysiologic Intraoperative Monitoring……………………………………………1006
182- Imaging Studies of Temporal Bone1…………………………………………………………1009
183- Imaging Studies of Temporal Bone2…………………………………………………………1015
184- Imaging Studies of Temporal Bone.…………………………………………………………..1020
185- Infections of the External Ear…………………………………………………………………….1031
186- Neoplasm of the Ear & Lateral Skull Base………………………………………………….1037
187- Congenital Aural Atresia…………………………………………………………………………….1045
188- Intracranial & Intratemporal Complications of OM……………………………………1050
189- Middle Ear & Temporal Bone Trauma………………………………………………………..1056
190- Cholesteatoma……………………………………………………………………………………………1061
191- Surgery of Mastoid & Petrosa…………………………………………………………………….1066
192- Reconstruction of TM & Ossicular Chain…………………………………………………….1074
193- Otosclerosis………..………………………………………………………………………………………1078
194- Acute Paralysis of Facial nerve…………………………………………………………………...1083
195- Otologic Manifestation of Systemic Diseases……………………………………………..1095
196- Infections of the Labyrinth…………………………………………………………………………..1101
197- Noise Induced HL……………………………………………………………………………………….1107
198- Ototoxicity……….…………………………………………………………………………………………1110
199- CPA Tumors………………………………………………………………………………………………..1112
200- Sudden Sensory Hearing Loss…………………………………………………………………….1120
201- Tinnitus………………………………………………………………………………………………………1123
202- Autoimmune Inner Ear Diseases……………………………………………………………....1127
203- Aging in the Auditory & Vestibular System……………………………………………....1129
204- Cochlear Implant & Other Implantable Prosthesis………….…………………………1132
205- Hearing Aid & Assistive Listening Devices………………………………………………….1138
206- PERIPHERAL VESTIBULAR DISORDERS……………………………….……………………….1143
207- CENTRAL VESTIBULOPATHY………………………………..........................................1147
208- MED. MANAGEMENT OF VEST. DISORDERS AND VEST. REHABILITATION….1151
209- SURGICAL MANAGEMENT OF VESTIBULAR DISORDERS…………………………….1153
210- Cumming's- TEMPORAL BONE NEOPLASMS AND LATERAL CRANIAL BASE
SURGERY…………………………………………………………………………………………………………………1156
211- Cumming's- AGING AND AUDITORY SYSTEMS – PRESBYCUSIS….……………….1160
212- CONGENITAL AURAL ATRESIA…………………………………………………..………………..1162
213- Ear & Temporal Bone………………………………………………………………….……………….1165
214- ELECTRONYSTAGMOGRAPHY……………………………………………………………………..1171
215- MENIERE’S DISEASE………………………………………………………………….……………..…1175
216- ELECTRONYSTAGMOGRAPH.,……………………………………………………………………..1177
217- FACIAL NERVE ANATOMY…………………………………………………………………………..1189
218- The Halmagyi (Head Impulse)Test ……………………………………………………………..1192
219- Head-Shaking Nystagmus (HSN) ……………………………………………………………....1193
220- Malignant Otitis Externa ………………………………………………………………………..….1194
221- NEOPLASMS OF THE EAR AND LATERAL SKULL BASE PATHOLOGY…………….1195
222- Otoplasty………………………………………………………………………………………………….…1197
223- PERIPHERAL VESTIBULAR DISORDERS……………………………………………….……...1198
224- TBD – Lateral Approach…………………………………………………………………….…..…..1208
225- TBD – Middle Fossa Approach……………………………………………………………………1213
226- Temporal Bone Anatomy……………………………………………………………………………1215
227- Vestibulo-Ocular Reflex (VOR)…………………………………………………………………..1230
-children < 2ya, pts with frequent OM, previous Abx within 3 months, seriously ill high dose
amoxcillin/clavulanate or ceftriaxone IM
-for high-penicillin-resistant pneumococcal strains:
-ceftriaxone IM or IV
-levo-gati-moxifloxacin (adults)
-vancomycin IV
-treatment course: 5 days usually
ACUTE MASTOIDITIS
1
CHRONIC SUPPURATIVE OTITIS MEDIA
-with TM perforation, with or without cholesteatoma
OTOMYCOSIS
2
NECROTIZING (“MALIGNANT”) OTITIS EXTERNA
PLUS
-oral antipseudomonas quinolone
(Cipro)
ACUTE RHINOSINUSITIS
-Hemophilus influenzae (38%) -for mild, no prior treatment -for moderate-severe or prior treated
-Streptococcus pneumoniae -amoxicillin +/- clavulanate -clavulin
(37%) -erythromycin plus TMP/SMX or -double dose amoxicillin (90
-other hemophilus sp (8%) doxycycline mg/kg/day children, 3-4 g/day
-Streptococcus pyogenes (group adults, in divided doses)
A - 6%) -respiratory quinolones
-Moraxella catarrhalis (5%) -levofloxacin
-alpha streptococci (3%) -gatifloxacin
-gram negative bacilli/mixed -moxifloxacin
anaerobes (3%) -cefpodoxim, cefdinir, cefuroxime,
cefditoren
-length of treatment: courses of 3, 4, 5 and 8 days yield similar cure rates as do 10 day courses
-nonresponders (in 5 days) will need to be switched to one or the alternative agents to treat virulent or resistant
bacteria for 10-14 days or more with even a third agent
3
MICROBIOLOGY, INFECTIONS AND ANTIBIOTIC THERAPY
ANTIMICROBIAL AGENTS
Penicillins
-pen G and V:
-highly active against:
-Strep pyogenes (B-hemolytic group A)
-Strep pneumoniae
-actinomycosis
-inactivated by penicillinase (B-lactamase):
-S. aureus
-H. influenzae
-M. catarrhalis
-S. pneumoniae: becoming increasingly resistant to penicillins and cephalosporins due to protein
binding
-antistaphylococcal penicillins
-methicillin, oxacillin, cloxacillin, dicloxacillin, nafcillin
-resist penicillinase
-aminopenicillins:
-ampicillin, amoxicillin
-extend activity spectrum to gram-negative organisms:
-Proteus, E. coli, H. influenzae
-resistance in B-lactamase producing organism
-augmented penicillins:
-clavulanate (amoxil) and sulbactam (ampicillin)
-for management of staphylococci, H. influenzae, M. catarrhalis, anaerobic organisms
Cephalosporins
-commonly and safely used by pts with history of penicillin rashes
-first generation:
-Keflex and Ancef:
highly effective against gram-positive organisms such as streptococci, pneumococci
except for penicillin-resistant strains, and staphylococci except MRSA
-mostly used for S. aureus
-second-generation:
-cefuroxime:
-highly active against gram-positive cocci
-H. influenzae and M. catarrhalis including pen-resistant strains
-penetrates blood-brain barrier fairly well
-third-generation:
-cefixime:
-oral agent highly effective against H. influenzae and M. catarrhalis
-ceftriaxone:
-parenteral agent effective against H. influenzae, M. catarrhalis, S. pneumoniae, N.
meningitidis, N. gonorrheae
-first choice for treating patients with intracranial and orbital complications of acute
sinusitis and otitis media
-usually less active against gram-positive bacteria
-anaerobic bacteria are also relatively resistant
4
Other B-Lactam Antibiotics
-imipenem and meropenem
-active against S. pyogenes, most S. pneumoniae organisms, S. aureus, H. influenzae, B. fragilis
and most anaerobic organisms and the coliforms including P. aeruginosa
-used as single agent against infection by unidentified organisms but CSF penetration is not assured
Macrolides
-has anti-inflammatory effect
-elevate theophylline levels
-erythromycin
-effective for respiratory infections d/t streptococci, most pneumococci, mycoplasmata and
chlamydiae, legionellosis, diptheria, and pertussis
-azithromycin and clarithromycin
-extend antimicrobial activity to include H. influenzae and M. catarrhalis
Clindamycin
-highly active against gram-positive cocci, including many but not all strains of penicillin-resistant
pneumococci
-effective against S. aureus and anaerobic infections of the aerodigestive tract (B. fragilis)
-risk of pseudomembranous colitis
Tetracyclines
-effective against Mycoplasma, Chlamydia, and Legionella
-stain enamel in forming teeth: avoided in children younger than 10 and pregnant women
Quinolones, Fluoroquinolones
-broad spectrum
-elevate theophylline levels
-potential for cartilage damage and arthropathy in children
-ciprofloxacin and ofloxacin:
-antipseudomonas quinolones
-levofloxacin, gatifloxacin, gemifloxacin:
-respiratory quinolones
-for respiratory and pharyngeal infections
-effective against B-hemolytic S. pyogenes, S. pneumoniae, S. aureus, H. influenzae, M.
catarrhalis , Mycoplasma, Chlamydia, Legionella, Bordetella pertussis
Vancomycin
-highly active against gram-positive cocci including MRSA, penicillin-resistant strains of pneumococci,
enterococci, and gonococci
-high concentrations in patients with renal impairment can cause ototoxicity
Metronidazole
-highly active against anaerobic bacteria
-B. fragilis
-all aerobic bacteria are resistant to this agent
-penetrates BBB well
Aminoglycosides
-used against P. aeruginosa and other hospital-acquired infections
-ineffective in anaerobic infections
-risk of ototoxicity (~10%)
5
Sulfonamides
-older agents effective in the management of H. influenzae but not of pneumococcal, streptococcal, and
staphylococcal infections
TREATMENT STRATEGIES
Otitis Media
-S. pneumoniae, H. influenzae, M. catarrhalis
-first line:
-amoxil:
-most strains of S. pneumoniae
-H. influenzae (20% resistant) and M. catarrhalis (80% resistant)
-second line:
-clavulin, 2nd generation cephalosporin
-macrolides
-high dose penicillin for penicillin resistant organisms
-for high-level resistance:
-vancomycin, levofloxacin, gatifloxacin, moxifloxacin, gemifloxacin
Sinusitis
-acute:
-same bacteria as in OM
-same drug choices
-intracranial or orbital complications:
-pneumococcal infection suspected Rx ceftriaxone, cefuroxime or trovafloxacin
-chronic:
-anaerobes and S. aureus
-clindamycin or clavulin
Pharyngitis
-caused by S. pyogenes in 30%
-also N. gonorrhoeae, Mycoplasma, Chlamydia and H. influenzae
Tonsillitis
-frequently caused by S. pyogenes
-clindamycin, cephalexin effective
Mastoiditis
-same treatment as AOM
-pneumococci and H. influenzae tend to intracranial extension Rx ceftriaxone
-chronic suppurative otomastoiditis including cholesteatoma: S. aureus, Proteus, B. fragilis and other
anaerobic organisms
-Pseudomonas
Suppurative Otitis
-necessitates combination drug therapy:
-polymyxin for pseudomonal infection and neomycin for S. aureus, Proteus organisms and others
6
DEGENERATIVE AND IDIOPATHIC DISEASES
Fibrous Dysplasia
-medullary bone replaced by fibroosseous tissue
-three clinical forms:
-monostotic FD (75-80%)
-polyostotic FD (20-25%)
-Albright syndrome:
-polyosotic fibrous dysplasia associated with abnormal skin pigmentation, precocious
puberty and other non-skeletal diseases
-20-25% of polyostotic pts
-onset usually <30 ya
-90% asymptomatic
-symptoms: local swelling, pain, displaced teeth or nerve-compression symptoms
-most commonly affected bones: ribs, femur for MFD; femur, tibia for PFD
-head and neck (25%): maxilla and mandible
-radiographic sign: expanded “ground glass” lesion
-histology: marrow replaced by whorled spindle cells with lack of “osteoblastic rimming”
-1/200 cases undergoes malignant degeneration osteosarcoma
-treatment: complete excision
Ossyfying Fibroma
-similar to fibrous dysplasia, but onset is 10 years later
-usually more discrete
-osteoblastic rimming present
-treatment: excision
Paget Disease
-most often occurs between 55-70 ya
-90% have polyostotic disease
-classic symptoms: enlarging skull, dorsal kyphosis, bowing of legs
-other symptoms:
-bone pain (most common)
-spinal root compression
-normal pressure hydrocephalus
-repeated fracture with nonunion
-disease process:
-lytic phase: increased osteoclastic activity with replacement with vascular stroma
-mixed phase: increased osteoblastic activity with osteoclastic activity “cotton wool” appearance
on X-rays
-osteoblastic phase sclerosis on X-rays
-elevated ALP levels and increased urine hydroxyproline levels; hypercalcemia
-occurs more commonly in skull than in face
-can undergo malignant transformation to osteosarcoma ~1-5%
-treatment: calcitonins, disodium etidronate or mithramycin
7
Fibrous Dysplasia Compared with Paget’s Disease
Characteristic Fibrous Dysplasia Paget’s Disease
8
Mikulicz Syndrome
-recurrent sialadenitis:
-unilateral, swollen, red, tender gland with purulent discharge
-sialography: dilation and focal narrowing of Stensen duct
-treatment:
-demonstration and removal of any stones
-antibiotics, warm compresses and sialogogues
-excision of gland in severe cases
-sialosis:
-recurrent bilateral nontender parotid swelling
-secondary to various conditions:
-cirrhosis, diabetes, alcoholism, malnutrition, ovarian insufficiency, thyroid
insufficiency, pancreatic insufficiency
-drugs: sulfisoxazole, phenalbutazone, catecholamines, iodide-containing compounds
-multinodular gland:
-autoimmune diseases
-granulomatous diseases: tuberculosis, sarcoidosis
-lymphoproliferative neoplasms
-Warthin’s tumour
-other tumours
Wegener Granulomatosis
-vasculitis, multinucleated giant cells and palisading histiocytes
-granuloma and typical polymorphonuclear cells
-tx: azathioprine, cyclophosphamide and steroids
Malignant Lymphoma
9
Idiopathic Midline Destructive Disease
-differentiated histologically from Wegener granulomatosis and lymphomatoid granulomatosis
-composed of sheets of typical polymorphs; no granuloma and no vasculitis
Polyarteritis Nodosa
-affects only small to medium-sized arteries
-rarely affects lungs
Foreign-Body Granulomas
-cocaine use; intranasal steroid injections for allergies
-multinucleated giant cells and presence of foreign material
-absence of vasculitis
Amyloidosis
-deposition of extracellular fibrillar proteins in various tissues
-rare in pediatric age group
-types:
-primary systemic form (56%):
-heart, tongue, GI tract
-secondary systemic form (8%):
-associated with chronic destructive diseases: tuberculosis, rheumatoid arthritis and
osteomyelitis
-kidney, adrenals, liver, spleen
-localized form (9%):
-any of above
-myeloma associated (26%):
-heart, tongue, GI tract
-histochemical studies: amyloid composed of light-chain immunoglobulins
-extracellular proteins that are green and birefringent under polarized light after staining with Congo red
-orbit most common site of deposition for localized amyloid in H+N
Sarcoidosis
-idiopathic disease characterized by noncaseating granuloma
-usually occurs in 3rd and 4th decade
-may be associated with impaired T-cell function, delayed hypersensitivity and energy
-H+N symptoms:
-cervical adenopathy (most common)
-deposits in supraglottic larynx dysphonia, dyspnea, dysphagia
-nasopharyngeal lesions
-parotid gland enlargement
-neurologic impairment
10
-orbital mass or lacrimal gland enlargement
-uveitis
-diagnosis:
-CXR - mediastinal lymphadenopathy
-hypercalcemia
-ACE (angiotensin converting enzyme) levels used to follow course of disease
-Kveim reaction: granulomatous reaction appearing 4 weeks after intradermal injection of sarcoid
spleen or lymph node extracts (experimental)
-treatment: oral steroids
Relapsing Polychondritis
-inflammation of cartilage and other tissues with a high concentration of glycosaminoglycans
-manifestations:
-auricular chondritis (50%)
-nonerosive polyarthritis (50%)
-nasal chondritis (15%)
-inflammation of ocular structures (15%)
-chondritis of respiratory tract (15%)
-cochlear and vestibular damage
-chondritis rapidly develops and resolves in 5-10 days
-involved cartilage becomes deformed: saddle-nose deformity; cauliflower ear
-mortality related to respiratory involvement (ie laryngeal collapse) or cardiovascular disease (eg. aneurysm
or valvular insufficiency)
-treatment: symptomatic; steroids for life threatening conditions
THYROIDITIS
Hashimoto Thyroiditis
-most common form of thyroiditis
-goitrous thyroiditis associated with elevated levels of antithyroid antibodies
-slowly progressive painless enlargement
-histology: lymphocytic infiltration with fibrosis and Hurthle cell change of follicular cells
-disease progresses to hypothyroidism
-most specific test: antimicrosomal antibody; positive in 90% of pts
-treatment: thyroid hormone replacement; FNA for solid lesions to r/o associated lymphoma or neoplasms
Subacute Thyroiditis
-two types:
-granulomatous
-thought to be caused by viral infection
-painful
-infiltration of giant cells
-transient hyperthyroidism transient hypothyroidism
-complete recovery in most cases; 10% have persistent goiter
-lymphocytic
-painless
-lymphocytic infiltrate
-permanent goiter and hypothyroidism more commonly seen than in granulomatous
thyroiditis
11
Acute Suppurative Thyroiditis
-mostly seen in immunocompromised
-typical pathogen: S. aureus
-treatment: antibiotics and surgical drainage
Reidel Thyroiditis
-rare fibrosing thyroiditis
-seen predominantly in women
-treatment: thyroid hormone replacement or surgical release of obstruction if required
12
CONNECTIVE TISSUE DISEASES
Autoantibody Relationships
-prevailing histopathologic feature is varying amount of connective tissue and blood vessel inflammation
with abundant fibrinoid deposits
Treatment
-rheumatologic assessment
-NSAIDS, topical and low-dose systemic steroids, antimalarial
-low-dose methotrexate
-high-dose steroids and azathioprine and cyclophosphamide reserved for visceral involvement
-oral ulcers:
-Klack’s solution: tetracycline, cortisone, diphenydramine, nystatin
RHEUMATOID ARTHRITIS
13
Treatment
-salicylates, NSAIDs, gold salts, penicillamine, hydroxychloroquine, immunosuppressive agents
SJOGREN SYNDROME
-see Ch 13 - Degenerative and Idiopathic Diseases
-increased (33-44 times) risk of lymphoma
-salivary gland biopsy best single criterion (spec 83%, sens 81%)
SYSTEMIC SCLEROSIS
Treatment
-symptomatic
-PPIs for reflux esophagitis
Treatment
-steroids for symptomatic patients
-methotrexate and other immunosuppressives
RELAPSING POLYCHONDRITIS
-see Ch 13 - Degenerative and Idiopathic Diseases
VASCULITIDES
Polyarteritis Nodosa
-rare: 1/100000 per year
-M=F; 5th or 6th decade
-involves small and medium-sized arteries
-ENT manifestations few:
-thromboembolic occlusion of end arteries of inner ear
14
-sudden bilateral SNHL
-vestibular disturbance
-cranial nerve palsies
Churg-Straus Syndrome
-allergic angiitis granulomatosis
-systemic small-vessel vasculitis, extravascular granulomas, hypereosinophilia
Hypersensitivity Vasculitides
-include hypersensitivity angiitis, Henoch-Schonlein purpura, cryoglobulinemia vasculitis
Wegener Granulomatosis
-1/100000 per year
-triad: respiratory tract granuloma, vasculitis, glomerulonephritis
-white; 5th decade
-typical clinical features: bilateral pneumonitis (95%), chronic sinusitis (90%), mucosal ulceration of
nasopharynx (75%) and evidence of renal disease (80%)
-most common oral cavity findings: hyperplasia of gingiva and gingivitis
-subglottic stenosis in 8.5%: poor prognostic sign
-otologic problems in 20-25%: serous otitis media, suppurative otitis media, SNHL, pinna changes
Behçet Disease
-vasculitis affecting Japanese and Mediterranean population
-3rd decade
-oral and genital ulcers and uveitis or iritis
-aphthous-like ulcers; punched out and covered with a pale pseudomembrane
-heal in a few days with scarring
-morbidity secondary to CNS involvement, arthritis, and large-vessel arthritis
-tx of ulcers: corticosteroid creams
Cogan Syndrome
-Meniere-like audiovestibular dysfunction, interstitial keratitis, and nonreactive tests for syphilis
-bilateral deafness results in 65% of cases
-accompanied by large- or medium-vessel systemic vasculitis
Kawasaki Disease
-mucocutaneous lymph node syndrome
-pediatric age group
-most common cause of acquired heart disease in children
-symptoms:
-fever (spiking despite Abx treatment)
-conjunctivitis
-red and dry lips
-erythema of oral mucosa
15
-polymorphous truncal rash
-desquamation of fingers and toes
-cervical lymphadenopathy
-“strawberry tongue”
-20-25% untreated children develop coronary artery dilatation or aneurysm
-death from rupture or thrombosis of coronary aneurysm from 2-12 weeks after onset of disease
-treatment with IV gammaglobulin and aspirin in first 10 days reduce incidence of coronary abnormalities
10-fold
16
GRANULOMATOUS DISEASES
OF THE HEAD AND NECK
NEOPLASTIC DISORDERS
Histiocytosis X
-sheets of polygonal histiocytes (Langerhans’ cells) with variable eosinophil, plasma cells, and
lymphocytes
-Langerhans’ cells = histiocytes containing cytoplasmic inclusions known as X bodies
-otitis media most frequent otologic finding
Eosinophilic Granuloma
-localized form of histiocytosis X
-affects children and young adults
-osteolytic lesions with predilection for frontal and temporal bones
-other symptoms:
-proptosis (sphenoid involvement)
-acute mastoiditis
-middle ear granulation tissue
-tympanic membrane perforations
-facial paralysis
-tx: surgical excision; XRT for inaccessible lesions
-excellent prognosis
Hand-Schuller-Christian Disease
-chronic disseminated form of histiocytosis X
-presents in children and young adults (rare in elderly)
-classic triad in 10%:
-skull lesions (polyostotic), exophthalmos and diabetes insipidus
-other symptoms:
-facial paralysis
-external auditory canal polypoid lesions
-tx: XRT, surgery, chemotx or combination
-mortality 30%
Letterer-Siwe Disease
-acute disseminated form of histiocytosis X
-children < 3ya
-uniformly fatal
-clinical:
-fever, proptosis, splenomegaly, hepatomegaly, exfoliative dermatitis, thrombocytopenia
-tx: radiation therapy and chemotherapy
Fibrous Histiocytoma
-painless mass lesion occurring in sun-exposed skin and orbital tissues
-histology:
-biphasic cell population of fibroblasts and histiocytes with spindle-shaped cells with elongated
nuclei arranged in cartwheel pattern
-tx: local excision with clear margins
17
Lobular Capillary Hemangioma
-risks: young males, postpubescent females, pregnancy
-circumscribed aggregates of capillaries arranged in lobules
-clinical:
-painless, friable, ulcerated or polypoid lesion on lips (40%), nasal cavity (30%, epistaxis), tongue
(20%), or oral mucosa (15%)
-mainly arise on septum
-female predominance in pts 18-39; based on hormonal factors
-in pregnant women, regresses after delivery
-tx: surgical excision
Necrotizing Sialometaplasia
-pathophysiology:
-infarct of mucosal salivary gland tissue resulting in a self-healing inflammatory process
-histology:
-metaplastic epithelial cells lining small salivary gland ducts with preservation of lobular
architecture
-lobular necrosis
-pseudoepitheliomatous hyperplasia
-most often occurs at junction of hard and soft palate
-lesion is sharply demarcated ulcer may be mistaken for SCCa
-spontaneous resolution over course of weeks to months
Sarcoidosis
-multisystem granulomatosis
-cause unknown
-clinical course variable
-most often in 3rd-5th decade
-histology:
-non-caseating epithelioid granuloma
-accumulation of T-cells
-mononuclear phagocytes
-derangement of normal tissue architecture
-symptoms:
-40% asymptomatic
-pulmonary involvement (88%, cough, hilar adenopathy, dyspnea)
-cervical adenopathy (25-50%, most common H+N presentation)
-salivary glands parotid mass, uveoparotid fever (Heerfordt’s disease)
-larynx supraglottic region most commonly affected in larynx (epiglottis most common);
submucosal infiltration
-other:
-uveitis, nasal mass, orbital mass, nasal perforations
-cutaneous lesions (erythema nodosum, rashes)
-“Darrier Rousey” nodule (subcutaneous lesion)
-hepatic and renal involvement
-splenomegaly
-cardiac (arrhythmia)
-bone lesions
-neuropathies
18
AUTOIMMUNE OR VASCULITIC DISEASE
Wegener Granulomatosis
-systemic disorder: ELK (ENT, Lungs,
HEAD AND NECK MANIFESTATIONS OF WG
Kidney)
-4th to 5th decade; M:F ~2:1 Nasal (60-80%) -chronic sinusitis, nasal crusting, bloody
-necrotizing granuloma with vasculitis in one rhinorrhea, PND, septal perforation
Otologic (20-25%) -SOM +/- SNHL 2o cochlear vasculitis
or more major organ systems
Ocular (40%) -granulomatous keratitis, uveitic, retinal
-granuloma, necrotizing vasculitis, artery involvement
and arthritis involving small arteries Tracheal -stridor from subglottic narrowing
must be demonstrated
-C-ANCA:
-cytoplasmic staining anti-neutrophil cytoplasmic antibodies
-used for diagnosis; high specificity (> 90%)
-used to monitor disease activity as levels parallel this
Goodpasture Syndrome
-antiglomerular basement membrane nephritis
-lacks sinus involvement
Relapsing Polychondritis
-intermittent inflammation of cartilage
-pinna, nose, trachea and larynx most commonly involved
-tx: NSAIDs, steroids or dapsone
Sjogren Syndrome
-autoimmune disorder of exocrine glands
-xerostomia, keratoconjunctivitis sicca and connective tissue disease
Periarteritis Nodosa
-fibrinoid necrosis of medium sized arteries with frequent involvement of kidneys
-non-specific nasal mucosal lesions
Churg-Strauss Syndrome
-triad: hyper-eosinophilia, allergic rhinitis, asthma and systemic vasculitis of medium and small muscular
arteries
-three phases:
-prodromal phase: atopy and allergic rhinitis
-hypereosinophilia
-systemic necrotizing vasculitis
-tx: high dose systemic steroids
19
Behcet Disease
-recurrent aphthous ulceration of upper aerodigestive tract and genitalia
-ocular inflammation
-cutaneous vasculitis
-no treatment known
Cholesterol Granuloma
-arise as consequence of inadequate ventilation with impaired drainage and haemorrhage of middle ear or
paranasal sinuses
-cholesterol precipitates from erythrocyte breakdown causes FB reaction with neovascularization and
formation of granulation tissue
Gout
-rare
-involvement of cricoarytenoid joint: pain, dysphagia, hoarseness, aspiration, stridor and possible airway
compromise
INFECTIOUS DISEASES
Bacterial Infections
Cat-Scratch Disease
-Rochalimae (Bartonella) henselae
-intracellular, pleomorphic, gram-negative, non-AFB
-seen with Warthin-Starry silver stain
-hx of cat exposure, primary inoculation site, regional adenopathy
-histology:
-suppurative and necrotizing granulomatous lymphadenitis with stellate abscesses
-tx: supportive with I+D for abscesses
Bacillary Angiomatosis
-young adults
-cutaneous papules and subcutaneous nodules
Brucellosis
-aerobic, gram-negative bacilli
-exposure from infected cattle (butter)
-tx: tetracycline
Rhinoscleroma
-Klebsiella rhinoscleromatis
-tx: tetracyline or streptomycin
20
Leprosy
-Mycobacterium leprae
-laryngeal ulcerations, lymphadenopathy, hyposmia, nasal collapse, fish-mouth deformity, facial nerve
paralysis, eyebrow and eyelash loss
-tx: dapsone
Nontuberculous Mycobacteria
HEAD AND NECK MANIFESTATIONS OF
-children aged 1-6 years more frequently TUBERCULOSIS
affected
-more commonly causes (1) corneal ulceration Lymph nodes -lymphadenopathy
and/or (2) cervical lymphadenopathy Larynx -granulomas or ulcerations, edema, polyploid
changes; most common site of involvement is
-transmission from soil to mouth or eye the arytenoids
-Dx: biopsy for C+S; AFB staining Eyes -conjunctivitis, keratitis, uveitic
Salivary glands -diffuse glandular involvement, usually of the
Tuberculosis parotid
Oral cavity -painful or painless ulcers, most frequently
-scrofula involving tongue
-rare in head and neck Ear -granulomas, tympanic membrane
-Dx: positive PPD, CXR, biopsy perforations, watery otorrhea, mastoiditis
-tx: isoniazid and rifampin daily for 9-12
months
Actinomycosis
-anaerobic or micro-aerophilic Actinomyces species
-from dental manipulation or trauma
-visible sinus tracts and lymphadenopathy
-purplish discolouration of overlying skin
-histology: sulfur granules
-tx: surgical debridement and Pen G IV x2-6 weeks
Syphilis
-Treponema pallidum
-dx:
-VDRL for screening
-dark-field examination
-fluorescent treponemal antibody-absorption test (ft-Abs)
-Warthin-Starry tissue staining
-histopathology:
-mononuclear infiltrate
-obliterative arteritis
-hydrops
-gummas and osteolytic lesions in otic capsule
-stages:
-primary:
-chancre at inoculation site, lymphadenopathy
-secondary: “Great Imitator”
-highly contagious, general malaise and fever, arthralgia, hepatosplenomagaly, genital
condyloma lata, nephrotic syndrome, “mucous patches”
-latent: asymptomatic phase
-tertiary:
-noninfectious stage
-may occur years after initial infection
-slow progressive
21
-neurosyphilis
-aortic involvement
-gummas
-H+N symptoms:
-lymphadenopathy
-laryngeal: laryngitis with mild edema of the larynx, vocal fold paralysis, dysphagia
-oral cavity: chancre, granulomatous infiltration of tongue, palate
-otologic: abrupt profound SNHL, Meniere’s symptoms, interstitial keratitis, TM perforation,
gummas of temporal bone
-nasal: saddle nose deformity, rhinitis, osseous and cartilaginous destruction, septal perforation
Anthrax
-Bacillus anthracis
-painless necrotic ulcer with surrounding edema +/- regional lymphadenopathy
Tularemia
-ticks, rabbits, deer
-photophobia, decreased visual acuity and cervical and preauricular lymphadenopathy
-exudative pharyngitis
-tx: streptomycin
Granuloma Inguinale
-Calymmatobacterium granulomatis
-tx: tetracycline, ampicillin or SMX-TMP
Fungal Infections
Histoplasmosis
-Histoplasma capsulatum
-airborne transmission
-endemic to Missouri and Ohio River Valley causes chronic pulmonary infection
-most infections are subclinical
-immunocompromised: granulomatous lesions of lips, gingiva, tongue, pharynx and larynx
-may mimic carcinoma
-dx: culture on Sabouraud’s medium, skin test, complement fixation test, latex agglutination
-tx: amphotericin B
Blastomycosis
-Blastomyces dermatitidis
-airborne transmission
-endemic to Central America and the Midwest USA)
-cutaneous disease, pulmonary involvement and constitutional symptoms
-oropharyngeal and verrucous laryngeal lesions
-histopathology:
-pseudoepitheliomatous hyperplasia
-intraepithelial microabscess
-single bifringent broad based bud (yeast form)
-tx: amphotericin B; itraconazole
22
Coccidioidomycosis
-Coccidioides immitis
-rare: skin, mucous membranes, thyroid, eyes, trachea, salivary glands, epiglottis
Candidiasis
-Candida albicans
-tx: nystatin or ketoconazaole
Rhinosporidiosis
-Rhinosporidium seeberi
-indolent, painless, warty excrescences on nasal, palatal and conjunctival mucous membranes
-tx: excision
Phycomycosis
-Mucor, Rhizopus or Absidia
-facial pain, fever, bloody rhinorrhea, facial swelling and sinus tenderness
-proptosis, visual loss, cranial nerve palsies and obtundation
-tx: amphotericin B and aggressive surgical debridement
Cryptococcosis
-Cryptococcus neoformans
-d/t immunosuppression
-rare: membranous nasopharyngitis, meningitis, hearing loss
Aspergillosis
-Aspergillus fumigatus
-allergic, noninvasive or invasive
Parasitic Infections
Leishmaniasis
-Leishmania from sandfly bites
-cutaneous or mucocutaneous lesions
-bloodborne spread to oral cavity and oropharynx
-progressive inflammation and destruction of soft tissues of mouth and nose may occur
Myiasis
-infestation of body by maggots and transmitted by screwworm fly
Toxoplasmosis
-Toxoplasma gondii
-from cat feces or infected poorly cooked lamb or pork
TRAUMA-INDUCED DISORDERS
Intubation Granuloma
-involve vocal process of arytenoids
-contact ulcer granuloma pedunculate polyp
23
Teflon Granuloma
-from vocal cord injections
Reparative Granuloma
-secondary to local trauma in oral cavity
Pyogenic Granuloma
-granulation tissue formed in response to minor trauma with secondary infection
24
GERIATRIC OTOLARYNGOLOGY
TYPES OF PRESBYCUSIS
Audiometric Profile
Cochlear Conductive All turns: basal > apical High-tone gradual slope Related to steepness of slope
-increasing number and decreasing cost of assistive listening devices are factors in improving quality of life
for pts with mild presbycusis
TINNITUS
-presbyastasis:
-disequilibrium
-degenerative changes such as vacuolization of sensory epithelium of SCC ampullae plus
fragmentation of otoconia
-morphologic changes in vestibular nerves, Scarpa ganglion, and cerebellum
-decreased sensory input, decreased integrating ability and weakened muscular function balance
problems
-atrophic changes
-voice quality deteriorates with aging -mostly in males
-anatomic and functional causes known: -increased pitch
-ossification of laryngeal cartilages -thin reedy voice
-limitation of arytenoid cartilage excursion -edema and polyploid change
-females
-incomplete glottic closure -lower pitched voice
-decreased number of collagen and elastin fibers -pharyngeal formants also lower
-atrophy of laryngeal muscles -smoking relationship
-fundamental vocal frequency increases but may decrease if -voice stability
-wobbling and tremolo (standard
there is edema or polyploid degeneration of vocal folds deviation from fundamental
-some changes in vocal quality may result from unsuccessful frequency and jitter)
efforts to compensate for effects of aging
25
-males:
-attempts to drop pitch
-gravelly, breathy, glottal fry
-easy fatigue
-apparently bowed vocal cords
-females:
-attempts to raise pitch
-squeezed, strained
-effortful voice
-variable ventricular band adduction
-older pts more likely to consult physicians for nasal drainage, postnasal drip, gustatory rhinitis, and
decreased olfactory ability
-diminished capacity of immune system is believed to be a factor in increased frequency and severity of
sinusitis in geriatric age group
PRESBYPHAGIA
PERIPHERAL NERVES
-general tendency to lose myelinated nerve fibers with increasing age, pathologic changes in Schwann
cells, an increase in cross-sectional area of nerves, and vascular changes (such as endothelial proliferation
and media fibrosis)
GERIATRIC IMMUNOLOGY
-with increasing age, immune system becomes less effective in protecting against infections and neoplastic
disease
-lymphocytes are not as effective in older people for the following reasons:
-function of helper and cytotoxic T-cell activity declines
26
-general response to antigens and immunogen decreases
-thymus gland involutes
-older T and B cells seem to produce a weaker response intrinsically
-quality of overall response is decreased (less IgG and fewer antibodies are produced)
27
HEADACHE AND FACIAL PAIN
CLINICAL SYNDROMES
Tension-type Headache
-bilateral
-stress related
-continuous nonpulsatile headache
-usually responsive to NSAIDs
-persists days or weeks, not disabling
Migraine
-premonitory symptom
-aura
-disabling unilateral headache
-often reported as a sick headache or sinus headache
-nausea and vomiting common
-photo- and phonophobia common
-precipitated by red wine and some foods
-preventive therapy initiated in pts suffering two or more attacks per month
-treatment strategies:
-aborting further development of pain by starting drugs shortly after first warning symptoms or at
earliest onset of pain
-treating pain if abortive therapy fails
-preventing headache by limiting predisposing events; promote healthy lifestyle
Cluster
-provoked by EtOH
-seasonal
-may be associated with allergy
-stereotypic attacks
-autonomic symptoms can cause confusion with sinusitis
Trigeminal Neuralgia
-lancinating pain along distribution of CN V
-brief but may result in significant functional impairment
-occurs in 5th, 6th and 7th decades
-triggers are small areas on face that precipitate an attack when touched
28
-not associated with any neurological impairment
-must rule out other neurological causes
-treatment:
-trials of carbamazepine, gabapentin, baclofen, phenytoin, sodium valproate, chlorphenesin
-2 week trial for a drug
-adjunctive therapy: TCA and NSAIDs
Glossopharyngeal Neuralgia
-unilateral lancinating pain located in posterior pharynx, soft palate, base of tongue, ear, mastoid or side of
head
-workup and treatment same as for trigeminal neuralgia
Post-traumatic Neuralgia
-most often include lateral parietal and occipital regions
-treatment includes same medications used for trigeminal neuralgia
-local infiltration of trigger points with bupivicaine can be effective
Postherpetic Neuralgia
-VSV infection of trigeminal nerve in childhood as chickenpox
-reactivation later in life by trauma or stress
-immunocompromised pts treated with acyclovir, NSAIDs or opioids for pain during acute phase
-other patients treated with 10d course of oral prednisone 40 mg/day, tapering after 5 days
-pain persisting > 2 months = postherpetic neuralgia
-opioid and NSAIDs often are of little use at this stage
-anticonvulsants most useful; combined with TCA or baclofen
Brain Tumour
-30% of pts with brain tumour have headache at time of diagnosis
-characteristic feature is crescendo quality of headache with greater intensity and frequency of pain along
with less response to analgesics over time
Subdural Hematoma
Subarachnoid Hemorrhage
Temporal Arteritis
-95% pts are > 60 ya
-daily moderate to severe headache, scalp sensitivity, generalized fatigue
-carotid artery pain, jaw claudication
-enlarged, thickened or tender scalp arteries
29
-treatment: prednisone (60 mg od)
Hypertension
-poor correlation between headache and chronic elevations in blood pressure
-acute headache associated with rapid rises in BP may be indication of pheochromocytoma, renal artery
stenosis, or hyperadrenalism
Post-traumatic Headache
-typically frontal and occipital, often present at some level day and night, poorly responsive to medications
-treatment: reassurance and a course of antidepressants (eg. TCA, SSRI)
30
MANIFESTATIONS OF AIDS
-HIV is a retrovirus that attaches to CD4+ cells marker of T-helper cells, macrophages, and other
immunological cells
-results in a decrease in T-helper lymphocytes and impaired function of macrophages, neutrophils, B-
lymphocytes and complement activation
-AIDS defining illness:
-candidiasis, CMV disease, Kaposi’s sarcoma, Pneumocystis carinii, etc..
-CD4+ count < 200 cells/ul
DERMATOLOGIC
-molluscum contagiosum
-pearly umbilicate papules; usually 2-5 mm, occasionally giant; predilection for eyelids
-tx: surgical excision, curettage or cryotherapy
-complics: frequent recurrence following treatment; can cause functional problems if extensively
involving and treated in eyelid areas
-bacillary angiomatosis
-subcutaneous nodules or friable papules; multiple organ involvement; negative cultures; classic
histopathologic appearance
-tx: erythromycin, 500 mg qid or rifampin 600 mg qd
-if unrecognized and untreated, can have multisystem involvement and possibly death
-cutaneous Cryptococcus
-most common dermatologic condition associated with HIV
-pustular or granulomatous lesions; histopathologic or culture identification
-tx: search for systemic infection, and treat systematically with amphotericin B and/or flucytosine
-complics: cryptococcal meningitis associated with 30% mortality rate even when treated
31
-seborrheic dermatitis
-white scaly plaques or patches with or without erythema and inflammation
-tx: hydrocortisone cream; ketoconazole cream
-complics: can become secondarily infected with S. aureus
-Kaposi sarcoma
-violaceous papular or ulcerated skin lesions, often multiple; can be associated with regional
adenopathy and mucosal lesions
-tx: low-dose XRT, systemic (vincristine or vinblastine), or intralesional (vinblastine)
chemotherapy
-complics: secondary infection produces severe symptoms; occasionally causes airway obstruction
or other functional problems
OTOLOGIC
-primary dermatologic conditions affecting EAC: KS and seborrheic dermatitis
-serous and acute otitis media most common otologic conditions
-ETD 2o to nasopharyngeal lymphoid hypertrophy
-Staphylococcus and Pseudomonas in acute or chronic OM is more common
-P. carinii and Candida have been cultured in middle ear aspirates of AIDS patients
-mild to moderate SNHL often reported: viral infection suspected
-Oral candidiasis:
-most common oral lesion in AIDS
-pseudomembranous plaques with underlying red inflamed mucosal surface
-tx: topical antifungal: nystatin tid or clotrimazole;
systemic antifungal: ketoconazole 200 mg qd or fluconazole
-can produce severe local symptoms; candida esophagitis must be considered
-Herpetic stomatitis:
-ulcerative, punched-out lesions occurring on any mucosal surface
-tx: oral acyclovir, 200 mg 5 times/day; topical analgesics
32
-frequent recurrence; may develop drug resistance
-Aphthous ulcers:
-usually single, but may be multiple; usually on mobile mucosal surface; may become extremely
large “giant apththous ulcers”
-tx: topical analgesics; topical steroids in Orabase; occasionally intralesional or systemic steroids
-can produce severe debilitating symptoms resulting in nutritional imbalance
-Hairy leukoplakia:
-whitish thickening of mucosa on lateral tongue; often has corrugated appearance
-usually asymptomatic
-EBV present in epithelium
-tx: none necessary; treat candidal superinfection when present; acyclovir may be beneficial
-Kaposi’s sarcoma:
-violaceus lesions; predilection for hard palate
-may be flat or nodular; may become ulcerated and secondarily infected
-tx: intralesional or systemic chemotherapy; palliative surgical or laser excision, radiation therapy
-can produce local symptoms when ulcerated or infected; occasionally causes airway obstruction
or severe dysphagia
-Non-Hodgkin’s lymphoma:
-second most common neoplasm associated with AIDS
-nodular, ulcerative; Waldeyer’s ring area often involved; biopsy diagnostic
-tx: chemo or XRT
-often causes local symptoms of obstruction or pain; frequent dissemination including
lymphomatous meningitis
LARYNX
NECK
33
-ddx lymphadenopathy:
-malignancy
-tuberculous, atypical mycobacterial infections
-histoplasmosis
-toxoplasmosis
-cat-scratch disease
34
F.Ling - POS notes and points (1)
Principles of Surgery
“69" other notes and points from previous exams ;)
1. Internal maxillary does pass through the deep lobe of the parotid
2. Aldosterone mechanism of action: resorption of sodium at cortical collecting duct (Ganong 345)
3. Non-caseating granulomas
-TB (can be caseating also) and sarcoid (Robbin 81)
4. Actinomycosis:
-draining sinuses
-involves skin sinus tracts with pus
-sulfur granules on histo
-tx: surgical drainage, penicillin for at least 8 weeks can be up to 1yr until drainage stops
-(Merck 1181)
5. Horner’s Syndrome: miosis, ptosis, anhydrosis, enophthalmos (Merck 652)
6. Early endoscopy is OK for caustic ingestion (Harrison 1585, Schwartz 1159)
7. Nasal fractures most common facial fracture in trauma; mandibular fracture second
8. Azathioprine causes cholestasis (Schwartz 430)
9. Renin (Ganong 421):
-factors that increase secretion: sympathetic activity, circulating catecholamines, prostaglandins
-factors that decrease secretion: hyperaldosteronism, angiotensin II, vasopressin, reabsorption across
macula densa, afferent arteriolar pressure
10. Melanoma treatment (Schwartz 525):
-Clark level I - < 0.75mm: 2cm margin, no lymph node dissection if not affected
-Clark levels II, III, IV - 0.76-4mm: excise with 2-3cm margin, lymph node dissection controversial
-Clark level V - > 4.0 mm: metastasis likely, no lymph node dissection
11. Most common type of melanoma: superficial spreading (70-80%)
12. Bites (Sanford 1997, Harrison 836)
-dogs:
- responsible for 80% domestic animal bites
-only 15-20% get infected
-bugs: strep viridans, staph, pasturella, anaerobes etc...
-cats:
-80% of bites get infected
-P. multocida most responsible
-humans:
-more frequently infected than other animal bites
-bugs: strep viridans (100%), staph epi (53%), staph aureus (29%), eikenella (15%), anaerobes
etc..
13. Presentation of CMV post transplantation:
-leukopenia with fever, pneumonia, gastroenteritis, hepatitis, retinitis, sepsis
35
F.Ling - POS notes and points (2)
14. Highest risk for surgery: CHF (Goldman index 11) > MI less than 6 months (Goldman index 10)
15. Indications for thrombolytics in PE (Way 800)
-shock, RV failure, severe pulmonary hypertension and may die with additional emboli
16. Pancreatic alpha cells rich in beta-adrenergic receptors (stimulation) glucagon
Pancreatic beta cells rich in alpha-adrenergic receptors insulin
17. Growth Hormone secretion:
-stimulated by: ACTH, thyroxine, alpha-adrenergic stimulation, glucagon
-inhibited by: hyperglycemia, FFA, cortisol, somatostatin
18. Effects of PTH:
- sCa: renal and intestinal resorption
- sPO4 via renal excretion
-1 hydroxylation of 25-OH vitamin D
-stimulates osteoclasts
19. ATN: hemegranular casts; SG < 1.015
Prerenal: hyaline casts; SG > 1.018
20. Amikacin for treatment of pseudomonas that is resistant to tobramycin or gentamicin (Merck 1174)
21. Oral Abx for pseudomonas: cipro (or other quinolones), oral indanyl carbenicillin
22. Persantine = dipyrimadole: decreases platelet aggregation, dilates coronary arteries
23. OCP and DVT (Merck 1998, Schwartz Ch 11):
-related to increases in blood clotting factors
-possibly increased platelet adhesion
-increased levels of globulins, particularly factors VII and X hypercoagulable state
-decreased antithrombin III
24. TTP (Merck 945)
-syndrome of: platelets, fragmented RBC, renal failure, fever, manifestations of ischemic damage (eg.
confusion, seizure, jaundice etc.)
-tx: plasmapheresis, steroids; if refractory, splenectomy, vincristine or cyclophosphamide have been used
25. Cytochrome P450 inducers: barbiturates, phenytoin, rifampin, carbamazepine
26. Cytochrome P450 inhibitors: cimetidine, INH, ketoconazole, allopurinol, erythromycin, MAOI, disulfiram,
verapamil
27. Thromboxanes synthesized in platelets; prostacyclines synthesized in endothelial cells
28. Serotonin found in enterochromaffin cells of the gut, CNS, and platelets
29. Arginine (Schwartz 246, Rush 48):
-helps to decreases protein catabolism
-reduces urinary nitrogen excretion
-improve immune function (T-cell proliferation)
-improve wound healing (?accelerates it)
-secretagogue activity on pituitary and pancreatic hormones: GH, PRL, glucagon, insulin, IGF,
catecholamines
30. Cryptococcus (Merck 1218)
-cannot be contracted via blood transfusion
-acquired by inhalation of soil contaminated with encapsulated yeast
-tx: Ampho B (with flucytosine)
31. Ionized calcium required for neuromuscular stability (Rush 15)
32. Preoperative TPN (Schwartz 444)
-increases wound healing
-increases risk of nosocomial and catheter related sepsis in non-severely malnourished individuals
-increases immune function pre-op and lowers mortality and decreases septic complications
33. Arthus reaction (Merck 1010)
-aka. Type III hypersensitivity
-due to presence of Ab that binds to injected Ag immune complex formation, complement activation and
neutrophil chemotaxis
36
F.Ling - POS notes and points (3)
37
F.Ling - POS notes and points (4)
38
F.Ling - POS notes and points (5)
67. Radiological signs of hyperparathyroidism aka osteitis fibrosa cystica (Harrison 2229):
-reabsorption of phalangeal tufts and subperiosteal absorption
-thinning of dura lamina of teeth
-salt and pepper appearance of skull
68. Tissue expansion (Schwarz 2105):
-epidermal thikening in first week goes back to normal
-decreased dermal thickness
-increases vascularity of skin
69. Hydrogen secretion in kidneys (Ganong 660-661):
-three major reactions to remove tubular fluid hydrogen:
a. HCO3 CO2+H2O
b. HPO4 H2PO4
c. NH3 NH4
39
Staging criteria: primary tumor (T)
Tx Minimum requirements to assess primary tumor cannot be
met
T0 No evidence of primary tumor
TIS Carcinoma in situ
T1 Tumor confined to antral mucosa of infrastructure with no
bone erosion or
destruction
T2 Tumor confined to suprastructure mucosa without bone
destruction, or to infrastructure with destruction of medial or
inferior bony walls only
Osama Marglani
T3 More extensive tumor invading skin of cheek, orbit, anterior
ethmoid sinus, or pterygoid muscle
T4 Massive tumor with invasion of cribriform plate, posterior
ethmoid sinus,
sphenoid sinus, nasopharynx, pterygoid plate, or base of skull
Inflammatory polyp.
Inverted papillomas and The medium-power microscopic
exophytic squamous papillomas appearance of this lesion is
are both characterized by characteristic of a nasal
proliferations of the same type inflammatory polyp. Note the
of epithelium. In inverted edematous connective tissue
papillomas, this epithelium filled with numerous eosinophils
characteristically grows down (bright pink granules) and
into preexisting mucosal plasma cells (blue cells with
glands, displacing and eccentric round nuclei and
replacing the normal epithelium perinuclear pink zone in the
as it proliferates. As the cytoplasm). The overlying
abnormal epithelium continues respiratory-type epithelium
to expand below the surface, it shows some reactive expansion
causes a broad-based mucosal (hyperplasia) of the basal cell
elevation. layer but the overlying ciliated
epithelial cells are still present.
Rhinosporidium
seeberi .
Rhinosporidiosis
occurs in the
Americas, Europe,
Africa, and Asia but is
most common in the
tropics, with the
highest prevalence in
southern India and Sri
Lanka.
R. seeberi is
visualized with fungal
stains such as
methenamine silver
and Periodic acid-
40
1
clival chordoma, "Large cells with
multiple vacuoles
depicting tumor and are called
cranial nerve 'physaliferous
relationships prior to cells' because of
a resemblance to
resection of the jellyfish.
petrous apex and These
removal of the tumor. neoplasms
arise from
remnants of
primitive
notochord .
41
2
! !
Cystic lesions The ameloblasts are
the palisaded cells
with the nuclei pulled
away from the
basement membrane
around a stellate
reticulum like tissue
and in a fibrous stroma
.
REVERSED
POLARIZATION.
" "
Psammoma body within a
papillary cancer . calcified sphere, or
large clear areas within the psammoma body
nuclei which look like "Little
Orphan Annie" eyes are
circled in blue .
Although these nuclear
features are
characteristic of
papillary carcinoma, Papillary thyroid
they are not carcinoma accounts
pathognomonic for about 80% of all
Papillary cancer (low thyroid carcinomas
resolution). Notice the
frond-like projections.
42
3
$ % & ' #
Medullary (C-cell) Follicular
carcinoma of the adenoma H/E
thyroid with amyloid preparation
stroma . x 100
Immunohistochemica
l anti-calcitonin Follicular
antibody stain of a carcinoma
medullary carcinoma accounts
showing strong red for less than
positivity 10%
Lymphocytic Anaplastic
infiltrate in the carcinoma
thyroid, with histology H/E
lymphoid follicle preparation
formation and x 200
fibrosis.
) " (
Schwannoma
(neurilemoma) is a
benign neoplasm of
the Schwann cells of
the neural sheath .
43
4
% ' )
(HE x100). Antoni type A tissue shows
fascicles of spindle-shaped
Typical cellular Schwann cells streaming
around numerous acellular,
groups ("Zellballen") eosinophilic areas
surrounded by a surrounded by paralleled or
palisaded spindled cells
capillary network. with blunt, elongated nuclei
Round, fairly regular The cells of these Verocay
bodies all orient their long
nuclei. Variable, axes toward the acellular
often granular area, and the areas
themselves are oval, linear
cytoplasm. or serpiginous in shape.
pleomorphic adenomas
originate from the
intercalated duct cells
and myoepithelial cells
oncocytic tumors
originate from the
striated duct cells
acinous cell tumors
originate from the acinar
cells,
Mucoepidermoid
tumors and squamous
cell carcinomas develop
in the excretory duct
cells.
44
5
The diverse microscopic pattern
of this lesion is one of its most pleomorphic
characteristic features.
Islands of cuboidal cells
adenoma showing
arranged in ductlike structures the epithelial (E) and
is a common finding.
the stromal (S)
Loose chondromyxoid stroma,
hyalinized connective tissue, components.
cartilage(,arrows) and even
osseous tissue are observed.
This neoplasm is typically
encapsulated, although tumor
islands may be found within the
fibrous capsule.
, + ( +
Warthin's tumor (benign Hodgkin's disease
papillary cystadenoma
lymphomatosum) is the involving the
second most common parotid
benign tumor of the parotid
gland. gland. Note the
It accounts for 2-10% of all Reed-Sternberg
parotid gland tumors. cell. (Fine needle
Bilateral in 10% of the aspiration, Pap,
cases.
630x)
may contain mucoid brown
fluid inFNA
45
6
High Power Mid Power
Lymphocytc
infilterates.
$
$
Mucoepidermoid carcinoma (MEC) is the MECs contain two
most common malignant tumor of the parotid major elements:
gland and the mucin-producing cells
and epithelial cells of
second-most common malignancy the epidermoid variety.
(adenoidcystic carcinoma is more common) MEC is divided into
of the submandibular and minor salivary low-grade (well
glands. differentiated), high-
MECs constitute approximately 35% of grade (poorly
salivary gland malignancy, and 80% to 90% differentiated)
of MECs occur in the parotid gland.
46
7
-
It is composed of uniform
basaloid epithelial cells with
a monomorphous pattern.
& &
A very high power Spider web.
view of the The buccal
dermoepidermal
mucosa
junction
involved most
Civatte bodies often
(arrows),
reticular form
keratinocyte
enlargement, and
most common
coarse collagen
bundles are illustrated.
47
8
ominous
characteristic of
squamous
carcinoma is its
ability to surround
nerves and to
infiltrate for long
distances in a
perineural fashion
48
9
Otolaryngology - Head and Neck Surgery Page 1 of 7
Dr. F. Ling's
Selected Pharmacopoeia
ANALGESI CS
Opioids
0.1 mg 0.1 mg
fentanyl n/a n/a n/a n/a
q1h q1h
0.015 0.06
1.5 mg 7.5 mg 1.5 mg 6 mg q3-
hydromorphone mg/kg q3- mg/kg q3-
q3-4h q3-4h q3-4h 4h
4h 4h
0.75
100 mg 300 mg 100 mg
meperidine n/r mg/kg q2- n/r
q3h q2-3h q3h
3h
30 mg 10 mg 0.2 mg/kg
oxycodone n/a n/a n/a
q3-4h q3-4h q3-4h
49
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Equianalgesic Table
Drug SC PO
Morphine 10 mg 20 mg
Hydromorphone 2 mg 4 mg
Oxycodone N/A 7.5-10 mg
Codeine 60 mg 120 mg
Fentanyl 100-150 ug TD
Meperidine 75 mg 300 mg
Methadone N/A 2 mg
Opioid Antagonists
ANAESTHESI A
Local Anaesthetics
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Antifungal Agents
fluconazole (Diflucan): 200 mg first day, then 100 mg IV/PO qd. Peds:
6 mg/kg first day, then 3 mg/kg qd
Antiviral Agents
Cephalosporins
Macrolides
51
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Penicillins
Quinolones
Sulfonamides
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Other
CARDI OVASCULAR
ACE Inhibitors
Beta-blockers
Diuretics
DERM ATOLOGY
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ENDOCRI NE
calcium supplementation
normal range: 2.2-2.6 mmol/L
mild depletion: 1.9-2.2 mmol/L
moderate depletion: 1.5-1.9 mmol/L
severe depletion: < 1.5 mmol/L
I V replacement
Hypocalcemia (severe or symptomatic)
100 to 200 mg of elemental calcium (approx. 4.5 to 9 mEq
or 10 to 20 mL of a 10% solution) injected slowly IV over
10 minutes
will usually raise serum total calcium by 0.25 mmol/L
(1 mg/dL) with levels returning to baseline in about
30 minutes
To maintain levels above baseline, intermittent boluses a
continuous infusion of 1-2 mg/kg/hour of elemental calcium
may be necessary
eg. 10 g calcium gluconate to 1L NS or D5W and run
at 50-100 cc/h (500-1000 mg/h ~ 45-90 mg elemental
Ca/h)
serum calcium will usually normalize with this
infusion regimen in 6-12 hours
infusion rate may need to be decreased to 0.3 to 0.5
mg/kg/hour of elemental calcium as the serum
calcium begins to approach normal levels
54
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1250 500 2
1500 600 2
Calcium citrate 950 200 5
Calcium gluconate 500 45 22
650 58 17
1000 90 11
Calcium lactate 325 42 24
650 84 12
Calcium 500 115 9
phosphate, dibasic
Calcium 800 304 4
phosphate, tribasic 1600 608 2
PULM ONARY
55
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!
" #
$ !$ % & ! ' () (
-hormone response pathways activated by:
-mediators released by injured tissue
-neural and nociceptive input originating from site of injury
-baroreceptor stimulation form intravascular volume depletion
! ( ! ! ! )! * +)
Corticotropin-Releasing Hormone:
-synthesis:
-stress (pain, fear, anxiety) paraventricular nucleus of hypothalamus CRH synthesis
-proinflammatory cytokines and ADH
-negative feedback: circulating glucocorticoid decrease CRH mRNA transcription
56
-secretion:
-stimulated by angiotensin II, neuropeptide Y, serotonin, ACh, IL-1, IL-6
-inhibited by GABA, substance P, ANP, endogenous opioids, l-arginine
-stimulates ACTH production and release
-mechanism:
-via cAMP production in ACTH producing corticotrophs
Cortisol/Glucocorticoids:
-cortisol essential for survival after significant physiological stress
-functions:
-potentiates actions of glucagon and epinephrine hyperglycemia
-promotes gluconeogenesis in liver (eg. inducing PEP-carboxykinase and transaminase)
-decreases insulin-binding to insulin receptors in muscles and adipose tissue
-induces proteolysis and augments release of lactate in skeletal muscle shifts substrate for hepatic
gluconeogenesis
-stimulates lipolysis and inhibits glucose uptake by adipose tissues
-adrenal insufficiency (Addison’s Crisis):
-from adrenal suppression secondary to exogenous glucocorticoid
-weakness, nausea, vomiting, fever, hypotension
-hypoglycemia (from gluconeogenesis), hyponatremia ( renal Na absorption), hyperkalemia
57
-thyroid hormone alteration in systemic inflammation not mediated by endogenous IL-1
-in severely injured or critically ill patients, a reduced free T4 concentration predictive of high mortality
-experiments have shown that thyroid hormone depletion significantly decreases cellular and humoral immunity
-repletion is associated with enhancement of both types of immunity
Growth Hormones:
-GHRH stimulates pituitary release of GH in pulsatile fashion during sleeping hours
-GH release also affected by:
-autonomic stimulation, thyroxine, ADH, ACTH, alpha-melanocyte stimulating hormone, glucagon, and
sex hormones
-physical exercise, sleep, stress, hypovolemia, fasting hypoglycemia, decreased circulating fatty acids, and
increased amino acid levels
-inhibited by:
-hyperglycemia, hypertriglyceridemia, somatostatin, beta-adrenergic stimulation, cortisol
-function:
-promote protein synthesis while enhancing mobilization of fat stores
-hepatic ketogenesis
-inhibits insulin release and decreases glucose oxidation elevated glucose levels
-role of GH during stress:
-promote protein synthesis while enhancing mobilization of fat stores
-direct stimulation
-potentiation of adrenergic lipolytic effects on adipose stores
-promote hepatic ketogenesis
-inhibit insulin release and decrease glucose oxidation
-protein synthesis:
-mediated by secondary release of insulinlike growth factor-1 (IGF-1)
-promotes amino acid incorporation and cellular proliferation
-attenuates proteolysis in skeletal muscle and liver
-IGFs:
-mediators of hepatic protein synthesis and glycogenesis
-adipose tissue: increases glucose uptake and lipid synthesis
-skeletal muscles: increases glucose uptake and protein synthesis
-promote incorporation of sulfate and proteoglycans into cartilage skeletal growth
-associated decrease in protein synthesis and observed negative nitrogen balance attributed to reduction in
IGF-1 levels
-IGF produced predominantly in liver; dysfunction may contribute to negative nitrogen balance after injury
Somatostatin:
-potent inhibitor of GH, TSH, renin, insulin, and glucagon release
-may regulate excessive nutrient absorption and activities of GH and IFG during convalescence form injury
58
Prolactin:
-GnRH and dopamine suppresses PRL secretion from anterior pituitary
-stimulants: CRH, TRH, GHRH, serotonin, VIP
-elevated levels seen after injury
-may account for amenorrhea frequently seen in women after injury or major operations
-has immunostimulatory properties
Endogenous Opioids:
-beta-endorphins attenuate pain perception; capable of inducing hypotension through a serotonin-mediated pathway
-enkephalins produce hypertension
-in GI tract: reduces peristaltic activity and suppresses fluid secretion
-in glucose metabolism:
-B-endorphins and morphine induce hyperglycemia, but also increase insulin and glucagon release by
pancreas
-endorphins influence immune system by increasing NK cell cytotoxicity and T-cell blastogenesis
-IL-1 activates release of POMC
-opioids compromise natural and specific immune system:
-inhibit proliferation and differentiation of lymphocytes and monocytes/macrophages
! ( ! ! ! )! * +)
Oxytocin:
-role in injury response unknown
-stimulates contraction of lactating mammary glands and induces uterine contractions in parturition
59
! &
Catecholamines:
-hypermetabolic state observed after severe injury has been attributed to activation of adrenergic system
-norepinephrine: from synaptic leakage during sympathetic nervous system activity
-epinephrine: from secretions of chromaffin cells of adrenal medulla
-functions:
-promotes stress-induced hyperglycemia
-liver: promotes glycogenolysis, gluconeogenesis, lipolysis and ketogenesis
-pancreas: decreased insulin secretion and increased glucagon secretion
-adipose: increases lipolysis
-skeletal muscle: inhibits insulin-facilitated glucose uptake
-other:
-thyroid: increase secretion of PTH, T4, T3
-secretion of renin
-inhibits release of aldosterone
-immune function:
-enhances leukocyte demargination with resultant neutrophilia and lymphocytosis
-lowers ratio of CD4 to CD8 T-cells
Aldosterone:
-mineralocorticoid
-synthesized, stored, and released in adrenal zona glomerulosa
-release induced by: AT II, hyperkalemia, and aldosterone stimulating factor (ASF) from pituitary
-ACTH is most potent stimulus for aldosterone release in injured patient
-function:
-maintain intravascular volume by conserving sodium and eliminating potassium and hydrogen ions
-early distal convoluted tubule: increases Na, Cl reabsorption and excretion of H+
-late distal convoluted tubule: Na reabsorption with excretion of K
-major effect on kidneys, but also acts on intestines, salivary glands, sweat glands, vascular endothelium,
and brain
Renin-Angiotensin:
-renin synthesized and stored in renal juxtaglomerular apparatus
-activation and release by:
-ACTH, AVP, glucagon, prostaglandins, potassium, magnesium and calcium
-barorecepors in JGA sense decrease in BP increase secretion
-angiotensin:
-angiotensinogen synthesized by liver
-renin converts angiotensinogen to angiotensin I
-angiotensin-converting enzyme on pulmonary endothelial surfaces converts AT I to AT II
-AT II:
-potent vasoconstrictor that stimulates aldosterone and vaspressin synthesis
-stimulates heart rate and myocardial contractility
-potentiates release of epinephrine by adrenal medulla, increases CRH release, and activates
sympathetic nervous system
-can induce glycogenolysis and gluconeogenesis
Insulin:
-derived from pancreatic beta islet cells
-released by certain substrates, autonomic neural input, and other hormones
-glucose major stimulant of insulin secretion
-others: amino aids, free fatty acids, and ketone bodies
-inhibition of release:
60
-epinephrine and sympathetic stimulation
-glucagon, somatostatin, GI hormones, beta-endorphins, IL-1
-function:
-global anabolic effect: promotes hepatic glycogenesis and glycolysis, glucose transport into cells, adipose
tissue lipogenesis, and protein synthesis
-in injured patient, biphasic pattern of insulin release observed:
-first phase: few hours after injury
-relative suppression of insulin, reflecting influence of catecholamines and sympathetic
stimulation
-later phase:
-return to normal or excessive insulin production with persistent hyperglycemia d/t
peripheral resistance to insulin
-ratio of insulin to glucose is used as a predictor of mortality and survival
-enhances T-cell proliferation and cytotoxicity
Glucagon:
-product of pancreatic alpha islet cells
-stimulants of secretion: plasma glucose concentrations and exercise
-function:
-stimulates hepatic glycogenolysis and gluconeogenesis
-promotes hepatic ketogenesis and lipolysis in adipose
-release after injury is initially decreased, but returns to normal 12 h later
'' #
, ' () (
-cytokines are produced by diverse cell types at site of injury and by systemic immune cells
-activity exerted locally via cell-to-cell interaction (paracrine)
-small polypeptide or glycoprotein; modulate gene transcription
-may be pro- or anti-inflammatory
-direct inflammatory response to infection and injury; actively promotes wound healing
-responsible for:
-fever, leukocytosis, hyperventilation, tachycardia (systemic inflammatory response syndrome SIRS)
-hemodynamic instability characteristic of septic shock
-metabolic derangements of injured patients (eg. muscle wasting and cachexia)
-contribute to end-organ injury multiple organ failure; death
Interleukin-1:
-TNF-a induced synthesis of IL-1 by macrophages and endothelial cells
-types:
-IL-1a: cell membrane-associated; exerts influence via cellular contact
61
-IL-1b: in circulation in greater quantities; induces characteristic systemic derangements after injury
-synergistic and similar effects to TNF-a
-half-life (~6 min) less than TNF-a
-effects:
-induces classic inflammatory febrile response to injury: stimulates local prostaglandin activity in anterior
hypothalamus
-anorexia effect on satiety center
-augments T cell proliferation by enhancing IL-2 production
-may influence skeletal muscle proteolysis: cachexia
-decrease pain perception: promote release of endorphin, increasing number of central opioid-like
receptors
-potent stimulant for ACTH and GC release via hypothalamus and pituitary gland
-regulated by IL-1 receptor antagonists (IL-1ra): competes for IL-1 receptor binding
Interleukin-2:
-promotes T-cell proliferation, immunoglobulin production, and gut barrier integrity
-not readily detectable in circulation during acute injury
-secretion impaired in: cancer and AIDS
-attenuated IL-2 expression contributes to transient immunocompromised state of the surgical patient
Interleukin-4:
-glycoprotein molecule
-produced by activated TH2 cells
-functions include:
-induction of B-lymphocyte proliferation
-enhances macrophage MHC class II (HLA-DR and LHA-DP) expression and adhesion molecules
-induces class switching in differentiating B-lymphocytes IgG4 and IgE
-also a potent anti-inflammatory cytokine:
-down-regulates effects of IL-1b, TNF-a, IL-6, IL-8, and superoxides production
-induce apoptosis in inflammatory macrophages (abrogated by IFN-gamma)
Interleukin-6:
-used frequently as an indicator of SIRS and predictor of preoperative morbidity
-levels proportional to extent of tissue injury during an operation
-induced by TNF-a and IL-1
-long half-life
-functions:
-with IL-1, important mediator of hepatic acute-phase protein response
-enhances C-reactive protein, fibrinogen, haptoglobin, amyloid A, a-1-antitrypsin, and
complement production
-induces PMN activation; may delay the phagocytic disposal of senescent or dysfunctional PMNs
-anti-inflammatory effects:
-attenuates TNF and IL-1 activity while promoting release of sTNFRs and IL-1ra
-prolonged and persistent expression of IL-6 associated with immunosuppression and postop
infectious morbidity
-can reduce plasma glutamine
Interleukin-8:
-has been proposed as an additional biomarker for the risk of multiple organ failure
-serves a PMN activator and potent chemoattractant
-does not produce hemodynamic instability characteristic of TNF-a and IL-1
Interleukin-10:
-important endogenous regulatory mediator during inflammatory response
62
-modulates TNF-a activity: reduces TNF-a levels and associated deleterious effects
-may promote sTNFR and IL-1ra production
Interleukin-12:
-promotes differentiation of TH1 cells and production of IFN-gamma
-prevents apoptosis in certain T-lymphocyte populations after their activation
Interleukin-13:
-pleiotropic cytokine sharing may properties of IL-4
-produced during TH2 responses
-with IL-4, modulates macrophage function, but no effects on T-cells
-can upregulate macrophage MHC class I and II antigens and other surface antigens, such as CD23
-can inhibit NO production and expression of proinflammatory cytokines; can enhance production of IL-1ra
-net effect of IL-13, along with IL-4 and IL-10 is anti-inflammatory
Interferon-gamma:
-TH cells activated by the bacterial antigens IL-2 or IL-12 readily produce IFN-gamma
-conversely, IFN-gamma can induce production of IL-2 and IL-12 by TH cells
-important role in activating circulating and tissue macrophages
63
-while induction of apoptosis via Fas/FasL cross-linking in activated immunocytes may be advantageous during
systemic inflammation, this activity at the tissue level may be detrimental to the host
! ) ( , !)
Cortisol/Glucocorticoids:
-glucocorticoid administration before or concomitantly with endotoxins infusion in healthy human beings is able to
attenuate the symptoms, catecholamine response, and acute phase response, but it increases IL-10 release
-increased IL-10 release may contribute to acute anti-inflammatory effect of glucocorticoid
-the proinflammatory cytokine IL-1 and TNF and IL-6 can activate the HPA axis and induce the release of CRH and
ACTH increased circulatory GC levels inhibit endotoxins-induced production of TNF at the level of mRNA
translation
-dexamethasone inhibits neutrophil apoptosis and prolongs their functional responsiveness
Catecholamines:
-inhibit endotoxins-induced macrophage production of TNF-alpha
-endogenous epinephrine or exogenous administration as a component of sepsis treatment may serve to limit
excessive proinflammatory effects of the cytokine network during the early phase of systemic infection
' " #
( +)+ ++' ( ) !
Prostacyclin:
-PGI2 an important endothelium-derived vasodilator synthesized in response to vascular shear stress and hypoxia
-derived from arachidonic acid
-causes vasorelaxation and platelet deactivation by increasing cAMP
64
Endothelins:
-produced by endothelial cell in response to:
-injury, thrombin, TGF-beta, IL-1, AT II, ADH, catecholamines, and anoxia
-potent vasoconstrictor properties
-ET-1 most biologically active and potent vasoconstrictors known
-increased serum levels of ET are correlated with the severity of injury after major trauma, major surgical
procedures, and in cardiogenic or septic shock
Platelet-Activating Factor:
-phopsholipid constituent of cell membranes that can be induced by TNF, IL-1, ADH, and AT II
-stimulates production of TxA2 promotes platelet aggregation and vasoconstriction
-increases glucagon and catecholamine activity experimentally
-can induce hypotension, increase vascular permeability, hemoconcentration, pulmonary hypertension,
bronchoconstriction, primed PMN activity, eosinophil chemotaxis/degranulation, and thrombocytopenia
-alters shape of endothelial cells, causing them to contract and increase permeability
-chemotactant for leukocyte adherence to vascular wall and facilitates migration out of vascular compartment
!) ++ +)! ' ( ) !
Heat-Shock Proteins:
-production induced by heat, hypoxia, trauma, heavy metals, local trauma, and haemorrhage
-presumed to protect cells from traumatic stress
-function intracellularly in the assembly, disassembly, stability, and transport of proteins
! &+) ) ! ' () !
Eicosanoids:
-oxidation derivatives of arachidonic acid
-secreted by virtually all nucleated cells except lymphocytes
-phospholipids –(PLP-A2) arachidonic acid
-two major pathways:
-cyclooxygenase: production of all prostaglandin and thromboxanes
-lipoxygenase: production of leukotrienes and HETE
-synthesis stimulated by:
-hypoxic and ischemic injury, direct tissue injury, endotoxins, norepinephrine, ADH, AT II, bradykinin,
serotonin, ACh, and histamine
-function:
-diverse effects systemically on endocrine and immune function, neurotransmission, and vasomotor
regulation
-major components of the inflammatory response in injured tissue, characterized by vascular permeability,
leukocyte migration, and vasodilation
65
Kallikrein-Kinin System:
-bradykinins are potent vasodilators produced through kininogen degradation by the serine protease kallikrein
-release stimulated by hypoxic and ischemic injury
-kallikrein activated (from prekallikrein) by:
-Hageman factor, trypsin, plasmin, factor XI, glass surfaces, kaolin, and collagen
-function:
-increase capillary permeability and tissue edema, evoke pain, and increase bronchoconstriction
-increase renal vasodilation and reduce renal blood flow
-increase glucose clearance by inhibiting gluconeogenesis
-may also increase nitrogen retention
Serotonin:
-tryptophan derivative found in enterochromaffin cells of intestine and platelets
-stimulates vasoconstriction, bronchoconstriction, and platelet aggregation
-also capable of acting as a myocardial chrono- and inotrope
Histamine:
-derived from histidine and stored in neurons, skin, gastric mucosa, mast cells, basophil, and platelets
-release activated by increased calcium levels
-H1 receptor binding:
-increased histamine precursor uptake (l-histidine)
-bronchoconstriction, intestinal motility, and myocardial contractility
-H2 receptor binding:
-inhibits histamine release
-both: induces vasodilation and increased vascular permeability
-hypotension, peripheral pooling of blood, increased capillary permeability, decreased venous
return, and myocardial failure
' - #
' ). + ) *
Substrate Metabolism:
-healthy 70 kg adult expends 1700-1800 kcal/day of energy
-sources: lipid, carbohydrate, protein
-obligate glycolytic cells (eg. neurons, leukocytes, erythrocytes)
-require 180 g glucose per 24 h for basal energy needs
-hepatic glycogen ~75 g glucose
-skeletal muscle:
-cannot directly release free glucose d/t lack of glucose-6-phosphatase
-fasting decreased serum glucose net effect of body to increase glucose production
-decrease insulin release
-increased glucagon and more transient elevations of GH, catecholamines, ADH, and AT II
-glucagon and epinephrine enhance cAMP promotes glycogenolysis
-cortisol and glucagon promote gluconeogenesis
-norepinephrine, ADH, ATII –(PIP3+Ca++) promote glycogenolysis
-reduction in anabolic growth factors (eg. IGF-1)
-gluconeogenesis:
-mainly by liver, but also by kidneys (up to 45% in late starvation)
-precursors: lactate, glycerol, amino acids (eg. alanine and glutamine)
-lactate sources:
-skeletal muscles via glycogenolysis and glycolysis
-erythrocytes and WBCs after aerobic glycolysis
66
-lactate converted to glucose in liver via Cori cycle
-protein metabolism:
-75 g protein must be degraded (mostly from skeletal muscle) daily during fasting and starvation to provide
gluconeogenic amino acids to liver
-proteolysis (results from insulin and cortisol) BUN excretion
-after 5d, rate diminishes to 15-20 g/day
-occurs as CNS and other tissues adapt to ketone oxidation as predominant energy source
-amount of protein required for GNG significantly reduced
-lipid metabolism:
-160 g TG provides energy requirements for GNG and basal enzymatic and muscular function
- insulin, glucagon and catecholamines promotes lipolysis
- free fatty acids and glycerol
-FFA and ketone bodies (from liver) source of energy for heart, kidney, muscle, and liver
-lipid stores provide up to 40% of caloric expenditure during starvation
-lipid oxidation reduces glucose requirements:
-decreased amount of mandatory glycolysis, which requirements for GNG and protein
degradation
-once initial obligatory neuroendocrine stress hormone response recedes, whole-body energy expenditure also
decreases during prolonged fasting
' ). + & ! !
Energy Balance:
-associated increase in energy expenditure and increased oxygen consumption
-d/t increased sympathetic activity
-may be related to influences on cell membrane sodium permeability the energy required for ion pump
action to maintain normal transmembrane concentrations
Lipid Metabolism:
-FFA principle sources of energy after injury
-lipolysis enhanced:
-d/t ACTH, cortisol, catecholamines, glucagon and GH; insulin; sympathetics
-hormone-sensitive lipase stimulated by catecholamines
-FFA can be oxidized by cardiac and skeletal muscle to produce energy
-lipoprotein lipase (clears plasma TG):
-suppressed in adipose tissue after trauma, but not in muscle
-suppressed in both in sepsis
-ketogenesis:
-decreased after major injury, severe shock, and sepsis
-suppressed by insulin and other energy substrates, uptake and oxidation of FFA
-increased after minor injury or mild infection
Carbohydrate Metabolism:
-systemic glucose intolerance after injury state of relative insulin resistance
-increases in plasma glucose levels proportional of severity of injury; correlated to survival
-d/t increased hepatic production and peripheral insulin resistance
-deprivation of glucose to non-essential organs (eg. skeletal muscles and adipose) mediated via catecholamines
-mediator-induced reduction of skeletal muscle pyruvate dehydrogenase AcetylCoA for TCA cycle
results in shunting of pyruvate to liver for GNG
-glucose provided for inflammatory and healing cells in the wound environment
67
-loss of lean tissues after significant injury:
-skeletal muscle is depleted while visceral tissues (eg. liver and kidney) are relatively preserved
-severe trauma, burns, and sepsis are associated with increased whole-body protein turnover and increased
net protein catabolism
-accelerated proteolysis and GNG persist after major injury and during sepsis
-after trauma, substrate cycling of amino acid occurs b/n skeletal muscle, liver, and the wound:
-major source is skeletal muscle
-proteolysis enhanced by:
-oxidative species and diminished antioxidant activities
-increased ubiquitin-dependent proteolytic pathways
-glutamine and alanine released:
-glutamine: major energy source for lymphocytes, fibroblasts, and GI tract
!* ! / !) )/
Catabolic Phase:
-adrenergic-corticoid phase:
- glucagon, GC and catecholamines with insulin
-rates of GNG, acute phase protein production, and immune cell activity are all still altered during the
catabolic phase
-administration of glucose produces little or no change in rate of protein catabolism
-glucose turnover increased
-Cori cycle activity stimulated: 3C intermediates glucose by pyruvate carboxylase and PEP carboxylase
-lipolysis and FFA oxidation
) ( 0 !
-history: -presence of weight loss and chronic illnesses or dietary habits influencing the quantity an quality
of food intake
-physical: -assess loss of muscle and adipose, organ dysfunction, and subtle change in skin, hair, or
neuromuscular function
68
-biochemical: -creatinine excretion, albumin, transferring
( ) ) (' ( &! ! )+ !
-reasonably well-nourished and otherwise healthy individual who undergoes an uncomplicated major operative
procedure has sufficient body fuel reserves to withstand the catabolic insult and partial starvation for at least 1 week
-requires: IV fluids /w min of 100 g glucose daily to minimize protein catabolism
-defined formula diets and TPN are unnecessary
-during early anabolic phase, pt needs adequate caloric intake of proper composition to meet energy needs
of the body and to allow protein synthesis
-chronically debilitated preoperatively from diseases or from malnutrition and patients who have suffered trauma,
sepsis, or surgical complications cannot maintain adequate caloric intake
-should receive consideration of nutritional support early
-in general, the indications for preoperative nutritional support appear largely confined to patients with
evidence of more severe erosion of lean body mass and adipose tissue stores
-enteral route should always be used when possible because it is considered to be more economical and well
tolerated in many patients
-NG, gastrostomy, and jejunostomy tube feedings for those with normal GI tract but cannot or will not eat
-ability to tolerate enteral feeds depends on:
-rate of infusion
-osmolality of feeds
-chemical nature of the product
-usually start with 30-50 cc/h then increased by 10-25 cc/h/d until optimal volume is delivered
-after full volume is attained, concentration is increased slowly to desired strength
-measure gastric residuals to monitor risk of aspiration
-decrease rate if abdo cramps or diarrhea occurs
-parenteral route used for supplementation in pt with limited oral intake or for complete nutritional management in
the absence of oral intake
-potentially enhances the magnitude of macroendocrine and microendocrine mediator responses to an
antigenic challenge
-loss of intestinal barrier function occurs
69
-experimental approaches for preserving GI mucosa integrity and gut mass:
-luminal stimulation by digestible or nondigestible substrates, and infusion of critical
intestinal fuel sources (eg. glutamine or short-chain fatty acids)
!)+ ( *
70
)! !)+ + )
-continuous infusion of hyperosmolar solution containing carbohydrates, proteins, fat, and other necessary nutrients
through indwelling catheter into SVC
-ratio of calories to nitrogen must be at least 100-150 kcal/g nitrogen and the two materials must be infused
simultaneously in order to maximize nitrogen use
-contraindications to hyperalimentation:
-lack of specific goal for pt management, or when instead of extending a meaningful life, inevitable dying
is prolonged
-period of cardiovascular instability or severe metabolic derangement requiring control or correction before
attempting hypertonic intravenous feeding
-feasible GI tract feeding
-patients in good nutritional status, in whom only short-term parenteral nutrition support is required or
anticipated
-infants with less than 8 cm of small bowel, since virtually all have been unable to adapt sufficiently
despite prolonged periods of parenteral nutrition
-patients who are irreversibly decerebrate or otherwise dehumanized
Fat Emulsions:
-derived from soybean or safflower oils are widely used as an adjunctive nutrient to prevent development of
essential fatty acid deficiency
-major energy source in TPN, but no evidence of enhanced metabolic efficacy if greater than 10-15% of calories is
provided as lipid emulsions
-pts with abnormal fa transport or metabolism, lipid nephrosis, coagulopathy, or serious pulmonary disease should
71
not receive fat emulsions
-limit administration to between 2.0-2.5 g/kg TBW/d
Special Formulations:
-renal failure patients (oliguric):
-final dextrose concentration of 40-45% and only essential L-amino acids
-hepatic failure:
-solutions contain increased levels of branched-chain amino acids and decreased concentrations of
aromatic amino acids to decrease encephalopathy
-cardiac cachexia:
-highly concentrated dextrose and amino acid formula that are low in sodium
Complications:
-sepsis secondary to contamination of CV catheter
-earliest signs: sudden development of glucose intolerance in a patient previously been maintained on
parenteral alimentation w/o difficulty
-if suspected, remove and culture catheter; replace at a different site
-problems with catheter placement:
-pneumothorax, hemothorax, or hydrothorax
-subclavian artery injury
-cardiac arrhythmia
-air embolism
-cardiac perforation and tamponade
-hyperosmolar nonketotic hyperglycemia:
-may occur with normal rates of infusion in patients with impaired glucose tolerance or in any pt if the
hypertonic solutions are administered too rapidly
-must monitor urine and blood glucose levels and electrolytes
-tx: volume replacement with correction of electrolyte abnormalities and administration of insulin
-excess calorie infusion may result in:
-carbon dioxide retention and respiratory insufficiency
-hepatic steatosis or marked glycogen deposition
72
! " #$ !
% & &
% '
-50-70% TBWt; ~ 60% (M), 50% (F)
-greater proportion of water in lean individuals
-newborns: 75-80% TBWt
(
-20% TBWt plasma (5% TBWt) + interstitial (15% TBWt)
-transcellular fluid (CSF, synovium) ~ 10% ECF = 1-2% TBWt
-principle cation: sodium
-principle anion: chloride and bicarbonate
)" ))
-proteins in plasma primarily responsible for effective osmotic pressure b/n plasma and interstitial fluid colloid
oncotic pressure
* & &
' ($ !
-normal individual consumes ~2000-2500 ml H2O/day; ~1500 ml by mouth
-daily water loss: 250ml stool, 800-1500 ml urine, ~600ml insensible loss
-insensible loss: skin (75%) and lungs (25%); by hypermetabolism, hyperventilation and fever
-can exceed 250ml/day per degree of fever
-unhumidified tracheotomy up to 1500ml/day
-gain in water: excessive cellular catabolism (up to 500ml/day)
)) )
-50-90 mEq (3-5g) as sodium chloride
-kidneys excrete excess salt
-gastrointestinal losses usually isotonic or slightly hypotonic
% & &
+ " $ ! )
-diagnosed by clinical examination
-indirect measurements:
-BUN rises with ECF deficit of sufficient magnitude to reduce GFR
-hematocrit: with ECF deficit; with excess
-[Na] NOT related to volume status of ECF
73
(1) Volume Deficit:
-most common causes of ECF deficit are GI losses from vomiting, NG suction, diarrhea, fistular drainage
-also sequestration of fluid in soft tissues injuries and infections, intraabdominal and retroperitoneal
inflammatory processes, peritonitis, intestinal obstruction, burns
$ ! )
-sodium primarily responsible for osmolarity of ECF
-clinical signs of hypo- or hypernatrema are not present until changes are severe
(1) Hyponatremia:
-acute symptomatic hyponatremia (<130) CNS signs of ICP; tissue signs of intracellular water
-risk of oliguric renal failure which may not be reversible if treatment delayed
(2) Hypernatremia:
-CNS and tissue signs characterize acute symptomatic hypernatrema
( + " , " )
"- ) $ ! )
./0 % ) %
Respiratory Acidosis:
-associated with retention of CO2 secondary to decreased alveolar ventilation
-inadequate ventilation:
-airway obstruction, atelectasis, pneumonia, pleural effusion, pain from upper abdominal incision,
abdominal distention
-narcotic use
Respiratory Alkalosis:
-hyperventilation secondary to apprehension, pain, hypoxia, CNS injury, assisted ventilation
74
-PaCO2 should not be allowed to fall below 30 mmHg
-dangers related to potassium depletion ventricular arrhythmias and fibrillation, particularly in
patients who are digitalized or have preexisting hypokalemia
-d/t entry of K+ into cells in exchange for H+; excessive urinary K loss in exchange for
Na
-shifting oxyhaemoglobin dissociation curve to left limits unloading of oxygen
-tetany and convulsions if ionized calcium significantly depressed
Metabolic Acidosis:
-retention or gain of fixed acids (DKA, lactic acidosis, azotemia)
-loss of base bicarbonate (diarrhea, small bowel fistula, renal insufficiency)
-develops when capacity of kidneys for handling a large chloride load is exceeded (biliary, pancreatic,
small-bowel secretions) and are maintained on parenteral fluids for an extended period
-use of Ringer’s solution indicated
-non-anion gap: loss of bicarbonate or gain of chloride acid (eg. administration of ammonium chloride)
-most common cause of elevated anion gap: shock or inadequate tissue perfusion
-common causes of severe metabolic acidosis in surgical patients: acute circulatory failure with
accumulation of lactic acid
-used of Ringer’s solution does not accentuate lactic acidosis
-indiscriminate use of bicarbonate during resuscitation of patients in hypovolemic shock is
discouraged:
-citrate in transfused blood and lactate in Ringer’s solution are metabolized to
bicarbonate by liver severe metabolic alkalosis can result if excessive bicarbonate
administered
-treatment: correct underlying disorder when possible
-indication for bicarbonate administration: severe metabolic acidosis after cardiac arrest
Metabolic Alkalosis:
-loss of fixed acids or gain of bicarbonate
-aggravated by any preexisting potassium depletion
-majority of pts have some degree of hypokalemia: influx of K+ into cells, efflux of H+ into serum
-hypochloremic, hypokalemic metabolic alkalosis:
-persistent vomiting or gastric suction in pt with pyloric obstruction
-results in urinary bicarbonate excretion net H+ resorption by renal tubular cells, with
K+ excretion
-volume deficit aldosterone mediated Na+ resorption with K+ excretion
-hypokalemia excretion of H+ paradoxic aciduria
-treatment: replace ECF volume with NS + KCl
.0 )) " , " )
Hyperkalemia:
-signs:
GI: nausea, vomiting, intermittent intestinal colic, diarrhea
Cardiac: ECG high peaked T waves, widened QRS, depressed ST segments
-disappearance of T waves, heart block, diastolic cardiac arrest
-treatment:
-1g of 10% calcium gluconate temporary suppression of myocardial effects
75
-bicarbonate/glucose/insulin (45 mEq NaHCO3 in 1000 ml D10W with 20 u regular insulin)
promotes cellular uptake of potassium
-cation exchange resins: Kayexalate
-dialysis
Hypokalemia:
-more common problem in than hyperkalemia:
1. excessive renal excretion
-occurs with respiratory and metabolic alkalosis
-K+ in competition with H+ for renal tubular excretion in exchange for Na+
-increased K+ excretion in alkalosis in exchange for Na+ permits H+ conservation
-hypokalemia may produce metabolic alkalosis: increased excretion of H+ when [K+] in
tubular cells is low
-renal tubular excretion of K increased when large quantities of sodium are available
2. movement of potassium into cells
3. prolonged administration of potassium-free IV fluids
4. TPN with inadequate potassium replacement
5. loss in gastrointestinal secretions
-signs:
-related to failure of normal contractility of skeletal, smooth and cardiac muscle
-flaccid paralysis, DTR, paralytic ileus
-sensitivity to digoxin, with cardiac arrhythmias and ECG signs of low voltage, flattening of T
waves, depression of ST segments
-treatment:
-prevention
-no more than 40 mEq/L; rate should not exceed 40 mEq/h
-potassium should not be given to the oliguric patient or to patients during first 24h after severe
surgical stress or trauma
Hypocalcemia:
-symptoms: numbness/tingling of circumoral region and tips of fingers and toes
-signs: DTR, +Chvostek’s sign, muscle and abdominal cramps, tetany with carpopedal spasm,
convulsions, prolongation of QT interval on ECG
-common causes:
-acute pancreatitis
-massive soft tissue infections (necrotizing fasciitis)
-acute and chronic renal failure
-pancreatic and small-bowel fistulas
-hypoparathyroidism
-other causes: severe magnesium depletion
-treatment:
-correction of underlying cause and repletion of deficit
-IV calcium gluconate or chloride
-majority of patients receiving blood transfusion do not require calcium supplementation; binding
76
of ionized calcium by citrate generally compensated by mobilization of calcium from body stores
-for rapid transfusion: 500 ml q5-10min 2ml 10% calcium chloride for every 500 ml
Hypercalcemia:
-symptoms: vague GI, renal, MSK, CNS origin
-easy fatigue, lassitude, weakness, anorexia, nausea, vomiting, weight loss coma
-severe headaches, pains in back and extremities, thirst, polydipsia, polyuria
-major causes:
-hyperparathyroidism
-cancer with bony metastasis: most frequently seen in patient with metastatic breast cancer
receiving estrogen therapy
-other causes: sarcoidosis, myelomas, lymphomas, leukemias
-treatment:
-IV fluids +/- furosemide administration
Magnesium deficiency:
-causes:
-starvation, malabsorption syndromes
-protracted losses of GI fluid
-prolonged IV therapy with Mg free fluids
-TPN with inadequate Mg
-other causes:
-acute pancreatitis
-treatment of DKA
-primary aldosteronism
-chronic alcoholism
-amphotericin B therapy
-protracted course after thermal injury
-functions: requirement for most enzyme systems
-signs and symptoms similar to calcium deficiency
-treatment:
-IV magnesium sulfate or magnesium chloride
-calcium chloride or calcium gluconate available to counteract any adverse effects of rapidly rising
serum magnesium level
Magnesium excess:
-commonly seen with severe renal insufficiency
-retention and accumulation of magnesium with impaired glomerular or renal tubular function
-other causes:
-magnesium-containing antacids and laxatives
-early thermal injury
-massive trauma or surgical stress
-severe ECF volume deficit
-severe acidosis
-signs and symptoms:
-lethargy and weakness with progressive loss of DTR
-ECG: PR interval, widened QRS, elevated T waves
77
-coma and muscular paralysis
death by respiratory or cardiac arrest
-treatment:
-correct co-existing acidosis
-ECF volume replenishment
-withholding exogenous magnesium
-acute symptoms temporarily controlled with IV 5-10 mEq of calcium gluconate
-peritoneal dialysis or hemodialysis if elevated levels persist
& &
Ringer’s Lactate:
-for replacement of GI losses and ECF deficits
-physiologic
-Na: 130 mEq; Cl: 109 mEq; lactate: 28 mEq
-minimal effects on body fluid composition and pH
Normal Saline:
-Na: 154 mEq; Cl: 154 mEq
-may induce dilutional acidosis by decreasing bicarbonate relative to carbonic acid
-ideal in correcting ECF deficit in presence of hyponatremia, hypochloremia, and metabolic alkalosis
- 3 $ -
78
restored by correction of volume deficit
-if hypervolemic, then water restrict patient
-Hypernatremia:
-if symptomatic, D5W infused slowly until symptoms relieved
-if ECF osmolarity reduced too rapidly convulsions and coma
-ideally correct with ½ NS
- 3 ! "
-blood should be replaced to maintain an acceptable RBC mass irrespective of any additional fluid and electrolyte
therapy
-replacement of ECF should begin during the operative procedure
-balanced salt solution needed during operation is approximately 0.5 to 1 L/h, but only to a maximum of 2-3 L
during a 4h major abdominal procedure, unless there are other measurable losses
) - 3 ! "
Volume Excesses:
-earliest sign of volume overload is weight gain during the catabolic period, when the patient should be
losing 1/4 to ½ lb/day
-circulatory and pulmonary signs appear late and represent a massive overload
Hyponatremia:
-hyponatremia associated with surgical procedures and traumatic injury is prevented by the replacement of
extracellular fluid deficits
-hyperglycemia may cause a dilutional hyponatremia
-endogenous water release: without adequate caloric intake, cellular catabolism causes pt to gain up to 500
cc/day of water between the fifth and tenth days
-intracellular shifts: bacterial sepsis precipitous drop in serum sodium concentration
Hypernatremia:
-high serum sodium level may indicate a significant deficit of total body water
-often the result of excessive or unexpected water losses
79
a. Excessive Extrarenal Water Losses:
-sweat; tracheotomy; burns etc..
b. Increased Renal Water Losses:
-hypoxic damage to distal tubules and collecting ducts or loss of ADH stimulation from damage to
CNS large volumes of solute-poor urine
c. Solute Loading:
-high protein intake increased osmotic load of urea excretion of large volumes of water
-prevent by an intake of 7 ml of water per gram of dietary protein
-excessive glucose administration, osmotic diuretics
Biochemical Abnormalities:
1. Metabolic acidosis results from failure of renal excretion of fixed acids and the inability to maintain respiratory compensation
2. Hyperkalemia d/t large amounts of intracellular potassium released in acute renal failure
3. Hyponatremia d/t production of metabolic water from metabolism of nutrients and liberation of water from intracellular
breakdown
4. Hyperphosphatemia and hypocalcemia d/t inadequate excretion and excessive release from injured tissue
5. Hypermagnesemia: kidney is the major organ for regulating magnesium balance
Predisposing Factors:
-Trauma:
-hypovolemic shock, myoglobinuria from rhabdomyolysis, intravascular haemolysis and
hemoglobinuria from transfusions
-Sepsis:
-endotoxins releases TNF produce renal failure
-Cardiopulmonary Bypass: hypoperfusion of kidneys
-Renal Transplantation:
-problems with renal artery, obstruction of urinary flow
-Urologic Surgery:
-obstruction in kidney, ureter, bladder, or urethra
-Vascular Disease:
-blood flow to kidney interrupted during clamp times of vascular surgeries
-Preexisting Renal Disease:
-nephrosclerosis, diabetes, chronic glomerulonephritis, chronic tubular interstitial nephritis
-Radiographic contrast agents
-Drugs:
-aminoglycosides, cyclosporine, amphotericin B, NSAIDs
Laboratory Studies:
-Urinalysis
-Urine osmolarity
-Urine urea and creatinine ratio:
-most useful in diagnosing acute renal failure postoperatively:
< 20 acute renal failure
> 40 prerenal azotemia
-Urine sodium:
-the underperfused kidney is sodium retaining, and a low urine sodium concentration is
characteristic of prerenal azotemia
80
Management of the Patient with Established Acute Renal Failure:
-correct reversible causes
-fluid and electrolyte management:
-treat hyperkalemia
-fluid intake should be restricted to replacing measured fluid losses plus 500-600 cc/d of
insensible losses
-hyponatremia: if below 120, dialysis is the only therapeutic endeavour that corrects
-metabolic acidosis
-use of dialysis:
-best initiated before the occurrence of life-threatening complications of acute renal failure such
as hyperkalemia, severe acidosis, uremic encephalopathy, or uremic pericarditis
-four forms:
-hemodialysis, peritoneal dialysis, continuous arterial-venous dialysis, continuous
venovenous ultrafiltration
81
! "# #" # $ #
! %
-Physiologic events in hemostasis: (1) vascular constriction; (2) platelet plug formation; (3) fibrin formation; (4)
fibrinolysis
& # #
-initial vascular response to injury
-vasoconstrictors:
-thromboxane A2 (TXA2) - powerful
-serotonin (5-hydroxytryptamine, 5-HT)
-bradykinin and fibrinopeptides
-contribution of pressure provided by surrounding tissues
-low perivascular pressures increased persistent bleeding:
-muscle atrophy accompanying aging, pts on steroids, Ehlers-Danlos syndrome
# #
-life span is 7-9 days
-Primary Hemostasis
-platelet plug formation on damaged intima within 15s of traumatic event
-requires vWF
-not affected by heparin
-principle mediators: ADP and serotonin
-plug process inhibited by cAMP
-Platelet release reaction stimulated by:
-ADP
-platelet factor 4
-trace thrombin on platelet surface
-Ca++, Mg++
-Release factors promote recruitment and aggregation and result in formation of amorphous plug:
-ADP, K+
-PDGF
-serotonin
-platelet factor 3:
-contributes phospholipid to several stages of coagulation cascade
-activates X (with IXa, VIII, and Ca++)
-activates II (with Xa, V, and Ca++)
-platelet factor 4 and B-thromboglobulin:
-inhibit heparin and modify fibrin formation
-Platelets provide lipoprotein surface:
-for conversion of prothrombin to thrombin
-initial activation of XI and XII
-Release inhibitor of plasminogen activation
82
#
-prothrombin thrombin: proteolytic enzyme which cleaves fibrinogen fibrin stabilizes platelet plug
-Intrinsic Pathway:
-starts with XII
-IXa + VIII + Ca++ (platelet surface): X Xa
-Xa + V + Ca++ (platelet surface): II (prothrombin) IIa (thrombin)
-Extrinsic Pathway:
-initiated by tissue lipoprotein
-thromboplastin + VII + Ca++: X Xa
-thromboplastin + Xa + V + Ca++: II (prothrombin) IIa (thrombin)
-Thrombin:
-activates XIII (fibrin stabilizing factor)
-cleaves fibrinopeptides A and B from fibrinogen fibrin
-makes VIII more potent
-XIIIa: cross-links fibrin monomers stable clot
-Actions of thrombin prevented by:
-antithrombin: binds thrombin to thrombomodulin on endothelium, preventing cleavage of fibrinogen
-activation of protein C: inactivates V and VIII
-circulating protease inhibitors
-Factors not synthesized by liver:
-thromboplastin, Ca++, most of factor VIII
-Vitamin K dependent: II, VII, IX, X
' # (
-dependent on plasmin
-lyses fibrin
-lyses others: fibrinogen, V, VIII
-split products interfere with normal platelet aggregation
-larger fragments incorporate into clot and form unstable clot
% )
#* #
(1) Autosomal dominant: von Willebrand’s disease, hereditary haemorrhagic telangiectasia, XI deficiency
(2) Autosomal recessive: deficiencies in factors X, V, VII, I
(3) Sex-linked recessive: hemophilia A (VIII) and B (IX, Christmas disease)
) $ #
-production: hereditary thrombocytopenia
-destruction: Wiskott-Aldrich syndrome
-von Willebrand disease: missing vWF
-Bernard-Soulier syndrome: normal vWF - missing glycoprotein I complex on platelet membrane receptor for vWF
-Glanzmann’s thrombasthenia: failed aggregation in presence of ADP; impaired mediation of factors in clot
retention
-Congenital afibrinogenemia: fibrinogen required for platelet aggregation
-Hermansky-Pudlak syndrome: storage pool disease platelets cannot store ADP
-oculocutaneous albinism, ceroidlike deposits in macrophages, bleeding diathesis
83
# # ) $ $ #
+, & ) $ # (- .* /
-male; sex-linked recessive; spontaneous mutations in 20%
-incidence 1:10000 to 1:15000
Clinical Manifestations:
-severity based on degree of deficiency: >5% of normal levels VIII: mild; 1-5%: moderately severe
-bleeding into joints (hemarthrosis), epistaxis, hematuria
-intracranial bleeding (trauma in 50% of cases): 25% of deaths
-vascular and neural compromise from pressure secondary to bleeding into soft-tissue closed space:
-Talipes equines contracture deformity: bleeding into calf
-Volkmann’s, flexion contractures of knees and elbos
-retroperitoneal bleeding: Psoas sign, hypovolemic shock
-intramural intestinal haematoma:
-n/v, crampy abdo pain, fever, WBC, “picket fence/stack of coins” appearance on UGI series
Treatment:
Replacement Therapy:
-half-life of VIII is 8-12h
-1 unit = amount present in 1 ml of normal plasma; FFP contains 0.6 u/ml; cryoprecipitates contain 9.6 u/ml
-minimum hemostatic level of VIII:
-mild haemorrhages: 30%
-joint and muscle bleeding and major haemorrhages: 50%
-major surgery and life-threatening bleeding: 80-100% pre-op and maintained > 30% x 2weeks
-amount given:
R = pt’s weight x [desired rise of VIII (% average normal)]/[total units of VIII in dose]
-half of R is subsequently administered q4-6h to maintain a safe level
0, 1 ) $ # (- * ) /
-X-linked recessive; accounts for 20% of hemophiliacs
-severe (50% of cases), moderate, mild forms according to level of IX
-prolonged PTT
Treatment:
-FFP or rarely, IX concentrates
-levels of 20-50% for severe haemorrhage for 3-5days then maintain at 10-20% for 10 days
-daily dose: 30-50 u/kg followed by 20 u/kg/d
-levels of 50-70% if operation required
-development of antibodies is a serious complication of treatment (10% of pts)
, 2 #3 ' #"4 ) 5
-autosomal dominant
-diminution of VIII:C (procoagulant) activity; variation in level may be noted
-prolonged bleeding time, prolonged aPTT
84
Clinical Manifestations:
-mild bleeding, epistaxis, menorrhagia
-serious bleeding after dental extractions, tonsillectomy
Treatment:
-cryoprecipitate (VIII R:vWF): 10-40 u/kg/12h
-replacement therapy should be begun 1 day pre-operatively
-aspirin must be avoided 10 days before operative procedure
) $ # $ #
0, # # 1 ) $ # (5
-rare autosomal recessive
-manifested by umbilical bleeding in the newborn and slow wound healing after an operation
-tx is FFP, cryoprecipitate, or XIII concentrates
6 ) % )
'#
-thrombocytopenia: most common abnormality of hemostasis that results in bleeding in surgical patient
-causes:
-disease processes: ITP, TTP, SLE
-hypersplenism/splenomegaly: sarcoid, Gaucher’s dz, lymphoma, portal hypertension
-reduced production in marrow: leukemia, uraemia, pts on cytotoxic therapy
-massive blood transfusion
-heparin induced: 0.6% of patients; after 4-15 days in pts given heparin for the first time
-impaired function: uraemia, thrombocythemia, PCV, myelofibrosis
-drugs: ASA, indomethacin, ibuprofen, dipyridamole, phenothiazine, penicillins, chelating agents,
lidocaine, dextran, beta-blockers, nitroglycerin, furosemide, antihistamines
-acute alcoholism
-viral infection
-vitamin B12 or folate deficiency
-no therapy for counts greater than 50000/mm3
-steroid therapy or plasmapheresis for idiopathic thrombocytopenia or SLE
-platelet transfusion:
-one unit = 5.5x1010 platelets: increases count by about 10x109/L
-4 to 8 units should be sufficient for adequate hemostasis
85
7 " (. $' # #
+, ) $' # # (#" 5
-Disseminated intravascular coagulation (DIC)
-caused by the introduction of thromboplastic materials into the circulation
-patchy necrosis of skin, hematuria and oliguria, confusion 2o cerebral ischemic, GIB, haemorrhage into adrenal
cortex acute hypotension
-causes: -retained dead fetus, premature separation of placenta, amniotic fluid embolus
-complication of dialysis, head trauma, mucin-producing and disseminated carcinoma, lymphomas,
thrombotic thrombocytopenia, rickettsial infection, snakebite, burns, aortic surgery, and shock from any
cause
-gram negative sepsis
-no lab test to confirm or exclude diagnosis; highly suggestive with combination of:
-low platelet count
-positive plasma protamines test presence of fibrin monomer-fibrinogen complexes
-reduced fibrinogen (<100mg/dL)
-context of patient’s underlying disease
Treatment:
-treat cause; supportive measures
-IV fluids + vasodilators
-plasma expanders if increased viscosity of blood
-active bleeding treated with FFP, cryoprecipitate (for fibrinogen), and platelet concentrates
0, ' # ( 5
-may occur in patients with metastatic prostatic carcinoma, shock, sepsis, hypoxia, neoplasia, cirrhosis, portal
hypertension, cardiopulmonary bypass
%( . $ 2 )
-major surgical risk for patients with marked thrombocytosis
-spontaneous thrombosis a complication of PCV: increased blood viscosity, platelet count and stasis
-myeloid metaplasia frequently represents part of the natural history of PCV
Treatment:
-thrombocyosis reduced with alkylating agents (eg. busulfan, chlorambucil)
-delay elective surgical procedures weeks to months after treatment
-emergency procedures: reduce RBC/plts by phlebotomy and replacement with RL
* )
-advanced cirrhosis:
-deficiencies in factors II, V, VII, X and XIII
-failure for liver to clear plasminogen activators increased fibrinolysis
-macroglobulinemia: abnormal production of proteins coat platelets
-multiple myeloma: cryoglobulins bind certain blood-clotting factors
# # #" ! "#
-spontaneous bleeding as a complication of anticoagulant therapy
-ecchymoses, petechia, or haematoma
86
+, " . # ( !(. *
-complications:
-overheparinization, heparin rebound, inadequate protamines neutralization, protamines excess,
thrombocytopenia
-two factors most important in triggering excessive bleeding: excessive fibrinolysis and platelet function
defects
-management:
-6 to 8 units of platelets
-if overheparinized: protamines
-excess fibrinolysis: EACA
% ) ! )
Platelet Count
-spontaneous bleeding only rarely for counts greater than 40000/mm3
-counts of 60000-70000/mm3 sufficient for hemostasis in surgery and trauma
Bleeding Time
-assessment of interaction b/n platelets and damaged blood vessel and formation of platelet plug
-abnormal in:
-thrombocytopenia
-qualitative platelet disorders
-vWD
-some patients with Vdeficiency or hypofibrinogenemia
-ASA ingestion
Prothrombin Time
-measures speed of the Extrinsic Pathway
-will detect deficiencies of factors II, V, VII, X and fibrinogen
Thrombin Time
-detects qualitative abnormalities in fibrinogen
-detects circulating anticoagulants and inhibitors of fibrin polymerization
-clotting time of pt’s plasma measured after thrombin added
Tests of Fibrinolysis
-fibrin degradation products (FDPs) measured immunologically
-euglobulin clot lysis time, dilute whole-blood or plasma-clot-lysis time: more sensitive, rapid evaluation of
fibrinolysis
& % 8
. 2 2 # $
-History:
-prolonged bleeding or swelling after biting lip or tongue
-bruises without apparent injury
87
-prolonged bleeding after dental extraction
-excessive menstrual bleeding
-bleeding problems associated with major and minor operations
-medical problems within past 5 years
-medications including aspirin within past 10 days
-relative with a bleeding problem
-Preoperative assessment:
Level 1: -negative history, minor procedure
-no screening test needed
Level 2: -negative history, major procedure
-platelet count, PTT
Level 3: -history suggestive, procedure where hemostasis is impaired (eg. cell savers)
-procedures where minimal bleeding could be injurious (eg. intracranial bleed)
-platelet count, bleeding time, PT/PTT
Level 4: -highly suggestive history
-hematologist consult, platelet count, bleeding time, PT/PTT
2 # $ 9 2 # . 2 $ . 2 ! "#
% * # "
-digital pressure
-haemostat and subsequent ligation with sutures or clips
-non-absorbable sutures evoke less tissue reaction and absorbable materials
-non-absorbable material in an infected wound can lead to extrusion or sinus tract formation
-cold packs promote hemostasis by inducing vascular spasm and increasing endothelial adhesiveness
* #
-heat denatures protein which results in coagulation of large areas of tissue
-advantage: time; disadvantage: more tissue is necrose
88
* #
-epinephrine: induces vasoconstriction; used on oozing sites in mucosa areas
-gelatin foam (Gelfoam), oxidized cellulose (Oxycel), oxidized regenerated cellulose (Surgicel), and micronized
collage (Avitene)
-fibrin glue (Tisseal)
* $ . # * .(
Platelet Concentrates
-indications:
-thrombocytopenia due to massive blood loss and replacement with platelet-poor products
-thrombocytopenia due to inadequate production
-qualitative platelet disorders
-may transmit infectious diseases and account for allergic reactions
-transfuse to elevate platelet levels to range of 50,000 to 10,000/mm3 for surgeries
-isoimmunity most important factor limiting usefulness
Concentrates
-antihemophilic concentrates
-albumin: 25 g osmotic equivalent of 500 ml of plasma; hepatitis free product
89
#" # $ . # $! " #
Volume Replacement
-restore circulating blood volume
-measurement of haemoglobin and hematocrit can be misleading and do not reflect severity of blood loss
-in OR: blood loss up to 20% replaced with crystalloids; above 50%, replaced with crystalloids, RBC, and albumin
or plasma +/- FFP if continued bleeding
. $ #" #
Massive Transfusion
-single transfusion greater than 2500 ml or 5000 ml transfused over a period of 24h
-complications:
-circulatory overload or DIC may occur
-dilutional thrombocytopenia, impaired platelet function, deficiencies of V, VIII, XI
-citrate toxicity: excessive binding of ionized calcium; rarely have a significant effect
-reduced 2,3-DPG increased affinity of RBC for O2 and less efficient delivery
-hypothermia decreases CO and rate
-hemolytic transfusion reaction
-infectious diseases
Routine Administration
-usually 5 ml/min for 1 min then 10-20 ml/min
-with marked oligemia: 500 ml over 10 min, second 500 ml over 10 min
-no practical advantage in intraarterial transfusion
Other Methods
-intraperitoneally: 90% enter circulation but uptake not complete for at least 1 week
-via medullary cavity of sternum and long bones: painful; limited rate
-cell saver: 250 ml in 5-6 min
-hemodilution: remove blood and maintain intravascular volume with crystalloids or colloid; removed blood may be
then retransfused
. #
90
Clinical Manifestation:
-pain, sensation of heat along vein; facial flushing, lumbar pain, constricting chest pain
-chills, fever, respiratory distress, hypotension, tachycardia
-if anaesthetized: abnormal bleeding and continued hypotension
-fall in platelet count, increased fibrinolysis, consumption of coagulation factors (esp V, VIII)
-Rudowski: oliguiria 56%; hemoglobinuria 56%; hypotension 50%; jaundice 40%; n/v 30%; flank pain 25%;
cyanosis and hypothermia 22%....
Treatment
-immediately stop transfusion
-send sample of patient’s blood to blood bank for comparison with pretransfusion samples
-determine bilirubin levels
-foley hourly urine measured
-initiate diuresis and alkalinize urine (mannitol or furosemide, 45 mEq bicarbonate)
-maintain hydration
(4) Embolism
-normal adult generally can tolerate embolism of 200 ml of air
-venous air embolism:
- venous pressure, cyanosis, “mill wheel” murmur over precordium, hypotension, tachycardia and
syncope
-tx: left lateral decubitus position in Trendelenburg
-arterial air embolism: dizziness and fainting, LOC, convulsions; air may be visible in the retinal arteries
(5) Thrombophlebitis
-discontinue transfusion and compress locally
91
-pathophysiologic condition: state of inadequate tissue perfusion
!"
-return of venous blood to heart produces ventricular end-diastolic wall tension, a major determinant of cardiac
output
-veins in skeletal muscles respond to external factors: gravitational forces and muscle pump
-exercise and increased sympathetic reflexively decrease the splanchnic capacitance
-salt and water balance from the kidneys via hormonal effects of renin, angiotensin and antidiuretic hormone
# $! !
-Frank-Starling curve: force of contraction dependent on initial muscle length
-affected by variety of disease states: MI, valve dysfunction, cardiac hypertrophy
!"
-force acting to resist myocardial work during contraction
-arterial pressure is the major component that influences the ejection fraction
-determined by precapillary smooth muscle sphincter
-in normal heart, stroke volume maintained in lieu of increased afterload by increased reload
# %
&' (! ) (' ((
1. -increased vascular tone elevates PVR redistribution of blood flow among organ systems
-“autoregulated” organs (heart, brain) preferred
92
7. -ACTH released (stimulated by various stresses)
-cortisol potentiates actions of epinephrine and glucagon, further stimulates mobilization of amino acids from skeletal muscle, and
results in renal sodium and water retention
$& !) ! * & (
Etiology
-ARDS is the final common pathway to various pulmonary insults
-initiation of inflammatory mediators increases microvascular permeability proteinaceous fluid deposition in
alveolar epithelial and pulmonary capillary endothelial interface V/Q mismatch
-fluid overwhelms pulmonary lymphatic clearance
-pulmonary edema refractory to diuretics and fluid restriction; colloid administration not useful
Diagnosis
-clinical suspicion
)' + &
$" ($( !
1. Ringer’s Lactate:
93
-lactate content will not aggravate lactic acidosis
-safe inexpensive, equilibrates rapidly throughout ECF
2. Colloid solutions:
-raise intravascular colloidal pressure intravascular influx of interstitial fluid
-more expensive, may bind and decrease ionized serum calcium, decrease circulating immunoglobulins,
decrease immune reaction to tetanus toxoid, decrease endogenous production of albumin
-may not necessarily be better for fluid resuscitation over crystalloids
-no clinical evidence that appropriate resuscitation with balanced slat solution is associated with
any harmful effects on pulmonary function
3. Hypertonic Saline:
-can be effective initial resuscitative solution but requires close monitoring of electrolytes to prevent
hypernatrema and hyperosmolar coma
-long-term benefits not established
4. Hetastarch:
-slow equilibration can lead to rapid fluctuations in CVP
-mild and transient coagulopathies noted
5. Dextran:
-greater risk of anaphylaxis; has produced coagulation defects and immunoglobulin depression
6. Blood substitutes:
-stroma-free haemoglobin (SFH) eliminates side effects secondary to erythrocyte stromal elements
-high affinity for oxygen, short plasma half-life, available only from human sources
-not a practical substitute
-perfluorodecalin:
-require emulsification to be water soluble
-use requires higher inspire oxygen concentrations
-effective substitute for haemoglobin
",$+! !')
(1) Vasopressors
-may elevate BP at expense of further PVR and tissue perfusion
-do not substitute for adequate fluid resuscitation
(2) ATP
-in experimental models, found to improve survival rates in potentially lethal shock (in combination with fluids)
-limited usefulness in clinical treatment since may result in marked homodynamic instability in hypovolemic pt
(3) Positioning
-Trendelenberg may interfere with respiratory exchange
-preferred position is elevation of both legs while maintaining head, trunk and arms supine autotransfusion of
pooled blood in venous circulation
94
(5) Pulmonary Support
-beneficial in patients with abnormal oxygen saturations: eg. PTX, pulmonary contusion, aspiration, a/w
obstruction, COPD etc..
(6) Antibiotics
-no support for protective mechanism against ravages of hypovolemia
-use in patients with open or potentially contaminated wounds
(7) Analgesics
-if causative injury produces severe pain, control of pain becomes mandatory
-small doses of narcotics should be given intravenously to prevent profound sedation
(8) Steroids
-specific instances, steroid depletion with hypovolemic shock may occur:
-elderly patient
-Addison’s disease, post-adrenalectomy, adrenal suppression with exogenous steroids
-IV hydrocortisone desirable in these cases
-steroids not indicated in trauma patient with hypovolemia
(9) Monitoring
-CVP:
-normal to depressed despite administration of fluids continuing hypovolemia
-elevated or rapid rise impairment of pumping mechanism
-if shock is refractory to treatment, must look for:
-continuing blood loss into chest or abdomen
-inadequate volume replacement
-inadequate clotting
-multisystem trauma with occult thoracic injuries (cardiac tamponade, hemopneumothorax)
-myocardial insufficiency (contusion or hypoperfusion)
!" *
-heart unable to generate sufficient cardiac output to maintain adequate tissue perfusion
-hypotension in the face of adequate intravascular volume
Pathophysiology
-secondary to valvular heart disease, cardiomyopathy, myocardial contusion
-AMI most frequent cause; fatal if >40% loss of left ventricular mass
-complications:
-papillary muscle dysfunction, ischemic ventricular septal defects, massive LV infarction,
arrhythmia
-vicious cycle created: increased myocardial oxygen demand, hypotension, shortened diastole, increased PVR and
afterload
Treatment
-initial therapy: optimizing ventricular reload by manipulating filling pressure, decreasing afterload in patient with
adequate sBP, correcting arrhythmia, improving contractility to sustain vital organ perfusion
95
-watch for pulmonary edema intubation and ventilation will myocardial oxygen demand from increased
work of breathing
2. Inotropic Agents:
-beta1-adrenergic receptors increased contractility and CO
-increases myocardial oxygen demand
-Dopamine:
- may reverse life-threatening hypotension and restore MAP to about 80 mmHg
-low doses:
2-5 ug/kg/min splanchnic, coronary, renal vasodilation
5-8 ug/kg/min adrenergic-mediated in contractility and heart rate
-high doses:
alpha-adrenergic effects: CVP and coronary vasoconstriction
-variable increase in heart rate
-can precipitate other arrhythmia
-Dobutamine:
-synthetic catecholamine with predominantly inotropic effect
-Digitalis:
-controversial; useful in supraventricular arrhythmia
-increased MO2: adds very little homodynamic benefit relative to therapy the sympathomimetic
agents
3. Vasodilator Agents:
-some patients with low CO and high filling pressures have near-normal arterial blood pressures
-systolic ventricular wall stress is high, and reducing afterload should increase cardiac output and decrease
myocardial work therefore can use nitroprusside, but with extreme caution in hypotensive patients
4. Mechanical Support
-intraaortic balloon pump: unloading LV and reduce myocardial work
-elevates diastolic BP: increases pulmonary perfusion, decreases myocardial work, increases
cardiac output distal to ventricle
-unclear if improves long-term survival
-good bridge until surgically correctable problems are addressed
-left ventricular assist devices: currently limited to cardiac surgery patients
5. Arrhythmias
-decreased ventricular EDP from decreased filling time
-digoxin drug of choice for atrial fibrillation or flutter - cardioversion if hypotension or hypoperfusion
-verapamil for tachyarrhythmias of atrial origin
-propranolol for sinus tachycardia
-defibrillation for ventricular fibrillation
-lidocaine for premature ventricular complexes which may lead to ventricular tachyarrhythmias
-bradyarrhythmias: electrical pacing
$ *
-occurs after serious interference with the balance of vasodilator and vasoconstrictors influences to the arterioles
and venules
-clinical syncope
-paralysis of vasomotor influences; eg. high spinal anaesthesia, spinal cord injury
-reflex interruption of nerve impulses: acute gastric dilatation
-low BP, low pulse rate, dry, warm, flushed skin
-decreased CO, decreased PVR
96
-can result in kidney failure and brain damage
Treatment
-gastric dilation NG tube insertion
-high spinal anaesthesia fluids, vasopressor (Neo-synephrine)
-spinal trauma maintain normal CVP that rises slightly with rapid fluid administration and using a vasopressor
judiciously to support arterial pressure
'
Clinical Manifestations
-normovolemic but has hypotension despite increased CO and good filling pressure
-paradoxical “warm shock”
-high CO associated with decrease in oxygen utilization and narrowed arteriovenous oxygen difference
-thrombocytopenia may be early indicator of gram-negative sepsis
-systemic illness may result form inappropriate systemic effects of mediators used to contain local infection
-myocardial depression despite hyperdynamic CO
Pathophysiology
-TNF is a central and proximal mediator of the host response to endotoxemia and bacteremia
-produced predominantly by cells of macrophage lineage
-reduction in membrane potential preceded onset of hypotension
-TNF-alpha:
-capable of inducing membrane depolarization in vitro
-important mediator of septic shock
-induces synthesis and secretion of secondary mediators: cytokines, PG, leukotrienes,
PAF, complement, coagulation cascade
-may synergise with lipopolysaccharide to induce many toxic effects mediated by TNF-alpha
-naturally occurring inhibitors of TNF-alpha activity: extracellular type I and II TNF receptors
shed from cell surface in response to inflammatory stimuli
-Interleukin-1
-key mediators of host response to infection, inflammation and injury
-IL-1 receptor antagonist (IL-1ra) blocks many functions of IL-1:
-lymphocyte proliferation, increased adhesion of endothelial cells for neutrophils and
eosinophil; synthesis of IL-1, TNF-alpha, IL-6, and IL-8 by monocytes; nitric oxide
production in SMC
-anti-endotoxins antibodies fail to confirm beneficial effects
-other potential mediators of septic shock: linins, endogenous opiates, other recently purified cytokines
Therapy
-antibiotics and early surgical debridement or drainage of abscess
-fluid therapy, vasoactive drugs as adjuncts
-broad spectrum should include anaerobic coverage
-steroids offer no advantage; use only in hypoadrenalism and stress coverage in those already taking steroids
1. Pharmacologic support
-dopamine: improves hypotension
-dobutamine: may not be tolerated by hypotensive patients
-use of pressors is primarily for transient support while primary definitive therapy with antibiotics and
drainage of surgical infection are being instituted
97
2. Manipulations of Humoral Responses
-difficult because of the complex and ill-defined interactions among a large number of mediators
-only a few showed statistical benefits in studies: HA-1A (human monoclonal IgM against lipid A of
endotoxins), E5 (murine monoclonal IgM against lipid A)
98
!
" # "$
-operative treatment generally required when host defences cannot function properly or when continuing
contamination with microorganisms
! %
99
&' ( $% "#
-cellulitis:
-spreading infection of skin and subcutaneous tissues
-local pain/tenderness, edema, erythema
-usually indistinct borders
-+/- systemic symptoms
-caused by: Strep. pyogenes, Staph. aureus, Strep. pneumoniae, Haemophilus influenzae, other
streptococci, aerobic and anaerobic gram-negative bacteria
-erysipelas:
-caused by strep. pyogenes
-intense erythema with sharp line of demarcation
-lymphangitis:
-inflammation of lymphatic channels
-presents as visible red streaks
)' *
-carbuncle:
-subcutaneous abscess from confluent infection of multiple contiguous hair follicles
-most commonly Staph. aureus
-felon:
-purulent collection in distal phalanx
-intense pain and pressure in compartment; treat with lateral incision
-breast abscess:
-usually Staph. aureus
-treat with incision and drainage and antibiotics
-perirectal abscess:
-infection of crypt glands that extends into perirectal space
-aerobic and anaerobic gram-negative bacteria
+' ,
-most caused by mixed aerobic and anaerobic gram-negative and gram-positive bacteria
-Clostridium sp. (C. perfringens, C. novyi, C. septicum) - gram positive rods
-most common, most dramatic infections, rapid progression, high mortality
-“gas gangrene”
-subcutaneous emphysema: anaerobic bacterial metabolism hydrogen, nitrogen, methane
-Strep. pyogenes
-Vibrio
-fungi necrotizing infections progress more slowly than bacterial infections
-surgical treatment requires debridement of all necrotic tissue
-hyperbaric oxygen: inhibits production of alpha toxin in Clostridia
-no improvement in patients with nonclostridial infection
-complications: middle ear injury, trauma to sinus, PTX, air embolism
-'
-caused by Clostridium tetani
-majority of cases appear after punctures, lacerations, and abrasions
-two toxins:
-tetanospasmin
-actons on anterior horn cells of spinal cord and brainstem
100
-blocks inhibitor synapses muscle spasms and hyperreflexia
-testanolysin
-cardiotoxic and causes haemolysis; not thought to be of major clinical importance
Clinical Manifestations:
-generalized muscle spasms generalized convulsions
-orthotonos, opisthotonos, emprosthotonos
-spasm of laryngeal and respiratory muscles fatal acute asphyxia
-mortality rate can exceed 50%
-diagnosis on clinical grounds; laboratory investigations not helpful in diagnosis
Treatment:
-tetanus immune globulin (TIG) 500-10,000 units ASAP
-ICU admission intubation, ventilation, paralytic drugs
-mild cases: sedation, muscle relaxants, analgesics
-(hyperbaric oxygen is ineffective)
-treat wound to remove C.tetani and nonviable tissue +/- antibiotics
Prevention:
> 3 doses No No No No
(Yes if > 10y (Yes if > 5y
since last dose) since last dose)
*such as, but not limited to, wounds contaminated with dirt, feces, soil, or saliva; puncture wounds;
avulsions; and wounds resulting from missiles, crushing, burns, or frostbite
. ($ / $
&' ( *( % *
-Primary peritonitis: caused by single organism; commonly seen in pts with ascites or renal failure on PD
-Secondary peritonitis:
-defect in GI tract
-requires operative intervention; antibiotics against aerobic and anaerobic enteric bacteria
-Tertiary peritonitis:
-peritonitis-like syndrome as a result of a disturbance in host’s immune response
-peritonitis without evidence of pathogens
-may also be caused by fungi or low-grade pathogenic bacteria
-Intraabdominal abscess: percutaneous or operative drainage along with Abx therapy needed
)' % "$ %
-causes:
-pneumonia (most common), pulmonary infact, septic embolic to lung, tracheal or bronchial
fistula, leaking esophageal anastomosis, hepatic abscess, subphrenic abscess, trauma, leaking
bronchial closure, infected hemothorax, paravertebral absces
101
-chronic empyema: dyspnea, fatigue, anemia, debility, clubbing of fingers
-treated with chest tube; may be converted to open drainage after 2 to 3 weeks
-open drainage if multiple pus pockets, thick pus, or inadequate drainage via CT
# ( " (
-septic arthritis
-suppurative pericarditis
# ! / (
-cardiac valves, pacemakers, vascular grafts, artificial joints
-total removal to eradicate infection
" 0 (1 % 2
-urinary tract infections (most common), wound infection, lower respiratory tract infection, bacteremia, cutaneous
infection
&' 3 (
Classification:
Dirty (28-40%)
-traumatic wound with retained devitalized tissue, FB, feces, delayed treatment
-perforated viscus
-acute bacterial inflammation with pus encountered during operation
102
Definition of Surgical Wound Infection:
Superficial:
-infection occurs at incision within 30 days after operation
-involves skin or subcutaneous tissue above fascial layer with any of the following:
-purulent drainage
-organism isolated from culture
-wound opened deliberately by the surgeon
Deep:
-infection occurs at incision within 30 days after operation (no prosthesis); within 1 year of an implant
-infection beneath fascial layer and any of the following:
-wound spontaneously dehisces or deliberately opened when T>38 and/or pain
-abscess seen on direct examination, operation, or histopathologic examination
-surgeon diagnoses infection
)' "#$ 4
103
Prophylactic Antibiotics:
-Principles:
1. Choose Abx effective against most likely pathogen
2. Abx with low toxicity
3. Give single, fully therapeutic dose IV 30-60 minutes preoperatively
4. Give second dose if surgery > 4h or twice half-life of Abx
5. Give 2-3 doses post-op; no need to extend beyond 24h
6. Use of Abx appropriate when infection frequent or when consequences of infection
unusually severe
-cephalosporins most commonly used because of broad spectrum
)' # " 0 (
5 .
&' % /
Staphylococcus
-facultative anerobes
-found on moist areas of body, anterior nares, mucous membranes
104
-TSS toxin-1 toxic shock syndrome
-catalase: resists H2O2-mediated intracellular killing
Streptococcus
-S. pyogenes, S. pneumoniae
-viridans group: S. mutans, S. mitior, S. salivarius, S. sanguis, S. milleri
-grouped according to:
a. Lancefield classification: cell surface antigens
b. Hemolytic ability on blood agar:
-alpha haemolysis: zone of green discolouration around colonies; intact RBC
-beta haemolysis: complete clearing of area around colonies; destroyed RBC
-gamma haemolysis: no haemolysis
Manifestations:
-pharyngitis scarlet or rheumatic fever
-erysipelas
-cellulitis, wound infection, endocarditis, UTI, bacteremia
-primary necrotizing soft tissue infections (although S. pyogenes an uncommon cause) and abscesses
)' * ( / $ * % / .
+' * .
105
-enterotoxins: C. difficile, C. perfringins
-neurotoxins: C. tetani, C. botulinum
6
-Herpesvirus family: CMV, HSV, VZV, EBV
-CMV: -causes most viral infections in organ transplant recipients
-ulcerative lesions of the GI tract bleeding or perforation
-EBV: -polyclonal B-cell lymphoma in transplant recipients
% %% ( $6
-retrovirus of lentivirus family
-RNA virus with cylindrical core containing RNA, RNA-dependent DNA polymerase (reverse transcriptase), and
core proteins
-GP-120: affinity for CD4+ receptor on TH cells
-infected CD4+ cells cannot carry immune functions opportunist infections, Kaposi’s sarcoma
and primary CNS lymphomas
-CD4 count < 200/mm3 = AIDS
5 .
! * % *
(1) Blood:
-concentration determined by rapidity of excretion and protein binding
-highly protein-bound antibiotics not excreted as rapidly do not have to be given as frequently
(2) Urine:
-sulfonamides, penicillins, cephalosporins, aminoglycosides, tetracyclines, quinolones, azoles
-excreted principally in urine and achieve high concentrations
(3) Bile: -besides urine, only bile regularly has antibiotic concentrations higher than serum levels
106
(4) Interstitial Fluid and Tissue:
-high, prolonged serum concentration and low protein binding favourdiffusion from serum into
extravascular tissue
(5) Abscesses:
-reduced antimicrobial efficacy d/t:
-acidic pH
-low redox potential
-large numbers of microbial and tissue products that can bind antibiotics
-drainage is key
* $
Prophylactic Antibiotics:
-discussed earlier
-administer to all patients with previously placed prosthetic devices such as cardiac valves or artificial
joints who are having any operation or dental procedure
! (%
Route: intravenous
Duration: most surgical infections can be treated effectively in 5-7 days of antibiotic therapy
Treatment Failure:
-wrong antibiotic, intraabdominal abscess, resistant bacteria, other causes (other sites of infection)
-inadequate dose, inappropriate route
Drug Toxicity:
-in renal failure, give a first dose of 80-100% then estimate timing and amount of second dose according to
various schedules based on the normal half-life of the antibiotic
107
-depth of injury proportionate to temperature applied, duration of contact and thickness of skin
!"!
108
Burn Center Referral Criteria:
1. Second- and third-degree burns > 10% TBSA in pts under 10 or over 50 yoa
2. Second- and third-degree burns > 20% TBSA in other age groups
3. Second- and third-degree burns involving face, hands, feet, genitalia, perineum, and major joints
4. Third-degree burns > 5% TBSA in any age group
5. Electrical burns, including lightning injury
6. Chemical burns
7. Inhalation injury
8. Burn injury in patients with preexisting medical disorders that could complicate management, prolong
recovery, or affect mortality
9. Any burn patients with concomitant trauma where burn injury poses greatest risk of morbidity or
mortality
10. Burn injury in children admitted to a hospital without qualified personnel or equipment for pediatric
care
11. Burn injury in patients requiring special social, emotional, and/or long-term rehabilitative support,
including cases involving suspected child abuse, substance abuse, etc.
# ! # $! %! !
(1) Airway:
-secure airway
-if suspicion of smoke inhalation 100% oxygen by mask
-endotracheal tube for unconscious patients
109
-CVP monitoring in pts with burns 50% TBSA, associated medical problems, very young or very old,
smoke inhalation
-Swan-Ganz catheters in pts with > 65% TBSA b/c of homodynamic instability
(6) Tetanus
-burns are tetanus-prone wounds
Chest Escharotomy:
-early respiratory distress may be due to compromise of the ventilatory function caused by a cuirass effect
related to a deep circumferential burn wound of the chest
-escharotomy: anterior axillary line bilaterally
Escharotomy of Extremities:
-circumferential burn wounds of extremities may lead to permeant, serious neurologic and vascular deficits
-intramuscular compartment pressure: treat if > 30 mmHg
-local anaesthesia unnecessary because 3rd degree eschar is insensate
-incisions along mid-medial or mid-lateral aspect of extremity; should extend to subcutaneous fat
-burn patients are at risk for developing compartment syndrome up to 72 h postinjury frequent
assessment of involved extremity needed
-burn extent, patient age, and depth of burn are primary determinants of mortality
Burn Size:
-Rules of Nines:
-upper extremity: 9% TBSA x 2 = 18%
-lower extremity: 18% TBSA x 2 = 36%
-anterior and posterior trunk: 18% TBSA each = 36%
-head and neck: 9% TBSA = 9%
-perineum 1% TBSA = 1%
TOTAL = 100%
-Hand ~ 2.5% TBSA: dorsal surface 1% TBSA, palmar surface 1%, vertical surface 0.5%
-infants: head almost 20% TBSA
Burn Depth:
-primary determinant of long-term appearance and function
-healing from remaining epithelium lined skin appendages: sweat glands, hair follicles with attached
sebaceous glands
110
-deeper the burn fewer appendages longer burn takes to heal
-burns taking > 3 weeks to heal often produce hypertrophic scars, functional impairment, and thin fragile
epithelial cover
-these burns should be treated surgically
-depth dependent on:
-heat of burn source
-thickness of skin
-duration of contact
-heat-dissipating capability of skin (blood flow)
$ %*
-hypovolemic shock and tissue trauma formation and release of local and systemic mediators vascular
permeability or in microvascular hydrostatic pressure
-Histamine:
-involved only in the very early increase in permeability
-released by mast cells immediately early after injury increased capillary permeability
111
-increased intravascular junction space in venules
-Serotonin:
-released immediately upon postburn platelet aggregation
-increases pulmonary vascular resistance
-indirectly amplifies vasoconstrictive effects of norepinephrine, histamine, angiotensin II, PG
-Prostaglandins:
-contribute to formation of burn edema
-PGE2 and PGI2 (prostacyclin) arterial dilatation in burn tissue blood flow and hydrostatic
pressure accentuate edema process
-Proteolytic cascades:
-coagulation, fibrinolysis, kinins, complement system
-Bradykinins: increase vascular permeability in the venule
-reduction of CO after burn injury is a result of hypovolemic and cellular shock, increased systemic vascular
resistance due to sympathetic stimulation and hypovolemia
-after successful resuscitation, CO normalizes after 18-24h and increases to supernormal levels during wound-
healing phase
! #+ % !, ! -
Hypermetabolism:
-glucose:
-metabolism elevated
-gluconeogenesis from alanine and glycogenolysis are increased
-plasma insulin levels elevated; hepatic insulin resistance basal rate of glucose production
elevated despite normal or elevated insulin level
-protein:
-excreted primarily as urea progressive depletion of protein stores
-proteolysis increased increased efflux of amino acids (particularly alanine)
-increased gluconeogenesis from amino acids makes them unavailable for reincorporation
of body protein
-wound repair requires amino acid protein synthesis and increased immunologic activity and may
require accelerated protein synthesis
-recommended protein intake: 1-2 g/kg/d
-fatty acids:
-released at rates in excess of requirement of fatty acids and energy substrates
-not oxidized but re-esterified into TG fat accumulation in liver
Neuroendocrine-Mediator Response:
-catecholamines are the major endocrine mediators of hypermetabolic response in thermally injured
patients
-thyroid hormonal serum concentrations not elevated in patients with large burns
Cytokine Cascade:
-after injury, a number of cytokines are induced rapidly, including TNF, IL-1 and IL-6
-TNF-alpha detectable early in burn shock; maximum level is of prognostic significance
-IL-1 and IL-6 are up regulated in inflammatory sites inducing PMN chemoattraction
-IL-2, a key cytokine in cellular immune response, is significantly suppressed in pts with large burns
-IL-6 induces hepatic synthesis of acute phase response proteins (eg. alpha-glycoprotein, C3, fibronectin)
112
Arachidonic Cascade:
-PGE2: major product after thermal injury
-produced by macrophages
-immunosuppressive effect by:
-inhibition of lymphocyte IL-2 production and T-cell activation
-down-regulation of IL-6
-massive increases in thromboxane B2
-leukotriene B4 is a potent neutrophil chemotactin produced after thermal injury
Cell-Mediated Immunity:
-impaired after burn injury
-functional capacity of T cels to perform their normal physiological response is impaired
Macrophages:
-function impaired after thermal injury
-products suppress mitogenic responsiveness in normal lymphocytes
Neutrophils:
-decreased Fc receptor expression, depressed intracellular killing capacity, and leukocyte chemotaxis
-CD16 (FcR, Fc, IgG receptors) and CD11 (adhesion molecules) on neutrophils is impaired
-baseline granulocyte oxidative activity is increased
Humoral Immunity:
-marked diminution of total serum IgG concentration
-levels return to normal between 10-14 days postburn
-low levels of IgG predictive of poor prognosis
-classical and alternative complement pathways are depleted
-production of GCSF and GM-CSF also impaired
113
(2) Hypertonic Saline:
-results in less edema because of smaller total fluid requirements
-advantages over RL controversial
(4) Dextran
Inhalational Injury:
-increases fluid requirements
-require 5.7 ml/kg/%burn
Rate of Administration:
-volume infused should maintain urine output of 30-50 cc/h in adults and 1 cc/kg/h in children
114
)
./0 # + 1 '!
-60-70% of deaths from house fires attributed to CO poisoning
-affinity for haemoglobin 200 times greater than oxygen and interferes with oxygen delivery:
1. prevents reversible displacement of oxygen on haemoglobin
2. shifts oxygen haemoglobin dissociation curve to the left decreasing oxygen unloading from at tissue
level
3. CO inhibits cytochrome oxidase a3 complex less effective cellular respiration
4. CO may bind to cardiac and skeletal muscle, causing direct toxicity
-COHb levels:
-< 10%: no symptoms
-20%: headache, nausea, vomiting, loss of manual dexterity
-30%: weak, confused, lethargic
-40-60%: coma
->60%: death
-half-life of COHb: room air 4-5 h; 100% O2 45-60 mins; HBO at 2 atm 30 min; HBO at 3 atm 15-20 min
-use of hyperbaric oxygen still controversial
.20 $! & # 3# -
-usually limited to upper airway:
-nasopharynx and oropharynx: very effective mechanism for heat exchange d/t relatively large surface area
and associated air turbulence, as well as their mucosa water lining that acts as a reservoir
-sudden exposure to hot air reflex closure of vocal cords reduces potential for lower airway injury
-greatest risk in those injured in an explosion and those who have been unconscious in a fire
-presence of significant intraoral and pharyngeal burns early intubation ETT for 3-5 days
.40 & *! $# #
-hydrogen cyanide: more effective inhibitor of cellular respiration than CO
-inhalation of aldehydes and caustic acids and bases mucosa coagulation and liquefaction necrosis
-direct epithelial damage: loss of bronchial epithelial cilia and decreased alveolar surfactant
-increase in bronchial blood flow with stimulation of alveolar macrophages
-airway edema, sloughing of necrotic epithelial mucosa, impairment of mucociliary clearance of secretions airway
obstruction V/Q mismatch hypoxia
-in the presence of burns, smoke poisoning approximately doubles the mortality from burns of any size
Diagnosis:
-anyone with flame burn and anyone burned in an enclosed space should be assumed to have smoke
poisoning until proved otherwise
-physical examination
-edema, strider, soot impaction smoke inhalation
-wheezing or rhonchi on chest auscultation injury to lower airways
-LOC decreased with hypoxemia, CO poisoning, or cyanide poisoning
-neurological deficits CO poisoning
-carboxyhemoglobin levels, ABG (to get P/F ratio)
Treatment:
(1) Upper Airway:
-in the presence of increasing laryngeal edema, nasotracheal or orotracheal intubation is indicated
-tracheotomy should never be used as an emergency procedure
-treatment of postextubation strider includes administration of racemic epinephrine and Heliox
(2) Lower Airway and Alveolar Damage:
-tracheobronchitis wheezing, coughing, retained secretions
115
-supplemental oxygen immediately
-efficacy of bronchodilators is questionable
-presenting sign of lower airway damage is hypoxemia
-treatment for smoke poisoning is supportive maintain ventilation with PEEP and oxygenation
until lung heals itself
-tracheotomy for those requiring long term ventilation (performed b/n 3 and 30 days after
intubation)
-anterior neck burns require excision and grafting 5-7 days prior to creation of
tracheotomy
./0 # 1% # ' #6
-for deeper burns, the eschar is surgically removed and the wound closed, with grafting techniques and
procedures for immediate placement of flaps tailored to meet patients’ individual needs
-early wound closure shortens hospital stay and duration of illness
.20 ! # 65 ' #!
Evidence Based Conclusions:
1. Small (<20%) full-thickness burns, and burns of indeterminate depth, if treated by an experienced surgeon, can be safely
excised and grafted with a decrease in hospital stay, cost to the patient, and time away from work or school
2. Early excision and grafting dramatically decreases the number of painful debridement required by all patients
3. Patients with burns between 20-40% TBSA will have fewer infectious wound complications if treated with early excision and
grafting
4. In animals with experimental burns, the depressed immune response and hypermetabolism associated with burns can be
ameliorated by early burn wound removal
Clinical Impressions:
1. Scarring is less severe in wounds closed early, leading to better appearance and fewer reconstructive procedures
2. Mortality from wound infection is lower in patients with major burns after early excision
3. Mortality from other complications of major burns may be lower with early excision and grafting
116
-Early Reconstruction:
-skin graft junctures should be avoided over joints, and grafts should be placed transversely when
possible
-thick skin grafts yield a better appearance than thin skin grafts:
-used for face, neck and other cosmetically important areas
-adjacent pieces of skin graft should be approximated carefully
-Donor Sites:
-with early excision the patient was spared the painful daily debridement, and with burn pain
diminished, patients concentrated on donor site pain
-all dressing seem to work, and difference in healing time are only 1 or 2 days
-complications: hypertrophic scarring, changed pigmentation, blistering, infections
-infections treated with systemic antibiotics and continuously moist dressings or silver
sulfadiazine
1. Cultured keratinocytes can be grown within 3 weeks and can be grafted successfully on a viable, non-infected excised burn
wound bed. For a massive burn with few or no available donor sites, this may be life-saving, especially in children
2. Take varies from poor to fair, with an optimistic range of 30-40%
3. Because epidermal cells lack a dermis, in early stages of wound healing, CEAs can provide only a barrier function to prevent
fluid exudation and bacterial invasion
4. The cover is fragile and must be protected from mechanical disruption for months, limiting daily activities and vigorous
physical and occupational therapy
5. CEAs are a temporary measure, permitting survival in the patients with massive burns.
Dermal Substitutes
-bovine collagen matrix with fiber size and distance similar to that of dermis, with a ground substance,
chondroitin 6-sulfate, filling the pores
-provides template on which native fibroblasts, endothelial cells, and macrophages can replace the collagen
with a dermal matrix resembling dermis
./0 # % !8 !& !
-hypermetabolism and hypercatabolism are universal consequences of injury
-magnitude of increase in metabolic rate is directly proportional to the size of burn injury
-requirements estimated from the Harris-Benedict equation
-routine determination of resting energy expenditure (REE) conducted at least twice weekly on burn patients for
proper adjustments of caloric needs
-caloric goal should be calculated at 120-130% of the measure REE
Carbohydrates:
-glucose is the best source of non-protein calories in the burn patient
-peripheral amino acids (alanine, glutamine and other glycogenic amino acids gluconeogenesis) and
wound lactate (glucose production by the Cori cycle) account for approximately one-half to two-thirds of
new glucose produced by the liver
-depletion of body protein during period of starvation leads to energy deficits and malfunctioning of
glucose-dependent energetic processes at the cellular level
117
Protein:
-energy and protein cooperatively contribute to improvement in protein conservation
-amino acid administration promotes synthesis of visceral and muscle protein without affecting the rate of
protein breakdown
-glucose retards whole-body protein breakdown and decreases the total amino acid pool, but exerts little
effect on protein synthesis
-both mechanisms improve nitrogen balance
-glutamine an important energy source for GI tract; broken down to alanine used in gluconeogenesis
-arginine may diminish protein catabolism and has secretagogue activity on pituitary and pancreatic
hormones improves immune function
Fat:
-appears to be a poor calorie source for the maintenance of nitrogen equilibrium and lean body mass in
hypermetabolic patients with large burns
-enthral tube feeding products are largely devoid of omega-3 fatty acids; alpha-linolenic deficiency has
been demonstrated in patients on long-term tube feedings.
.40 ! 6 '& #
-seems to influence outcome
-TPN used only when patient’s needs cannot be wholly met by enteral route
-functionally intact alimentary tract always should be used
-safest route for infusion of nutrients is distal to the ligament of Treitz
-advantages of enteral route over TPN:
-maintains integrity of GI tract
-increased hepatic protein synthesis may reduce incidence of bacterial translocation from the gut
-preserves gut mucosa mass and maintains digestive enzyme content
-stimulates trophic hormones, particularly gastrin
-initiate greater insulin release and promotes anabolism
-blunts intensity of hypercatabolic response and more effectively maintains preinjury weight
-prolonged postresuscitation ileus, overuse of narcotics, and constipation are frequently causes of failure of
successful enteral alimentation
-sepsis is associated with ileus and severe glucose intolerance
.90 % # # ,, !# !
-burn patients require higher ambient temperatures for comfort because of the apparent change in the hypothalamic
set point of thermal neutrality
-warming burn patients to 38.2oC decreases the metabolic rate and corresponding energy requirements
-warming blankets, and heat lamps may be required
-administration of narcotics reduces metabolic rate associated with pain
-systemic infection requires additional calories to maintain nitrogen balance
-vigorous physical therapy promotes preservation of muscle bulk and must be provided on a daily basis to all
patients requiring prolonged hospitalization
118
-burns cause severe immunosuppression that is directly related to the size of the burn wound
!' % 6 6!%
-extent of burn injury is one of the major demographic predictors of outcome
-presence of inhalation injury correlates highly with infection and mortality
-burns involving less than 10-20% TBSA in otherwise healthy burn patients are almost never associated with life-
threatening infection
%# # 6! #
-diagnosis remains one of infection because many of the cardinal signs of sepsis are also present in uninfected burn
patients
-thrombocytopenia is one of the major manifestations of infection
-a precipitant onset of hyperglycemia, fall in blood pressure, and decrease in urinary output should suggest the
possibility that the patient is becoming unstable
-if associated with hypothermia, leukopenia, and falling platelet count, the patient is probably developing
sepsis
5 ' 6!%
-gram-negative bacteria (Pseudomonas species) is the dominant organism causing fatal wound infections
-pathological feature of burn wound sepsis is invasion of the organisms into viable tissue
spread to perivascular structures capillaritis and vascular occlusion haemorrhagic necrosis
-likelihood of septicaemia increases in proportion to the size of the burn wound
! & #
-respiratory tract most common locus of infection
-diagnosis confirmed by presence of characteristic CXR patterns, and presence of offending organisms and
inflammatory cells in sputum
-damaged lung tissue from inhalational injury can become infected
-antibiotic prophylaxis only selects resistant organisms and does not reduce the incidence of pneumonia
,, # "! $ & + ,$ !+
-major cause of sepsis in burn patients in up to 5% of major burns
-associated with use of IVcatheters
#% ! # ' %# '
-should be suspected in patients with positive blood cultures and no other identifiable source of bacteremia
-systemic antibiotic therapy should be instituted and continued for at least 4 weeks
# #% 6!%
-the majority of patients with positive urine cultures do not require antimicrobial treatment
-candiduria in the absence of signs of systemic infection can be treated with bladder irrigations with amphotericin B
$ ' 6 $! #
-rare complications
-a conservative approach with drainage of the helix centrally, in an attempt to preserve the out cartilages, is usually
successful
!# & ! 6 6!%
-definitive treatment of the septic burn wound is the expeditious excision of the wound
119
Topical Antimicrobial Therapy:
-proved wide-spectrum antimicrobial activity:
-silver nitrate:
-associated with electrolyte imbalances and methemoglobinemia (unusual)
-mafenide acetate:
-able to penetrate eschar; only agent capable of suppressing dense bacterial proliferation
beneath eschar surface
-disadvantage is strong carbonic anhydrase inhibition interferes with renal buffering
mechanisms
-silver sulfadiazine: most common agent used
Spectrum of Antimicrobial Gram (-) - good Gram (-) - good Gram (-) - variable
Activity Gram (+) - good Gram (+) - good Gram (+) - good
Yeast - good Yeast - poor Yeast - good
Antibiotics:
-indiscriminate use of multiple agents promotes overgrowth of Candida species, enterococci, and multiple-
antibiotic-resistant organisms in the patient and in the burn center
-infection caused by an identified organism is treated by a single antibiotic
-altered pharmacokinetics of antibiotics in burn patients result in lowered serum drug levels when the usual
recommended dose is used inappropriate peak levels should prompt alterations in the dosage
120
!% %#
Wound Management:
-early surgical treatment indicated:
-massive deep tissue necrosis which will not clear up with standard resuscitation techniques, major
debridement and/or amputation may be necessary
-compartment syndrome
-otherwise definitive surgical procedures can be done between days 3 and 5, before bacterial contamination occurs
and after the tissue necrosis is delineated
$!& %#
Emergency Care:
-involved clothing should immediately be removed and the burns thoroughly flushed with copious amounts of water
-will limit severity of the burn
-neutralizing agents may cause burns themselves; they frequently generate heat while neutralizing the offending
agent
-chemical burns cause progressive damage until the chemicals are inactivated by reaction with the tissue, or diluted
by flushing with water
-chemical burns considered deep dermal or full-thickness, until proven otherwise
-phenol: can have severe systemic effects
-hydrofluoric acid: may cause death from hypocalcemia
121
)
# # !& ! 6
122
Feet: -ROM important
-elevate feet when not walking
Perineum:
-require hospitalization for 24-48h for observation of urinary obstruction secondary to edema
Complications:
-most complications in small burn injuries result from overtreatment:
-too-vigorous dressing changes that pull off newly formed epithelium, or the use of a variety of topical and
systemic antibiotics that can cause secondary infection or formation of a pseudomembrane
# # !& ! 6 '! # ! #-
-pharmacological modalities:
-hypnotics and analgesics: morphine, methadone, codeine, acetaminophen, NSAIDs
-anesthetic agents: ketamine, fentanyl
-antianxiety drugs, major tranquillizers and antidepressants
-non-pharmacological modalities:
-verbal and/or physical comfort
-relaxation therapy
!$#+ #
Inpatient Therapy:
-maintaining function and preventing the complications of prolonged immobility are the specific goals of the
rehabilitative treatment of burn patients
-position of maximal comfort promotes the formation of scar contractures
-edema is reduced by compression and elevation
-active and passive exercises implemented
-scar hypertrophy can be retarded by the use of custom-fitted pressure garments over healed scars
123
Outpatient Therapy:
-continuous follow-up of persisting functional deficits
-evaluation for corrective surgical procedures
-modification and evaluation of rehabilitation therapy
Psychological Support:
-anxiety, depression, denial, withdrawal, regression
-post-traumatic stress disorder:
-in nearly half of older children and adults suffering burn injury
-recurrent intrusive recollections, avoidance of circumstances that invoke memories of event, loss of
interest in daily activities, feelings of isolation, hyperalertness/vigilance, memory impairment, sleep
disturbances
-psychosocial support is critical for the burn patients for the duration of the course of treatment and follow-up
$ % + !&
Marjolin’s Ulcer:
-chronic ulceration leading to malignant degeneration
-squamous cell carcinoma is most common
-rare tumours: malignant fibrous histiocytoma, sarcoma, neurotropic malignant melanoma
-chronic breakdown of a healed burn wound scar should lead to suspicion of malignant degeneration
-~30% of burn scar carcinomas occur in the head and neck
-adjuvant radiotherapy improves survival
Heterotopic Ossification:
-occurs in up to 13% of burn patients; ossification of soft tissue
-most commonly involves patients with full-thickness burns greater than 20% TBSA, and is found adjacent to the
involved joint 1-3 months after injury
-elbow most commonly affected joint
-limited physical activity precedes radiographic evidence of calcification
Fractures:
-up to 10% of burn patients have associated fractures
-treated with splints and traction until resuscitation complete
124
!" # !
-acute: “normally proceed through an orderly and timely reparative process that results in sustained restoration of
anatomic and functional integrity”
-chronic: “wounds that have failed the above”
$% !
Primary Closure:
-approximates the acutely disrupted tissue with sutures, staples, or tape
Delayed Primary Closure:
-approximation of wound margins is delayed for several days after the wound has been created
-prevents infection in wounds in which there is significant bacterial contamination, foreign bodies,
or extensive tissue trauma
-during the time the wound is open, events occur that will significantly decrease the chances of
wound infection after closure
Secondary Wound Closure:
-margins of the open wound move together by the biologic process of contraction
& "' ( ) )
Epithelialization:
-keratinocytes migrate and then divide to resurface partial-thickness loss of skin or mucosa
Contraction:
-spontaneous closure of full-thickness skin wounds or constriction of tubular organs after injury
Connective tissue matrix deposition:
-fibroblasts are recruited and produce a new connective tissue matrix
' !
*+, #
-damaged vessels and lymphatic trigger a cascade of events:
-vasoconstriction; mast cell release of vasoactive compounds: bradykinin, serotonin, histamine;
diapedesis of cells into wound; hemostatic clot of platelets
-platelets release clotting factors to produce fibrin; also produce several essential cytokines which modulate
the subsequent wound healing events
*-, ! (( #
-migration of leukocytes into the wound
-24h: predominantly PMNs, then by macrophages
*., / %
-fibrous protein collagen is synthesized
-cross-linking of collagen provides strength and integrity
-increased synthesis within 10h of injury
-synthesis peaks after 5-7 days and then declines gradually
(4) Remodelling
-acute and chronic inflammatory cells diminish gradually, angiogenesis ceases, and fibroplasias ends
-equilibrium between collagen synthesis and collagen degradation is gradually restored
125
$# 0
Cytokine Source Functions
Platelet Derived Growth Platelets, macrophages, -chemotactic for PMNs, macrophages, fibroblasts, and SMCs
Factor (PDGF) including endothelial cells, keratinocytes, -activates PMNs, macrophages, and fibroblasts
isoforms AA, AB, and BB smooth muscle cells -mitogenic for fibroblasts, endothelial cells, and SMCs
-stimulates production of MMPs, fibronectin, and HA
-stmulates angiogenesis and wound contration
-remodelling
-inhibits platelet aggregation
-regulates integrin expression
Transforming Growth Platelets, T lymphocytes, -chemotactic for PMNs, macrophages, lymphocytes, fibroblasts, and SMC
Factor Beta (TGF-B) macrophages, endothelial cells, -stimulates TIMP synthesis, keratinocyte migration, angiogenesis, and
including isoforms b1, b2, keratinocytes, SMCs, fibroblasts fibroplasias
b3 -inhibits production of MMPs and keratinocyte proliferation
-regulates integrin expression and other cytokines
-induces TGF-B production
Epidermal Growth Factor Platelets, macrophages, saliva, -mitogenic for keratinocytes and fibroblasts
(EGF) urine, milk, plasma -stimulates keratinocyte migration and granulation tissue formation
Keratinocyte growth factor Fibroblasts -stimulates keratinocyte migration, proliferation, and differentiation
(KGF; aka FGF-7)
Insulin-like Growth Liver, macrophages, -stimulates synthesis of sulfated proteoglycans, collagen, keratinocyte
Factor-1 (IGF-1) fibroblasts,a nd others migration, and fibroblast proliferation
-endocrine effects similar to growth hormone
Connective tissue growth Endothelial cells, fibroblasts -chemotactic and mitogenic for various connective tissue cells
factor (CTGF)
Interleukins (IL-1 etc..) Macrophages, mast cells, -chemotactic for PMNs (IL-1) and fibroblasts (IL-4)
keratinocytes, lymphocytes, and -stimulates MMP-1 synthesis (IL-1)
many tissues -angiogenesis (IL-8)
-TIMP synthesis (IL-6)
-regulates other cytokines
126
PDGF: platelet derived growth factor
-initiates many wound healing events and stimulates production of several other cytokines
-chemotaxis for fibroblasts, neutrophils, macrophages, SMC
-stimulates production of fibronectin and hyaluronic acid
-may stimulate wound contraction
-collagen is the major component of the extracellular matrix of all soft tissues, tendons, ligaments, and bone
-matrix also contains glycosaminoglycancs, proteoglycans, fibronectin, laminin, elastin
Synthesis:
-transcription mRNA translation on RER proline hydroxylation glycosylation (galactose/glucose)
procollagen (soluble) secretion into extracellular matrix cross-linking (lysyl oxidase) and cleavage of
amino and carboxyl terminals (procollagen peptidase) collagen (insoluble)
-three polypeptide chains: glycine-proline-X
-hydroxyproline important for collagen stability; ascorbic acid and oxygen required for
hydroxylation process
Degradation:
-breakdown mediated by matrix metalloproteinases (MMPs)
-MMPs synthesized by variety of cells: inflammatory cells, fibroblasts, epithelial cells
-MMP-1, 8, and 13: initiate degradation of collagen by splitting molecule into specific 3/4 and 1/4
fragments (TCA and TCB fragments)
-after this initial split, other nonspecific proteases further degrade collagen
-MMPs are zymogens which are activated by other proteases such as plasmin
-MMPs inhibited by alpha-2-macroglobulins and tissue inhibitors of metalloproteinases (TIMPs)
Ground Substance:
-proteoglycans and glycosaminoglycans
-molecular “shock absorbers”, provide for moisture storage, and also sequester cytokines
# "#
Mechanism:
-myofibroblasts: peak during and after the process of wound contraction
-extracellular matrix also important in contraction process
127
-precise mechanism of contraction not fully understood
Clinical Approaches:
-for scar revision, must assess maturity of scar:
-mature scar: soft and pliable
-skin graft may be used to correct contracture
-FTSG contracts much less than STSG
-splinting of wound required
-immature scar: stiff, indurated, hypertrophic, tender
-still contains inflammatory cell components and myofibroblasts that contribute to
contracture
-use musculocutaneous flap to fix defect or wait until scar matures
% #' 2#
Mechanism:
-healing by migration and mitosis
-epithelial destruction scab for dermal protection
-migration of cells from margins of wound and from hair follicles and sebaceous glands
-cells flatten out and send cytoplasmic projections into surrounding tissue
-epithelial cells, secrete proteases and migrate as a sheet of cells
-fibronectin and vitronectin support migration
-move by actin-myosin contractile system
-mitosis begins when there are not enough cells for further migration
-factors involved:
-bFGF, PDFG, TGF-a and EGF stimulate keratinocyte migration and mitosis
-TGF-B inhibits epidermal cell proliferation but stimulates motility
##
(( %%
-only a small number of immunosuppressed patients actually manifest clinical wound healing problems
-chemotherapeutic anticancer drugs inhibit healing
-malignancies deplete nutrients and also inhibit wound healing directly
128
#" ! "#) & #/ (
Factors that Affect Healing in Surgical Practice Factors that Contribute to Wound Infection
Local Factors General Factors Surgeon
Surgical technique
Blood supply Age Devitalized tissue
Denervation Anemia Impaired local circulation
Hematoma Anti-inflammatory drugs Hematoma
Infection (local) Cytotoxic drugs Foreign body
Mechanical stress Hormones Organism
Protection (eg. Dressings) Infection (systemic) Infective nature
Surgical technique Jaundice Source: (a) Endogenous, eg. skin, biliary, colorectal
Suture material and technique Malignant disease (b) Exogenous (cross-infection)
Type of tissue Malnutrition Patient
Obesity Disease: eg. DM, neoplasia, malnutrition, anemia,
Temperature chronic granulomatous disease
Trauma, hypovolemia, hypoxia Medications: eg. steroids, cytotoxics, intensive antibiotic
Uremia therapy, radiotherapy
Vitamin deficiency Immune response of individual
Trace metal deficiency Remote active infection
3 &
# # # "#
Anatomy:
-inner mucosa layer for absorption
129
-outer muscularis mucosa layer for motility
-both wrapped by serosa layer
Layers:
-Epithelium: one-cell thick; regenerates q8days
-Laminia propria: collagen types I, III, and V and elastin
-Muscularis mucosa
-Submucosa
-Muscularis propria: densely packed SMC with types I and III collagen
-Serosa
Factitious Wounds:
-self-mutilation
130
Marjolin’s Ulcer:
-nonhealing wound in an area of previous trauma may represent squamous cell carcinoma
-normal immunologic surveillance decreased because of dense scar unable to destroy malignant
transformation within scar
3
-injury haematoma formation, edema, and pain
-migration of cells into and neovascularization into fracture site
-formation of soft callus: fibrocartilaginous splint of granulation tissue and cartilage
-endochondral ossification over 6-8 weeks by osteoblasts from periosteum and medullary canal
-remodelling over years
-rigid internal fixation: no soft callus formation direct bone to bone healing across injury without endochondral
ossification
-delayed union of nonunion (factors):
-site of fracture, presence and degree of soft-tissue injury, bone loss, inadequate reduction, inadequate
immobilization, infection, previous radiation, malignant growth at the fracture site, poor blood supply to
the fracture
-bone grafts:
-Osteogenesis: formation of new bone by cells that survive in the graft
-Osteoconduction: blood vessels and cells from the surrounding tissue grow into the bone graft scaffold
-osteoinduction: transformation of local, undifferentiated cells into bone-forming cells
#
-has little propensity to heal
-deep injury to articular cartilage that goes into subchondral bone produces exuberant inflammatory and healing
response fibrocartilage intermediate hyaline cartilage formed over time
' "
Pathophysiology:
-arise form physical and biochemical insults of extended duration
-prolonged inflammatory stage of wound repair extensive tissue damage and impaired healing by PMNs
-products released by PMNs continue to degrade extracellular matrix and prevent or impair the migration
of other reparative cells in to the wound
Pressure Ulcers:
-pressure and hear forces over bony prominences cell death in least vascularized tissues
-can be complicated with osteomyelitis
-Marjolin’s ulcers rarely occur in these chronic ulcers
131
-spinal cord injury patients at risk: do not have normal leukocyte response to injury below level of
enervation
-fecal and urinary incontinence maceration and skin breakdown
-antibiotics should not be used to treat these wounds unless they are causing systemic toxicity
Classification:
Stage I: Non blanchable erythema of intact skin, the heralding lesion of skin ulceration
Stage II: Partial-thickness skin loss involving epidermis and/or dermis
Stage III: Full-thickness skin loss involving damage or necrosis of subcutaneous tissue that may extend
down to, but not through, underlying fascia
Stage IV: Full-thickness skin loss with extensive destruction, tissue necrosis, or damage to muscle,
bone, or supporting strictions (eg. tendon, joint capsules, etc..)
Diabetic Ulcers:
-typically present as foot ulcers
-neuropathy is most important causative element
-tissue trauma and pressure are promoting factors
-lack of sensation results in increased mechanical stress, prevents timely detection of skin
punctures, or improper shoes, or the detection of foreign bodies in shoes
-angiopathy: capillaries are thicker and more permeable
-partial-thickness wounds require semiocclusive dressings to provide moist environment for epithelialization
-combining an absorbent dressing material with the polyurethane film or hydrocolloid alleviates the
problem of excess wound fluid
-occlusive/semiocclusive dressings may exacerbate infection when covering areas in which the bacterial count is
higher than 100,000/g of tissue.
-dressings are used to deride:
-exposed tendon: slower more gentle process needed use hydrogens to keep wound moist
-eschar use hydrocolloid; debridement through autolysis
132
&
-tissue reactivity to particular sutures and its significance in the healing process has never been validated
-woven suture material should not be used in the closure of contaminated wounds
-more likely to facilitate infection than a smooth suture
-staples must be removed within a few days if permanent skin marks are to be avoided
-tape strips may be used to substitute dermal sutures as long as wound edges are well approximated
133
-orthotopic transplantation: graft placed into its normal anatomic location (eg. heart transplant)
-heterotopic transplantation: graft placed in a different site (eg. kidney transplant)
-syngeneic: transplantation b/n individuals of identical genetic strain
-allogeneic: transplantation b/n genetically different members of same species
-xenogeneic: transplantation b/n different species
-autotransplant: one site to different site within same individual
! "#
-epitope: molecular unit of specific immune recognition (carbohydrate/peptide moiety)
-antigen: epitope containing molecules that can be bound by T-cell receptors or antibodies of B-cells
-may contain several epitopes
-major histocompatibility complex (MHC):
-cluster of genes on chromosome 6
-known as human leukocyte antigen (HLA)
-polymorphic gene: differ in detail while conforming to the same basic structure
$ $ % &!!' #
Cellular Immunity:
-TCR recognizes processed peptide antigens bound to MHC molecules
-parenchymal cells express class I MHC molecules
-display peptides from within (eg. viral replication)
-bind to T-cells /w CD8 molecule
-hematopoeitic cells express class II MHC molecules
-display peptides that have been phagocytized from surrounding extracellular spaces
-bind to T-cells /w CD4 molecules
-CD4+ T-cells are first alerted of an invasion of the body by antigen presenting cells (APCs) and activate CD8+ T-
cells to search the body for cells that have been infected by this invader
Humoral Immunity:
-B cells bind soluble antigens and secrete soluble forms (Abs) to bind these foreign molecules
-material bound by Ab is opsonized for destruction by cells of the innate system of immunity
-ie. macrophages, monocytes, PMNs
-activate complement system membrane destroyer
134
( ) '( ' * ( ( & "
-antigens responsible for human allografts rejection are encoded by HLA region of chromosome 6
-class I molecules (HLA-A, B, and C)
-class II molecules (HLA-DR, DP, and DQ)
-other genes encoded by HLA:
-TNF-alpha and beta
-components of complement cascade (class III molecules)
-heat-shock protein (HSP-70)
-peptide transporter proteins TAP 1 and TAP 2; proteosome proteases LMP 2 and LMP 7
-other polymorphic transplant antigens: ABO blood group
-Class I molecule:
-single polymorphic gene + nonpolymorphic protein B2-migcroglobulin (from chr 15)
-30-50 alleles per locus
-structure:
-expressed as single MHC-encoded, transmembrane alpha chain (/w 3 domains alpha 1, 2 and 3),
in combination /w B2M
-binding via groove made by alpha 1 and alpha 2 domains
-binds peptides synthesized in the endoplasmic reticulum
-found on all nucleated cells except neurons
-Class II molecule:
-two chains: alpha and beta
-differ by alleles represented at each locus and in number of loci present in HLA class II region
-structure:
-formed by two MHC-encoded chains (alpha and beta) each /w two domains
-binding site via alpha 1 and beta 1 domains
-binds peptides derived from endocytosed proteins
-found primarily on cells of the innate immune system (phagocytes, macrophages, monocytes)
-can be upregulated to appear on other parenchyma cells by cytokines
135
-matching donors and recipients /w regard to HLA type has been shown to improve outcome after kidney, heart, and
pancreas transplantation
-no such correlation for liver transplantation
-matching may reduce overall survival:
-HLA compatibility potentiates the inflammation during viral reinfection after
transplantation for viral hepatitis and increases the chances for clinical recurrence of the
original disease
T-Cell Receptor:
-T-cells formed in fetal liver and bone marrow
-migrate to thymus during 1st trimester
-at thymus, a series of DNA rearrangement and recombination occurs (V, J, D and C regions)
-individual cells recombine to express a single TCR /w a single specificity
-results in population of T-cells capable of binding 109 different specificities: essentially all
combinations of MHC and peptide
-now also able to express CD4 and CD8
-after recombination, thymic selection occurs to avoid “self-destruction”
-cells initially interact /w MHC-expressing cortical thymic epithelium
-first positive selection occurs: if no binding cells are useless (unable to function in
periphery) apoptosis occurs
-then negative selection: surviving cells move to thymic medulla
-lose either CD4 or CD8
-if binding to self-MHC occurs apoptosis results
-only cells released into periphery are those that can bind self MHC /wout activation
Antibody:
-maturation occurs in the bone marrow
-two light-chain loci (kappa and lambda) each /w V, D, J, and C regions
-types: IgM, IgG, IgA, IgE, or IgD; defined by heavy chain usage
-Fc portion: binds cells of the innate system
136
-in IgM and certain classes of IgG can activate complement
-isotype switching: alteration of heavy-chain gene usage from IgM to either:
-IgG: significant soluble mediator of opsonization
-IgA: mucosa immune responses
-IgE: mast-cell mediated immunity
-IgD: primary cell-bound Ab
-affinity maturation:
-D and J regions undergo random additions resulting in clones that have altered antigen affinity
-those /w increased affinity are retained for future encounters; will have a more vigorous response
T-Cell Activation:
-initial binding to APC or endothelial cell is non-specific and mediated by adhesion molecules (eg. ICAM-
1, VCAM-1, LFA-1)
-MHC recognition:
-single interaction of TCR /w an MHC is not sufficient for activation
-~8000 TCR ligand interactions /w same antigen must be reached
-initiation of a series of intracytoplasmic protein tyrosine kinases (PTK)
activation of phosphokinase C-gamma hydrolysis of PIP2 IP3 + DAG
-IP3 binds to ER release of Ca++ induces calmodulin to bind to and activate
calcineurin initiate transcription of IL2
-IL2 autocrine activation of T-cell potentiates DAG activation of protein
kinase C (PKC) gene regulatory steps in cell cycle
-also requires second confirmatory signal by binding CD28 (on T-cell) /w B7 molecules (on
APC) potentiates the TCR-initiated tyrosine phosphorylation
-reduces the number of binding events of TCR-MHC from 8000 to 1500
T-Cell Amplification:
-cytokines (particularly IL-2 and IFN-gamma) recruit other T-cells
-T-cells develop one of two phenotypes:
-Th1 cells:
-mediate cytotoxic responses (eg. delayed-type hypersensitivity)
-express IL-2, -12, -15, and IFN-gamma
-Th2 cells:
-support the development of humoral or eosinophilic responses
-express IL-4, -5, -10, and -13
-immunosuppression produces artificial patterns of gene expression, resulting in nonphysiologic patterns of
cytokine secretion
-in the late phases of rejection, the inflammatory response recruits cells /w nonspecific cytotoxic activity to
the organ
-IL-8, released by activated macrophages and T cells, also recruits PMNs to the scene to remove necrotic
tissue
T-Cell-Mediated Cytotoxicity:
-amplification generally performed by CD4+ T-cells: best suited to interact /w class II expressing APCs
-cytotoxicity best mediated by CD8+ T-cells
-in the artificial situation of transplantation, both CD4+ and CD8+ mediate cytotoxicity
-Ca++ mediated exocytosis of cytolytic granules: contain perforin and serine proteases called
granzymes
-T-cells can also induce apoptosis
-after activation, non-MHC-restricted, T-cell-mediated cytotoxicity occurs other T-cells /wout the
specific TCR can participate in cytotoxicity
137
-T-cells expressing the gamma-delta TCR are prominent effector of non-MHC-restricted cytotoxicity
-this is induced by high levels of IL-2
Antibody-Mediated Cytotoxicity:
-Ab serves as anchoring site for complement C1q:
-Classical Complement Activation Cascade:
-two Fc bind C1q and activate it C3 activation formation of membrane attack
complex (MAC) of polymerized C5, 6, 7, 8, and 9
-results in disruption of cell membrane and cell lysis
-several byproducts of C3 cleavage serve as chemoattractant to phagocytic cells and as
opsonins potentiating antigen phagocytosis
-Ab can act as opsonin
-phagocytic cells have receptors for Fc portion of IgG Ab-dependent cellular cytotoxicity
-Ab binding to endothelium complement activation on endothelial cell cellular retraction and exposure
of underlying matrix potentiates platelet activation and aggregation
microvascular thrombosis, a hallmark of the tow Ab-mediated graft rejections: hyperacute
rejection and acute vascular rejection
( ,( # ) !
Acute Rejection:
-caused primarily by T-cells
-evolves over days to weeks; most common in the first 6 months
-T-cells bind antigen via TCR (either directly or after phagocytosis of donor tissue and re-
138
presentation of MHC peptides by self APC) cell activation
-results in massive infiltration of graft of T-cells, /w destruction of the organ
-incidence of acute rejection declines /w decreasing MHC disparity, but any mismatch can cause T-cell
mediated destruction. Therefore T-cell specific immunosuppression required
-treatment leads to graft restoration in 90-95% of cases
-monitoring for acute rejection mus be intense, particularly during the first year after transplantation
-unexplained graft dysfunction should prompt biopsy and evaluation for lymphocytic infiltration
and graft parenchyma necrosis characteristic of acute rejection
Chronic Rejection:
-poorly understood
-insidious onset: months to years
-pathophysiology undefined, untreatable
-heightened immunosuppression not effective in reversing or retarding progression
-characterized by parenchymal replacement by fibrous tissue /w a relatively sparse lymphocytic infiltrate
-direct cell-mediated tissue destruction is not a primary mechanism
-requires re-transplantation
!!' '
-the event occurring at the time of transplantation are the most critical in establishing the state of immune
unresponsiveness necessary for long-term graft survival
-immunosuppression is extremely intense in the early post-op period and subsequently tapers
-induction immunosuppression: usually involves deletion of T-cell response completely and
cannot be maintained indefinitely /wout lethal consequences
-maintenance immunosuppression: well tolerated if dosed appropriately
-rescue agents: immunosuppressant used to reverse an acute rejection episode (same as agents
used for induction)
Corticosteroids:
-used in conjunction /w other agents, improves graft survival
-can contribute significantly to the morbidity of transplantation
-anti-inflammatory agent
-bind to an intracellular receptor after nonspecific uptake into the cytoplasm
-prevents the function of NF-KB, a key activator of proinflammatory cytokines
-prevents the primary mechanism by which lymphocytes amplify their responsiveness
-block transcription of IL-1 and TNF-alpha and IFN-gamma production, PMN migration, and
lysosomal enzyme release by PMNs
-inhibits PLA2 and arachidonic acid cascade
-mutes upregulation of MHC
-do not have a significant influence on Ab production
-most commonly used is prednisone or methylprednisolone
-effects of steroids:
-suppressed HPA axis
-need coverage /w steroid preparation in the amount equal to their endogenous adrenal
capacity; should not exceed 50 mg hydrocortisone q8h
-impaired glucose tolerance
-delayed wound healing
-salt and fluid retention
-hypertension
-CNS effects (insomnia, depression, nervousness, euphoria)
-chronic effects:
-Cushing’s syndrome, cataracts, muscle wasting, and growth retardation n prepubertal
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children
-peptic ulcers
-osteoporosis (inhibition of bone matrix formation and intestinal absorption of calcium)
-HLA-identical donors: no need for steroids
-pts who have survived a year /wout a rejection episode can be considered for /wdrawal from steroids
Antiproliferative Agents:
Azathioprine:
-hepatic conversion azathioprine 6-mercaptopurine (6-MP) 6-thio-inosine monophosphate (6tIMP)
-inhibits DNA synthesis by alkylating DNA precursors and inducing chromosomal breaks through
interference /w DNA repair mechanisms
-inhibit conversion of IMP to AMP and GMP
-effects are nonspecific
-effectively inhibits rejection as a maintenance agent but, has no value as a rescue or induction agent
-1-3 mg/kg/day
-toxicity: bone marrow, gut mucosa, liver
-decrease dose as total WBC or leukopenia (< 0.3)
-hold in the presence of infection
-hepatotoxin: rarely used in liver transplantation
Calcineurin Inhibitors:
Cyclosporine:
-mainstay immunosuppressant in most maintenance regimens
-mechanism of action:
-binds to cytoplasmic cyclophilin (cis-trans peptidyl-prolyl isomerases critical for protein folding)
-does not effect immunosuppression but is related to toxic side effects
-cyclosporin-cyclophilin complex binds to calcineurin-calmodulin complex
-prevents Ca++-dependent phosphorylation and activation of transcription-regulating
factor NF-AT
-prevents transcription of IL-2 and other genes critical for T-cell activation
-reversible inhibition of T-cell-mediated immune responses, but does not prevent antigen recognition by T
cells. Effects can be overcome /w exogenous IL-2
-ineffective as rescue agent b/c effects are abolished in the presence of IL-2
-metabolised by cytochrome P-450 of liver:
-concentrations increased by inhibitors (eg. ketoconazole, erythromycin, CCBs)
-concentrations decreased by inducers (eg. rifampin, phenobarbital, phenytoin)
-side effects:
140
-renal:
-causes dose-related nephrotoxiciy d/t vasoconstrictors effect on proximal renal arterioles
-idiosyncratic reaction producing hemolytic uremic syndrome
-hyperkalemia
-hypertension
-neurologic:
-tremors, paresthesia, headache, depression, confusion, somnolence, seizures
-hypertrichosis
-gingival hyperplasia
-hepatotoxicity: increased LFTs
Tacrolimus (FK506):
-macrolide produced by Streptomyces tsukubaenis
-blocks NF-AT arrests T-cell activation
-intracellular target is an immunophilin distinct from cyclophilin
-100x more potent in blocking IL-2 and IFN-gamma production than cyclosporine
-mainly maintenance agent; has shown promise as rescue agent
-side effects:
-similar to cyclosporine wrt renal and hepatic toxicity
-tremors and mental status changes
-diabetogenic effect
-effective in liver transplants (drug of choice)
Antilymphocyte Preparations:
OKT3:
-murine monoclonal Ab to the signal transduction subunit on human T cells (CD3)
-mechanism of action:
-binds to CD3 and prevents signal transduction of T-cell receptor antigen binding event and
arrests amplification of a rejection episode
-downregulates TCR complex “blind” T-cell
-blocks cytotoxic activity of already activated T cells through inappropriate activation and
degranulation
-dose 5 mg/day for 10-14 days
-pre-treat /w methylprednisolone to prevent adverse reactions
-monitor /w flow cytometry to measure percentage of CD3+ cells
-good rescue agent (better than steroids) but limited to steroid-resistant rejection b/c of side effects
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Rapamycin:
-macrolide antibiotic derived from Streptomyces hygroscopicus
-similar to tacrolimus; have been shown to antagonize each other
-interacts /w FK-BP but does not affect calcineurin activity
-does not inhibit expression of NF-AT or IL-2, but impairs signal transduction by the IL-2
receptor
-prevents T-cells from entering the S phase of cell replication
-advantage: interrupts T-cell activation even if IL-2 is present from an exogenous source or ongoing
rejection
-hypertriglyceridemia may be a significant side effect
Deoxyspergualin:
-isolated form Bacillus laterosporus
-has the strongest antiproliferative properties via anti-monocyte-anti-macrophage effect
-prevents the nuclear translocation of NF-KB
-inhibit antigen presentation or the costimulatory function of APCs
-effective in prolonging allografts survival in animal models of renal, pancreas, liver, and heart transplant
-side effects:
-GI disturbances
-headache, fatigue, perioral numbness, decreased white blood cell and platelet counts and
hematocrit
-synergistic /w cyclosporine
Brequinar:
-selectively inhibits T- and B-cell proliferation
-inhibits enzyme dihydro-rotate dehydrogenase interferes /w pyrimidine synthesis
-inhibits lymphocyte DNA synthesis and interrupts rejection process at level of clonal expansion
-synergistic /w cyclosporine
-side effects: leukopenia
Anti-IL-2 Strategies:
-high-affinity IL-2 receptor is dependent on up-regulation of 55-kD subunit Tac
-induction /w anti-Tac Abs has prevented and reduced frequency of early rejection when used in
combination /w cyclosporine
-synergistic /w cyclosporine, may reduce the dose of cyclosporine
-other Abs: 33B3.1, BT563
Costimulation Blockade:
-interruption of the CD28 pathway of costimulation may selectively energize only those cells undergoing
binding to the allografts, leaving non-reactive cells unaffected
-agents under investigation include Abs directed against B7-1 and B7-2, CD28, CD40, gp39, and fusion
protein, CTLA4-Ig
Concordant Xenografts:
-derived form closely related species, such as Old world monkeys and apes
-most of the critical molecular elements responsible for antigen presentation and T-cell-mediated rejection
are revolutionarily conserved in mammals
-feasible /w available immunosuppressive pharmaceutical agents
-widespread application of concordant xenografts would quickly deplete the supply of nonhuman primates
-concern that zoonotic transfer of disease would put the pt and the public at undue risk
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Discordant Xenografts:
-rapid HAR, generally from IgM Abs directed against atypical carbohydrate residues
-intervention at all levels of innate and acquired immunity will be required for successful engraftment
-transgenic alteration of pigs to express human proteins is the key for future clinical applications of
discordant xenografts
. .
-Vascular grafts
-used as autografts
-replacement of damaged or atherosclerotic arteries
-vein grafts (eg. saphenous) are optimal conduits for CABG
-autografting of arteries used occasionally for arterial replacement of diseased renal artery (hypogastric
artery)
-allogenic arterial conduits are the ideal replacement material for transplant renal artery stenosis
-Nerve grafts
-serves as a route along which the pt’s own nerve can regenerate
-prevention or amelioration of systemic complications may be possible by achieving more precise glucose control
-most successful approach to restoring normal long-term glucose homeostasis in Type I diabetes is whole-organ
pancreas transplantation
Historical Background:
-using a whole pancreaticoduodenal allografts /w anastomosis of the duodenal segment to the bladder is the safest
and most popular method of handling exocrine secretions
Indications:
-Type I insulin-dependent diabetics younger than 45 years
-no significant CAD
-no major amputations or severe visual impairment
-contraindications: untreated malignancy, active infection, HIV seropositivity
-three circumstances:
-pancreas transplantation alone (PTA) - in the non-uremic pt /w normal kidney
-pancreas transplantation after successful kidney allografting (PAK)
-offered to young diabetics /w tow ore more end-organ complications, who have undergone prior
living-related or cadaveric renal transplantation
-simultaneous pancreas-kidney transplant (SPK) - in uremic pt
-~90% are SPK
Operative Procedure:
-most widely used duct management technique of pancreas transplantation is bladder drainage, in which a
duodenal segment is anastomosed side-to-side to the dome of the bladder
-advantages of bladder drainage:
-urinary amylase determinations as screening test for rejection
-avoidance of enteric anastomosis and spillage of bowel contents
-reduced potential for peripancreatic infections
-advantages of enteric drainage:
-avoidance of post-operative urologic complications
-avoidance of chronic dehydration and need for bicarbonate replacement
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-early removal of foley
-technique:
-vascular reconstruction of pancreatic blood supply is performed /w donor iliac artery “Y” graft to
donor splenic artery and superior mesenteric artery
-duodenum segment is shortened to approximately 10-12 cm
-spleen removed by ligating splenic artery and vein
-intraabdominal placement of graft
-pancreas usually is placed into the right iliac fossa, and the kidney, if transplanted
simultaneously, is implanted on the left side
-venous anastomosis performed: portal vein of graft to distal inferior vena cava or iliac
vein
-arterial anastomosis: iliac “Y” graft /w recipient iliac artery
-bladder drainage side-to-side anastomosis of duodenal segment to dome of bladder
-enteric drainage side-to-side anastomosis to ileum
-generous IV doses of mannitol and albumin administered to limit reperfusion injury and tissue
edema
-irrigation /w antibiotic solution, including amphotericin B, miconazole, and cephalothin, to
minimize risk of peripancreatic infection, abscesses, and mycotic aneurysm
Postoperative Management:
-quadruple drug regimen: ATGAM or OKT3, MMF, cyclosporine or tacrolimus, and steroids
-antibiotic therapy for 10-14 days post-op
-acute rejection in 70-80% of pts, usually in the first year
-rescue: high-dose steroids x 2 days; if no response, OKT3 or ATGAM
-/w early treatment, 90% reversible
-lymphocytic infiltrates initially involve exocrine portion of gland; islet cells removed later
-monitor exocrine secretions of amylase in urine; a consistent drop > 25% strongly suggests possibility of
rejection, but it is not a reliable indicator of rejection
-obtain biopsies (gold standard) b/c only 55% of hypoamylasuria have biopsy evidence of rejection
-diagnosis of rejection after SPK transplantation relies almost entirely on serum creatinine and renal biopsy since
rejection of pancreas graft alone is unusual
Complications:
-urologic complications most common
-hematuria:
-early: usually mild and self-limiting
-late: d/t suture granulosa, urinary tract infection, or ulceration of duodenal segment
-if persists despite appropriate therapy, conversion to enteric drainage indicated
-postoperative urinary leak:
-three sites: urethral implantation site, duodenocystostomy anastomosis, duodenal segment
-early: usually located in bladder-duodenum suture line
-late (> 4 weeks): lateral duodenal staple lines or as the result of an ulcer /win duodenal segment
-significantly elevated serum amylase and development of pancreatic ascites discernible on CT
scan are highly suggestive
-diagnosis /w voiding cystourethrogram (VCUG)
-tx: Foley catheter bladder decompression for 2-3 weeks
-may require re-exploration and conversion to enteric drainage
-urinary tract infections:
-d/t alkalinization of urine secondary to bicarbonate and exocrine secretions, presence of a
diabetic neurogenic bladder /w incomplete emptying, mucosa injury at the bladder anastomosis,
and prolonged catheter drainage
-persistent urethritis:
-digestive action of pancreatic enzymes on urothelium
-treat /w Foley drainage for several weeks; may require conversion to enteric drainage
144
-early postoperative hyperamylasemia:
-may cause ARDS from preservation-induced pancreatitis
-late graft pancreatitis:
-sudden-onset lower abdo pain; elevation of serum amylase; absence of leak; evidence on
CT scan of gland edema and retroperitoneal inflammation and peripancreatic
inflammation, /wout evidence of abscess or fluid collections; resolution of symptoms
/win 24h of Foley catheter drainage
-metabolic acidosis:
-result of excessive urinary loss of bicarbonate-containing exocrine fluids
-tx /w oral replacements and fluids
-peripancreatic fluid collections:
-drained if suspicion of infection
-exocrine secretions of the pancreas transplant must be converted from bladder drainage to enteric drainage in 10-
25% of pancreas transplant recipients
-common indications are persistent hematuria and urinary leaks from the duodenal segment
Results:
-two most significant factors affecting graft survival are the circumstances in which the pancreas transplant occurs
and the duct management technique used
-good pancreatic graft survival: > 75% 1-year graft survival
Potential Candidates:
-pts /w short-bowel syndrome
-Crohn’s disease, mesenteric thrombosis, trauma (adults)
-Necrotizing enterocolitis, intestinal pseudoobstruction, gastroschisis, volvulus, intestinal atresia (children)
Operative Procedures:
-three methods:
-pts w/o liver failure isolated intestinal grafting
-/w liver failure combined liver intestine transplant
-multivisceral procedure
Donor Issues:
-most clinicians consider an identical ABO blood type mandatory b/c of previously reported hemolytic reactions
-a limiting factor is the required size match between donor and recipient (for children)
145
Preservation:
-University of Wisconsin solution used for preservation
-intestines more sensitive to ischemia and reperfusion injury
-good results for up to 16h cold ischemic time
-it is recommended that the intestine be transplanted /win 12h of retrieval
Immunology:
-problems /w graft-versus-host disease (GVHD) and host-versus-graft disease (rejection)
-reducing the number of lymphocytes by using shorter segments, irradiation, or poly/monoclonal Abs affects the
severity of GVHD and possibly reduces its incidence
-cyclosporine or tacrolimus has been used
-prednisone and azathioprine insufficient; tacrolimus significantly improved the out come after intestinal
transplantation
Diagnosis of rejection:
-symptoms: fever, abdo pain, elevated WBC, ileus, increased stomal output, gastrointestinal bleeding, positive
blood cultures
-intestinal biopsies: cryptitis, shortening of villi, mononuclear infiltrate, mucosal sloughing
-immunopathology: increased class II or IL-2 receptor expression
-Loss of mucosal integrity: measures of intestine permeability: 99mTc-DTPA po and urinary excretion measured
value greater than 5% indicates increased permability and possibly an acute rejection
Results:
-1-year graft survival: 65%
-3-year graft survival: 29%
Indications:
-indicated for treatment of irreversible liver failure from acute or fulminant disease or chronic liver disease
-fulminant disease: cause usually unknown, but may be secondary to viral hepatitis, Wilson’s disease, hepatotoxins,
or alcoholic hepatitis
-posthepatitic cirrhosis resulting from hepatitis B or C is associated /w the risk of recurrence of viral hepatitis and
cirrhosis in the transplanted liver.
-strategies to prevent recurrence of hep B: hep B hyperimmune globulin, interferon, lamivudine
-tranplant for PBC associated /w high success rate; primary dz may recur and is difficult to distinguish from chronic
rejection
-PSC should be treated before cholangiocarincoma develops
-alcoholic liver disease account for 75% of liver failure; a period of abstinence and evidence of family and social
support are required before the candidate can be eligible for transplantation
-tranplantation for cancer is controversial; immunosuppression usually favors the reemergence of underlying
malignancies
Preoperative Evaluation:
-signs and symptoms of liver failure
-pts /w stage IV coma must be managed aggressively to prevent cerebral edema or hemorrhage
-increased INR and thrombocytopenia: bleeding should be treated /w FFP and platelets
-GIB related to underlying portal hypertension constitutes an indication for liver transplantation
-ascites: diuretics and paracentesis
-hepatorenal failure, is reversible after liver transplantation; search for any underlying cause of renal dysfunction
-pts /w liver failure are immunocompromised; SBP can be treated /w antibiotics
-patient /w advanced cirrhosis often have a substantial loss of their non-parenchymal liver mass and
reticuloendothelial system, rendering them highly susceptible to sepsis, particularly by translocation across
146
the gut
-hyperdynamic state: elevated CO and low systemic vascular resistance; pulmonary hypertension may develop
risk for cardiac-related intraoperative death
Contraindications:
-multisystem organ failure
-sepsis outside the liver, although pts /w a septic focus /win the liver may appropriately be treated /w liver
transplantation
-noncompliance /w medical therapy (eg. Active alcohol or drug abuse)
-severe cardiac or pulmonary disease
-disseminated cancer
Immunologic Considerations:
-graft failure more frequently due to primary nonfunction, recurrence of original disease, or biliary and vascular
complications; usually not d/t immunologic rejection
-rejection episodes common during first 3 months posttransplant
-ABO blood groups compatibility is required, but this is not absolute; ABO-incompatible liver transplants have been
performed successfully
-ABO compatible but non-identical liver (eg. blood type O donor to type A recipient) may be associated /w a self-
limited graft-versus-host reaction, leading to haemolysis of recipient RBCs
-HLA matching is not a consideration in liver transplantation b/c the shorter preservation times required make it a
practical impossibility
Postoperative Management:
-avoidance of vasoconstrictive inotropic agents, such as epinephrine, norepinephrine, phenylephrine, or high-dose
dopamine will reduce blood flow to the liver
-prostaglandin E1 infusions may be useful for increasing renal and hepatic perfusion in the immediate postoperative
period
-diuretics in the first 24-48 h to help mobilize fluids sequestered as a result of cirrhosis
-maintenance immunosuppression: cyclosporine or tacrolimus
147
-tapering steroids also used
-induction /w ALG or OKT3 is optional; may be useful in pts recovering form hepatorenal failure allows a delay
in starting nephrotoxic agents such as cyclosporine or tacrolimus
-elevations in LFTs prompt percutaneous liver biopsy
-rejection typically responds to bolus steroid therapy; steroid-resistant rejection treated /w ALG or OKT3
Complications:
-primary nonfunction: high INR, low fibrinogen level, high ammonia level in first several days posttransplant
-pts develop hepatic encephalopathy progressing to coma
-urgent transplant required
-portal vein thrombosis:
-rare complication
-marked rise in serum ammonia level or variceal bleeding
-diagnosed by Doppler ultrasonography
-required thrombectomy, restoration of portal flow, and evaluation of the cause of thrombosis
-hepatic artery thrombosis:
-5% in adults; higher incidence in pediatric liver transplantation
-early: d/t technical problems; late: immunologic injury of hepatic arterial tree
-results in ischemic changes of bile ducts leading to plugging and obstruction biloba formation liver
abscess and sepsis
-mx: retransplant or observation
-bilomas can be drained percutaneously, and strictures of the common bile duct can be treated /w
resection and Roux-en-Y drainage
-bile leaks:
-must be treated immediately may lead to peritonitis, sepsis and graft loss
-tx /w operative intervention or by ERCP /w papillotomy and temporary stenting of the CBD
-recurrence of original disease: PBC, Hep B and C
-hepatoma or cholangiocarcinoma recurring in a transplanted liver contraindicates retransplantation
-posttransplant lymphoproliferative disorder (PTLD)
Results:
-certain indications, such as PBC in adults and biliary atresia in children, are associated /w higher-than-average
success rates
Recipient Selection:
-long waiting lists; ~15-20% mortality rate among pt on the waiting list
Indications:
148
General Indications Warranting Consideration for Adult Cardiac
Transplantation
Severe cardiac disability despite maximal medical therapy
-History of recurrent hospitalization for CHF
-New York Heart Association functional class III or IV
-Peak metabolic oxygen consumption <15 mL/kg/min
Symptomatic cardiac ischemic refractory to conventional treatment
-Unstable angina not amenable to coronary artery bypass grafting or PTCA /w left
ventricular ejection fraction < 30%
-Recurrent symptomatic ventricular arrhythmias
Exclusion of all surgical alternatives to cardiac transplantation
-Revascularization for significant reversible ischemic
-Valve replacement for critical aortic valve disease
-Valve replacement or repair for severe mitral regurgitation
-most cardiac transplant recipients suffer from end-stage, inoperable coronary artery disease (38%) or
idiopathic cardiomyopathy (40%)
-other diagnoses: defined cardiomyopathy (eg. viral, postpartum, familial), congenital anomalies, and
valvular disease
-peak oxygen consumption, a function of peak cardiac output and peripheral oxygen extraction, correlates
well /w functional class and is an independent predictor of outcome in heart failure pts
-if < 15 mL/kg/min (< 50% normal), then 1 -year mortality rate exceeds 50%; these pts would
benefit from transplantation
Contraindications:
-advanced age, irreversible hepatic, renal, or pulmonary dysfunction, active or extrapulmonary infection,
severe peripheral or cerebral vascular disease, unresolved malignancy, severe, pulmonary hypertension,
psychiatric illness or history of medial noncompliance, drug or alcohol abuse, current tobacco use, and
cachexia or morbid obesity
-studies demonstrated that older pts (>60years):
- more likely to die of late infectious complications or malignant disease after transplantation
-higher risk for developing steroid-induced diabetes and clinically significant osteoporosis
-severe COPD: FEV1 < 1L or 50% or predicted
-chronic infective agents (eg. hep Ba nd C, HIV) preclude transplant
-previous malignancies < 5 years of cure (except SCC of skin)
-severe fixed pulmonary hypertension: increased incidence of posttransplant RV failure
-higher mortality rates /w transpulmonary pressure gradient > 15 mmHg
-these pts should be considered for combined heart-lung transplantation
Medical Management:
-goal: relieve debilitating symptoms; preserve organ function and optimize pt’s condition for
transplantation
-usually treated /w digoxin, diuretics, vasodilators, and ACEi +/- anticoagulants
-amiodarone has improved survival in pts /w end-stage heart failure /wout increasing perioperative risk
149
Mechanical Support:
-intraaortic balloon pump (IABP)
-improves coronary perfusion and reduces afterload and mitral regurgitation
-cannot be used for extended periods of time
-ventricular assist system (VAS)
-intermediate ro long-term circulatory support for pts in severe ventricular failure
-considered when:
- CI < 2.0 L/min/m2 BSA
-ventricular filling pressure > 20 mmHg
-u/o < 20 cc/h
-systemic vascular resistance is > 2100 dynes sec/cm-5
-reduced mortality rates in those awaiting cardiac transplantation
Criteria:
-irreversible brain death
-tests: ECG, ABG, echo, serologic screening (eg. HIV, hepatitis, HBsAg, hep C Ab, HSV, CMV,
toxoplasma), pancultures
-normal cardiac function and absence of significant cardiac history and significant coronary atherosclerosis
-absolute contraindications:
-severe coronary or structural disease, prolonged cardiac arrest, prior MI, CO-Hb > 20%, SaO2 <
80%, metastatic malignancy, HIV+
Management:
-maintenance of hemodynamic stability
-IV fluids to maintain CVP b/n 5-12 mmHg
-DI is common and requires IV vasopressin (0.8-1.0 U/h)
-dopamine, alpha agonists may be used judiciously
-blood tranfusion sparingly to maintain Hb ~ 10g/dl
-avoid hypothermia
Donor-Recipient Matching:
-parameters include ABO compatibility and body size
-ABO mismatch hyperacute rejection
-size matching and graft ischemic time particularly important for recipients /w elevated pulmonary vascular
resistance
-grafts from donors whose weight is < 80% of that of recipient or /w ischemic times longer than 2 h are avoided
-no upper donor size limit in adults
-recipient is screened for preformed Abs against a standardized panel of random donors
Operative Procedures:
Procurement:
-median sternotomy pericardial well created
-heart inspected and palpated for contusions, perforations, thrills, and CAD
-intravenous heparin administered at a dose of 300 u/kg and allowed to circulate for 3-5 min
-ligation and division of vessels
-hyperkalemic cardioplegic solution at 2-4oC rapidly infused into aortic root @ 150 mmHg arrest in
diastole
-cold saline at 4oC poured onto heart and into pericardial well
-remainder of pulmonary vessels divided
-heart removed and placed in cold saline medium
150
Orthotopic Transplantation:
-pt prep: CV access via (L) IJ vein; sparing right for future endomyocardial biopsies
-median sternotomy; routine cannulation of aorta and vena cavae
-see Fig 10-23
Heterotopic Transplantation:
-operative technique bypasses the left heart and involves anastomoses between the left atria, aorta,
pulmonary arteries, and donor superior vena cava to recipient right atrium
-indications:
-irreversible severe pulmonary hypertension
-diminished donor heart function anticipated b/c of size mismatch or prolonged ischemic time
Postoperative Management:
Graft Physiology:
-de-nervated heart (from sympathetic and parasympathetic plexus) is isolated from normal autonomic
regulatory mechanisms
-resting HR higher b/c of absence of vagal tone, sinus arrhythmia and carotid reflex bradycardia
-increased sensitivity to catecholamines increased B-adrenergic receptor density and loss of
norepinephrine uptake in postganglionic sympathetic neurons
-cardiac output at low end of normal range
-delayed increase in heart rate
Immunosuppression:
-“triple drug” combination: cyclosporine, azathioprine, glucocorticoid
-high dose, then taper
-cyclosporine:
-inhibits T lymphocyte activation (blocking release of IL-2 from helper T cells)
-trough serum concentration of 150-250 ng/ml x first few weeks 50-150 ng/ml
-side effects: nephrotoxicity, hypertension, hepatotoxicity, hirsutism, increased incidence of
lymphoma
-azathioprine:
-cytotoxic agent and bone marrow suppressant
151
-dosed to maintain WBC < 5000 mm3
-side effects: generalized bone marrow depression (leukopenia, anemia, thrombocytopenia)
-glucocorticoid:
-potent immunosuppressive effects by inhibiting leukocyte elaboration of inflammatory mediators
-methylprednisone bolus 500 mg IV then 125 mg IV q8h x 24h
-then 1.0 mg/kg/day during first week 0.2 mg/kg/day if no acute rejection
-side effects: cushingoid features, hypertension, diabetes, osteoporosis, peptic ulcer disease
-addition of OKT3 to triple-drug regimen over first 10 post-op days has delayed time to first rejection and
has reduced early rejection rates, but has not resulted in significant differences in overall recipient survival
-side effects: hypotension, bronchospasm, fever
-premeditate /w acetaminophen, antihistamines, corticosteroids
-most side effects are manageable or reversible /w dose reduction
Postoperative Complications:
Acute Rejection:
-major cause of death after cardiac transplantation
-highest incidence during first 3 months
-using OKT3 /w triple therapy reduces rejection from 84% to 75%
-after 3 months: incidence ~ 1 episode per pt a year
-endomyocardial biopsy is gold standard for diagnosis
-acute rejection characterized by:
-lymphocytic infiltration and myocytic necrosis
-treatment:
-severe or moderate in early posttransplant period: pulsed steroid dosing
-methylprednisone IV @ 1000 mg/d x 3d
-subsequent severe or moderate rejection episodes on routine surveillance:
-steroid pulsing or by po prednisone to 100-200 mg/day x 3d taper over 2 weeks
-mild rejection not treated unless persistent
-refractory rejection to steroids:
-ATG or OKT3
-MTX and total lymphoid irradiation
-repeat biopsy q 10-14 days after antirejection therapy
Chronic Rejection:
-accelerated atherosclerosis major limiting factor
-may lead to arrhythmias, MI, sudden death, or impaired LV function and CHF
-angina not experienced b/c graft is de-enervated
-risk factors for developing CAD:
-older donor age
-older recipient age
-incompatibility at HLA-A1, A2 and DR loci
-hypertriglyceridemia
-frequent acute rejection episodes
-recipient CMV infection
-elevated levels of antiendothelial Abs correlate /w graft CAD
diffuse vascular narrowing; concentric intimal proliferation /w SMC hyperplasia
-coronary angiograms on a yearly basis; intracoronary ultrasonography is a sensitive test for graft
atherosclerosis
-tx: PTCA or CABG for proximal lesions; retransplantation for diffuse disease
Infection:
-leading cause of morbidity and mortality
-risk peaks during first few months after transplantation
152
-early infections (first month after transplantation)
-bacterial (gram negative bacilli)
-pneumonia, mediastinitis, catheter sepsis, urinary tract and skin infections
-late infections:
-opportunistic viral, fungal, and protozoan pathogens
-CMV infection most common viral infection (73-100% transplant pts)
-reactivation ~ 1-4 months after transplant
-donor organ though to be most common vector of primary CMV infections
-leukopenia /w fever, pneumonia, gastroenteritis, hepatitis, and retinitis
-CMV pneumonitis most lethal (13% mortality)
-retinitis most refractory to treatment
-trigger for accelerated graft CAD and inhibitor of cell-mediated immunity
-tx: ganciclovir (DHPG) and hyperimmune globulin
-fungal infection:
-tx: amphotericin B, fluconazole and flucytosine
-infection prophylaxis:
-vaccinations: pneumococcal, hepatitis B and DPT boosters; annual influenza vaccine
-in children, MMR before transplantation
-perioperative antibiotics: cefazolin
-long-term prophylaxis: nystatin for thrush, SMX-TMP for opportunistic bacterial and
Pneumocystis carinii infections, and antiviral agents such as acyclovir or ganciclovir
Neoplasm:
-recipients predisposed to skin cancer, B-cell lmphoproliferative disorders, carcinoma in situ or cervix,
carcinoma of vulva and anus, and Kaposi’s sarcoma
-appear ~ 5 years after transplantation
-lymphomas frequently seen in recipients < 20 ya
-thought to be d/t EBV infection in setting of T-cell suppression
-tx /w reduction in immunosuppression and antiviral agent (acyclovir or ganciclovir)
Retransplantation:
-indications are graft failure from accelerated graft CAD or recurrent acute rejection
) ( ) (
-indications:
-acquired dilated cardiomyopathy
-congenital heart disease
-blood type and donor size are most important considerations in donor-recipient matching
-moderate oversized heart grafts are preferred for recipients /w and elevated pulmonary vascular resistance
-immunosuppression therapy similar to adults; steroids are tapered more quickly to minimize growth retardation
and infectious complications
-acute rejection treated /w pulsed steroids; antilymphocyte preparations, total lymphoid irradiation, and methotrexate
reserved for refractory cases
153
' " ) ' "
Preoperative Considerations:
154
Donor-Recipient Matching:
-parameters include ABO compatibility and body size
-matching donor and recipient height seems to be the most reproducible method of selecting
appropriate donor lung size
-donor lungs should not be > 4 cm over similar measurements
-panel-reactive Abs (PRA) level greater than 50% prompts prospective specific crossmatch between the
donor and recipient
Operative Techniques:
-see Schwartz pg. 413-415
Management of Recipients:
Immunosuppression:
-protocols similar to those used in cardiac transplantation
-induction therapy /w anti-lymphocytic Ab preparations can be used
Postoperative Complications:
-early morbidity and mortality most commonly caused by infection, graft failure, and heart failure
-mortality after 1 year caused most commonly by obliterative bronchiolitis, infection, and malignancy
-majority of acute rejection occurs in first 3 months
-fever, dyspnea, impaired gas exchange: PaO2, FEV1, interstitial infiltrate on CXR
-dx /w bronchoscopy /w transbronchial parenchyma lung biopsy and BAL
-lymphocytic perivascular infiltrates
-tx /w IV steroid boluses; persistent rejection treated /w ATG or OKT3
-pulmonary and cardiac rejection present asynchronously in most cases
-transbronchial biopsy: 89% sensitivity in predicting cardiac rejection
-endomyocardial biopsy: 34% sensitivity in predicting lung rejection
-chronic lung rejection:
-obliterative bronchiolitis (OB): dense eosinophilic submucosa scar tissue that partially or totally
obliterates lumina of small airways
-decreases in PaO2 and FEV1
-no effective treatment; augmentation of immunosuppression
-dx in 20-50% of long-term lung transplant survivors
Infection:
-bacterial, viral, fungal infections leading causes of M+M
-bacteria:
-gram-negative: predominate during early post-op period
-lack of cough reflex in denervated lung, abnormal mucociliary clearance mechanisms, and
deficiencies in lymphatic drainage predispose grafted lungs to infection
-invasive infections caused by organisms cultured form donor
-viruses:
-CMV most common and clinically significant
155
-b/n 2 weeks and 100 days after transplant
-primary infection in previously seronegative recipients more serious than reactivation in
seropositive pts
-dx /w BAL or transbronchial biopsy
-tx /w ganciclovir
-prophylaxis: ganciclovir, acyclovir, and polyvalent immune globulin
-Herpes Simplex pneumonia: tx /w acyclovir
-risk of developing lymphoproliferative disease; in association /w EBV infection
-treat by lowering immunosuppression and administering acyclovir
-fungal infections:
-peak in frequency b/n 10 days and 2 months posttransplant
-Candida albicans and Aspergillus
-tx /w fluconazole, itraconazole or amphotericin B
-prophylaxis: inhaled amphotericin B
-Pneumocystis carinii: prophylaxis /w oral TMP/SMX or inhalational pentamidine
-most common airway complications are partial anastomotic dehiscence and stricture
-dx during bronchoscopic examination
-tx: dehiscence: reoperation or close observation and supportive care
stricture: laser ablation or dilation /w rigid bronchoscopy or balloon and bougie dilators
Preoperative Management:
Histocompatibility Testing:
-blood group typing and HLA typing
156
-for living donor transplants, exception is ABO subtype A2 less antigenic
-/w plasmapheresis and preoperative preparation, an A2 donor kidney can be transplanted into a
non-A2 recipient
-HLA-typing:
-lymphocytotoxic serologic test
-potential recipient’s cells are tested against a battery of sera (from multiparous women or as
monoclonal Ab preparations)
-all cadaveric and potential living donors are HLA typed as well
-class I antigens HLA-A,B and C and class II antigens HLA-DR, DP, and DQ
-not necessary to type every antigen in a living-related donor situation b/c all HLA
antigens are found together on chromosome 6
-HLA-A,B and DR is sufficient
-siblings: zero-, one- or two-haplotype match
-parents and children: always one haplotype match
-two-haplotype matched living donor kidneys have near 100% graft survival /w extremely low rate
of acute rejection
-if a healthy donor is available that is blood-group-compatible, the pt should be considered even
/w a poor HLA match
-one year survival advantage for six-antigen matches over completely mismatched cadaveric
transplants is ~5%
-serum screening for anti-HLA Abs
-multiparous women who have lost a transplant are at highest risk for sensitization
-test pt’s serum against a panel of lymphocytes selected to represent the known HLA antigens
-an important factor in predicting the likelihood of finding a suitable donor for a given recipient:
-if panel reactive Abs (PRA) > 90% will likely have reactivity against 90% of potential
donors
-final crossmatch
-cells from potential donor and serum from recipient incubated together
-Ab binding detected using a cytotoxic technique or flow cytometry or antihemophilic globulin
(AHG) est
-performed before proceeding /w transplantation
-a positive T-cell crossmatch is considered an absolute contraindication to transplantation
-along /w blood typing, the final crossmatch constitutes the most important histocompatibility test
and is mandatory before all renal transplants
Renal Donor:
157
Evaluation of the Cadaver Donor:
-account for ~ 75% of all kidney transplants
-marginal donors may be used:
-older and may have other dz not affecting kidneys, including low-grade brain tumours
-mild renal dysfunction or acute tubular necrosis
Donor Nephrectomy:
-most common complications after live donation: UTIs, wound infections, and PTX
Organ Preservation:
-hypothermia is the cornerstone of organ preservation
-however, hypothermia induced cell swelling may occur b/c Na-K pump is slowed
-mechanisms of preservation injury:
-loss of energy-generating capabilities resulting from mitochondrial damage b/c of loss of precursors for
ATP regeneration
-oxygen free radicals in reperfusion injury
-activation of catabolic enzymes
-activation of arachidonic acid cascade and production of cytotoxic products such as thromboxane and
leukotrienes
-two basic methods of preservation: cold storage and machine perfusion
-majority of kidney transplant centers still cold-store kidneys
Surgical Procedures:
Preoperative Preparation:
-cardiac stress testing or cardiac catheterization:
-for long-standing diabetes, hx of cardiac dz, age > 50
-bilateral native nephrectomy before transplantation:
-poorly controlled hypertension, chronic pyelonephritis and hydronephrosis
-polycystic kidney disease: if pain, hematuria, and UTI accompany disease
-cystoscopy, cystometrogram or VCUG may be required for those /w urologic history
-pts /w hx of pancreatitis: pancreatic U/S or CT scan and w/u for hyperparathyroidism
-cholecystectomy before transplant in pts /w symptomatic cholelithiasis
-pretransplant sigmoid colectomy: hx of diverticulitis, esp. pts /w PKD (higher incidence of diverticulosis)
-active hepatitis or chronic liver diseases and cirrhosis are not candidates
-but, those /w hepatitis B who are HbeAg negative and /w chronic persistent hepatitis C may be considered
Anesthesia:
-Swan-Ganz catheter and art line for older pts and those /w significant hypertension, diabetes, or previous CABG
-avoid succinylcholine in hyperkalemic pts: may exacerbate hyperkalemia and result in cardiac arrest
-renal-dose dopamine may be used to enhance renal transplant perfusion
-pts usually are given methylprednisolone, mannitol, and furosemide before removal of vascular clamps and
reperfusion of the kidney
Postoperative Care:
Immediate Care:
-u/o (from obligatory diuresis) usually is replaced /w half-normal saline solution /w 5% dextrose /wout potassium
-replace u/o plus 30 ml/h (insensible losses) not exceeding 200 ml/h
-early delayed graft function occurs in approximately 25% of cadaveric transplants
-fluid replacement linked to u/o will help to prevent fluid overload and the need for urgent hemodialysis
-anuria/oliguria in live donor kidney should alert to serious problem b/c these are expected to function immediately
-assess for any blood clots in Foley – irrigate or replace FC
158
-assess volume status; if CVP < 12 mmHg – give fluid bolus (500 cc) until CVP rises
-trial of furosemide (up to 200 mg) if no response from fluid boluses
-if no change in u/o despite above, then doppler U/S of kidney to assess blood flow
-if blood flow ok, then obstruction or urine leak (usually at UV junction) assessed /w U/S or
nuclear scintigraphy
-delayed graft function if above evaluation unremarkable: managed /w hemodialysis
Technical Complications:
-early: graft thrombosis, urine leaks, bleeding, wound infections
-late: lymphoceles, ureteral strictures, renal artery stenosis
-graft thrombosis:
-arterial or venous thrombosis
-technical in origin
-abrupt cessation of u/o
-dx on U/S
-early post-op bleeding:
-dysfunctional platelets in uremic pts
-DDAVP at time of operation to help /w platelet function if operative field not dry
-urine leaks:
-at UV junction most commonly
-usually technical failure, but also occur b/c of distal ureteral slough from inadequate blood supply
-dx: decreasing u/o, lower abdo pain, scrotal or labial edema, and rising serum creatinine
-U/S: fluid collection; renal scan: extravasation of radioisotope beyond collecting system
-tx: early exploration and repair
-UV leaks: reimplantation
-bladder leaks: primary closure
-lymphoceles:
-perinephric collections of fluid in ~5% transplants
-result of excessive iliac dissection and failure to ligate lymphatics overlying iliac artery
-may present as swelling over transplant, unilateral leg edema from iliac vein compression, increased
creatinine level from ureteral compression
-dx: aspiration: high protein content and creatinine concentration equal to serum
-drainage if symptomatic (ie. Causing compression)
-options: sclerosis /w tetracycline or peritoneal window for intraabdominal drainage
-renal artery stenosis:
-in 10%; usually in first 6 months
-primarily presents /w HTN
-may also have fluid retention, bruit over transplanted kidney
-worsening renal function when ACEi are used to treat HTN
-dx: angiogram; U/S and MRI angio may be used as screening tools
-may occur distal to anastomosis from rejection, atherosclerosis, and clamp or perfusion cannula injury
-more common if end-to-end anastomosis used vs end-to-side
-tx: >80% can be corrected /w balloon angioplasty at time of angiography; else repaired surgically
-ureteral obstruction:
-rising Cr /w hydronephrosis
-d/t lymphocele or stricture in distal ureter
-strictures d/t ischemia and sometimes rejection;
-dx: antegrade pyelogram
Immunosuppression:
-antithymocyte globulin (ATG), OKT3, cyclosporine, tacrolimus, azathioprine, mycophenolate mofetil, prednisone
-numerous protocols for cadaveric transplants
-triple therapy:
159
-azathioprine (or MMF), cyclosporine and prednisone
-cyclosprine 5-8 mg/kg po bid
-MMF 1000 or 1500 mg po bid (watch for GI sxs and leukopenia)
-prednisone 500-1000 mg IV then rapid taper to 5-10 mg od after 3-6 months
-steroids usually for life
-quadruple therapy:
-addition of ATG or OKT3
-to avoid nephrotoxic effects of cyclosporine and tacrolimus
-cyclosporine or tacrolimus not given until Cr level < 3.0 mg/dL; overlapped /w ATG or OKT3 until target
cyclosporine levels achieved
-two-haplotype living-related protocols:
-cyclosporine-based protocol /w azathioprine or MMF; steroid /wdrawal
-one-haplotype and living-unrelated protocols similar to cadaveric protocols
Treatment of Rejection:
-rejection occurs in 40-50%
-first line: high-dose steroids (usually methylprednisolone 500-1000 mg for 3-5 days)
-second line: OKT3 effective in reversing 90%
-polyclonal preparations such as ATG used in those /w Abs to OKT3 or serious side effects from OKT3-
induced cytokine release
-OKT3 as first line if biopsy-proven vascular rejection
-if rejection, then switch pt to MMF
-if refractory to steroids and OKT3, then treat /w tacrolimus (reversal in 75% of pts on tacrolimus)
Long-term Complications:
-most common causes of death: cardiovascular disease, infectious disease, malignancy
-noncompliance responsible for 10-15% of late graft losses
-recurrence of disease
-cardiovascular dz more common in pts /w DM, HTN, elevated serum cholesterol and triglyceride levels, and
smokers
-risk of IHD 3-4x greater in posttransplant pts than general population
-prevention is key:
-reduce hyperlipidemia /w diet and weight loss +/- statins
-minimized use of steroids, treatment of HTN, exercise
-hepatic dysfunction:
-common after transplantation; may be secondary to hep B, C, or drug toxicity (azathioprine, cyclosporine)
-hep B: progression to cirrhosis accelerated /w immunosuppression: may enhance viral replication
-hep C: more common than hep B; causes chronic liver disease in majority of pts
-hepatotoxicity from azathioprine/cyclosporine uncommon
-azathioprine: cholestatic pattern (d/c drug)
-cyclosporine: increased bilirubin and transaminase levels (usually responds to decreasing dose)
-may also be caused by pancreatitis, cholelithiasis and choledocholithiasis
-bone and mineral metabolism:
-hypophosphatemia and hypercalcemia (may be from persistent hyperparathyroidism)
-subtotal parathyroidectomy if: severe mental status changes, renal stones, fractures, pancreatitis, serum
calcium > 12.5 mg/dl after 1 year
-severe osteopenia or osteonecrosis
-minimize steroid dosage and correct hyperparathyroidism
-estrogen and calcium supplements in post-menopausal women
-may require etidronate and nasal calcitonin
-hyperglycemia:
-secondary to steroids: increase glucose production, impair peripheral use, and increase glucagon levels
-cyclosporine and tacrolimus decrease beta cell excretion and cause peripheral insulin resistance
-malignancies:
160
-lymphomas (1-2%)
-carcinoma of colon, rectum, prostate, breast and lung NOT increased
-skin cancer (esp. SCC) up to 20x higher
-higher incidence of Kaposi’s sarcoma and genital neoplasm (eg. Vulvar, vaginal, and cervical carcinomas)
-Posttransplant lymphoproliferative disease (PTLD):
-driven by EBV
-polymorphic B-cell hyperplasia nuclear atypia malignant monoclonal B-cell lymphoma
-occurs more frequently in those who have received antilymphocyte preparations (eg. ALG, ATG, and
OKT3)
-tx by lowering or stopping immunosuppression
-may respond to antiviral treatment /w acyclovir or ganciclovir
Special Problems:
Diabetes:
-diabetics at higher risk for HD and PVD
-all should have noninvasive cardiac evaluation for ischemia
-transplantation contraindicated if diffuse coronary disease (not amenable to surgery) /w LV dysfunction
-diabetic candidates for renal transplantation should be evaluated for combined kidney-pancreas transplantation
-juvenile diabetics /w transplants have 5 year survival rates ~80% (vs ~30% in non-transplanted pts on dialysis)
Pediatric Pts:
-pediatric pts /w functioning kidneys grow more normally, have significant catch-up growth, and potentially can
have more normal lifestyles
-work-up similar to adults, but less need for evaluation for comorbid conditions
-look for urologic as well as neurologic (eg. spina bifida) abnormalities
-recommended that pts < 1 year be allowed to grow before consideration for transplant
-pediatric pts have poorer overall graft survival than adult pts, particularly in cadaveric tx
-outcome better /w living-donor transplants
-high risk of non-compliance
Retransplant Pts:
-retransplant recipients have poor overall graft survival compared to first transplant recipients
-factors which increase graft loss in retransplant:
-extremely short survival of first transplant d/t acute rejection in < 6 months
-high PRA levels: generalized sensitization from a previous failed graft
-best outcomes have been demonstrated /w induction therapy, and the use of OKT3 or ATGAM can be
recommended for these pts
161
-ideal preservation solution:
-presence of impermeant molecules that suppress hypothermically induced cell swelling
-ion pumps slow down, loss of electrical potential across membranes, and entry of Cl down its
chemical gradient leads to accumulation of water in cell swelling organ damage
-appropriate biochemical environment
-University of Wisconsin (UW) solution:
-lactobionic acid as primary impermeant:
-large MM (358 kD)
-negatively charged
-also contains raffinose, hydroxyethyl starch, adenosine (stimulates ATP synthesis during reperfusion of
the organ)
-machine perfusion for kidneys decreases delayed graft function (<10% vs 25-30% seen in simple cold storage)
-gluconate is used in place of lactobionic acid
162
! "
-sum total of abnormalities of all organ systems and their interactions that determine the outcome of an operation
#$ % &
-estimation using Goldman’s cardiac risk index
-risk of surgical cardiac death:
-no previous MI: 1.0-1.2%
-MI > 6 months: 6.0%
-MI (transmural) < 3 months: 16-37%
#'$ ( &
-risk factors:
1. smoking
2. obesity
3. advanced age
4. industrial exposure
5. PCO2 > 45 mmHg diffusion defect
6. abnormal PFTs:
-FVC < 70% predicted
-FEV1 < 2.0L or < 70% predicted
-PEFR < 200 L/min
-FEV1/FVC < 65%
7. PAP > 30 mmHg
-exercise oxygen consumption (prior to thoracotomy) (VO2) > 20 ml/kg/min less likely to have post-op pulmonary
complications
-8 weeks smoking cessation prior to surgery beneficial
#)$ * &
-serum abnormalities of BUN and Cr are not manifest until > 75-90% of renal reserve lost
-creatinine clearance (ml/min) = [1.23 x weight (140-age)]/creatinine in umol/L
163
-correct reversible causes: infection, uncontrolled hypertension, obstruction, and dehydration
-peritoneal, hemodialysis, or continuous ultrafiltration occasionally required
#+$ * &
-patients with cirrhosis
-Child-Pugh criteria: based on presence of ascites, bilirubin, encephalopathy, nutritional status, albumin
-class A < 5%; B 5-10%; C 20-50% mortality following non-cardiac surgery
-generally die of high-output CV failure and low peripheral resistance
-see Table 11-4
-measures that can be taken:
-abstinence from alcohol important prior to elective procedures
-improve protein tolerance by use of branched-chain amino acid
-control ascites:
-spironolactone and lasix combined with fluid restriction to 1500 ml/day
-limit sodium to 2g/day
#-$ . */*
-difficult to assess
-severely malnourished patient:
-weight loss > 15% over previous 3-4 months
-serum albumin < 3.0 g/dL
-energy to injected skin-test antigens
-serum transferring level < 200 mg/dL
-if severely malnourished, then enteral or parenteral (only if severe) nutrition for 4-5 days preop
-normalize retinol binding protein, thyroxin-binding prealbumin, and transferring
#0$ ! &# 1 2 * 2 $
-no definite guidelines
-see appendix
. 3 4
Pathophysiology:
-lack of metabolically effective circulating insulin
-deficient utilization of glucose by peripheral tissues
-increased output of glucose by liver
-increased fatty acids ketones urine
-glycosuria osmotic diuresis loss of sodium and potassium
-anaesthetic agents can cause an exaggerated hyperglycemic epinephrine response and an increased
resistance to exogenously administered insulin
-stress of operation aggravates hyperglycemia
-epinephrine: glycogenolysis
-glucocorticoid: mobilized protein, anti-insulin effect
-growth hormone
Management:
-DM pts should have preference on operative schedule to minimize effects of fasting and ketosis
-mild DM frequently do not require insulin; dietary control sufficient
-pts using OHA should continue their use until day before operation
164
Insulin Therapy:
-see appendix for protocols
Ketoacidosis:
-IV hydration, insulin therapy, and electrolyte replacement (potassium)
-need for potassium usually does not exceed 80 mEq
Pathophysiology:
-disorder of normal body thermoregulation
-controlled by anterior hypothalamus
-?protective mechanism to combat infection
-all pyrogens evoke common mediator IL-1 (endogenous pyrogen)
-alters activity of temperature-sensitive neurons raises set-point increased body temperature
-vasoconstriction chills, shivering
Perioperative Fever:
-fever in the immediate postoperative period usually is not serious, is not very high, and is self-limited
-usually ascribed to atelectasis
Malignant Hyperthermia:
-incidence ~ 1/100000 general anaesthetic procedures
-succinylcholine, halothanes metabolic acidosis and electrolyte imbalances
-hypercalcemia, hypotonicity, hyperthermia (~40OC), oxygen denaturation, hypercapnia, cardiac
dysrhythmia
-treat with dantrolene IV 1 mg/kg, repeat to total dose of 10 mg/kg prn
-supportive measures; ventilation/oxygenation, treatment of possible myoglobinuria
165
5 . 4
5 % /*
Predisposing Factors:
-staphylococcus aureus most frequently involved offending organism
-enteric organisms in bowel surgery; other less common pathogens: enterococci, Psedomonas, Proteus,
Klebsiella
-hemolytic strep responsible for 3% of wound infections
Prevention:
-skin preparation: -clipping (2% infection rate) preferred over shaving (5%) of hair
-bowel preparation: -clear liquids, cathartics, antibiotic regimens
-prophylactic antibiotics
-maintenance of temperature: -warming blankets, warm fluids
-meticulous technique: -gentle handling of tissue, hemostasis
-appropriate drainage
Clinical Manifestations:
-infections usually evident between 5th and 8th POD; may manifest after weeks if pt on antibiotics
-necrotizing fasciitis or clostridia myositis can occur within 24 hours
Management:
-open incision and pack wound with gauze
-cellulitis and edema add antibiotics; Gram stain may help guide treatment
-if hemolytic strep penicillin for 1 week
-clostridia myositis/necrotizing fasciitis surgical debridement
166
-Fournier’s gangrene: necrotizing fasciitis of perineum or groin in diabetic patients
-30-70% mortality rate
5 % *
-inadequate hemostasis
-provide good culture medium for bacteria
-early haematomas return to OR ligate responsible vessel primary closure of wound
-late haematomas manage patient expectantly with hope that haematoma has not become contaminated
5 % *
-lymph collections
-aspiration and pressure dressings
-continuous closed-suction drainage
5 % . *1 * *
-< 45ya: 1.3%; > 45ya: 5.4%
-generally caused by a technical factor
-contributory factors:
-malnutrition, hypoproteinemia, morbid obesity, malignancy with immunologic deficiency, uraemia,
diabetes, coughing with increased abdominal pressure, remote infection
-local factors: hemorrhage, infection, excessive suture material, poor technique
-monofilament sutures have lower incidence of disruption than braided sutures
-vitamin C deficiency: 8x increase in wound dehiscence
-zinc deficiency associated with poor healing
-steroids interfere with wound healing; use vitamin A to counteract these effects
-chemotherapeutic agents inhibit wound healing
-usually wait 1-2 weeks post-op before chemotherapy started
-radiation causes obliteration of small vasculature and fibrosis
Clinical Manifestations:
-salmon-coloured fluid draining from wound at 4th or 5th POD (85% of the time)
Treatment:
-depends on pt’s condition
-if no evisceration non-operative treatment with sterile occlusive wound dressing and binder
-evisceration moist sterile towels applied and pt returned to OR
-perioperative broad-spectrum antibiotics should be given
4 4
( **
-requires release of alpha-adrenergic receptors in SMC of bladder neck and urethra and parasympathetic stimulation
to contract bladder
-stress, pain, spinal anaesthesia, and various anorectal reflexes conspire to increase alpha-adrenergic stimulation
-if retention urinary catheter used
* * *
Etiology:
-inadequate resuscitation: -sympathetics decreases renal blood flow; RAA system will shunt blood away
from afferent arterioles
167
-drug toxicity: aminoglycosides, vancomycin, amphotericin B, high doses of penicillin G or sulfonamides
-see Table 11-12 for other nephrotoxic drugs
Prerenal:
-BUN/Cr 20:1
-commonly observed with dehydration
-hepatorenal syndrome:
-two mechanisms: hypovolemia (type I) and maldistribution of blood flow (type II)
-Type I: deficiency in intravascular volume secondary to blockage of liver outflow ascites
-Type II: failing liver, elevated bilirubin, other stigmata of cirrhosis; CO and low PVR
-kidneys are normal; recovery is rare and depends on recovery of intrinsic liver disease
Intrinsic Damage:
-acute tubular necrosis:
-most common cause in surgical setting is renal perfusion d/t prolonged and sustained
hypotension (from sepsis, blood los, hypovolemia, dehydration, or myocardial infarction)
-mechanism:
-kidney tries to maintain glomerular blood flow afferent dilatation and efferent
constriction of arterioles
-perceived hypoperfusion angiotensin by RAA system afferent constriction
- sympathetics norepinephrine afferent constriction
-this results in tubular ischemic and hypoperfusion of renal cortex ATN
-myoglobinuria and transfusion reaction (free Hb) may complicate renal injury
-other causes:
-radiocontrast dyes with dehydration
-atheromatous embolic during aortic vascular surgery
-clamping of renal artery
Postrenal Failure:
-ureteral clots or stones; BPH
Manifestations:
-oliguria with u/o of 0.4-0.5 cc/kg/h in adult
-anuria: uncommon; usually from ATN as a result of renal artery thrombosis or obstructive uropathy
-fractional excretion of sodium (FENa) = [UNa / PNa] / [UCr/PCr]
-if > 1% intrinsic renal damage
-UNa < 10 mEq/L prerenal cause or intrinsic liver disease
-intrinsic UNa > 40 mEq/L, FENa > 3%
Management:
-if diagnosis is uncertain:
-volume challenge if suspect hypovolemia
-once adequate volume status established furosemide (20-40 mg) to improve u/o
-stop nephrotoxic drugs
-established renal failure:
168
-treat hyperkalemia: infusion of calcium, hypertonic dextrose solution, and insulin then resins
-maintenance of nutrition in patients with ATN: enterally or parenterally
-IV “Giordano-Giovannetti diet” of essential AA and hypertonic dextrose, with minimum
of fat, decreases mortality in patients with ATN
-dialysis for critical ionic excesses, volume overload, or BUN concentration > 80-100 mg/dl
Pathophysiology:
-VC and FRC may be reduced after upper abdominal surgery (50-60% and 30% respectively)
-postoperative pain alters mechanics of respiration
-closing volume (lung volume at which airway closure is first detectable) decreases in the postoperative
period
-other physiologic causes of insufficiency: diffusion defects, abnormalities in V/Q, reduction in CO with
persistent shunt, alterations in Hb level and persistent shun, and shunting that is anatomic or related to
atelectasis
Predisposing Factors:
**
-collapse of alveoli resulting from anaesthesia, diaphragmatic dysfunction, postoperative incisional pain, and patient
positioning
-prevention is key:
-coughing and deep breathing, chest physiotherapy, incentive spirometry,
-intermittent positive pressure breathing, and CPAP
-medication for prophylaxis:
-expectorants: provide more liquid secretions
-detergents and mucolytic solutions: alter surface tension of secretions and render their elimination more
likely
-bronchodilators: eliminate bronchospasm
*
-third most common nosocomial infection (after wound and UTI)
-pathogens include Psueudomonas, Serratia, Klebsiella, Proteus, Enterobacter, Streptococcus
-use of H2-blockers may breakdown acid barrier, allowing overgrowth and colonization of the stomach by intestinal
flora (gram negatives)
Clinical Manifestations:
-fever, productive cough, dyspnea, pleuritic chest pain, and purulent sputum
-if hypotensive, consider gram negative pneumonia
169
Management:
-cultures obtained via routine ETT suctioning have little predictive benefit in correctly identifying the
pathogen responsible for noscomial pneumonia
-empiric therapy with aminoglycoside and antipseudomonal penicillin initiated until definitive culture
results obtained (via BAL ideally)
-most likely setting is during emergency induction of anaesthesia, particularly in pts with GERD or hiatal hernia
Clinical Manifestations:
-presence of gastric contents in mouth followed by wheezing, hypoxia, bronchorrhea, and cyanosis
-CXR: progression of local damage and infiltration accute respiratory failure results
-causes chemical pneumonitis that results in bacterial colonization with subsequent development of
pneumonia
Management:
-prevention: empty stomach and neutralization of gastric contents
-suction then ETT to complete clearance of tracheobronchial tree
( %*
-pulmonary-capillary hydrostatic pressure exceeds plasma oncotic pressure
-most common causes: fluid overload or myocardial insufficiency secondary to MI
-others: sepsis, valvular dysfunction, neurogenic stimulation, and hepatic failure
-increased capillary permeability:
-sepsis, ARDS, acute pancreatitis
Clinical Manifestations:
-two peak phases:
-during resuscitation if too aggressive with fluid replacement
-post-operative when fluid mobilization occurs
-rales, distended neck veins, cyanosis, peripheral pitting edema
-CXR: vascular redistribution, septal lines (Kerley’s B lines), peribronchial and perivascular cuffing
Management:
-depends on inciting cause
-for overload:
-pulmonary catheter may aid diagnosis and management
-PAWP 18-25 mmHg; CI decreased with increased PVR
-if PAWP normal or low, look for other causes
-?ARDS
-ECG look for evidence of pump failure
-treat with diuretics, IV nitroglycerin ( venous capacitance and preload)
-dobutamine or amrinone may improve cardiac output
-consider afterload reduction with nitroprusside if above maneuvers fail to produce a sufficient CI
2 ( % *
-fat embolism extremely common pathologic finding after trauma
-26% in patients with single fracture to 44% in patients with multiple fractures
-fat embolism syndrome with pulmonary dysfunction, coagulopathy, and neurologic disturbances associated with
increased circulating fat globules is ncommon
170
Pathophysiology:
-long bone fractures with release of marrow fat into circulation
Clinical Manifestations:
-respiratory insufficiency
-CXR shows characteristic bilateral alveolar infiltrates
-may evolve into ARDS
-CNS involvement in 86% confusion and disorientation with eventual progression to coma
-characteristic petechial rash occurs in axillae, neck , and skin folds
-fat globules in urine not specific for fat embolism syndrome
-associated findings:
-unexplained drop in hct, thrombocytopenia, hypocalcemia, and hypoalbuminemia
Management:
-immobilize any long bone fracture
-early surgical fixation decreases incidence of pulmonary complications of fat embolism
-oxygenation and supportive measures
* * (. * ( % *# . $
-pt incapable of maintaining adequate oxygenation, adequate ventilation, adequate tissue delivery, or some
combination of these defects
-syndrome that includes:
-lung injury, acute in nature
-bilateral infiltrates on frontal chest radiograph
-PaO2/FIO2 < 200
-PCWP < 19 mmHg with no evidence of CHF
-may be due to specific single cause or may represent endpoint of a poorly understood pathway with a common final
denominator of lung damage and subsequent decompensation of oxygenation and ventilation
Management:
-reduce volutrauma:
-early use of PEEP adjusted to the inflection point (as seen on pressure-volume curve)
-pressure-limited ventilation with plateau pressures less than 35 cmH2O
-permissive hypercapnia
-use of inhalational NO
-PEEP has remained the mainstay of treatment of ARDS
-recruits collapsed alveolar units
-attenuates lung injury associated with PPV
-may prevent loss of FRC and prevent alveolar collapse at end-expiration
-permissive hypercapnia limits potentially detrimental effects of increased peak airway pressures, the
number of breaths necessary per minute, which reduces the risk of barotrauma and volutrauma
171
-inhalation of NO at mall doses has reduced pulmonary hypertension and improved oxygenation in a
variety of patients
-newer modalities using partial liquid ventilation (PLV) and perfluorocarbon-assisted gas exchange
(PAGE)
. 4
4( % /
-mortality from perioperative MI ranges from 54% to 89%
-presence of coronary artery disease: risk of perioperative MI increased from 0.1-0.7% to 1.1%
-patients over 40: infarction rate is 1.8%
-previous MI: infarction rate 27% (within 3 months); 11% (b/n 3 and 6 months); 5% (> 6 months)
Clinical Manifestations:
-most cases occur on operative day or during first 3 PODs
-most important precipitating factor is shock risk of coronary thrombosis and myocardial ischemic
-chest pain only in 27% of patients b/c may be masked by narcotics
-may manifest as a sudden appearance of shock, dyspnea, cyanosis, tachycardia, arrhythmia, or CHF
-evaluate with ECG, serial cardiac enzymes, ABG (rule out respiratory causes)
Management:
-pre-operative:
-optimize CHF (digitalization for pts with enlarged hearts)
-treat anemia
-optimize fluid and electrolyte balance
-continue beta-blockers until morning of operation
-operation after 6 months of an MI
-intra-operative:
-regulation of BP important
-avoid hypoxia, hypotension, haemorrhage, dehydration, electrolyte disturbance and arrhythmias
-treatment:
-+/- monitoring in ICU
-pain relief: morphine and sedation
-+/- heparin, ASA; nitro and beta-blockers
-hypoxia relief: oxygen
-shock treated by vasopressor agents
-early emergency cardiac catheterization, angioplasty, or stenting may reverse an evolving MI
1( 1
-sinus tachycardia (not an arrhythmia) is the most common disturbance of rhythm, followed by PVC and sinoatrial
arrhythmia
Etiology:
-intrinsic cardiac disease
-perioperative release of catecholamines d/t stress or pain
-organ manipulation that stimulates reflex response
-electrolyte abnormalities and metabolic disturbances:
172
-hypokalemia PACs and PVCs
-hyperkalemia conduction abnormalities
-hypocalcemia QT interval ventricular arhythmias
-hypercalcemia bardycardia and heart block
-cardiac medications:
-digitalis toxicity supraventricular-atrial flutter with varying block, PVCs, VT or VF
-antihypertensive meds sinus bardycardia or induction block
-anaesthetic agents:
-halothanes ventricular dysrhythmias
-parasympathetic stimulation (neostigmine, physostigmine, succinylcholine) bardycardia
-other factors:
-hypercapnia may suppress sinoatrial node function ectopic pacemaker or aberrant reentry
mechanisms
-thyrotoxicosis atrial fibrillation
-pheochromocytoma
Sinus Tachycardia:
-find and treat cause: pain, hypovolemia, hypoxia, acidosis, sepsis, CHF, hypoperfusion, hypercapnia
Atrial Fibrillation:
-lack of “atrial kick” may result in 10-15% decrease in cardiac output
-causes:
-thyrotoxicosis, valvular heart disease, hypertension, CAD, PE, MI
-common after pneumonectomy
-cardioversion if hemodynamically unstable
-anticoagulate if long standing A-fib
-control rate (eg. with CCB, BB) and rhythm
173
Sustained Supraventricular Tachycardias:
-may be a result of digitalis toxicity
-obtain serum potassium and digitalis levels
Atrial Flutter:
-if unstable cardioversion
-digitalis used to maintain heart rate once controlled
( * *
Preoperative Hypertension:
-preoperative hypertension that is untreated or poorly controlled does increase the risk of perioperative
blood pressure lability, which may result in increased incidence of stroke, TIA, arrhythmias, post-op MI,
and possibly post-op renal failure
Postoperative Hypertension:
-systolic pressures > 200 mmHg result in bleeding from suture line, haemorrhagic cerebral infarction,
myocardial ischemic or infarction, and acute renal failure
-~ 80% of post-op HTN episodes occur within first 3 h of emergence form anaesthesia
-d/t ETT, inadequate analgesia, acute bladder distention, fluid overload
-tracheal stimulation, hypothermia, hypercapnia, hypoxemia
-if uncontrollable sodium nitroprusside or labetalol is given
-late post-op:
-d/t hypervolemia 2o fluid mobilization into intravascular space, inadequate analgesia, or failure to
resume previous antihypertensive medications
174
3
6 *% ( * 2* *
Heparin-Induced Thrombocytopenia:
-form of consumptive platelet activation
-not dose dependent
-mechanism: autoantibody formation directed toward heparin and platelet surface antigens
-mild: occurs 2-4 days after heparin exposure
-severe: 6-12 days after exposure and associated with thrombosis
-arterial thrombosis common
-significant mortality rate
-phlegmasia cerulea dolens amputation rate up to 30%
-treatment: stop heparin; +/- surgical thrombectomy; Greenfield filter, anticoagulation with warfarin
1* *% 1 2 . %*
Antithrombin-III Deficiency:
-AT-III the most important inhibitor of coagulation
-inactivates thrombin, Xa, IXa, XIa, plasmin, kallikrein, XIIa
-deficiency is autosomal dominant
-recurrent thrombosis in 60%; pulmonary embolus in 40%
-treatment: heparin; if OR FFP to raise level of AT-III
Protein C Deficiency:
-Protein C: vit K-dependent inhibitor of procoagulant system
-inactivates V and VIII
-seen in 4-5% of patients < 45y with unexplained venous thrombosis
-deficiency is autosomal dominant: (CRM-: lack of protein; CRM+: dysfunctional protein)
-significant when serum activity < 70%
-treatment: warfarin
Protein S Deficiency:
-Protein S: vit K-dependent; produced by hepatocytes and megakaryocyte
-cofactor for Protein C
-significant when serum activity < 60%
!
-associated with high mortality related mainly of primary disease
-75% of pts are > 70y
-causes: poor oral hygiene, dehydration, use of anticholinergic agents, lack of oral intake
-staphylococci infection via probable transductal inoculation of parotid gland
-routes of spread for suppurative parotitis:
-downward into deep fascial planes of the neck
-backward into external auditory canal
175
-outward into skin of face
Clinical Manifestations:
-swollen tender parotid
-may progress rapidly to severe cellulitis on affected side of face and neck
-may require tracheotomy if airway compromised
Management:
-prophylaxis: adequate hydration, good oral hygiene
-start with broad spectrum Abx against staph; take C+S of pus
-surgical drainage; should not be delayed beyond 5th day
Prognosis:
-mortality approximated 20%, but his was frequently related to the patient’s basic disease
* % 3 7* 2
-small bowel normally does not manifest ileus post-op, because it continues to function throughout and after
operation
-tube feedings may start almost immediately after operation
-if inflammation or several anastomoses in small bowel 24h ileus might be experienced
-gastric ileus: 24-48h
-colonic ileus: 3-5 days
-caused by:
-surgical manipulation, inflammation, peritonitis, blood in peritonem
-blood in retroperitoneum
-hypokalemia, hypocalcemia, hyponatremia, hypomagnesaemia
-opiates and phenothiazine
-treatment:
-correct underlying disorder, if any; mostly supportive treatment
-long tube decompression
-measure serum albumin prolonged ileus in hypoalbuminemic patients
-12.5g q8-12h to raise albumin > 3.0 mg/dL often results in return of bowel function
* & %
General Considerations:
-factors that increase likelihood of anastomotic leakage:
-emergency procedures, poorly prepared patients, inadequately resuscitated patients, prolonged
intraoperative hypotension, hypothermia
-etiological factors: poor surgical technique, distal obstruction, inadequate proximal decompression
176
Intestinal Leaks and Fistulas:
Leaks: -fever, leukocytosis, unexplained ileus in absence of intestinal obstruction, complicated post-op course
-if patient is in jeopardy, sepsis uncontrolled, no effective drainage abdomen re-explored
-anastomosis must be resected and redone
-if hemodynamically unstable separation of both ends and diversion should be done
Fistula: -increased wound pain and redness/drainage on POD #4-5
-usually result from operations involving inflammatory bowel disease, cancer, or lysis of adhesions
-allow fistula to close spontaneously
1. Stabilization:
-resuscitation using crystalloids, RBC, and albumin
-Abx only if septic
-sump-type drain placed around skin; skin protected with Stomadheisve and ion exchange paste to keep
pH acidic and prevent activation of pancreatic enzymes that require basic pH
-TPN: 5-6% AA, 15-25% dextrose, 20% fat
-nutrition can be monitored with RBP, TBP, transferring
-enteral feeds may be attempted but they must be supplemented with TPN
3. Decision:
-somatostatin used to promote closure
-if short-turnover protein levels are increasing, the serum albumin concentration is approaching 3.0 g/dl,
and the patient is maintaining the albumin level without infusions of exogenous albumin, operation can
take place
-failure to maintain or increase in levels of transferring, retinol-binding protein, and thyroxin-binding
prealbumin indicative of mortality
4. Operation:
-mortality ~10-11% if operated during first 10 days or after 4 months; ~20% between 10 days and 4months
-resection and end-to-end anastomosis; protection with omentum onlay
-for duodenal fistula: vagotomy and gastrojejunostomy, feeding jejunostomy and gastrostomy, area of
fistula drained
-chronic pancreatic fistula:
-excise fistula down to pancreas, identify leak, distal pancreatectoy and splenectomy
-Roux-en-Y anastomosis can be used to provide internal drainage for the pancreatic fistula
5. Healing:
-feeding delayed 7-10 days
-difficulties eating:
-lack taste sensation: use zinc sulfate or lactate
-may be necessary to allow alcohol to induce eating
177
Colocutaneous Fistulas:
-fluid and electrolyte abnormalities and skin digestion are rare, but infectious complications are significant
-percuaneous drainage of intraabdominal abscesses and local care of wound infections
-antibiotics as indicated
-spontaneous closure likely
-persistence if sepsis, distal obstruction, anastomotic dehiscence, Crohn’s disease, or carcinoma present
-lack of spontaneous close by 5 weeks surgical repair
-resection of fistula and affected colonic segment with primary anastomosis and temporary
diversion of the fecal stream by colostomy
* ( ( % *
Dumping:
-loss of pyloric valve that normally prevents hyperosmolar material from entering duodenum and small
bowel
-d/t pyloroplasty, pyloromyotomy, gastrojejunostomy, gastric resection, Billroth I or II anastomosis
-results in release of vasoactive substances:
-serotonin, bradykinin, substance P, peptides (VIP, pancreatic polypeptide, insulin, glucagon,
neurotensin, enteroglucagon)
-results in decreased plasma volume hypotension; hypokalemia
-symptoms:
-early postprandial bloating, borborygmus, cramps, sensation of light-headedness, palpitations,
sweating, hypotension
-eating solids at meal and drinking liquids afterwards diminishes symptoms
-avoid carbohydrates which are more likely to provoke dumping
-in severe cases, long-acting octreotide may oppose some of the action of released peptides and ameliorate
the symptoms
-surgical treatments: conversion of BII to BI; 6 cm reverse loop of jejunum to slow transit of hypertonic
solution
Postvagotomy Diarrhea:
-5-20% of patients have troublesome diarrhea post-truncal vagotomy
-factors:
-dysmotility or dysfunction of small bowel motility stasis and overgrowth of bacteria,
malabsorption of fat, increased and incoordinate bile flow into small bowel
-treatment difficult:
-antibiotics have little success
-10-cm reversed jejunal loop 100 cm distal to ligament of Treitz has been advocated
178
Alkaline Reflux Gastritis:
-stomach sensitive to bile; eating associated with burning epigastric pain
-large amounts of bile emanating form afferent loop
-acute and chronic inflammation, evidence of decreased parietal cells, and increase in mucous-secreting
cells, and intestinalization of the gastric glands
-most effective treatment: cholestyramin and sucralfate
-if medically unmanageable: Tanner-19 procedure with vagotomy and long bile-containing loop
anastomosed 60 cm down stream
Nutritional Complications:
-fat malabsorption chronic nutritional deficiency, failure of absorption of fat-soluble vitamins, chronic
bile salt diarrhea
-iron and calcium absorbed primarily in duodenum
-after BII many pts hypocalcemic and iron-deficiency anemic
-loss of intrinsic factor monthly B12 injections required
-may require conversion of BII to BI
Recurrence of Disease:
-complications for ileostomies: ulcerative colitis 4%; Crohn’s disease 30%
-Crohn’s: granulomatous, ulcerations; peristomal fistulas
-ciprofloxacin and metronidazole should be initiated
-no point in resiting stoma recurrence will likely happen again
Skin Complications:
-usually result of siting and inability to obtain appropriate seal around stoma
-Caraya powder, ion exchange paste, +/- nystatin powder and systemic fluconazole (if yeast) are helpful
-cellulitis requires antibiotics
Stomal Stricture:
-development of serositis in immediate postoperative period
-most common cause of stricture is necrosis or retraction, resulting in mucocutaneous separation, exposure
of the serosa, and subsequent serositis
-tx: stoma separated from skin, skin opening enlarged, new maturation performed
-if stricture at fascial level, fascial opening enlarged
4 3 4
( % * / * * * / % * *# . $
-most common metabolic complication after surgery
179
-may result in CNS damage, seizures and death
-secretion of ADH is more prolonged or more intense than after normal operative procedures
-management:
-if slight edema and [Na] ~125-130 fluid restriction is all that is required
-if CNS disturbance:
-symptoms not severe mannitol given slowly provokes diuresis of excess water secreted with
minimum of sodium; furosemide can be added
-if severe 3% saline; small increments 50-100 ml over 3-4 hours
-permanent CNS damage can occur if rapid correction of hyponatremia
-prevention: avoid overresuscitation of patients; limit free water
. %* / 1( %4* 2
Thyroid Storm:
-mortality of 10-20%
-occurs in patients with existing thyrotoxicosis that is unrecognized or uncontrolled
-any traumatic event, such as surgery, infection, or embolism, may complicate thyrotoxicosis and provoke
thyroid storm
-once hypotension supervenes, it is a preterminal event
-irreversible cardiac failure usually is the mode of death
-tx: -control of catecholamine-induced cardiac symptoms: propranolol IV 1mg/min to max of 10 mg
to control HR
-dobutamine may be necessary
-PTU 200 mg and KI 5-10 gtts given to decrease T3 and T4 release
-hydrocortisone 200 mg IV followed by 100 mg q8h diminishes thyroid hormone release
Myxedema Coma:
-pts with chronic hypothyroidism that is unrecognized or inadequately controlled; provoked by stress of
operation
-inciting factors: trauma, infection, GIB, surgery, narcotics and phenothiazine
-tx: -warming, hydration, assisted ventilation
-L-thyroxine 300-500 mg IV then 50-100 mg/d
%* // * (
-d/t suppression of pituitary-adrenal axis by previous administration of steroids or destruction or exhaustion of
adrenal glands
-in patients with carcinoma, bilateral adrenal metastasis may occur
-symptoms:
-unexplained hypotension, fever, abdominal pain, light-headedness, weakness, palpitations, mental status
changes, nausea, and vomiting
-lab findings:
-hypoglycemia, hyponatremia, occasionally hyperkalemia
-tx: -measure serum cortisol and initiate treatment
-hydrocortisone 200 mg IV
-hypotension should resolve in 1-2h if dx is correct
-400 mg hydrocortisone in divided doses over 24h should b given if hypotension not resolved
8* *
-most common cause is pre-existing liver disease
-cirrhosis, alcoholic hepatitis, fatty infiltration
-general anaesthesia should be avoided in patients with established liver dz:
-portal vein’s contribution is diminished and hepatic artery supplies at least 50% of hepatic flow
180
-splanchnic vasoconstriction of hepatic artery markedly decreases hepatic flow
-therefore, regional or epidural anaesthetic is preferred
-liver failure usually on 3rd or 5th POD
-somnolence, jaundice, u/o, ascites
-treatable reversible causes:
-hypovolemia, hypokalemia, hypomagnesaemia, GIB, constipation, remote infection
-must r/o SBP
-tx: -correct lytes, administration of neomycin, cathartic, or lactulose, and provision of nutritional support
-enteral feeds preferred:
-modified low aromatic, high branched-chain amino acid formulation
-hepatorenal syndrome type II can complicate hepatic failure; if liver does not recover post-op death
-delirium (20%), depression (9%), dementia (3%), functional psychosis (2%) of elderly post-op patients
Clinical Manifestations:
-manifestations are extremely variable
-delirium: occurs most commonly in elderly patients and those who are immobilized for long periods
-depressive reactions: pt characteristically uncooperative or recovery may be impeded by listlessness,
anorexia, and disinterest
-suicide a major risk in pts with depressive reaction
-paranoid psychotic disorder
Management:
-efforts should be directed at removing toxic causes of the acute brain syndrome, removing unnecessary
stimuli without isolating the patient, and providing psychologic or pharmacologic tranquillization
-consultation with psychiatry is indicated in the case of any acute and severe emotional disturbance
.* * * % 1* /. *
-delirium usually follows operation within 48h but may be delayed
-hyperactivity with irritability, delusions, hallucinations, restlessness, and agitation
-cause is multifactorial
-Haldol 2-15 mg PO bid or 1-5 mg IV followed by 5-10 mg/h may help agitation
-prophylactic medication with lorazepam should be administered in the perioperative period to patients with severe
alcoholic histories who are candidates for DTs
.* *
-characteristically occurs late in the post-op period
-use of SSRIs are useful
*
-very yound gan old patients are particularly vulnerable to the development of psychiatric complications after
surgical treatment
Pediatric Surgery:
-severe anxiety states may be precipitated by the shock of operation
-emotional needs must be attended to
-maturity is important and decreases post-op anxiety reactions
181
Surgery in the Aged:
-more prone to become emotionally disturbed when confronted with new situations, esp. if inadequate
comprehension and generalized feeling of insecurity
Cancer Surgery:
-two major threats: disease and extensive surgical treatment
-depression is related to an anticipated interference with valued activities
-tendency toward seclusion, withdrawal, and nonparticipation
-depression frequent
Cardiac Surgery:
-serious psychiatric disturbances observed with considerable frequency afte mitral valvulotomy and open-
heart surgery
-manifestations usually after initial lucid interval of 3-5 days; resolve shortly after transfer from CICU to
ward
-postoperative incapacitation and increased time on heart-lung machine are factors increasing the
likelihood of delirium ?organic brain damage from operation
182
! " # $ $ "
Indications:
1. Continuous monitoring of blood pressure
-shock, acute hypertensive crisis, use of potent vasoactive or inotropic drugs, high levels of
respiratory support, high-risk patients undergoing extensive operations, controlled hypotensive
anaesthesia, rapidly changing cardiac function
2. Frequent sampling of arterial blood
-any acute illness involving cardiovascular or respiratory dysfunction
Clinical Utility:
-observation of arterial pressure waveform may permit a qualitative assessment of cardiovascular status
Sites of Catheterization:
-radial artery:
-mean and end-diastolic radial pressures usually accurate estimates of aortic pressure
-systolic pressure often much higher than that of aorta d/t overshoot caused by resonant behaviour
of radial artery
-test collateral supply with Allen’s test (6s return of blood or less)
-axillary artery:
-long-term direct arterial pressure monitoring
-better representation of aortic pressure waveform and minimal systolic pressure overshoot
-because of extensive collateral circulation, thrombosis will not lead to compromise in distal arm
-femoral artery:
-easier localization and cannulation
-dorsalis pedis artery:
-relatively small size and overestimation of systolic pressure at this level
-superficial temporal artery:
-surgical exposure required for cannulation
-risk of cerebral embolization has been reported in infants
-brachial artery is not used often because of high complication rate:
-may lead to loss of forearm and hand if collateral flow is not sufficient
Complications:
-failure to cannulate, haematoma formation, disconnection from monitoring system with bleeding
-increased of radial artery occlusion:
-female gender, low CO states, vasoconstrictors drugs, severe PVD, small wrist circumference,
insertion by surgical cut-down, multiple puncture attempts, haematoma formation, and increased
duration of cannulation
-increased risk of infection:
-placement > 4 days, insertion by surgical cut-down, local inflammation
183
" $ '" # $ " " &$
Indications:
-secure access for fluid therapy
-drug infusions
-parenteral nutrition
-CVP monitoring
-other: aspirate air embolism, placement of cardiac pacemakers or IVC filters, hemodialysis access
Clinical Utility:
-CVP:
-can differentiate pericardial tamponade from hypovolemia
-tracing:
-absent a-wave: A-fib
-prominent v-wave: tricuspid insufficiency
-used to measure RAP; indirectly measures RVEDP, and estimates RVEDV
-cannot be used to assess LV function
Sites of Catheterization:
-subclavian vein:
-easiest to cannulate, but risk of PTX and inability to compress vessel if bleeding occurs
-internal jugular vein:
-lower risk of PTX; good compressibility
-risk of arterial puncture
-external jugular vein:
-high incidence of failure
-femoral vein:
-risk of infection and thrombosis continue to limit general acceptance of long-term cannulation
Complications:
-long-term: infection or thrombosis
-three types of thrombi:
-mural thrombus
-catheter thrombus
-sleeve thrombus
Indications:
-in general, a PA catheter indicated whenever the data obtained will improve therapeutic decision making
without unnecessary risk
-see Table 12-1
Clinical Utility:
-measures directly:
- CVP, PADP, PASP, MPAP, CO, PAWP, mixed venous blood gases, continuous mixed venous
oximetry
-others:
-LAP:
-PAWP is a reliable index of LAP even in the presence of elevated pulmonary vascular
184
resistance
-if measuring in West’s Zone I or II, then PAWP may reflect alveolar pressure and not
LAP (esp. if low pulm. vasc. pressures or high PEEP)
-must be in West’s Zone III (catheter should be below LA in supine position) to
accurately measure LAP
-LVEDP:
-in absence of MV dz or premature MV closure d/t AR, LAP reflects LVEDP
-LVEDV:
-if no alterations in LV compliance, LVEDP will reflect LVEDV
-intrathoracic pressures introduces artifact that affects all intrathoracic vascular pressures:
-if respiratory insufficiency:
-“stiff” lungs do not transmit alveolar pressure as readily to pulmonary circulation
-PEEP artifact should not exceed 1 mmHg for every 5 cmH2O PEEP applied
-hypovolemic patients:
-may cause greater discrepancy higher measured PAWP than actual
-intravascular measurements should be performed at end-expiration and obtained from a calibrated
oscilloscope rather than digital display which may average artifact
Catheter Insertion:
-mean PAWP should be lower than the MPAP and lower than or equal to the PADP
Complications:
-development of dysrhythmias (up to 50% of patients, but <1% are serious)
-RBBB seen in 3-6%, therefore need for transvenous pacemaker on standby
-coiling, looping or knotting in RV
-infections
-thromboembolism
-pulmonary artery rupture:
-more likely in elderly patients and those with hypertension
-other: thrombocytopenia, cardiac valve injuries, catheter fracture, balloon rupture
185
'" $
Lung Volumes:
-Tidal volume (VT): volume of air moved in or out of lungs in any single breath
-Vital capacity (VC): maximal expiration following a maximal inspiration
-reduced in diseases involving respiratory muscles or their neural pathways, obstructive and
restrictive ventilatory impairment, and in pts who fail to cooperate fully
-Minute volume (VE): total volume of air leaving lung each minute
-increase in VE required to maintain normal PaCO2 suggests increased dead space relative to VT or
an abnormally high CO2 production
-Dead space (VD): portion of tidal volume that does not participate in gas exchange
-the VD/VT ratio ~ 0.33-0.45 in healthy subjects
-increased in ARDS, emphysema, PE, shock with low CO, PPV with excessive PEEP
-if > 0.6, usually wearable from ventilator
Pulmonary Mechanics:
-Maximal inspiratory force: maximal pressure below atm exerted against an occluded airway
-more negative than -20-25 cmH2O used as one clinical parameter to confirm recovery from NM
block after general anaesthesia
-more negative than -30 cmH2O predict successful weaning from mechanical ventilation
-limited power in predicting weaning outcome; assess only strength without taking into account
the demands placed on respiratory muscle pump
-Compliance:
-change in volume divided by a change in pressure
-decreased values are observed with disorders of the thoracic cage or a reduction in the number of
functioning lung units (resection, bronchial intubation, PTX, atelectasis, pulmonary edema)
-Work of breathing:
-measure of the process of overcoming the elastic and frictional forces of the lung and chest wall
Blood-Gas Analysis:
-pulmonary and cardiac function must be assessed to evaluate any given set of ABGs accurately
-a decreasing PaO2 without a change in PaCO2 suggests that blood oxygenation is deteriorating
despite constant alveolar ventilation
-usually attributable to V/Q imbalance or intrapulmonary shunting
-oxyhaemoglobin dissociation curve:
-right shift: increased DPG, temperature, PCO2; decreased pH
-left shift: carboxyhemoglobinemia; decreased temperature and PCO2; increased pH
-little evidence that shifts of oxyhaemoglobin dissociation curve are clinically significant in the
majority of patients
-hypercapnia ( PaCO2):
-d/t hypoventilation (ie. CNS depression), increased CO2 production (eg. hyperthermia,
hyperthyroidism), increased physiologic dead space
-mixed venous blood:
-mixture of all blood that has traversed the capillary beds capable of extracting oxygen
-reflects total body balance between oxygen delivery and oxygen consumption of perfused tissues
186
Capnography:
-patients with COPD and other derangements associated with increased dead space have increased arterial
to end-tidal CO2 gradient [P(a-ET)CO2]
-PETCO2 (end-tidal CO2 gradient):
-determine proper ETT placement
-in CPR an increase from zero (circulatory arrest) provides an immediate bedside validation of the
efficacy of CPR; provides earliest evidence of successful resuscitation
-detection of increased CO2 production in malignant hyperthermia
-detection of disconnection or malfunction of anaesthesia breathing circuit
Pulse Oximetry:
-in the presence of elevated carboxyhemoglobin or methemoglobin levels, SPO2 overestimates fractional
saturation at all saturation values
-methemoglobinemia maybe induced by a large number of drugs, including local anesthetics (prilocaine,
benzocaine), NTG, phenacetin, phyenytoin, Pyridium, and sulfonamides
-Gastric tonometry has been propsed as a relatively noninvasive monitor of the adequacy of aerobic metabolism in
organs whose superficial mucosa lining is extremely vulnerable to low flow and hypoxemia and in which blood
flow is sacrificed first in both shock and the systemic inflammatory response syndrome
-intramucosal pH (pHi) is measured
Clinical Utility:
-in critically ill patients, used as predictor of organ dysfunction and mortality
-better predictor of mortality than base deficit, lactate, oxygen delivery, and oxygen consumption
-can provide metabolic end point of resuscitation
RENAL MONITORING
187
Glomerular Function Tests:
-BUN:
-affected by GFR and urea production
-may be increased in UGIB, catabolic states induced by trauma, sepsis, or steroids
-may be lowered during starvation and in advanced liver disease
-not a reliable monitor of renal function in critically ill patients
-Creatinine:
-inversely related to GFR
-not influenced by protein metabolism or the rate of fluid flow through the renal tubules
-plasma creatinine level will double with a 50% reduction in GFR (constant production of Cr)
-acute reductions are not immediately reflected, 24-72h required for equilibration to
occur
-CCr = (140-age) x weight in kg / 72 x PCr multiply by 0.85 for females
Electrophysiologic Monitoring:
-EEG used in:
-CEA, cerebrovascular surgery, open heart surgery, epilepsy surgery, induced hypotension for a
variety of surgical procedures
-somatosensory evoked potentials:
-reflect integrity of dorsal spinal columns and sensory cortex
-useful for monitoring during resection of spinal cord tumours, spine instrumentation, CEA, and
aortic surgery
-brainstem auditory-evoked potentials:
-reflect integrity of CN VIII and auditory pathways
-monitoring for surgery in posterior fossa
-visual evoked potentials:
-monitor optic nerve and upper brainstem
-pituitary surgery
188
Jugular Venous Oximetry:
-invasive method of continuously monitoring jugular venous bulb oxyhaemoglobin saturation
-provides a measure of the relationship b/n total cerebral blood flow and total cerebral oxygen consumption
Measurements:
-the ratio of CO2 production to oxygen consumption is the respiratory quotient (RQ)
-average ~ 0.8
-monitoring oxygen consumption and CO2 production and calculating the RQ provide inferences into the
adequacy of total calories as well as the mixture of substrates:
-prolonged starvation fat metabolism: RQ ~0.6-0.7
-excessive carbohydrate administration RQ > 1.0
-no great method of measuring this all prone to errors
189
F.Ling - POS notes and points (1)
Anaesthesia
190
F.Ling - POS notes and points (2)
Pharmacology
1. Bethanacol contraindicated in CAD and bladder outlet obstruction
-negative inotrope and chronotrope
-smooth muscle constriction in bronhioles, bladder and uterus
2. Ciprofloxacin:
- theophylline levels
-s/e: n/v, diarrhea, headache, dizziness, insomnia
3. Ampicillin and amoxicillin ineffective in the presence of penicillinase
4. Penicillinase resistant: methicillin, nafcillin, oxacillin, cloxacillin
-others: clavulin, sulbactam, tazobactam, vancomycin
5. Vancomycin least likely to become resistant to bacteria producing penicillinase
6. Advantage of 3rd generation cephalosporins: better gram negative coverage and CSF penetration
7. Cephalothin (1st generation cephalosporin) most likely side effect: hypersensitivity
191
F.Ling - POS notes and points (3)
192
F.Ling - POS notes and points (4)
1. Sodium deficit:
-Na = %body water x TBW(140-[Na])
-%body water = 50% female, 60% male (note previous exam may give volume of distribution of Na as
20%)
2. Plasma volume in 70kg male = 3.5L (5% body weight)
3. Blood volume is ~7% body weight (hct 40%, plasma 60% blood volume)
4. SIADH:
-hyponatremia, urine Na concentration, urine K, urine osmolality
5. Hypokalemia caused by all: lasix, hydrochlorothiazide, mannitol, ventolin
- except: metoprolol
6. Hypermagnesemia:
-hyporeflexia
-CNS: lethargy, coma, paralysis
-CVS: ECG changes and cardiac alterations similar to Ca
7. Hypomagnesemia:
-increased DTR, cardiac dysrhythmias, weakness, mental status changes, seizure
8. Patient with post-op, receiving only IV fluids: Na 112, Cl 105, K 3, BUN 12. Cause is dilutional
hyponatremia
9. Use calcium IV for cardiac effects of hyperkalemia
10. 70% of CO2 is transported in the blood as HCO3-
11. Most common cause of hypercalcemia:
-outpatient: parathyroid adenoma
-inpatient: metastatic disease (esp. breast cancer)
12. pH from 7.0 to 7.4, [H] less than half; from 7.4-7.0, [H] more than double
13. Pyloric stenosis: hypokalemic, hypochloremic, metabolic alkalosis
-signs and symptoms: projectile vomitting, non-bilous, olive mass, stomach peristalsis
14. Four year old boy with pyloric stenosis and 25% dehydration. Fluid for resuscitation: D5 0.45NS with 30
mEq Kcl at 25cc/h
15. Neonatal nutritional needs:
-90-120 kcal/kg/day
-Free H2O
-Na 3-5 mmol/kg/day
-K 2-3 mmol/kg/day
-protein 2-3.5 g/kg/day
16. When giving contrast dye, to avoid renal insufficiency: ensure patient is well hydrated
17. Ringer’s lactate: Na 130, Cl 109, Ca 3, K 4, HCO3- 28
18. Emphysema does not cause respiratory alkalosis
19. Urinary Na > 40 suggests renal cause to acute renal failure
20. Hypoaldosteronism (Addisonian crisis): everything decreased except K (will be )
21. Hyperaldosteronism: hypokalemia, hypertension, Na and H2O retention
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Nutrition
194
F.Ling - POS notes and points (6)
1. Best pre-operative screening for bleeding risk: history and physical (ie. prior bleeding problems)
2. Heparin actions:
-inhibition of antithrombin III
-increases PTT
3. Coumadin:
-vitamin K antagonist
-prevents carboxylation of factors II, VII, IX, and X (“1972")
4. Major crossmatch: mixing donor RBC with recipient serum
5. Minor crossmatch: mixing donor serum with recipient RBC
6. Patient with obstructive jaundice and hypoprothrombinemia: due to poor fat absorption (unable to absorb
vitamin K)
7. Acute DVT management: Heparin 5000u IV bolus followed by 800-1000u/h infusion
8. Most common cause of transfusion related death: Hepatitis C
9. Management of hemolytic transfusion reaction:
-most important: stop transfusion
-least important: Lasix
-others: IV hydration, alkalinization of urine, Lasix or Mannitol, Foley
10. Patient with VonWillebrand’s disease going for surgery:
-DDAVP prior to surgery
-if active bleeding, use cryoprecipitate
11. Woman with hypernephroma, on coumadin for MVP, presents with gross hematuria. 4 units PRBC given
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F.Ling - POS notes and points (7)
and she is now stable with INR 2.2, Hb 98. Next step is: give FFP
12. VonWillebrand’s disease: autosomal dominant, most common bleeding disorder (1% population), variable
expression
13. Risk of infection from donor increases with number of units transfused
14. Defect in CRF hemostasis: Quality of platelets bleeding time prolonged
15. Papaverine does not affect platelet function
16. Sickle cell disease: presence of fetal hemoglobin does not promote sickling
17. Side effects of protamine:
-hypotension (most common)
-pulmonary hypertension
-anaphylaxis, n/v
18. Most common complication of massive transfusion: dilutional thrombocytopenia/hypothermia
19. Most common coagulation defect: dilutional thrombocytopenia
20. Most common cause of asystole from massive transfusion: hypothermia
21. Most common cause of febrile transfusion reaction: WBCs in donor blood
22. Patient with hemophilia going for surgery. Need 30-60% factor VIII activity before, during and after surgery
for at least 2 weeks. Ideally for surgery, levels should be 80-100%.
23. Classical hemophilia: mild (>5% factor VIII activity); moderate (2-5%); severe (<2%)
24. Most characteristic in classical hemophilia: prolonged PTT (normal PT and bleeding time)
25. Platelet transfusion can transmit syphilis if stored at room temperature (should be stored at 4oC)
26. Albumin and plasma proteins do not transmit hepatitis and syphilis
27. Patient receiving transfusion intra-op begins bleeding from operative field and decreased urine output
-hemolytic transfusion reaction
-stop transfusion, infuse saline and mannintol/lasix etc.. (“all except: steroid”)
-check recent hemolytic reaction: urine free hemoglobin
28. Father with hemophilia: all his sons will be normal, his daughter will be carriers
29. Oral contraceptives predispose to DVTs by:
- antithrombin III levels
- protein S
- fibrinolytic activity
- coagulation factors (fibrinogen, VII, VIII, IX,X)
30. Platelets secrete:
-alpha granules: PDGF, TGF-B, IGF-1, fibronectin, fibrinogen, thrombospondin, vWF
-dense bodies: serotonin
-lysosomes: hydrolases and proteases
31. Heparin-induced thrombocytopenia:
-due to antibody formation directed towards heparin and platelet surface
-treatment: stop heparin (can use danaparoid, hirudin, or LMW heparin)
32. Post massive transfusion (48h): pCO2 40, CVP 15, pO2 50 on 100% most likely cause is pulmonary edema
33. Primary fibrinolysis: euglobin lysis time, fibrinogen, FDP
34. EACA inhibits plasminogen activation - for treatment of primary fibrinolysis
35. Factor VIII:C produced by endothelial cells (also in liver); other coagulation factors made by liver
hepatocytes
36. TTP improves with steroids and splenectomy; high success rate with plasmapheresis
37. Elevated PT in: coumadin use, extrinsic pathway defects, VII deficiency
38. DIC: diffuse bleeding, PT and PTT, fibrinogen, FDP; must treat primary cause
39. Blood volume increases with all except: hepatic venous congestion
40. Hypofibrinogenemia is associated with DIC, cancer of prostate, advance liver disease
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F.Ling - POS notes and points (8)
Surgical Infections
1. Clean contaminated operations:
-entering respiratory tract, GI, GU, gyne procedures
2. Antibiotics given 30 mins prior to incision
3. Endocarditis prophylaxis prior to GU procedure: Penicillin (Vancomycin if allergic) and Gentamicin
4. Best method to diagnose C.difficile colitis: C.difficile toxin
-tx: oral or IV metronidazole: oral vancomycin
5. Subcutaneous air NOT pathognomic for clostridial myonecrosis
6. Skin preparations:
-best for persistent effect: Chlorhexidine
-immediate reduction of bacterial counts: Alcohol
7. Shave 24 hours before surgery increases chance of wound infection
8. Tetanus:
-booster every 10 years
-2yo never vaccinated, with laceration: tetanus toxoid and TIG at different site (plus future doses)
9. Endocarditis prophylaxis required for esophagoscopy with sclerotherapy injection
10. Abscess secondary to Bacteroides fragilis, best Abx: Clindamycin
11. Parotitis: most common organinsm is Staph. aureus; best Abx is cloxacillin
12. Strep gives diffuse erythematous rash use penicillin
13. Central line infection, most likely organism: Staph. epidermidis
14. Pre-op antibiotics for inguinal hernia repair: 1st generation cephalosporin (Ancef)
15. Patient with chills and fever 6 hours after insertion of Foley catheter, first thing done: blood cultures
16. Most suitable agent to sterilize surgical instruments: glutaraldehyde
17. Rabies:
-single stranded RNA virus
-Boy bitten by neighbourhood dog, best management: quarantine dog for 10 days do not treat for rabies
-Treatment if not vaccinated: local wound management, HRIG 20IU/kg (½ in wound, ½ IM gluteal), and
vaccine (HDCV or RVA) 1.0 ml deltoid for 5 doses (days 0,3,7,14 and 28)
18. Most common etiology of CJD: corneal transplant
19. Post-splenectomy organisms: S. pneumonia, H. flu, Neisseria sp. (encapsulated organisms)
20. Punctured right index finger swollen finger: tenosynovitis
21. Most common etiology for isolated aortic regurgitation: Endocarditis
22. C-section: prophylactic antibiotics given after cord is clamped
23. Patient does not need prophylaxis for cardiac catheterization
24. Strep causes erythema with serous exudate, even with bacterial count of 103/gm tissue
25. Most likely cause of wound infection from domestic animal bite: Pasteurella multocida
26. Most likely cause of wound infection from human bite: Staph and strep; Eikenella corrodens (15%)
27. Least likely to require prophylactic antibiotics: history of rheumatic fever as child
28. Most common cause of empyema is pneumonia
29. Central line infection:
-staph epi: can use sterilized line again
-staph aureus: remove line, 48 hours w/o line, Abx for 6 weeks
30. Toxic shock syndrome staph aureus toxin
31. Most common nosocomial infection: UTI
32. Most common organism causing nosocomial pneumonia: gram negatives (pseudomonas)
33. Systemic candidiasis frequently seen in immune suppressed patients
34. Treatment of chlamydia: doxycyline
35. Pseudomembranous colitis associated with any antibiotics (esp. clindamycin, ampicillin, cephalosporins)
36. Patient with tissue expander, presents with redness and discharge from area. Management: remove expander
37. Patient had C-section, on 1st generation cephalosporin and develops temperature post-op. Additional
coverage for: ?gram-negatives vs. enterococcus
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F.Ling - POS notes and points (9)
Trauma
1. Basically intubate everyone with airway problems
2. Most common cause of hypotension post trauma: hypovolemia
3. Child with head injury, decision to sending patient home based on length of time he was unconscious
4. Child with poor IV access:
-percutaneous peripheral vein, saphenous vein, venous cut down
-intraosseus up to 6 years (emergency)
5. Aortic tear most commonly in decelerating injuries at the level of ligamentum arteriosum distal to left
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F.Ling - POS notes and points (10)
subclavian artery
6. 40yo male, MVA, HR 140 RR 40 deviation of trachea: 14 gauge needle to 2nd ICS followed by chest tube in
5th ICS AAL
7. Revised trauma score, Triage score and Abbreviated injury scale take all into account except: urine output
8. Hemotympanum: mostly associated with base of skull fracture
9. MVA, widened mediastinum and loss of left CVA aortogram
10. Complete tracheo-bronchial disruption presents as: Massive air leak in chest tube with no lung expansion
11. Signs of ruptured diaphragm: air fluid level in lower lung field with NG tube in lung on CXR
12. Woman 36 wks gestation involved in MVA. Abdominal pain, uterus hard tender, bleeding PV: abruption
13. Treatment of neurogenic shock does not include MAST pants
14. Management of patient with spinal cord injury. First thing to do is manage airway
15. Best time to get critical x-rays in trauma is: after primary survey
16. Pathophysiology of neurogenic shock: increased venous capacitance due to decreased peripheral resistance
17. Most common complication of CSF leak: meningitis
18. Patient with knee dislocation and absent distal pulses. After reduction, pulse returns but remains weak do
femoral angiogram
19. DPL positive except: amylase level 20IU (should be over 80IU)
-poor for assessing retroperitoneal hematoma
20. Goal of CPR: maintain cerebral perfusion
21. Carotid sheath exposed due to injury. Best managed by: primary closure
22. Know GCS scoring
23. Cephalic vein should be catheterized for hypotensive MVA patient
24. Pelvic fracture, still showing signs of hemorrhage despite volume resuscitation. Next step: apply external
fixator.
25. Chest tube drains 1200cc blood originally followed by 600cc in next 3 hours. Next step: thoracotomy
-most common source of bleeding: intercostal artery
-indications:
->1500 cc initially
->200cc/h for 4 hours
->100cc/h for 8 hours
26. Relief of symptoms immediate with aspiration of pericardial effusion
27. Spinal cord injury having intact sensation, flaccid paralysis in upper limbs and able to hold lower limbs
against gravity. Patient has: central cord injury
28. Patient with extensive facial fractures:
-fixation can be delayed until patient is more stable
-CT is best method for evaluation
29. Revised Trauma Score: GCS, RR, BP
30. Cranial nerve injury most commonly seen with intracranial injury: olfactory (I)
31. Cranial nerve injury most commonly seen with increased ICP: abducens (VI)
32. Compartment syndrome:
-most reliable sign: pain out of proportion to injury and on passive movement
-least reliable sign: absent pulses
33. Child with supracondylar fracture of humerus. Suspect Volkmann’s ischemic contracture. Confirm with:
pain on passive extension of fingers
34. Treatment for frostbite: rapid rewarming of extremities
35. Child presents with frost bite hands and feet, you should: elevate the core temperature if significantly reduced
36. Post MVA, bleeding at urethral meatus with comminuted fracture of pelvis: retrograde urethrogram
37. Common finding in IVP for trauma patient: decreased perfusino with renal contusion
38. Most sensitive indicator of pericardial tamponade is: ?pulsus paradoxus
39. The following ICP in trauma: hyperventilation, elevating HOB, loosen tight clothing around neck, mannitol
-except: steroids
40. Most common solid abdominal organ injured in blunt injury: spleen
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41. Most common viscus abdominal organ injured in blunt injury: duodenum
42. Most common organ abdominal injured in penetrating injury: liver
43. Coverage for distal 1/3 of tibia: musculocutaneous free flap
Burns
1. A man with 1st degree burns to face, 2nd degree burns to anterior thorax and abdomen, circumferential burns
to right thigh and lower leg. Body surface affected: 36%
2. STSG will have better take on contaminated surface than FTSG
3. Less contraction with FTSG, better cosmetic results (skin colour matching)
4. Respiratory complications most common cause of death in burn patients
5. Most common cause of pneumonia is via bronchoalveolar route (vs. hematogenous route)
6. Parkland formula for burns: 4cc/%burn/kg. 50% in first 8 hours and 50% in next 16 hours.
7. Patient with inhalational injury, first step in management: secure airway
8. Patient with inhalational injury, all execpt: tracheostomy
9. Unconscious patient with head injury in a house fire is most likely to have inhalational injury
10. Inhalational injury will require more fluids than calculated by Parkland formula
11. Most sensitive sign of inhalational injury: carbonaceous sputum
12. Severity of inhalational injury proportional to time of exposure, closed room
13. Most important s/e of silver sulfadiazine: leukopenia (neutropenia)
14. Alkali causes liquefaction necrosis; acids causes coagulation necrosis
15. 14 yo with 25% partial thickness burns to left side of face, chest and upper arm. Most appropriate initial
management: assessment and treatment of respiratory system
16. Patient with 3% full thickness burns secondary to molten metal in the middle of the back. Treatment of
choice: early excision and skin grafting
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F.Ling - POS notes and points (12)
10. Keloids extend beyond the margins of the surgical wound; best treated by steroid injections; difficult to
distinguish microscopically from hypertrophic scars
11. Best moisture barrier: keratinocytes in epithelium
12. Effect of delayed wound healing due to radiation caused by: Damaged endothelium
13. Steroid effects:
-inhibit inflammatory response
-inhibit fibroblast proliferation
-inhibit protein synthesis in wound
-delays wound contracture
-alters t-cell function
-decreases tensile strength of closed wound
-retards epithelialization and angiogenesis
14. Chronic steroid use causes thinner dermis than normal with less collagen
15. Steroid effects can be reversed by: Vitamin A
16. Hypertrophic:
-increased water content, beta-growth factor
17. In urine, best indication of collagen breakdown: hydroxyproline
18. Donor site on thigh for STSG heals by epithelialization
19. Severity of contracture which could affect the patients function is influenced by: site and depth of the wound
20. Pyoderma gangrenosum:
-hypersensitivity vasculitis seen in Crohn’s, UC, RA, lymphoma, leukemia
-50% idiopathic
-tx: dapsone, steroid therapy and local wound care
21. Best indicator of muscle viability is bleeding after incision
22. Staples, suture and tape provide same strength to healing wound
23. Staples better than sutures when it comes to wound infection
24. Bone remodelling continues even after 6 months. Osteoclastic activity is the dominant force.
25. Regeneration can occur from cell of the following except: ?dermal papilla
26. Macrophages digests tissue within an abscess
27. Wound infection most likely to occur from normal flora of skin
28. Most important factor to prevent wound dehiscence is: surgical technique
29. Dermal papillae: basal cell layer; does not contribute to epithelialization
30. Repair of peripheral nerve, the least and last function to be retained: two point discrimination
31. Vitamin C required in hydroxylation of proline and lysine in collagen synthesis
Oncology
1. Transcription of mRNA from DNA occurs in the nucleus catalysed by RNA polymerase
2. Translation occurs on ribosomes; synthesis of protein from mRNA sequence
3. Most specific finding for malignancy histologically: mitotic figures and prominent nucleoli
4. Tumour arising from sympathetic nervous system in pediatric population: Neuroblastoma
-most common abdominal tumour in children between 2-4 years
5. Tumour associated with SIADH: small cell (oat cell) ca
6. Symptomatic malignant pericarditis: treat with intraoperative pericardial window
7. Alkylating agents: non-cell cycle specific
-cyclophosphamide, busulphan, cisplatin, dacarbazine, chlorambucil, mustard gas
8. Most serious side effect of 5FU (cell-cycle specific): myelosuppression
9. Most important side effect of bleomycin: pulmonary fibrosis
10. Most important effect of doxorubicin: cardiac toxicity
11. Vincristine (cell-cycle specific, m-phase):
-prolonged ileus, peripheral neuropathy, alopecia, mild myelosuppression, ADH effect, vesicant
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F.Ling - POS notes and points (13)
12. Cyclophosphamide:
-alkylating agent, non-cell cycle specific
-s/e: hemorrhagic cystitis, neutropenia, n/v, alopecia, infertility
13. Most likely tumour to cause hemorrhage after metastasis to brain: melanoma
14. Colon carcinoma least likely to metastasize to bone (PTBLK)
15. Aneuploidy:
-absence of normal complement of DNA
-most common genetic aberration seen in malignant cells
16. Brachytherapy gives least radiation to the skin
17. Multiple ports used in radiation therapy because it protects radiosensitive tissue
18. Molecular oxygen enhances the effects of radiation
19. Radiotherapy most dependant upon:
-adequate oxygen tension
-mitosis
-vascularity
-temperature
20. Most common neoplasm associated with Paget’s disease: Osteosarcoma
21. 35yo with previous history of radiation, has solitary asymptomatic thyroid nodule, cold on thyroid scan and
FNA consistent with thyroiditis. Next step: thyroidectomy
22. Sero-sanguinous discharge from single breast duct. Concerned about cancer.
23. Mortality from cancer in females: lung breast colorectal
24. Mortality from cancer in males: lung prostate colorectal
25. Incidence of cancer in males: prostate lung colorectal
26. Patient with lump in breast 2 cm in size, last month 3 cm in size. Next step: FNA
27. Patient with 2cm neck mass in upper cervical nodes of 2 months duration. Plan should be: examination of
aerodigestive tract first, then FNA
28. Pain control in cancer patients: use of ASA may potentiate the effect of narcotics
29. Fractionation of radiation allows normal tissue to heal between doses
30. Oncogenes: genes that, when expressed, contribute to the development of malignancy
31. Proto-oncogenes: genes found in normal tissues that, when activated may lead to transformation of the cell to
a malignant phenotype
32. Best method to perform anterior scalene lymph node biopsy: borders of dissection should include internal
jugular vein lateral, omohyoid muscle superior
33. Most common cause of SVC obstruction: small cell ca
34. Antidote to methotrexate: folinic acid (leucovorin)
35. Barrett’s esophagus: most predictive of malignancy in severe dysphagia
36. Pathological changes in radiation pneumonitis:
-1h-1day: immediate release of surfactant
-1-3 months: compensatory swelling of type II cell
->3 months: disappearance of type II cell and alveolar collapse
37. Malignant melanoma: ratio of white:black = 20:1
38. 2cm lesion on bone scan can been because of: osteoblastic activity
39. Nasopharyngeal carcinoma most commonly presents as: neck mass (60%)Changes in skin secondary to
radiation:
-end arteritis obliterans, atrophic skin changes, erythema, hyperpigmentation
40. Radiomimetic chemotherapy: alkylating agents
41. Anti-tumour agent produces its effect on tumour cells by decreasing the number of tumour cells by a constant
fraction
42. Neoadjuvant chemotherapy: chemo used prior to definitive tx (eg. surgery or radiation)
-benefits: size of tumour, determines response to chemo to predict the efficacy in an adjuvant setting
43. Lesions associated with malignant melanoma: Lentigo maligna, congenital nevus, dysplastic nevus
44. 40 year old asymptomatic, CT scan shows 2 cm adrenal mass. Most likely adenoma
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Surgical Complications
204
F.Ling - POS notes and points (16)
25. Most likely finding in patient with early ARDS: refractory hypoxia
26. Most common source of bleeding from tracheostomy: inferior thyroid artery
27. Most common source of massive bleeding from tracheostomy: innominate artery
28. Damage to thoracic duct NOT seen in catheterization of right IJ
29. PE causes less than 10% infarction
30. Cause of hypoxia in PE is due to no perfusion of ventilated alveoli
31. Least sensitive method of diagnosing DVT in legs: history and physical
32. Persanten is NOT and acceptable method for DVT prophylaxis
33. Platelet inhibitors are not effective in DVT prophylaxis
34. Pathophysiology of high output renal failure: retention of BUN
35. Best method to follow glucose levels in a diabetic patient post-op: blood sugar
36. Most likely cause of hypoxia post-op in patient with known IHD: pulmonary edema (2o CHF)
37. Patient with urinary retention, foley inserted giving 1300cc urine. Patient continues to have u/o, most likely
cause: post-obstructive polyuria
38. Patient administered penicillin and develops urticaria and faints. Initial management: epinephrine
39. Most common site for DVT: calf vein (soleus and posterior tibial and peroneal veins)
40. Steroid therapy produces muscle wasting seen first in: pelvic and shoulder region (proximal muscle
weakness)
41. Contrast reaction: urticaria, hypotension, chest pain, dyspnea
42. 30 year old with bilateral hilar adenopathy and non-caseating granulomas on mediastinosopic biopsy:
sarcoidosis
43. Most likely cause of acute scrotum in 30 year old: acute epididymal orchitis
44. ATN: secondary to ischemia, septicemia, tubular toxins (myoglobin, contrast, drugs), acute pancreatitis,
prolonged hypotension
45. All can cause paralytic ileus: peritonitis, retroperitoneal hematoma, opioids, myxedema
46. Gynecomastia caused by: renal failure, liver failure, Kleinfelter’s, adrenal cortical tumours, spironolactone
47. Superficial femoral embolism, definitive treatment is embolectomy
48. Least effective drug in preparing patient with thyrotoxicosis for surgery: phenylephrine
49. Air embolism:
-100-300cc produce typical features
-IV line can be used to release air; place patient in LLD position
-hypocapnic secondary to hyperventilation
50. Pathology seen in ARDS:
-small stiff wet lungs
-atelectatic changes
-patchy diffuse hemorrhages
-alveolar infiltrates
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10. 57yo male has infected appendectomy. Several days later he is hypotensive with SVR 600 and CVP 8, most
likely diagnosis: Septic Shock
11. Patient with massive PE and in shock. What would suggest he is a candidate for thrombolytic therapy: he
requires inotropic support
12. Brain death: absence of cerebral blood flow on cerebral angiogram
13. Coronary blood flow is determined by myocardial oxygen demand
14. Diastolic blood pressure is dependent on peripheral vascular resistance
15. Phenylephrine acts on alpha-receptors to cause vasoconstriction
16. Intra-aortic balloon pump:
- MAP, coronary blood flow, peak diastolic pressure, afterload
-contraindicated in severe aortic regurgitation, aortic stenosis, ventricular aneursym, dissection of aorta,
ventricular septal defect, recent prosthetic graft in aorta within 12 months
17. Effects of PEEP:
-prevent alveolar collapse by maintaining FRC above critical closing volume; improves lung compliance
- V/Q mismatch
- venous return CO
- afterload
- EDV
- ICP, CVP
18. Young male with disappearance of distal pulses following exercise can best be explained by: redistribution of
peripheral vascular resistance
19. GFR affected by:
-arterial oncotic pressure, interstitial oncotic pressure, AV pressure difference, renal blood flow
-except: reflux
20. Oxygen dissociation curve:
-SaO2 vs oxygen tension
-right shift: T, [H], CO2, DPG
-left shift: T, [H], CO2, DPG, carboxyhemoglobin
21. ARDS: 4 stages:
-I: hypoxia and hypocapnia
-II: hypoxia and hypercapnia
-III: x-ray changes
-IV: massive x-ray changes
22. ARDS earliest and best indicator: refractory hypoxemia
-PaO2:FiO2 < 200
23. Best method to assess capillary perfusion in a patient with shock: urine output
24. Patient developed A-fib with rapid ventricular response, most effective treatment initially:
-unstable: cardioversion
-stable: digoxin (old)
25. Interstitial pulmonary disease: FEV1, pO2, pCO2, residual volume
26. Best indicator of alveolar ventilation: pCO2
27. Starling’s law: SV relationship to EDV
28. Best treatment for mild digitalis toxicity: stop the drug
29. Cerebral auto-regulation: regulation of brain blood flow according to variation in arteriovenous pressure
30. Best non-invasive test to differentiate primary pulmonary hypertension from thromboembolic pulmonary
hypertension: radioisotope perfusion/ventilation scan
31. At sea-level, mixed venous oxygen of 40 mmHg considered normal
32. One gram of 100% saturated Hb contains 1.39 ml of O2
33. Indications for artificial ventilation:
-PO2 < 70 on oxygen mask
-PCO2 > 50
-alveolar-arterial difference 60 after 100% O2
206
F.Ling - POS notes and points (18)
Statistics
207
Methods of Fractionation
Conventional Fractionation:
-1.8-2.2 Gy per day for 5 days/week for 5 weeks (45-55 cGy total)
Method Fractions Dose per Total Total Acute side Late side
per day fraction treatment treatment effects effects
dose time
An additional rationale for hyperfractionation is to allow radiosensitization through redistribution. The greater the
number of fractions, the greater the likelihood that the tumor will be in a sensitive phase of the cell cycle at some
time during the treatment. This strategy invariably results in more intense acute reactions when compared to
conventional treatment.
In the accelerated fractionation schemes, the dose per fraction is unchanged while the daily dose is increased, and
the total time for the treatment is reduced. Three basic variations are possible.
Continuous hyperfractionated accelerated radiation therapy (CHART) is an intense schedule of treatment, where
multiple daily fractions are administered within an abbreviated period of time. An intense acute reaction develops in
most patients. This reaction usually limits the total dose.
In a concomitant boost technique, the first fraction of the day is administered in a larger volume, while the second
fraction is targeted to a reduced-boost field of treatment. The boost may be administered early in the course of
therapy or toward the end of treatment. This regimen is based upon the recognition that the treatment can induce an
accelerated repopulation of the tumor cells so that reduction of the overall treatment time results in improved
control.
Clinical trials are in progress with the goal of evaluating these various altered fractionation patterns and comparing
them to conventional treatment. Preliminary results from the recently completed randomized trial, RTOG-9003,
supports the benefit of altered fractionation over conventional treatment for head and neck cancer.
208
ANTIMICROBIAL TREATMENT GUIDELINES
FOR ACUTE BACTERIAL RHINOSINUSITIS 2004
Sinus and Allergy Health Partnership
ADULTS
Beta-lactam allergic
TMP/SMX 83 84
Telithromycin 77 73
Mild disease with recent antimicrobial use (past 4-6 weeks) or moderate disease
Gatifloxacin/levofloxacin/moxifloxacin 92 100
Ceftrizxone 91 99
Beta-lactam allergic
209
CHILDREN
Cefuoxime axetil 85 87
Cefdinir 84 86
Beta-lactam allergic
Mild disease with recent antimicrobial use (past 4-6 weeks) or moderate disease
Beta-lactam allergic
Clindamycin 79 78
210
OLFACTORY FUNCTION AND DYSFUNCTION
INTRANASAL CHEMOSENSATION
-granule cells: maintain synaptic contact between tufted cells and mitral cells
211
OLFACTORY DISORDERS
Terminology
-anosmia: loss of ability to smell
-hyposmia or microsmia: decreased ability to smell
-total anosmia: inability to smell all odorants on both sides of nose
-dysosmia: distorted smell perception
-2/3 of causes due to prior URI, head trauma, nasal and paranasal sinus disease; usually permanent
-other causes:
-congenital:
-familial dysautonomia
-Kallmann’s syndrome
-autosomal dominant
-hypogonadotrophic
-anosmia secondary to incomplete olfactory bulb and stalk, hypothalamus, or
olfactory epithelium -
-iatrogenic: septoplasty, rhinoplasty, turbinectomy, XRT
-intranasal neoplasms
-intracranial tumours
-olfactory groove meningiomas, frontal lobe glioma, pituitary adenoma, meningioma)
-epilepsy
-psychiatric disorders
-exposure to environmental chemicals, medications
-smoke, sulfur dioxide, putrid gases, cocaine, cadmium, heavy metals, radiation,
chemotherapy
212
CLINICAL ASSESSMENT AND PATIENT MANAGEMENT
Olfactory Testing
-reliability of a number of olfactory tests is low
-UPSIT (University of Pennsylvania Smell Identification Test)
-4 booklets containing 10 odorants a piece
-multiple choice (forced choice) with 4 response alternatives
-chance performance = 25%
-very low scores reflect avoidance, and hence recognition of the correct answer
-high reliability
-Electrophysiologic Tests:
-still experimental
-OERPs: odor event-related potentials; not reliable, non-localizing
DETECTION OF MALINGERING
PATIENT MANAGEMENT
213
NASAL FUNCTION AND EVALUATION
Vasomotor Control
Sympathetic
-norepinephrine (primary neurotransmitter)
-avian pancreatic polypeptide
-neuropeptide Y
Parasympathetic
-acetylcholine (primary neurotransmitter)
-vasoactive intestinal polypeptide
-peptide histamine isoleucine
Other
-substance P
-stimulation of smooth muscle, vasodilation and stimulation of nasal secretion
-H1 and H2 histamine receptor agonist vasodilator
-leukotriene D2 vasodilator
RESPIRATION
-nasal vestibule
-aka: external nasal valve
-skin-lined region beginning anteriorly at nares and extending to level of caudal end of
upper lateral cartilage
-dilator nares muscles prevents collapse from negative inspiratory pressure
-potential cause of obstruction during inspiration
-nasal valve
-aka: internal nasal valve, limen nasi
-borders: nasal septum, caudal end of upper lateral cartilage, anterior end of inferior
turbinate, nasal sill
-narrowest segment of nasal airway (50% of total nasal resistance)
214
-nasal cavum
-region posterior to piriform aperture
-engorgement of inferior turbinates contributes to resistance
-resistance can change with posture, disease, physiologic state and psychologic factors
-major sites for regulation of airway resistance:
-dilator nares muscles
-venous sinusoids of nasal turbinates
Nasal Cycle
-intrinsic variability of nasal airway resistance that occurs in cyclic pattern in as may as 40% of persons
-duration 2-6 hours
-positional effect:
-congestion of nasal chamber in lower position
-d/t neural response to stimulation of pressure receptors on surface of body
History
-character of nasal obstruction:
-onset and duration
-constant vs intermittent
-unilateral (tumours, normal nasal cycle) vs bilateral
-associated mouth breathing, snoring, anosmia/hyposmia/taste disturbances, tearing (nasolacrimal
duct obstruction or allergy)
-contributing factors:
-potential toxin and allergen exposure Common Classifications of Drugs that Cause
-known drug allergies Rhinorrhea and Nasal Congestion
-medications -antihypertensives
–history of immunodeficiency, asthma, sinusitis, -psychotropic medications
otitis media, allergy, sleep disturbances, facial -oral contraceptives
trauma or surgery -chronic nasal decongestants: rhinitis
medicamentosa
-associated symptoms: -cocaine: local vasoconstriction
-allergic component (sneezing, itchy and watery -tobacco: irritates mucosa and impairs ciliary
eyes, clear rhinorrhea) clearance
-antithyroid medication
-sinus involvement (facial pain, headaches)
-aspirin: activates peripheral chemoreceptors
-acute infection (fevers, malaise, purulent or -marijuana
odorous rhinorrhea, pain)
-other head and neck symptoms:
-sore throat, postnasal drip, cough, ear complaints, halitosis, ocular pain, hoarseness
Physical Exam
-external nasal exam:
-external deformities, nasal flaring, nasal airflow
-anterior rhinoscopy:
-examine with and without topical decongestion
-quality of turbinates, nasal mucosa
-nasal septum
-osteomeatal complex obstruction
-foreign bodies, nasal masses, choanal opening
-quality of nasal secretions:
-purulent or thick (infectious)
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-watery and clear (vasomotor rhinitis, allergy)
-salty and clear (CSF leak)
-H&N exam:
-facial tenderness, tonsil and adenoid hypertrophy, cobblestoned posterior pharynx, cervical
adenopathy, otologic exam
Ancillary Test
-allergy evaluation
-paranasal plain films
-CT/MRI
-biopsy of nasal mass
-ciliary biopsy and mucociliary clearance tests
-nasal secretion protein and glucose (evaluate CSF leak if suspected)
-culture and sensitivity
-pulmonary function tests
-olfactometry
-rhinomanometry: provides an objective measurement of airway resistance, largely not utilized in clinical
practice since highly time consuming, not cost effective, and inaccurate
Rhinomanometry
-used to measure pressure needed to produce airflow through nasal airway ie. resistance
-does not measure location of nasal obstruction
-anterior rhinomanometry:
-measurement of transnasal pressure at anterior end of nose
-differential pressure transducer inserted into occluded nostril, difference between atmospheric
pressure and nasal pressure = pressure difference b/n nasopharynx and air = driving pressure for
airflow through unobstructed nostril
-limitations:
-cannot be used in cases of complete occlusion of one nasal passage
-septal perforation or marked flaccidity of septum
-posterior rhinomanometry:
-air pressure in nasopharynx measured with catheter placed in mouth
-interpretation:
-two major types of nasal obstruction: mucosal hypertrophy/congestion and structural deformity
-resistance measured before and after decongestion to determine relative importance of the above
two factors
-nasal resistance greater than 0.3 Pa/cm3/s usually symptomatic
-threshold for subjective obstruction varies
Effect of Decongestion:
-if decongestion causes less than 35% decrease in resistance, a structural cause can be inferred
-eg. septal deformity, conchal hypertrophy, stenosis, concha bullosa
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Airway Collapse:
-typical rhinomanometric finding of collapse is an asymmetric nasal pressure-flow curve
-collapse only occurs during inspiration, therefore higher inspiratory resistance c/f expiratory resistance
Acoustic Rhinometry
-noninvasive measurement of cross-sectional area of regions of nasal airway
-can help identify location of flow-limiting segments in nasal airway
-results reproducible and accurate
-graph produced of nasal cross-sectional area as function of distance
-able to find narrow segments of airway
-acoustic pulse is introduced and reflected pulse measured
-does not measure effect of narrow regions on airflow dynamics or airway resistance
-area distal to severe constriction may not be accurately estimated
-Characteristics of Rhinograms:
-initial flat tracing = nosepiece
-first depression (I notch) = nasal valve
-second trough (C notch) after a small peak = head of inferior turbinate
-upward slope (climbing W) with small peaks and troughs = posterior nasal cavity and its
increasing cross-sectional area
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SINUS ANATOMY AND FUNCTION
-maxillary and ethmoid sinuses are the only sinuses at birth which are large enough to be of
clinical significance
Maxillary sinus:
-first sinus to begin development (65th day GA)
-not evident on x-ray until 4-5 months of age fluid filled
-biphasic growth:
-first 3 years of life
-second growth acceleration between 7-12 ya pneumatization laterally
-slow expansion until 18 years
-adult dimensions: 34x33x23 mm; 15 ml
Frontal sinus:
-begins development during 4th month
-visible usually after 2nd year on radiographs
-sinus invades frontal bone by 5 ya, reaching adult size in late adolescence
-dimensions: 17x28x27; 6-7ml
-4-15% of population: developmental failure of one frontal sinuses present
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Sphenoid sinus:
-pneumatization begins at 3 ya
-growth to sella turcica by 7 ya
-adult size by 18 ya
-dimensions: 23x20x17 mm; 7.5 ml
ANATOMY
Ethmoidal Sinus
-lateral wall: lamina papyracea
-medial wall: functions as lateral wall of nose
-midline vertical plate of ethmoid bone:
-superior portion termed crista galli
-inferior portion termed perpendicular plate of ethmoid bone
-roof of ethmoid bone = horizontal plate: separates anterior cranial fossa from nasal cavity
-thin medial portion: cribriform plate
-thick lateral portion: fovea ethmoidalis
-lateral lamella: extremely thin lateral part of cribriform plate
-Keros classification:
-Type I: cribriform plate 1-3 mm below fovea ethmoidalis
-Type II: 4-7 mm below
-Type III: 8-16 mm below
-anterior vertical attachment of middle turbinate to horizontal plate separates cribriform plate from lateral
lamella and fovea ethmoidalis
-dissecting lateral to turbinate prevents entrance into horizontal part of cribriform plate
-presence of Keros type II or III ethmoid roof risk of entering anterior cranial fossa through
lateral lamella
-anterior cells:
-drain into ethmoid infundibulum of middle meatus
-frontal recess cells:
-most anterior cells
-0-4 cells
-form frontal sinus, supraorbital air cells
-infundibular cells:
-next most anterior
-1-7 cells
-agger nasi cells extend outside ethmoid capsule
-represent superior remnant of the first ethmoturbinal
-in close proximity to frontal recess
-often opened during FESS to get better view of nasofrontal duct
-can obstruct outflow of frontal sinus
-bullar cells
-1-6 cells
-consistent location in middle meatus
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-form bulla ethmoidalis
-may form suprabullar recess if anterosuperior wall of bulla does not reach ethmoid
roof
-uncinate process:
-thin semilunar piece of bone; part of ethmoid bone
-remnant of first ethmoturbinal
-middle turbinate:
-concha bullosa:
-pneumatization of middle turbinate; in 12% of population
-may result in nasal obstruction
-anterior end attaches to horizontal plate
-posterior end inserts laterally on lamina papyracea
-divides anterior from posterior ethmoid cells
-sinus lateralis or retrobullar recess: occurs if posterior wall of bulla ethmoidalis does not
contact third basal lamella
-posterior cells:
-drain into superior meatus
-Onodi cell:
-posterior ethmoid cell that can pneumatize an area of sphenoid bone superior and lateral
to sphenoidal sinus in 9-12% of population
-optic nerve and carotid artery can be exposed and injured during dissection in this area
-vasculature:
-anterior and posterior ethmoid arteries
-maxillary and ethmoid veins (cavernous sinus)
-innervation:
-anterior and posterior ethmoidal nerves (from nasociliary nerve, V1)
Maxillary Sinus
-supraorbital nerve dehiscent in 14% of population
-Haller cell:
-pneumatization of ethmoid complex into the roof to the maxillary sinus
-may occlude ostia
-1st and 2nd molars: two most dehiscent teeth in maxillary sinus (2.2% and 2.0% of persons, respectively)
-removal of teeth may result in oral-antral fistula
-accessory ostia present in 15-40% of cases
-Vasculature:
-maxillary and facial artery
-facial vein
-Innervation:
-infraorbital nerve (V2)
Frontal Sinus
-develops from anterosuperior ethmoidal cells
-frontal recess:
-medial wall: middle turbinate, uncinate process
-lateral wall: lamina papyracea
-posterior wall: anterior face of bulla ethmoidalis
-anterior wall: agger nasi cells
220
-drainage pattern:
-A: UP LP (80%); drainage medial to uncinate process to middle meatus
-B: UP base of skull; drainage lateral to uncinate process to infundibulum
-C: UP middle turbinate; drainage lateral to uncinate process to infundibulum
-vasculature:
-supraorbital and supratrochlear arteries
-ophthalmic (cavernous sinus) and supraorbital (anterior facial) veins
-innervation:
-supraorbital and supratrochlear nerves (V1)
-structure of sinus variable
-anterior wall is strongest, twice as thick as posterior wall
-drainage ostium in posteromedial portion of sinus floor
-Foramina of Breschet: small venules that drain the sinus mucosa into the dural veins
Sphenoidal Sinus
-anatomical relationships of sphenoid ostium:
-face of sphenoid sinus lies 7 cm from nasal sill at 30o angle with floor of nasal cavity
-empties into sphenoethmoidal recess via small ostium
-adjacent to posterior border of nasal septum
-adjacent to posterior border of nasal septum
-0.5-4 mm in diameter
-located 10-15 mm above sinus floor or 30 degree above floor of nasal cavity
-1/3 up from choana to base of skull
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-maxillary vein (pterygoid plexus)
-innervation:
-sphenopalatine nerve (parasympathetic fibers and V2)
222
PHYSIOLOGY
Sinus Epithelium
-pseudostratified ciliated columnar epithelium
-four basic cell types:
-ciliated columnar epithelial cell:
-50-200 cilia per cell; 9+2 microtubule doublets; 10-20 beats/s
-nonciliated columnar cells:
-contain microvilli that expand surface area to improve humidification and warming of
air
-basal cell:
-may be primitive stem cell that can differentiate into other epithelial cells
-goblet cell:
-produce thick mucous after stimulation by irritating substance
-higher amount in maxillary sinus than other sinuses
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-submucosal glands: serous and mucinous glands penetrate lamina propria
-parasympathetics thick mucous
-sympathetics thin mucous
-density highest at ostia of maxillary, sphenoid, and anterior ethmoidal sinuses
Mucous Blanket
-two layers:
-sol layer:
-thin, periciliary fluid allowing cilia to be mobile
-produced by microvilli
-gel layer:
-upper layer of thick mucous (mucoglycoproteins) that supplies insertion point for tips of
the cilia
-produced by goblet cells and submucosal glands
-provides protection against low humidity and cold
-traps foreign particles and bacteria
-IgA inhibits adherence of bacteria to epithelial surface
-causes agglutination then clearance by phagocytosis
-IgG and interferon to provide antiviral role
-lactoferrin
-transports iron into bacteria antioxidant activity
-lysozyme
-secreted by serous cells
-mucociliary clearance:
-3-25 mm/min towards natural ostium
-maxillary sinus: star-shaped drainage pattern from sinus floor superiorly to ostium
-frontal sinus: medial wall of frontal recess roof lateral downward and medially toward
sinus ostium
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A. External Nose
Framework
Cartilages: greater alar (lower lateral), septal, lateral nasal (upper
lateral), lesser alar, sesamoid.
b. Bones: Nasal, maxillary, frontal
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Blood supply
External carotid
external maxillary: lateral nasal, angular, alar, septal, external
nasal.
Internal carotid
ophthalmic, which gives rise to anterior ethmoid, posterior
ethmoid, and dorsal nasal vessels
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B. Internal Nose:
Floor
floor of nose is formed by hard palate
nasal cavity extends as far back as soft palate, where posterior
choanae opens into nasopharynx.
Roof
roof of nose is adjacent to anterior cranial fossa
cribriform plate contains numerous tiny perforations which transmit
sensory fibers to olfactory bulbs
posteriorly, roof slants downward as anterior wall of sphenoid sinus.
Lateral Walls
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Blood Supply
Anterior ethmoid - to roof and anterior superior portion of septum
and lateral wall.
Sphenopalatine - to lateral wall of nose
Nasopalatine - supplies roof, septum, and floor
Lateral nasal - supplies lateral nasal wall anteriorly.
Descending palatine - supplies lateral nasal wall posteriorly.
Pharyngeal - supplies roof posteriorly
Posterior ethmoid - supplies septum and lateral nasal wall superiorly
Septal - supplies septum inferiorly and floor
Nerve supply
Medial internal nasal - to septum, anterosuperiorly
Lateral internal nasal - to lateral wall, anterosuperiorly
External nasal - to skin of back of nose
Posterior superior nasal - supplies septum and lateral wall
posteroinferiorly, to middle turbinate
Posterior inferior nasal - to floor and inferior turbinate
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Pharyngeal - to choana
Anterior superior alveolar - to inferior meatus
Infraorbital - to vestibule
Lymphatics: drained by
Facial venous drainage
Retropharyngeal
Superior deep cervical
Submandibular
PARANASAL SINUSES
These are air- filled, mucosal- lined cavities which develop in facial and cranial
bones. spaces communicate with nasal airway. Their function is unknown but has
been subject to a great deal of speculation. They could serve to decrease weight
of skull or to function as resonators for voice. In lower animals with a more acute
sense of smell, sinuses are largely lined by olfactory epithelium. Sinuses may
have originally developed to increase available surface area for sense of smell.
Therefore, in humans, with olfaction limited to a much smaller area, sinuses may
be vestigial anachronisms.
C. Ethmoid - Numerous cells in superior and lateral walls of nose, and in medial
walls of orbits.
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D. Sphenoid - Paired, in sphenoid bone. Sella turcica projects into this space.
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NASAL SEPTAL ABNORMALITIES
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NONALLERGIC RHINITIS
Bacterial Rhinitis
-common pathogens: pertussis, diphtheria, group A strep, chlamydia
-tx: antibiotic regimen, symptomatic therapy similar to viral rhinitis
Rhinoscleroma
-pathogen: Klebsiella rhinoscleromatis (Frisch’s bacillus)
-endemic to East Europe, North Africa, South Asia, Central and South America
-SSx and stages:
-catarrhal: persistent purulent rhinorrhea, nasal honey comb-colour crusting
-granulomatous: small, painless granulomatous nodules in upper respiratory tract (including glottis
and subglottis)
-sclerotic: lesion heals with extensive scarring (dense fibrotic narrowing of nasal passage)
-dx: biopsy and culture
-histopathology:
-Mikulicz’s cell: foamy histocytes continuing the bacteria, “moth eaten” cytoplasm
-Russell bodies: bloated plasma cells with bifringent inclusions
-pseudoepitheliomatous hyperplasia
-tx: long-term antibiotics, debridement, consider laser excision or cryotherapy
233
Rhinosporidiosis
-pathogen: Rhinosporidium seebri
-endemic to Africa, Pakistan, India, Sri Lanka, spread from contaminated water
-SSx:
-friable, “strawberry” red polypoid nasal lesion
-epistaxis, obstruction
-dx: culture and biopsy
-histopathology:
-pseudoepitheliomatous hyperplasia, submucosal cyst, fungal sporangia with chitinous shells
-tx: surgical excision with cauterization of the base and oral antifungal angents, corticosteroid injections,
may consider dapsone
Hormonal Rhinitis
-causes:
-hypothyroidism (myxedema)
-elevated estrogen 2o pregnancy
-OCP
-menstrual cycle
- estrogen inhibits acetylcholinesterase ACh in parasympathetic ganglia edema, hypersecretion and
vascular engorgement of nasal mucosa
-manifests near end of first trimester and resolves after delivery
-tx: refractory to most regimens, conservative management (nasal saline irrigations, avoidance of allergens,
may consider nasal steroids), avoid decongestants (may place fetus at risk)
Vasomotor Rhinitis
-low nasal eosinophil counts and negative skin test results for allergy
-theory: abnormal functioning of parasympathetic input to turbinate and septal mucosa
-SSx:
-similar symptomatology to allergic rhinitis except with negative allergy evaluation, morning
rhinorrhea, alternating sides, pale nasal mucosa
-triggers:
-environmental conditions: cold air, high humidity, irritants
-medications: antihypertensives, antipsychotics, cocaine
-psychotropic: anxiety, stress, exercise
-diagnosis of exclusion
-tx:
-attempt to eliminate irritants and address causal factors if possible
-medical management:
-anticholinergic sprays
-corticosteroid sprays
-hypertonic saline sprays
-may consider short course of oral and topical decongestants or antihistamines
-surgical procedures:
-surface turbinate cautery
-septoplasty: removes mechanical points of irritation
-vidian neuronectomy (efficacy controversial)
-partial turbinectomy or turbinate ablation
-total turbinactomy risks atrophic rhinitis
234
-symptoms of perennial rhinitis
-dx: allergic symptoms with negative allergic tests
-tx: symptomatic relief similar to allergic rhinitis (nasal corticosteroids, antihistamines, decongestants)
Occupational Rhinitis
-nasal discharge or congestion due to exposure to airborne substance at work
-allergic or non-allergic
-treatment: identification and avoidance of offending irritant
Drug-induced Rhinitis
-caused by systemic drugs
-antihypertensives most often implicated
-reserpine, guanethidine, phentolamine, methyldopa, prazosin, chlorpromazine, beta-blockers,
ACEi
-Rhinitis medicamentosa:
-from prolonged used of topical vasoconstricting agents (> 7 days)
-pathophysiology:
-causes down-regulation of alpha-adrenergic receptors “rebound effect”
-refractory vasodilation of mucosal blood vessels
-increased parasympathetic activity
-increased vascular permeability
-mucosal injury can result: loss of cilia, metaplasia, fibrosis
-may be irreversible if vagale tone becomes atonic
-treatment:
-cessation of topical vasoconstrictors
-replacement with nasal saline
-acute nasal obstruction: some administer high burst of prednisone with rapid taper to
reduce mucosal edema
-may add oral antihistamines and/or steroid sprays
Gustatory Rhinitis
-food allergy possible but rare
-alcohol has direct vasodilating effect
-spicy foods watery rhinorrhea via vagally mediated mechanism
235
-secondary causes:
-over-aggressive nasal surgery
-chronic rhinosinusitis
-granulomatous disease of the nasal cavity
-radiation
-tx:
-saline irrigations, oil based ointment impregnated nasal tampons, vitamin A and D and iron
supplements, systemic or topical antibiotics (for secondary infections), consider nasal
vestibuloplasty or periodic nostril closure for failed medical therpy
DIFFERENTIAL DIAGNOSIS
-allergic rhinitis
-rhinosinusitis
-anatomic nasal obstruction
-choanal atresia
-adenoid hypertrophy
-septal deviation, turbinate enlargement, neoplasia
-polyps (Samter syndrome: asthma, nasal polyposis, asthma)
-systemic disease:
-Wegener granulomatosis
-sarcoidosis
-relapsing polychondritis
-granulomatous obstruction: tuberculosis, leprosy, sporotrichosis, blastomycosis, histoplasmosis,
coccidiomycosis, rhinoscleroma
CLINICAL EVALUATION
History
-PMHx, medications, FHx (immunodeficiency, ciliary dyskinesia, CF)
-onset: allergic rhinitis usually before age of 20 y
-unilateral fixed obstruction: structural cause
-daytime congestion: occupational rhinitis
-cyclical: nasal cycle
-onset of symptoms with relocation: environmental factors
-hyposmia or anosmia: polyposis
-mucopurulent discharge: primary or secondary rhinosinusitis
-epistaxis: neoplasm
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Physical Examination
-otology: SOM, TM retractions from allergy-induced ETD
-nasal exam:
-“allergic salute”: transverse crease across bridge to nose
-boggy pale mucosa typical of allergic rhinitis
-hyperaemia: infection or abuse of topical decongestants
-submucosal bumpiness and crusting suggestive of granulomatous disease
-watery secretions indicative of rhinitis
-nasal endoscopy
Other Tests:
-serum IgE and serum eosinophil levels: controversial clinical use because of unexceptional sensitivity or
specificity
-nasal cytology
-eosinophil allergic etiology
-neutrophils infectious etiology
MANAGEMENT
Antihistamines
-first line therapy in children with allergic rhinitis
-reduce symptoms of allergic rhinitis
-second generation H1 antagonists:
-non-sedating
-cetirizine, fexofenadine (Allegra), loratadine (Claritin), desloratadine (Aerius)
-no efficacy in management of nonallergic rhinitis
-intranasal antihistamines to relieve nasal congestion
Decongestants
-topical:
-phenylephrine, oxymetazoline, xylometazoline
-for short term use only: infectious rhinitis, ETD and acute exacerbations of allergic
rhinitis
-oral:
-pseudoephedrine, phenylephrine, phenylpropanolamine
-used alone for vasomotor rhinitis and infectious rhinitis
-used in combination with antihistamines in allergic rhinitis
-avoid in pts with hypertension, CAD, glaucoma, diabetes, urinary retention or
hyperthyroidism
-contraindicated with MAO inhibitors or TCAs
Corticosteroids
-topical:
-control congestion, rhinorrhea, itching and sneezing
-systemic absorption is ~2% but becomes rapidly metabolized
-no suppression of HPA axis
-inhibition of inflammation through inhibition of PLP A2 and subsequent release of
arachidonic acid
237
-oral:
-high burst with rapid tapering no more than 2 weeks
-used mostly for polyposis
Intranasal Anticholinergics
-for parasympathetically mediated rhinitis: gustatory or vasomotor rhinitis
-also can be used in allergic rhinitis
-contraindicated in pts with narrow-angle glaucoma or those taking another anticholinergic agent
238
ALLERGIC RHINOSINUSITIS
-pathophysiology:
-allergens contact nasal mucosa
-early-phase response (IgE mediated)
-occurs within 5 minutes of allergen exposure with maximum effect at 15 minutes
-cross-linking of IgE receptors on mast cells causes degranulation:
-histamine
-leukotrienes (LTC4, LTD4, LTE4)
-PGD2
-PAF
-HETE5
-cytokines
-increases local vascular permeability and proteolysis
-late phase response
-starts 5-7 h and peaks at 6-8 hours after allergen challenge
-cytokines recruit eosinophil, neutrophils and basophil
DIAGNOSIS OF ALLERGY
Adjunctive Tests
-nasal smear:
-obtained from inferior turbinate mucosa
-eosinophil (>25%) allergy
-neutrophils infection
Skin Testing:
-scratch test: not widely used
-prick test:
-series of allergens inserted by needle into skin
-positive “wheal-and-flare” reactions compared to controls
-grading is subjective
-risk of anaphylaxis
239
-intradermal testing:
-similar to prick test except allergen is placed intradermally
-more sensitive than prick test
-grading is subjective and risk of anaphylaxis
-serial dilution endpoint titration:
-quantitative
-multiple solutions with differing concentrations given intradermally to titrate to a
positive response
-time consuming process
-test results obscured by histamines
In Vitro Testing:
-radioallergosorbent test (RAST)
-antigen bound to surface of paper disc
-pts serum obtained binds to antigen
-radiolabelled anti-IgE identifies specific antigen-IgE complexes
-enzyme-linked immunosorbent assay (ELISA)
-similar to RAST except fluorescing agents are used for markers of antigen-IgE
complexes
-indications:
-equivocal skin tests results
-high risk of anaphylaxis
-skin disorders
-failed immunotherapy
-uncooperative patient
-advantages:
-highly specific, no risk of anaphylaxis, no effect from skin condition or medications
-disadvantages:
-less sensitive, requires up to 1-2 weeks for results, more expensive
Anaphylaxis
-ABCs: airway, oxygenation, IV access
-inject up to 0.3 ml of epinephrine intramuscularly
-consider dopamine for hypotension
-add diphenhydramine (Benadryl) 50 mg, dexamethasone 4 mg, and cimetidine 300 mg through IV
Environmental Control
-pets out of primary living and sleeping areas
-clean for dust
-avoidance of smoke
-nasal saline to cleanse mucous membranes
First-line Pharmacotherapy
-OTC medications: antihistamines, decongestants, cromolyn
240
Second-generation and Third-generation Antihistamines
-lipid insoluble: do not cross BBB
-loratadine
-cetirizine
-fexofenadine
Topical Glucocorticoids
-reduce local inflammation
Cromolyn:
-stabilizes mast cells preventing release of mediators in acute and late phase reactions
-effective only for prophylaxis
241
-requires a chronic regimen (3 years)
-risk of worsening symptoms and anaphylactic shock
-contraindications:
-pregnancy
-autoimmune disorders
-immunological compromised patients
-B-blockers (increases sensitivity to allergens)
-easily avoidable allergens
-noncompliant patients
-involves parenteral administration of antigens to stimulate formation of allergen-specific IgG-blocking
antibodies, which eventually compete with IgE antibodies for target sites on mast cells of basophil
-polyps
-sinusitis
-asthma
-otitis media
-allergic fungal sinusitis
-fungal immunotherapy has been shown to prevent recurrence and minimize dependence on
systemic glucocorticoids
242
NASAL OBSTRUCTION
-respiratory epithelium:
-goblet cells: -produce protective mucous layer containing salts, glycoprotein,
polysaccharides, and lysozymes
-ciliated cells: -removes wastes for digestion and excretion
-others: -stromal cells, inflammatory cells, nerves, blood vessels, arteriovenous
anastomoses, venous sinusoids
243
EVALUATION AND ASSESSMENT
History
-onset, duration, unilateral vs bilateral, duration, contributing factors
-rhinorrhea/epistaxis
-nasal or orbital pain
-history of middle ear disease, respiratory illness
-drug/smoke
-nasal surgery/trauma
Physical Examination
-Cottle manoeuver: widening alae with index finger and thumb restoration of nasal patency
-obstruction that resolves with decongestion caused by mucosal abnormality
Differential Diagnosis
Congenital Tumour
-neurogenic tumours -papilloma
-glioma -polyps
-encephalocele -hemangiomas
-meningocele -pyogenic granulomas
-dermoid -JNA
-choanal atresia -malignancy
-congenital cysts
-Tornwaldt cyst Endocrine
-nasolacrimal duct cyst -hypothyroidism
-teratoma -pregnancy
-diabetes
Infectious/Idiopathic
-infectious rhinitis Neurologic
-chronic sinusitis -vasomotor rhinitis
-adenoid hypertrophy
-rhinoscleroma Systemic
-tuberculosis -Wegener’s
-syphilis
Toxin/Trauma -sarcoidosis
-septal hematoma -tuberculosis
-septal deviation -fungal infection
-septal perforation -allergy
-medication side effects -cystic fibrosis
-rhinitis medicamentosa -relapsing polychondritis
-synechia
-environmental irritants
-foreign bodies
-valvular collapse
244
SPECIFIC ETIOLOGIES OF NASAL OBSTRUCTION
Anatomic Abnormalities
Turbinate Hypertrophy
-bony and/or mucosal
-bony hypertrophy may be long term result of prolonged hypertrophy of mucosal tissue or result of
traumatic injury to septum with associated enlargement of nasal turbinates
-50% of inspired air flows along inferior extent of inferior turbinate or between middle and inferior
turbinates
-morbidity associated with radical inferior turbinate resection: haemorrhage, ozena, atrophic rhinitis
-inferior turbinoplasty:
-conservative submucous turbinate resection
-provides 3-5 years of relief without previously mentioned sequelae
-does not address mucosal hypertrophy
-performed when inferior turbinate projects medially and obstructs nasal cavity or when
hypertrophic turbinate mucosa remains unresponsive to vigorous medical management
-chronic hyperplastic mucosal disorders (eg. vasomotor rhinitis)
-available therapy: intraturbinal injection, cryotherapy, electrocautery, laser ablation
Septal Perforation
-causes:
-septoplasty (most common cause, > 50%)
-infections (tertiary syphilis)
-trauma (nose picking)
-neoplasms
-granulomatous disease, vasculitis
-cocaine abuse
-chrome inhalation septal perichondritis
-dx: consider biopsy of granulation tissue or abnormal mucosa to evaluate for malignancy, sarcoidosis,
tuberculosis and other granulomatous diseases
-tx:
-saline irrigation
-antibiotic ointment can be used to control crusting and bleeding around perforation
-polymeric silicone button used to stop whistling
-surgical repair:
-contraindications:
-cocaine abusers
-malignancy
-granulomatous or vascular diseases
-rotation flaps from septal cartilage or bone, nasal floor and lateral nasal wall
-transposition of inferior turbinate flap
245
Valvular Collapse
-nasal valve is narrowest portion of nose
-insufficient cartilage support negative pressure will cause collapse
-surgical reconstruction via open approach, can include
-internal spreader cartilage grafts
-suture repair of drooping upper lateral cartilage
-autogenous cartilage grafts to support columella
-spanning grafts or simple lateral crus onlay grafts to support lateral crura (alar batten grafts)
Choanal Atresia
-see Congenital Anomalies of the Nose
Adenoidal Hypertrophy
-“adenoid facies”
-associated with improper orofacial development: dry, thin upper lip, retrognathic mandible,
narrowed maxilla, broad nasal arch, upturned nose
Nasal Polyposis
-associated with:
-Samter triad: ASA sensitivity, asthma, nasal polyposis
-cystic fibrosis (strongly suggested if polyps seen in children)
-medialization of medial maxillary sinus wall by polyps
-fungal sinus infection
-pathogenesis:
-characterized by chronic eosinophilic inflammation
-inflammatory cytokines and mediators increase polyp water retention by increasing
sodium ion uptake
-ASA believed to block COX metabolism of arachidonic acid while stimulating 5-lipooxygenase
overproduction of leukotrienes increase vascular permeability, increase mucous secretion and
bronchoconstriction
-treatment:
-medical management:
-topical corticosteroids
-decrease capillary permeability
-decrease excretion in response to cholinergic stimulation
-suppress cytokine synthesis in eosinophil, basophil and lymphocytes
-inhibit influx of eosinophil and basophil into nasal epithelium and decrease
production of inflammatory mediators arachidonic acid production
-oral corticosteroids
-used for recurrent conditions
-short high burst with rapid taper
-surgical management:
-FESS with polypectomy
Mucosal Disease
-allergic and nonallergic rhinitis
246
Miscellaneous Causes of Nasal Obstruction
Septal Hematoma
-risk of vascular septal cartilage necrosis saddle nose deformity
-treatment: I+D via Killian incision through perichondrium, nasal packing, prophylactic antibiotics
Septal Abscess
-from untreated haematoma
-complications:
-septal perforation
-cavernous sinus thrombosis
-intracranial infection
-saddle nose deformity
-most common pathogen: Staphylococcus aureus
Foreign Bodies
Relapsing Polychondritis
-nasal obstruction secondary to loss of cartilaginous support in the nasal septum
Granulomatous Disease
-polymorphic reticulosis, nonhealing lethal midline granuloma, Wegener granulomatosis, rhinoscleroma,
sarcoidosis, tuberculosis
-infections: blastomycosis, coccidioidomycosis, histoplasmosis, leprosy, sporotrichosis, syphilis
Rhinoslceroma
-granulomatous stage: antibiotics (eg. streptomycin, tetracycline)
-fibrotic stage: surgical treatment: resection of fibrotic tissue and intranasal stent placement
Sarcoidosis
Tuberculosis
-intranasal infection usually involves anterior portions of turbinate and septum
-histopathology:
-caseating necrosis in center of granuloma containing epithelioid cells and multi nucleated giant
cells
247
SINUS SURGERY
CALDWELL-LUC OPERATION
Indications:
-mycotic maxillary sinusitis
-multiseptate maxillary sinus mucocele
-antrochoanal polyp
-oroantral fistula closure
-revision procedures
-preparation for transantral sphenoethmoidectomy, orbital decompression, exploration of pterygomaxillary
fossa
Technique:
-nasal mucosa decongested
-superior buccogingival sulcus and lateral wall of interior meatus infiltrated with 1% lidocaine with
1:100,000 epi
-incision made from canine to second molar
-canine fossa exposed, infraorbital nerve protected
-antrum entered through canine fossa
-nasoantral window can be made in central third of inferior meatus
Complications:
-edema and ecchymosis of cheek
-infraorbital nerve dysesthesia
-oroantral fistula
-epiphora
-antral contracture due to fibrosis and bony thickening of antral walls can make revision surgery difficult
Indications:
-nasal polyposis with hyperplastic pansinusitis
-recurrent and chronic suppurative sinusitis
-uncomplicated frontoethmoid mucopyocele
-access for intranasal sphenoethmoidectomy
Technique:
-standard nasal decongestion; eyes and medial canthal regions observed throughout procedure
-uncinectomy followed by dissection proceeding posteriorly into ethmoidal bulla
-anterior ethmoidal artery against fovea ethmoidalis and lamina papyracea are key preserved landmarks
-anterior attachment of middle turbinate is not to be disrupted to preserve the frontal recess
-middle turbinate preserved: pain and crusting appear to be more common among patients with total
resection of middle turbinate
Complications:
-retrobulbar hemorrhage
-optic nerve injury
-CSF leak
-intracranial hemorrhage
-horizontal gaze diplopia: trauma to medial rectus with subsequent fibrosis
248
EXTERNAL ETHMOIDECTOMY
Indications:
-frontoethmoid mucopyocele or sinusitis with orbital involvement
-revision surgery with absent or distorted landmarks - distortion can increase risk of intranasal procedure
-CSF leak repair
-anterior skull base lesion
Technique:
-Lynch incision:
-incision beginning at inferior margin of medial aspect of eyebrow, curves down toward medial
canthus, angles acutely back on to side of dorsum of nose
-incision carried to periostium
-angular vessels secured and supraorbital bundle preserved
-periosteal elevation medially and laterally - periosteal elevation ensures integrity of medial canthal
ligament and trochlea
-anterior ethmoidal artery encountered in frontoethmoidal suture line ~24 mm posterior to anterior lacrimal
crest clipped and divided
-posterior ethmoidal artery encountered ~10 mm posterior to anterior artery and ~ 5 mm anterior to optic
foramen
-exposes: lacrimal bone, frontal process of maxilla, lamina papyracea, orbital process of frontal bone
-ethmoid entered through lacrimal fossa
-frontoethmoid suture identifies level of anterior cranial fossa
-lamina papyracea taken down to allow complete exenteration of ethmoidal cells
Complications:
-same as for intranasal ethmoidectomy
-risk of orbital injury and intracranial penetration lower with external approach
-hypertrophic scar formation, medial canthal scarring, rounding of medial canthus
-injury to lacrimal apparatus uncommon
TRANSANTRAL ETHMOIDECTOMY
Indications:
-orbital decompression
Technique:
-exposure of floor of orbit via Caldwell-Luc operation
-delicate bone at junction of posterior orbital floor and medial antral wall gently perforated with
Wilhemlminski punch, and entrance into ethmoidal sinuses carefully enlarged with fine biting forceps
-exposure of ethmoid sinus is limited to anterior cells
249
-risk of recurrent mucocele formation from stenosis of nasofrontal duct
Riedel Method
-removal of frontal sinus floor and anterior wall (disfiguring)
-allows for complete obliteration
Killian Method
-modification of Riedel by preserving a bridge at the supraorbital rim to reduce deformity
Lothrop Method
-creates a large drainage opening into the nasal cavity be removing bilateral anterior ethmoids, middle
turbinates and frontal septum
250
MIDLINE NASAL MASSES
NASAL ANATOMY
Neurogenic Tumours
Glioma None No Negative No Solid mass of glial tissue with a fibrous stalk
Encephalocele Always Yes Positive Yes Ependyma-lined space that communicates with
ventricles
Dermoid Rare Rarely Negative Rare Fluctuating cyst with sinus track leading to skin
-Nasal Glioma
-60% extranasal; 30% intranasal; 15% connect to dura by fibrous stalk
-pathophysiology:
-sequestered glial tissue or “pinched-off encephaloceles” results in unencapsulated
collection of heterotrophic glial cells
-SSx:
-intranasal or extranasal firm mass
-does not become larger with crying or straining (negative Furstenburg)
-CT/MRI scan mandatory for preoperative evaluation to r/o intracranial extension
-tx: surgical excision
-small tumours:
-transnasal endoscopic resection with immediate repair of skull-base defect with
free mucosal graft, pedicled mucosal flap or conchal cartilage with fibrin glue
and nasal packing for 3 weeks
-large tumours:
251
-extranasal approach
-may require neurosurgical consultation for intracranial involvement
-Encephalocele
-contains ependyma-lined space with CSF
-communicates directly with ventricles
-meningocele contains meninges
-meningoencephalocele contains meninges and brain
-meningoencephalocytocele contains meninges, brain and part of ventricular system
-clinical features:
-positive Furstenberg test: compression of jugular veins increase size of mass
-transillumination of mass
-types by location:
-occipital:
-most common
-defect occurs over occiput
-sincipital:
-defect occurs between frontal and ethmoid bones at foramen cecum
-involves frontoethmoid area and is external
-defect is anterior to crista galli in region of foramen cecum
-subtypes:
-nasofrontal (glabellar lesion)
-nasoethmoid (lateral nose)
-nasoorbital (medial orbital wall)
-basal:
-lesions are internal
-defect in floor of anterior cranial fossa between cribriform plate and clinid
process or through superior orbital fissure
-subtypes:
-transethmoidal
-transsphenoidal
-sphenoethmoidal
-sphenomaxillary
Neurofibroma
-usually associated with generalized neurofibromatosis
-excision only when tumours large enough to produce facial asymmetry, visual disturbances or severe pain
Dermoid Cyst
-entrapment of epithelial elements as dural tract resorbs
-cysts can occur anywhere from nasal tip to foramen cecum
-simple cysts: involve only skin and nasal bones
-complex cysts: extend through cribriform plate to the dura
-SSx:
-presents at birth
-forms a fistulous tract, pit or cyst on midline or off-midline of nasal dorsum or septum
-tuft of hair may protrude from pit
-dx: CT/MRI to evaluate for intracranial extension
-tx:
-meticulous excision, must excise complete tract
-craniotomy for known dural connections
252
Hemangioma
-sclerosing therapy has been a mainstay of treatment
NASOPHARYNGEAL MASSES
Nasopharyngeal Cysts
-three types described:
-intra-adenoidal
-extra-adenoidal - located deep in the pharyngobasilar fascia
-branchial cleft cysts from 1st and 2nd pharyngeal pouches
-treatment: excision if infected
Nasopharyngeal Teratoma
-50% of H+N teratomas occur in the nose
-F>M ~ 6x
-hair, skin, bone, cartilage and teeth can be found in teratomas
Infection
Furuncle
-most common infectious lesions of nasal vestibule
-Staph aureus
-complications: septal abscess, septal chondritis, saddle-nose deformity, cavernous sinus
thrombosis
-tx: I+D; antistaphylococcal antibiotics
Septal Abscess
-caused by furuncle or trauma with resultant septal haematoma
-tx: surgical drainage; Abx
-complication: saddle nose deformity, cavernous sinus thrombosis, meningitis, septal perforation
Rhinoscleroma
-Klebsiella rhinoscleromatis
-stages:
-catarrhal: purulent rhinorrhea lasting weeks to months
-granulomatous: formation of soft nodules in the nose, pharynx, larynx and
tracheobronchial tree
-may cause progressive airway obstruction
-histology:
-Mikulicz cells: foamy histiocytes containing intracellular Klebsiella
organisms
-sclerotic: dense fibrotic narrowing of nasal passages
-treatment:
-tetracycline for 4 weeks (effective in 70% of patients)
Rhinosporidiosis
-Rhinosporidium seeberi
-public bathing inoculates nasal epithelium with colonizing fungi
253
-small tumour-like masses in nose, nasopharynx and eye
-tx: surgical extirpation with cautery at base
Leprosy Mycobacterium leprae dapsone, rifampin congestion followed by atrophy of the mucosa,
confused with atrophic rhinitis
Tuberculosis Mycobacterium rifampin, isoniazid, ethambutol nonspecific sinusitis, ulcers, and polyps
tuberculosis common
Inflammatory
Rhinophyma
-massive hypertrophy of sebaceous glands (form of acne roascea
-associated with Demodex folliculorum
-SSx:
-begins with coarsening of nasal skin over cartilaginous portion of nose
-develops into large protuberant lobular swelling of nasal tip
-nasal obstruction
-tx:
-surgical full thickness excision (laser, cold scalpel, or dermabrasion) until normal nasal
contour
-may require STSG
Benign Lesions
Papilloma
-verrucous lesions cause by HPV (types 6 and 11)
-managed by surgical excision or laser ablation
-for septal keratotic papilloma, a cuff of normal mucoperichondrium should be taken with lesion
254
to avoid recurrence
Inverting Papilloma
-M>F ~ 3x
-arise from lateral nasal wall
-malignant growth occurs in as many as 15% of cases
-SSx:
-unilateral obstruction, sinusitis, epistaxis, rhinorrhea, diplopia, typically presents on
lateral nasal wall (rarely on nasal septum), may be associated with a benign nasal polyp
-histopathology:
-cristae-laden senescent mitochondria
-inflammatory cells throughout epithelium
-endophytic growth of epithelium
-complications:
-malignant degeneration
-extension into sinuses, orbit, or intracranial and skull base
-treatment:
-surgical removal by medial maxillectomy via lateral rhinotomy or endoscopically
-recurrence rate of 44%, therefore multiple procedures might be required
-radiation therapy ineffective
Angiofibroma
-occurs exclusively among boys and men
-non-metastasizing tumour that is locally aggressive
-high risk of uncontrollable haemorrhage with biopsy
-tx:
-preoperative embolization
-surgical removal: open or endoscopic
255
Benign Neoplastic Lesions Manifesting as Midline Nasal Masses
Lesion Characteristics Treatment Complications
Inverting papilloma unilateral nasal mass, confused wide excision recurrence, SCC
with simple polyp
Salivary tumour relatively rare, pleomorphic type wide excision minor gland tumours have high rate of
most common malignancy
Angiofibroma juvenile males, obstruction plus embolization, wide excision recurrence, haemorrhage, especially with
epistaxis biopsy
Malignant Lesions
Mucoepidermoid Carcinoma
-rare
-manage like SCCa
256
Neuroectodermal Lesions
Olfactory Neuroblastoma
-arise for olfactory tissue, possibly bipolar neurons
-lobular pattern of uniform cells surrounded by vascular stroma
-aggressive local growth with occasional metastasis to regional lymph nodes
-tx: radical surgery with chemotherapy and radiation therapy
Malignant Melanoma
-second only to SCCa
-primary endonasal site of origin is nasal septum pigmented masses
-50% recurrence rate with poor prognosis
-median survival 2 years; 5-yr survival 25%
-tx: wide local excision; lymph node dissection not usually used for N0 disease b/c low incidence
of nodal metastasis
Hemangiopericytoma
-arises from pericytes of Zimmermann (small cells external to capillary endothelial cells)
-tx: preoperative embolization and en bloc resection of tumour
Kaposi Sarcoma
-dark-brown nodules appear on skin or mucosa
-histology: capsule surrounding spindle cells with prominent nuclei
-tx: excision
Lymphoreticular Tumour
-lymphoma
-Hodgkin disease
-extramedullary plasmacytoma
Salivary Adenoid cystic carcinoma pain common, hematogenous metastasis poor prognosis, aggressive treatment
Mucoepidermoid carcinoma rare lesion low grade has good prognosis; high
grade has poor prognosis
Neuroectodermal Olfactory neuroblastoma pink or brown friable lesion aggressive radical surgery
Malignant melanoma nasal septum pain and swelling 50% recurrence rate
Mesenchymal Hemangiopericytoma lobulated mass, Zimmermann cells, epistaxis embolization, en block resection
257
SINUS IMAGING
Acute Sinusitis
-thickening of sinus mucosa alone is specific for neither
acute nor chronic inflammatory change
-presence of an air-fluid level if there has been no
recent antral lavage suggests acute inflammation
Chronic Sinusitis
-long-standing chronic inflammatory disease can
produce osteitic changes of sinus walls that result in
bony thickening
-bone erosion can occur with chronic inflammatory
disease and often is associated with polyposis
-erosion into retromaxillary space is extremely unusual
and suggests presence of neoplasia or a mucocele
-osteomeatal complex, sphenoethmoidal recess, and frontal recess become prime areas of interest
-complete or partial obstruction of these outlets causes inflammatory changes in associated sinus
cavities
-anatomic variations that can contribute to disease:
-concha bullosa cell
-septal deviation and spur
-lateral convexity of middle turbinate (paradoxical turbinate)
-pneumatization and inversion of uncinate plate
-prominent agger nasi cell
-prominent ethmoidal bulla and Haller cell
GRANULOMATOUS SINUSITIS
258
FUNGAL SINUSITIS
-entities:
-invasive fungal sinusitis in immunosuppressed pt
-associated with mucormycosis or aspergillosis
-acute, fulminant destructive disease marked by vascular invasion and necrosis
-chronic indolent sinusitis
-in pt with normal immune function
-tissue-invasive infection, typically unilateral and not responsive to antibiotics
-mycetoma
-noninvasive fungal ball that causes complete or near-complete opacification of a sinus
cavity
-organisms: Aspergillus fumigatus, Pseudallescheria boydii, Alternaria
-CT:
-can be associated with thickening of sinus walls
-usually hyperdense and contains calcifications in 25% of cases
-MRI:
-hypointense on MRI (T1and T2)
-allergic fungal sinusitis
-pt with heightened immune function or atopy
-hypersensitivity reaction to fungal antigens
-CT:
-involved sinus contains peripheral
rim of low density
-edematous mucosa and complete
opacification of central cavity by
homogeneous high-attenuation
material corresponding to thick
allergic mucin
-often scattered flecks of calcific
material
-sinus walls can be surprisingly
expanded and destroyed
-MRI T2:
-mucin is extremely hypointense,
mimicking an aerated sinus cavity
RETENTION CYSTS
POLYPOSIS
259
MUCOCELE
-occur as obstructive complications of chronic sinus inflammation, polyposis, trauma, surgery, or tumour
-CT: mucocele contents have low density and do not enhance
-MRI: intensity characteristics vary with protein content of mucocele and degree of hydration
NEOPLASTIC DISEASE
-malignant disease of nose and paranasal sinuses account for less than 1% of all malignant lesions in the
body and 3% of all H+N tumours
-MRI particularly useful, because nearly 95% of all sinonasal tumours are low to intermediate in signal
intensity during T2-weighted sequence
260
Malignant tumours of bony origin
-most common malignant bone tumours of paranasal sinuses are multiple myeloma, osteogenic sarcoma,
and chondrosarcoma
261
RHINOSINUSITIS: CURRENT CONCEPTS AND MANAGEMENT
-function of sinuses:
-dampening of sudden increased intranasal pressure
-voice resonance
-possible participation in olfaction
-humidification of inspired air
-decreasing weight of skull
-frontal sinus:
-varies greatly in size and shape
-nasofrontal duct drains into frontoethmoidal recess of middle meatus
-10-12% of adults have rudimentary frontal sinus or lack pneumatization of frontal bone
-ethmoid sinus:
-most developed at birth
-anterior and middle ethmoidal cells drain to middle meatus
-posterior cells drain to superior meatus
-maxillary sinus:
-present at birth
-drains into middle meatus
-sphenoid sinus:
-begins developing in 2nd or 3rd year of life
-completely pneumatized by 17th or 18th year
-drains into sphenoethmoidal recess
PATHOPHYSIOLOGY
262
-osteal patency:
-hypo-oxygenation and osteal obstruction accumulation of secretions in sinus ideal culture
medium for bacteria
-mucociliary layer:
-double layer:
-superficial viscid gel layer
-underlying serous sol layer
-nasal mucous produced by:
-goblet cells
-submucosal mucous-producing glands
Local
-impairment of mucociliary transport function
-cold/dry air
-medications
Regional
-suppurative sinusitis: apical dental infection (main predisposing factor)
-nasal/midface trauma (alters anatomic configuration of OMU)
-septal pathology mechanical obstruction
-choanal atresia interferes with drainage of nose
-edema 2o to URTI
-barotrauma produces edema of sinus ostium
-swimming in contaminated water
-nasal polyps, FB, nasal packing, nasal tumours
-immotile cilia syndrome
-congenital: disorientation of cilia and abnormalities of dynein arms
-sinusitis and bronchitis
Systemic
-general debilitation:
-malnutrition, long-term steroid therapy, uncontrolled diabetes, blood dyscrasia, chemotherapy
-critically ill patients:
-regional obstruction from NG tubes
-colonization of UGI and URT by gram negative bacilli
-immune deficiencies (eg. IgG deficiency, AIDS)
-pseudomonas in HIV patients; microsporidium, CMV, Aspergillus (invasive), histoplasma,
Cryptococcus, atypical mycobacteria
-non-Hodgkin lymphoma in HIV patients
CLASSIFICATION OF SINUSITIS
Five axes:
a) clinical presentation (acute, subacute, chronic)
b) anatomic sites of involvement (ethmoid, maxillary, frontal, sphenoid)
c) responsible organism (viral, bacterial, fungal)
d) presence of extrasinus involvement (complicated, uncomplicated)
e) modifying or aggravating factors
263
-Acute sinusitis: 1 day to 4 weeks
-management is medical, rarely surgical
-drainage if orbital or intracranial complications threaten
-Subacute sinusitis: 4 weeks to 3 months
-medical management indicated
-Chronic sinusitis: > 3 months
-sinusitis that is uncontrolled or inadequately managed
-process irreversible without surgical intervention
-osteal patency must be restored surgically to allow clearance of mucopus from sinus
CLINICAL EVALUATION
History
-Acute sinusitis:
-pain: nasal, facial, headache
-ethmoidal pain: medial portion of nose or retro-orbital area
-sphenoidal pain: vertex or bitemporal headaches
-nasal obstruction/discharge
-fever, malaise, lethargy
-diagnosis depends on presence of > 2 major factors or 1 major and 2 minor factors:
Major factors:
-facial pain or pressure
-facial congestion or fullness
-nasal obstruction
-nasal purulence or discoloured PND
-hyposmia or anosmia
-fever
Minor factors:
-headache
-halitosis
-fatigue
-dental pain
-cough
-ear pain, pressure, or fullness
-fever
-Chronic sinusitis:
-mucopurulent discharge and symptoms of mild nasal obstruction
-pain and systemic symptoms are conspicuously absent
Physical Examination
-mucosal edema and erythema
-+/- mucopurulent discharge
-facial pain/tenderness over affected sinuses
-look for periorbital edema, malodorous breath
-nasopharynx: adenoidal obstruction, tumours, choanal atresia, PND
-look for otitis media or serous otitis media
-transillumination not reliable
-nasal endoscopy: pus in middle meatus
264
-periorbital edema; blindness can be a complications of sinusitis
-children much less likely to report classic sinus headaches
-“cold” lasting more than 7-10 days, daytime cough with nocturnal exacerbation, mucopurulent
nasal discharge, fetid breath, low grade fever
Investigations
-plain radiography:
-indications: screening study for acute sinusitis
-evaluates presence of air-fluid levels, opacification, and bone destruction
-high rate of false positives and false negatives to evaluate for chronic sinusitis
-CT of paranasal sinuses:
-indications:
-complications of severe acute sinusitis
-medical failure of chronic sinusitis
-diagnosis of epistaxis, nasal or sinus tumours, nasal polyps
-CSF leaks
-trauma
-preoperative films
-MRI of paranasal sinuses:
-improved soft tissue detail, poor bone resolution
-indications:
-complicated sinusitis (intracranial and intraorbital extension)
-evaluation of soft tissue masses
-fungal sinusitis (hypodensity in T2-weighted sequences form the presence of metallic
proteinaceous material, magnesium, iron, and calcium)
Ancillary studies
-sinus cultures:
-obtained through an anterior maxillary puncture or from an endoscope
-indications:
-failed medical management
-complicated sinusitis (sepsis, orbital infection, intracranial extension)
-immunocompromised patients
-immunological profile:
-qualitative immunoglobulins including IgG subclasses
-ciliary biopsy
-allergy testing
MICROBIOLOGY OF SINUSITIS
-little correlation between culture results with specimens from nose or nasopharynx and those from sinus
aspiration
-antibiotic management of acute sinusitis usually empiric
265
-Acute (nosocomial):
-Pseudomonas aeruginosa, enteric gram-negative bacilli (KEEPS), Staph. aureus, Candida,
streptococci
-anaerobes
-Chronic sinusitis:
-anaerobes (Bacteroides, anaerobic cocci), fungus (1-2%)
-alpha streptococci, H. influenze, S.aureus, S. pneumoniae, M. catarrhalis
-Immunosuppression:
-usual organisms plus: Pseudomonas, S. aureus, Listeria monocytogenes, Leigionella
-CMV
-Fungi (fulminant): Aspergillus, Candida, Mucor, Phaehyphomycosis, Rhizopus
-Atypical mycobacteria
-Microsporidia, Cryptococcus
-Cystic Fibrosis:
-P. aeruginosa, S. aureus
Viral sinusitis
-often follows viral rhinitis
-rarely requires treatment except in immunosuppressed (eg. with CMV infection)
Fungal sinusitis
-types:
-noninvasive: (1) mycetoma and (2) allergic fungal sinusitis
-invasive: (3) fulminant (immunosuppressed); (4) indolent (immunocompetent)
-modifying factors can predispose a patient to sinus infection or can prevent complete resolution of
infection:
-eg. atopy, immunosuppression, ciliary dyskinesia, mechanical obstruction
Mycetoma:
-pathogens: Aspergillus fumigatus (most common), Pseudallescheria boydii, Alternaria
-SSx: unilateral chronic or recurrent sinusitis, unilateral proptosis, facial hypesthesia
-dx: CT/MRI, biopsy with culture
-aspergillosis histology:
-septated 45 degree, Y-shaped (Sabouraud’s agar stain)
-tx: adequate surgical debridement, consider adjuvant less toxic antifungal medications
266
-promotes polyp growth
-sinus imaging:
-often unilateral involvement of one or two sinuses
-CT: areas of hyperdensity in opacified sinus cavities
-MRI: hypointensity on T1 and signal void on T2
-erosion of bony sinus wall frequently encountered:
-osteolytic factors secreted by fungi
-cytokine-mediated osteoclast activation
-long-standing pressure on sinus walls
Major Criteria:
1. testing or history positive for fungal atopy (RAST, skin testing)
2. nasal polyposis
3. CT showing hyperdense material in sinus cavity and possible sinus wall erosion
4. allergic mucus with eosinophilic preponderance
5. identification of fungus
6. no histologic evidence of tissue invasion
Minor Criteria:
1. chronic rhinosinusitis
2. CT scan demonstrating serpiginous areas of high attenuation especially in
ethmoidal and maxillary sinuses, with bone thinning and erosions with
dislocation of adjacent structures
3. MRI showing decreased signal intensity leading to hypointense T1-weighted
and markedly hypointense T2-weighted images with typical void signal
Treatment
-ethmoidectomy
-middle meatal antrostomy with extirpation of allergic mucous and polypectomy
-post-op steroid sprays and saline irrigations
-systemic anti-fungals are of no use because fungi are not invasive
-consider immunotherapy for refractory cases
267
-risk factors: immunocompromised host (diabetic ketoacidosis, chemotherapy, HIV, bone marrow
transplant)
-SSx:
-necrotic black turbinates and soft palate, epistaxis, cranial nerve involvement, progresses
rapidly into obtundation and death
-mucormycosis histology:
-non-septated, 90 degree broad branching hyphae
-tx:
-correct metabolic abnormality if present
-urgent surgical debridement
-IV amphotericin B
MANAGEMENT
Acute rhinosinusitis:
-First-line empiric therapy:
-Amoxicillin:
-covers H. influenzae, M. catarrhalis, S. pneumoniae
-does not cover strains that have beta-lactamase enzyme
-Erythromycin and a sulfonamide
-cephalexin and a sulfonamide
-Amoxicillin-clavulanate
-for beta-latamase producing strains of H. influenzae and M. catarrhalis, but not
effective against penicillin-resistant pneumococci
-second-generation cephalosporins: cover beta-lactamase producing organisms
-Second-line therapy:
-amoxicillin-clavlanate
-clarithromycin and second-generation cephalosporin
-respiratory quinolones (levofloxacin, gatifloxacin, moxifloxacin), ciprofloxacin
-contraindicated in children and pregnant women - interference with cartilage
development
-Orbital or intracranial complications:
-IV Ceftriaxone: excellent penetration of BBB
-IV Flagyl: better CSF penetration than clindamycin
-Nosocomial sinusitis:
-cover gram-positive, gram-negative (eg. Pseudomonas), and anaerobic bacteria
-IV Flagyl + ampicillin + ceftazidime, cefotaxime, or ciprofloxacin
-imipenem
-piperacillin-tazobactam
268
-analgesics for pain
-humidification, mucolytics and expectorants, saline nasal irrigation to help clear secretions
Chronic sinusitis
-Antibiotics for 3-6 weeks:
-clavulin
-clindamycin
-cephalexin and metronidazole
-ciprofloxacin
-itraconazole
-cefuroxime
-clarithromycin
-nasal corticosteroid sprays
-nasal hypertonic saline irrigations
-oral decongestants and mucolytic agents
-allergy management
-surgical management frequently required
Kartagener’s disease
-aggressive antibiotic therapy
-avoid functional antrostomies (no mucociliary clearance)
-consider “gravity dependent” inferior antostomies for refractory disease
SURGICAL MANAGEMENT
-main indication for maxillary sinus irrigation is the presence of mucopurulent material in an
immunosuppressed patient or a patient with suspected subacute or chronic maxillary sinusitis or acute
sinusitis that has not responded to antibiotic therapy
-surgery for acute maxillary sinusitis is indicated if the pain persists for more than 24-48h despite
appropriate antibiotic therapy or if ophthalmic and neurologic complications occur
COMPLICATIONS
269
-direct lymphatics
-orbital cellulitis, abscess, proptosis
-subperiosteal and orbital abscess
-blindness, loss of ROM, increased IOP
-osteomyelitis
-mucoceles
1. Periorbital/Preseptal Cellulitis:
-eyelid edema, erythema, tenderness
-no vision changes, chemosis, proptosis, or restriction of ocular muscles
-tx: IV ABx and concurrent aggressive sinusitis regimen
2. Orbital Cellulitis:
-proptosis, chemosis
-may cause vision changes (anterior pupillary defect)
-may limit extraocular muscles
-tx: IV ABx and concurrent aggressive sinusitis regimen +/- FESS
3. Subperiosteal Abscess:
-collection of pus between bone and periosteum
-chemosis, proptosis
-restricted extraocular motion
-decreased vision
-tx: urgent surgical decompression
4. Orbital Abscess:
-collection of pus in orbital soft tissue
-proptosis, chemosis, restricted extraocular motion
-decreased vision
-tx: urgent surgical decompression
5. Cavernous Sinus Thrombosis:
-pathogens:
-S. aureus (most common), hemolytic Streptococcus and type III Pneumococcus
-SSx:
-spiking fevers, toxaemia
-proptosis, facial edema, ophthalmoplegia
-tx:
-IV ABx
-may require ligation of IJV if septic emboli
-anticoagulants (controversial)
-sinus surgery
Neurologic (rare)
-intracranial pathways
-congenital dehiscence
-trauma
-direct extension
-lymphatics
-olfactory nerve sheath
-venous system
-foramina of Breschet
-meningitis (most common intracranial complication)
-epidural or subdural abscesses
270
-brain abscess, cavernous sinus thrombosis
-venous sinus thrombosis
EMERGENCIES
Ophthalmologic:
-orbital cellulitis/abscess
-ethmoid sinus most common sinus contributing to orbital complications
-third nerve palsies may be result of sphenoid sinusitis
-IV Abx, surgical drainage, early consultation if any present:
-visual changes
-change in ocular mobility
-change in ocular pressure
-proptosis
-acute ethmoidal sinusitis with orbital complications probably best managed through external
ethmoidectomy approach; if no complications then endoscopically and intranasally is reasonable
Neurologic:
-abscess (epidural/subdural/intraparenchymal), meningitis, cavernous sinus thrombosis
-IV Abx, surgical drainage, early consultation if any present:
-CN involvement (II, III, IV, VI)
-papilledema
-altered mental status/LOC
-nuchal rigidity
271
ENDOSCOPIC SINUS SURGERY
-agger nasi:
-ascending (frontal) process of maxilla forming a thick bony ridge inside the nose
-agger nasi cells: cells anterior to opening of frontal sinus
-ostiomeatal unit:
-medial border: anterior middle turbinate
-lateral border: lateral nasal wall
-uncinate process bisects region
-anteriorly joined to posteromedial portion of lacrimal bone by membranous attachment
-may attach anterosuperiorly to LP or to skull base
-inferolaterally fused with medial wall of maxillary sinus
-ethmoidal infundibulum:
-lateral wall is medial wall of orbit and antrum
-posterior aspect empties into inferior hiatus semilunaris
-ethmoid bulla:
-constitutes posterior boundary of inferior hiatus semilunaris
-bony medial wall of maxillary sinus:
-natural ostium of maxillary sinus
-anterior (inferior to inferior limb of uncinate process) and posterior (superior to inferior limb of
uncinate) fontanelles
-usually covered by mucosa
-perforated in 10-28% of patients accessory ostium
-frontal recess:
-typically drains medially to uncinate process and laterally to middle turbinate
-occasionally drains into inferior hiatus semilunaris
-sinus lateralis = retrobullar recess
-most posterior aspect of anterior ethmoidal cells
-basal lamella:
-lateral, sigmoid, bony attachment of middle turbinate to medial orbital wall
-separates anterior and posterior ethmoidal air cells
-ethmoidal roof classification (Keros)
-type 1: cribriform plate is 1-3 mm
-type II: 4-7 mm deep
-type III: 8-16 mm deep
-Onodi cell = sphenoethmoidal cell
-pneumatization of sphenoid bone by an ethmoidal air cell
-clinical bony dehiscence of cavernous portion of carotid canal occurs among 22% of patients
PREOPERATIVE EVALUATION
272
-second pass:
-between middle turbinate and inferior turbinate
-visualize anterior and inferior portions of middle turbinate and meatus
-natural opening to sphenoidal sinus viewed
-third pass performed during withdrawal of scope
-visualize ethmoidal bulla, inferior hiatus semilunaris and uncinate process
-natural ostium of maxillary sinus usually hidden behind uncinate process
Radiographic Evaluation
-optimal time to perform CT is during
Preoperative Radiographic Checklist
quiescent phase of disease
-pts should undergo comprehensive medical 1. Shape of skull base and orbit
therapy before CT scan -medially down-sloping versus flat, particularly in region of
lateral lamella of cribriform plate
-fungal disease suspected if:
-metal-like or diffusely increased 2. Relative thickness of skull base and orbit in different areas
densities within soft tissues of along roof of ethmoid bone and presence of medial orbital or
involved sinuses bone dehiscence along skull base
-reduced signal intensity of a T2- 3. Position of anterior ethmoidal neurovascular bundles
weighted image -look just behind globe on true coronal CT scans
273
Relative Contraindications to Endoscopic Surgery
-absence of defined ostiomeatal abnormality
-osteomyelitis
-inaccessible lateral frontal sinus disease
-frontal sinus disease accompanied by stenosed internal ostium
-threatened intracranial or intraorbital disease
ANAESTHESIA
SURGICAL PROCEDURES
Complete Sphenoethmoidectomy
-indicated for extensive disease
Concurrent Septoplasty
-usually begun after endoscopic procedure is completed on side away from septal deflection
-hemitransfixion incision made on side contralateral to deflection
274
-anterior ethmoidal artery typically just anterior to vertical portion of basal lamella, immediately below
base of skull and posterior to frontal recess
-tight nasal packing should be avoided when integrity of orbital wall is in question: blood can dissect into
orbit and cause delayed haematoma and vision loss
-base of skull usually thinnest where anterior ethmoidal artery crosses from medial orbital wall to
cribriform plate
275
APPROACHES TO THE SPHENOIDAL SINUS
ANATOMY
-classification: three types of pneumatization; incidence
varies depending on series
-Harnberger:
-sellar (86%)
-presellar (11%)
-concha (3%)
-Congdon:
-postsellar (67%)
-presellar (24%)
-conchal (5%)
-conchal pneumatization not a contraindication to sphenoid
surgery
-dehiscent carotid artery in 4%
-dehiscent optic nerve in 4%
-Cavernous Sinus:
-contents:
-internal carotid artery
-indents posterior inferior surface of sphenoid sinus
-abducens nerve travels in close association with lateral wall of artery
-oculomotor nerve
-trochlear nerve
-abducens nerve
-ophthalmic division of trigeminal
-maxillary division of trigeminal
PREOPERATIVE EVALUATION
-active sinus infection if the main contraindication to a transnasal intracranial procedure
OVERVIEW OF APPROACHES
-transseptal:
-sublabial
-intranasal
-external rhinoplasty
-transantral
-transethmoidal
-external
-intranasal
-endoscopic:
-intranasal sphenoethmoidectomy
-transantral sphenoehtmoidectomy
-transpalatal
276
TRANSSPHENOIDAL HYPOPHYSECTOMY
Transseptal Approaches
-indications:
-large pituitary neoplasms with extensive suprasellar involvement
-total removal impossible, but tissue diagnosis and decompression of optic chiasm can be
obtained
-pituitary microadenoma
277
Previous Septal Surgery
-strategies to avoid septal perforation:
-avoidance of problem area using traditional septoplasty techniques to go around scar tissue
-careful dissection through adherent mucosal areas; usually feasible when reoperation needed
soon after initial procedure
-lateral displacement of septum
Transantral Approach
-not commonly used at present
-allows widest exposure and is 1-2 cm closer to sphenoidal sinus than transeptal approach
-increased risk of damage to cavernous sinus, optic nerve and anterior cranial fossa
Transethmoidal Approach
-external and intranasal
-only external route appropriate for hypophysectomy (not popular)
-same disadvantages as transantroethmoidal route
-intranasal approach used for extensive nasal polyposis
278
Endoscopic Approaches to the Sphenoid Sinus
-sphenoidal sinus lies at medial inferior portion of posterior ethmoid cell
-anterior wall ~7 cm posterior to anterior nasal spine
-posterior wall ~9 cm
-approach transethmoidal or direct
Intranasal Sphenoethmoidectomy
-middle turbinate infractured
-Glasgow forceps used to enter middle ethmoid cells
-dissection continued medial to turbinate
-ostium is enlarged toward midline with Kerrison forceps
Transantral Sphenoethmoidectomy
-used by some to manage chronic hyperplastic disease, especially if extensive benign maxillary disease
encroaches on ethmoidal and sphenoidal sinuses
-antral cavity entered through sublabial canine fossa approach
-removal of nasoantral wall
-anterior sphenoid wall is opened to expose the sinus
SPHENOID TUMOURS
Transpalatal Approach
-for neoplasms of nasopharynx, posterior
pharyngeal wall, and choanae
-tumours isolated to sphenoidal sinus and
sella are better resected with alternative
methods
-Dibble and King:
-midline palatal split; hard palate,
posterior vomer removed as
necessary
-palate closed in two layers, muscle
and nasal mucosa first, followed by
oral mucosa
-Mullan:
-U-shaped incision at junction of
soft and hard palate
-hard palate resected
-incision closed in two layers
-preserves palatal motor function
best, but exposure is limited
inferiorly
-Kennedy:
-S-shaped incision originating along
lingual alveolus and curing back
across palatal aponeurosis to dive
soft palate off midline
279
Sphenoidal Mucocele
-transsphenoidal endoscopic approach successful in management of sphenoidal and ethmoidal mucoceles
with orbital and intracranial extension and with cholesterol granuloma of petrous apex
COMPLICATIONS
Nasal
-poor appearance (saddle and tip deformities)
-septal perforation
-infection
-epistaxis
Neurologic
-injury to optic nerve and cranial nerves III, IV, V1, V2
-trauma to optic chiasm
-late prolapse of chiasm into sella
-trauma to hypothalamus
-CSF leak
Vascular
-haemorrhage from internal carotid artery
-haemorrhage from cavernous sinus
EMERGENCIES
Preoperative:
-acute sinusitis with meningitis or other neurologic signs surgical drainage
-developing visual loss in sellar or parasellar tumour surgical decompression, radiation therapy
Intraoperative:
-retrobulbar haemorrhage with proptosis and visual compromise lateral canthotomy, ophthalmologic
consultation
-persistent haemorrhage from sphenoid or cavernous sinus region interventional arteriography
280
SPHENOID SINUS DISEASE
DEVELOPMENT
-begins early in third month of fetal development and continues throughout first decade of life
-progressive pneumatization after age 3
ANATOMY
-neighbouring structures of the sphenoid sinus
-dura
-pituitary
-optic nerve and chiasm
-rests against superolateral wall
-bone overlying optic canals becomes increasingly dehiscent with increasing age
-cavernous sinus
-internal carotid artery
-located within medial aspect of cavernous sinus
-passes directly across lateral wall and produces a medial deflection of the lateral wall
into the lumen of the sinus (carotid sulcus)
-abducens nerve
-oculomotor nerve
-trochlear nerve
-ophthalmic nerve
-maxillary nerve
-sphenopalatine ganglion
-sphenopalatine artery
-pterygoid canal and vidian nerve
-sphenoid ostium:
-1.5 cm above sinus floor on anterior wall
-drainage dependent on mucociliary flow
INFLAMMATORY DISEASE
281
-cerebral infarction
-blindness
Mycetomas
-fungal balls
-occur despite adequate host immunity and are noninvasive
Chronic Sphenoiditis
-from obstructive polyposis
-obstruction, mucin stasis, chronic bacterial infection
-tx: removal of obstructing polyps, regular saline irrigations, use of nasal steroids, extended course of
antibiotics
Mucoceles
-treatment requires creation of wide sphenoidotomy with decompression of the mucocele
NEOPLASTIC DISEASE
Fibrous Dysplasia
-bony encroachment on optic nerve and ocular muscles
Chordoma
-typically arise from clivus and extend by direct expansion
-derived from notochordal remnants
-treatment involves surgical removal and XRT
282
OPERATIVE TECHNIQUES
Open Approaches
-transseptal approach
-columellar incision or sublabial incision
-via ethmoid air cells:
-transmaxillary approach
-transorbital approach
-transpalatal approach
Endoscopic Approaches
-minimally invasive
-Bolger technique:
-relies on entering superior meatus through basal lamella, allowing identification of anteroinferior
aspect of superior turbinate
-dissection proceeds laterally to define posterior limit of lamina papyracea
-Bolger’s parallelogram:
-medial limit: lateral aspect of superior turbinate
-lateral limit: lamina papyracea
-superior limit: skull base
-inferior limit: horizontal portion of superior turbinate (attaching to lateral nasal wall)
-anterior face of sphenoid sinus is posterior wall of this box
-natural ostium located by gently removing inferior portion of superior turbinate
-safe area of entry: medial-inferior portion of parallelogram
283
COMPLICATIONS OF SINUS SURGERY
RELEVANT ANATOMY
Intranasal Ethmoidectomy
-blindness, permanent diplopia, CSF fistula with meningitis, brain injury, major vessel injuries
-synechiae, orbital hematoma, subcutaneous emphysema, loss of smell, hemorrhage
-contributing factors: repeated procedures, extensive disease, loss of landmarks
284
Transantral Ethmoidectomy (TE) and External Ethmoidectomy (EE)
-fewer major complications because of direct vision
-distance to ethmoidal and sphenoidal sinuses through transantral approach is half that of an intranasal
approach
-EE: orbital edema, supraorbital anesthesia, hemorrhage, wound infection
-TE: intracerebral hemorrhage, pneumocephalus, CSF fistula
Sphenoidotomy
-injuries to carotid artery, cavernous sinus, optic nerve, and brain can be catastrophic but they are rare
-CSF fistula, blindness, carotid artery injury, carotid cavernous fistula, meningitis
Caldwell-Luc Procedure
-most common immediate: facial swelling, cheek discomfort
-most common long-term: recurrent sinusitis, recurrent polyps, facial paresthesia, dacryocystitis,
-other: fever, hemorrhage, facial asymmetry, oroantral fistula, gingivolabial fistula, devitalized teeth,
recurrent polyps, blindness
ORBITAL COMPLICATIONS
Orbital Hematoma
-risk of hematoma with retention in retrobulbar space increases greatly with penetration of the periorbita
-most frequently caused by trauma to orbital veins lining lamina papyracea
-rarely by injury to anterior and posterior ethmoidal arteries (quick hematoma formation)
-orbital septum:
-fibrous membrane dividing eyelid into anterior and posterior chambers
-preseptal hematoma: darker and more diffuse and produces more lid edema
-postseptal hematoma: proptosis, conjunctival changes such as chemosis, pupillary changes,
mydriasis, and a dilated pupil
-most cases of orbital hematoma do not have associated proptosis and pupillary changes - these findings
signal increased orbital pressure and potential damage to the optic nerve
-ecchymosis usually resolves in ~ 7-10 days
Blindness
-direct (optic nerve injury) or indirect (orbital hematoma)
-temporary or permanent
-from increased orbital pressure compromised vascular supply to optic nerve
-retinal tolerance:
-venous hematoma: 60-90 minutes
-arterial hematoma: 15-30 minutes
-neural tissue vulnerable to ischemic injury
-intranasal procedures:
-right-handed surgeon more prone to cause injury on right side
-left ethmoidal sinuses are actually more medial than appreciated by a right-handed surgeon
-do not over pack nose if dehiscence present may press into periorbita and posterior chamber
-treatment: fast arterial hematoma:
-Medical treatment:
-eye consultation
-mannitol 1-2 g/kg in 20% infusion
-orbital massage: redistributes orbital blood
-remove nasal
-high dose steroids (controversial): dexamethasone 1-1.5 mg/kg/24h
285
-Surgical treatment:
-lateral canthotomy
-medial external (lynch) decompression
-endoscopic decompression
-control bleeding artery (anterior ethmoidal artery)
Diplopia
-injury to ocular muscles: medial rectus and superior oblique
-direct muscle injury or injury to nervous or vascular supply to muscle
-persistent diplopia rare complication with poor prognosis
Subcutaneous Emphysema
-from resultant fracture or perforation of lamina papyracea
-observe for orbital hematoma
-treatment in most cases is simple observation and reassurance
-emphysema resorbs within 7-10 days
INTRACRANIAL COMPLICATIONS
286
-treatment for persistent leaks: bedrest +/- lumbar drain
-use of antibiotics is controversial and should be used with caution so as not to select out resistant
organisms
-conservative management often allows CSF fistula to heal without surgery
-if persists for 2-3 weeks should be closed surgically
Intracranial Infections
-meningitis
-brain abscess
Anosmia
-three types of causes:
-interference with access of odorant to olfactory nerve
-damage to olfactory nerve
-damage to central olfactory pathway
Hemorrhage
-one of the most common complications during or after sinus surgery
-preoperative sedation and vasoconstriction with a topical spray improves blood pressure control and
decongestion and diminish any systematic reaction to topical cocaine
-only diseased tissue should be removed
-areas of injury:
-sphenopalatine
-carotid
-ethmoid
-carotid-cavernous fistulas
-posterior septal artery:
-runs below sphenoid bone and feeding into posterior middle turbinate can cause marked
intraoperative and postoperative hemorrhage
-tx:
-if bleeding is too great then operation is terminated and nasal packing instituted
-electrocautery
-consider embolization for carotid injuries
287
SYNECHIA
-although growth disturbance and retarded sinus development have occurred in animals, no clinical study
has shown growth problems
OTHER COMPLICATIONS
-residual disease
-facial edema
-aspiration of packing material
-toxic shock syndrome
-osteomyelitis
-tooth numbness and pain (Caldwell-Luc)
-embossment (frontal sinus obliteration)
288
EPISTAXIS
ANATOMY
a) Internal Carotid
-internal carotid a. opthalmic a.
-branches (within orbit):
posterior ethmoidal a. (absent in 31%)
anterior ethmoidal a. (absent in 7-14%)
-posterior ethmoid artery enters posterior ethmoidal foramen within 4-7 mm of the optic nerve > 80% of
the time
-anterior ethmoid artery enters anterior ethmoidal foramen 14-22 mm posterior to maxillo-lacrimal suture >
80% of the time
-ethmoidal arteries branch into medial and lateral branches in ethmoidal cells
-medial branches: supply superior septum and Little’s area
-lateral branches: supply superior and middle turbinates
b) External Carotid
- facial artery superior labial artery
nasal arterial branches
medially to septum
laterally to ala
- maxillary artery
sphenopalatine a.: supplies septal mucosa
posterior nasal a.: supplies lateral nasal wall and turbinates
anastomosis superiorly with ethmoid arteries
anastomosis inferiorly with pharyngeal branches of maxillary artery
(Woodruff naso-nasopharyngeal plexus)
pharyngeal artery
descending palatine a. (greater palatine canal and foramen) greater palatine a.
(supplies septum and floor of nose) incisive foramen
Little’s area
289
-Kiesselbach’s plexus (Little’s area) anastomosis of:
-sphenopalatine artery
-greater palatine artery
-anterior ethmoid artery
-nasal branches of facial artery
ETIOLOGY
Local Factors
-trauma
-digital manipulation
-septal perforation turbulence and impaired
laminar airflow drying, scab formation
epistaxis
-nasal fracture
-probably posttraumatic pseudoaneurysm of internal carotid artery triad of prior
monocular blindness, ipsilateral orbital fractures, delayed epistaxis
-local inflammation
-decongestants and nasal steroids
-foreign bodies
-tumours: eg. juvenile angiofibroma, nasopharyngeal carcinoma
290
-chemical inhalants
-nasal prong O2, CPAP
-surgery: septoplasty and FESS
Systemic Factors
-vascular disorders:
-Osler-Weber-Rendu:
-autosomal dominant: mucocutaneous telangiectasias and epistaxis
-thin vessel walls without smooth muscle, increased angiogenesis resulting in vascular
proliferation, arteriovenous fistulae, mucosal fragility
-most common disease of vascular structures leading to recurrent epistaxis
-aging:
-fibrosis of muscular tunica media of arteries
-atherosclerosis NOT a risk factor
-hypertension NOT a significant risk factor for anterior epistaxis
-some possible association of increased risk for posterior epistaxis
-blood dyscrasias:
-VonWillebrand disease
-most common hereditary bleeding disorder associated with epistaxis
-AD
-epistaxis in 60%
-recommended presurgical prophylaxis: desmopressin
-Hemophilia A and B
-hematologic malignancies: leukemia, multiple myeloma, thrombocytopenia
-malnutrition
-alcohol
-drugs: ASA, NSAIDS, anticoagulants, chloramphenicol, carbenicillin, dipyrimdamole
-infectious/inflammatory:
-TB
-syphilis
-Wegener’s
-periarteritis nodosa
-SLE
MANAGEMENT
Exsanguinating Epistaxis
-due to severe midfacial trauma with maxillary artery laceration
-ABCs
-anterior nasal packs followed by oro- and nasopharyngeal pack (after airway has been secured)
-radiographic embolization
291
Electric Cauterization
-induces a deeper penetration and more tissue destruction than silver nitrate
-repetitive cauterization increases likelihood of septal perforations
Laser Photocoagulation
-argon and neodymium:yttrium aluminum garnet laser
-multiple treatments required
-photocoagulates abnormal subepithelial arteriovenous reticulum, preserving the overlying mucosa and
underlying cartilage
Nasal Packing
-Anterior
-local anesthesia may decrease the risk of apnea, bradycardia, and hypotension by blocking the nasal-vagal
reflex
-patients with chronic mucosal pathology from HHT, coagulation d/o, or leukemia should be managed
without packing in anticipation of future multiple treatments
-use Surgicel, Oxycel or Avitene
-Posterior
-patients who fail anterior packs
-main purpose is to stabilize the anterior packing
-complications/pitfalls of nasal packing:
-hypoxia; aspiration of packs
-toxic shock syndrome
-sinusitis
-alar necrosis
-septal perforation
-synechiae
-cerebral ischemic
-cardiovascular complications
-failure to control bleeding
-vasovagal syncope
-septal hematoma
-eustachian tube dysfunction; otitis media
Balloon Packs
Endoscopic Management
-endoscopic control under local anaesthesia for posterior epistaxis
-preliminary studies show effective control of bleeding
-benefits:
-precise localization of bleeding site and direct visualization of the injection, cauterization,
lasering, or packing
-treatment localized to smaller area
-disadvantages:
-expertise required
-expense and limited availability of instrumentation
292
Maxillary Artery Ligation
-causes decrease in intravascular pressure gradient, resulting in hemostasis of posterior nasal cavity unless
anastomoses exist with continued high pressures
-ligation of maxillary artery and distal branches:
-descending palatine, sphenopalatine, posterior nasal arteries
-note: sphenopalatine and posterior nasal arteries may bifurcate at sphenopalatine foramen or earlier
-procedure:
-Caldwell-Luc approach
-removal of posterior maxillary wall area enlarged with mastoid curettes
-identify and clip vessels within pterygopalatine fossa
-overall average success rate of 87%
-indications:
-failed medical management after 72 hours
-pts requiring more than three units of blood transfusion
-nasal anomaly that precludes nasal packing
-continued bleeding despite nasal packing
293
Septodermoplasty
-grafting technique
-telangiectatic mucosal surfaces removed with preservation of perichondrial and periosteal vascular bed
-STSG then grafted
-used mainly for patients with Osler-Weber-Rendu disease
294
MANIFESTATION OF SYSTEMIC DISEASES OF THE NOSE
(Cumming’s Ch 44)
GRANULOMATOUS DISEASES
Wegener’s granulomatosis
-necrotizing granulomas and vasculitis of the upper and lower respiratory tract
-three main forms:
-Type 1: limited form of WG.
-URTI persisting for several weeks, unresponsive to antibiotics
-associated serosanguineous nasal drainage and pain
-expression of very large nasal crusts in both sides of nose
-no disease other than WG with such severe crusting
-when crusts are removed mucosa is very friable
-Type 2: sicker patient with more systemic symptoms
-nasal involvement similar as type 1 but other organs are involved
-hemoptysis and cavitating lesions
-Type 3: widely disseminated
-involvement of multiple organs including airway, pulmonary, renal, and sometimes
cutaneous lesions
295
Histopathology of Wegener’s granulomatosis
-vasculitis necrosis with an inflammatory background
-typically involves medium and small vessels
-necrosis is granulomatous in nature
-small microabscesses that enlarge and coalesce until typical necrosis has developed
-necrotic center surrounded by palisading histiocytes and scattered giant cells
Sarcoidosis
-chronic systemic granulomatous disease
-capable of involving almost any organ in the body:
-eye (episcleritis, uveitic)
-various neuropathies (sudden deafness, unilateral or bilateral facial palsy)
-salivary glands (parotid swelling)
-oropharynx (tonsillar hypertrophy)
-larynx (epiglottic swelling and subglottic stenosis)
Nasal involvement
-external
-raised, papular lesion on the nose; firm and elastic
-lupus pernio
-chronic, violaceous cutaneous lesions with a predilection for cold-sensitive
areas such as nose, cheeks, ears, and fingers
-internal
-diffuse nasal crusting or a vasomotor-like appearance to the nasal mucosa
Diagnosis
-diagnosis of exclusion
-pt’s clinical and radiographic presentation compatible with sarcoidosis
-nasal biopsy material noncaseating granuloma
-other causes for granulomatous changes need to be excluded
-bronchoalveolar lavage (BAL)
-pts with > 28% T lymphocytes in BAL fluid: high-intensity alveolitis
-pts with < 28% T lymphocytes have low-intensity alveolitis
-ACE:
-seems to correlate with the clinical activity of sarcoidosis in some patients
-not diagnostic
-other studies:
-increased ESR
-hypercalcemia and hypercalcuria may occur (10% of cases)
-hypergammaglobulinemia noted in 20-25%
-ECG abnormalities: prolonged P-R interval, bundle-branch block, arrhythmias, and
296
nonspecific sinus tachycardia (ST)-segment changes
Management
-involvement of the intranasal mucosa, epiglottis, and subglottis responds to aerosols containing
cortisone
-corticosteroids
-low dose MTX
Churg-Strauss Syndrome
-granulomatous vasculitis
-eosinophil-rich, granulomatous inflammation and necrotizing vasculitis of the upper respiratory tract
affecting small to medium vessels associated with asthma and eosinophilia
-three phases:
-prodromal phase that may persist for years
- allergic disease (e.g., allergic rhinitis and nasal polyposis, frequently followed by
asthma)
-peripheral blood and tissue eosinophilia, chronic eosinophilic pneumonia, or eosinophilic
gastroenteritis
-life-threatening systemic vasculitis
-c-ANCA and p-ANCA tests always negative
-Histopathology:
-prominent eosinophilia of vessels and perivascular tissue
-vasculitis of the small arteries and veins
-fibrinoid, necrotizing epitheloid eosinophilic granuloma
-tx:
-responds well to corticosteroids; not cyclophosphamide
Rhinoscleroma
-Klebsiella rhinoscleromatis
-chronic granulomatous disease of the respiratory tract
-also involves larynx, trachea, and bronchi
Nasal involvement
-1. catarrhal stage:
-foul-smelling, purulent rhinorrhea for weeks or months
-2. atrophic stage:
-large nasal plaques or crusts that simulate the lesions in atrophic rhinitis
-3. granulomatous stage:
-multiple granulomatous nodules are found throughout the nose, pharynx, larynx,
trachea, or bronchi. These nodules can enlarge and coalesce
-4. fibrosis and stenosis
-often complete stenosis of the nostrils
Diagnosis
-high index of suspicion and the finding of coalescent, enlarged granulomatous nodules at or near
the nasal vestibule
-cultures of infected tissue yield K. rhinoscleromatis in 98% of cases; this is diagnostic
-identification of Mikulicz’s cell in biopsy specimens is not definitely pathognomonic because
this cell can be found (though rarely) in other disorders.
297
Histopathology
-characteristic fibrosis and eosin-staining Russell bodies
-vacuolated Mikulicz’s cell: a large, foamy histiocyte that stains well with hematoxylin and eosin.
-easiest to identify during granulomatous stage
Treatment
-Streptomycin (1 g/day for 4 weeks) plus tetracycline (2 g/day)
-Corticosteroids and radiotherapy are not effective.
Tuberculosis
Nontuberculous mycobacteria
-less virulent
-more likely to infect individuals who have altered host defences
-less susceptible to standard antituberculosis drugs
-most common infections:
(1) corneal ulcers caused by Mycobacterium fortuitum
(2) cervical lymph nodes infected by nontuberculous mycobacteria (Mycobacterium
scrofulaceum, Mycobacterium szulgai, and Mycobacterium xenopi)
Nasal involvement
-usually affects anterior septum or anterior part of turbinates
-perforations of cartilaginous portion of septum
-lupus vulgaris (an indolent and chronic form of tuberculosis of the nose) scarring is more severe
Management
-2-month course of therapy with three drugs: isoniazid, rifampin, and either streptomycin or
ethambutol
Histoplasmosis
-primarily involves larynx and tongue; can involve any part of head and neck
Nasal involvement
-accompanied by pulmonary involvement characterized by cough, chest pain, and hoarseness
-CXR: diffuse miliary or a localized type of infiltrate
-nasal involvement consists of either nodules or ulcers composed of masses of organisms in
macrophages
Histopathologic features
-lesion is an epithelioid or histiocytic granuloma
-periodic acid–Schiff, Gridley, or Grocott-Gomori methenamine-silver nitrate stain to identify
organism
Treatment
-amphotericin B, in a dose of 1 mg to 10 mg per day and progressing to 1 mg/kg for a total dose of
2 g administered during a 2- to 3-month period
Rhinosporidiosis
-caused by Rhinosporidium seeberi
-contracted by immersion in contaminated waters in Asia and Africa
-nasal mucosal lesion is flat and sessile, then enlarges painless polypoid growth that fills nasal cavities
-mx: complete surgical excision; no medical management effective
298
-microscopically: pseudoepitheliomatous squamous cell metaplasia overlies numerous multisized,
microscopic globular cysts called sporangia
Mucormycosis
-caused primarily by fungi of the order Mucorales and of the genera Mucor, Rhizopus, and Absidia
-occur in diabetics and immunosuppressed patients
-broad, nonseptic hyphae (typical of Mucorales) on tissue sections stained with periodic acid–Schiff or
Grocott-Gomori methenamine-silver nitrate stain confirms the diagnosis
-prognosis is poor, with a reported death rate as high as 50%.
-amphotericin B only effective antifungal drug treatment
-aggressive surgical debridement mandatory
Clinical diagnosis
-lymphoma lesions more likely to be unilateral, with extension into soft tissue of nose, upper lip,
oral cavity, and maxillary sinus, with or without orbital involvement
-lesions are ‘‘explosive,’’ rapidly progressive
-in T-cell lymphoma otologic, tracheal, and renal involvement is extremely uncommon
-histology: polymorphic lymphoid infiltrate with angiocentric and angioinvasive features
Treatment
-XRT for localized lesions
-multiorgan involvement best treated standard leukemia protocol
299
CEREBROSPINAL FLUID LEAKS
CLASSIFICATION
PATHOPHYSIOLOGY
-CSF rhinorrhea is more common than CSF otorrhea in most reported series
300
-most frequent sites: cribriform plate and roof of ethmoid
-tumours may cause CSF rhinorrhea through direct erosion of bone
DIAGNOSIS
Symptoms
301
Cerebrospinal fluid otorrhea
-traumatic:
-94% of those who ultimately developed CSF otorrhea after trauma had an immediate onset
-symptoms may consist of hearing loss, pressure sensation in ear, or dizziness
-postop CSF otorrhea:
-leakage from incision site, a fluctuant mass at surgical site, or meningitis
-CSF otorhinorrhea after surgery for acoustic neuroma occurs in approximately 10% to 20%
-nontraumatic:
-congenital CSF otorrhea
1. petromastoid canal
2. wide cochlear aqueduct
3. Hyrtl’s fissure
4. facial canal
-children who have congenital CSF otorrhea frequently have a form of Mondini inner ear malformation and
a history of recurring episodes of meningitis
-may have a congenital dehiscence of fallopian canal or Hyrtl’s fissure
-tympanomeningeal fissure
-a congenital cleft that runs between hypotympanum and posterior cranial fossa passing
in proximity to jugular bulb
-adults who have normal inner ear function, have a CSF fistula as a result of ruptured
meningoencephaloceles that present through congenital defects in tegmen of temporal bone
Diagnostic studies
1. ‘‘Halo sign’’:
-classic sign of CSF leakage:
-clear fluid area surrounds a blood stain when CSF mixed with blood is absorbed onto
paper
2. Biochemical studies on fluid:
-testing for glucose content in suspicious fluid: >30 mg/ml confirmatory for CSF
-collecting adequate amounts of fluid to analyze for chemical content difficult
-glucose content of tears may be a confounding factor
3. B2 transferring identification:
-immunoelectrophoretic identification of B2 transferrin in fluid suspected to be CSF
confirms diagnosis of a CSF leak
-other tissue fluids that contain B2 transferrin:
-aqueous and vitreous humor in eye
-perilymph in cochlea
4. CT cisternography with nonionic contrast
-radiologic diagnosis of extracranial CSF
5. Radionuclide cisternography
-injection of radioactive isotopes (radioactive sodium, 111In-DTPA [diethylenetriamine
pentaacetic acid] 99mTc-DTPA) into subarachnoid space
-combined with scintigraphy of pledgets placed intranasally
-overall success rate of 25% to 65% and has been useful in patients with intermittent
rhinorrhea not diagnosable by other means
302
Localizing site of leakage
-leak occurring in only one side of nose generally correlates with side of defect
-leakage from nose when head is upright or tilted backward suggests that leak is through cribriform plate,
ethmoid roof, or frontal sinus
-leakage only on tilting head forward suggests that leakage is coming from sphenoid sinus or through
middle ear
-use of radioactive isotopes injected into subarachnoid space is not very accurate in localizing site of
leakage
-false-positive result is common because of absorption of radioactivity within bloodstream and
redistribution of this activity through nasal mucosa to pledgets
MANAGEMENT
Traumatic
-majority of traumatic CSF fistulas heal without surgical intervention
-if no evidence of resolution of CSF leakage by end of 1 week, probably will require surgical
exploration and closure of leak
-pts who develop CSF rhinorrhea days or weeks after trauma generally do not heal without
surgical intervention
-adjacent facial fractures should be reduced early, and reduction may result in cessation of CSF
leakage without further therapy
-indications for repair:
-failed conservative management > 2 weeks
-recurrent meningitis
-gunshot wounds
-large defects in skull base with herniation of brain and evidence of a spicule of bone penetrating
brain
-early onset that is associated with meningitis or a pneumocele (controversial)
-pts in whom injury to dura is not suspected until postoperatively when CSF rhinorrhea occurs,
conservative therapy is indicated because majority of these leaks will close
-prophylactic antibiotics have not been shown to be effective in prevention of meningitis and are not
recommended in posttraumatic patients
303
Nontraumatic
-conservative therapy rarely helpful in nontraumatic or delayed CSF rhinorrhea
-high-pressure CSF rhinorrhea:
-decrease high intracranial pressure rhinorrhea resolves in most patients
-surgical exploration if no resolution
-normal-pressure CSF rhinorrhea:
-leaks rarely close with conservative therapy and almost always require surgical exploration and
closure
Operative approaches
-intracranial and extracranial approaches
Frontal sinus
-best repaired through an extracranial approach using an osteoplastic flap
Sphenoid sinus
-best approached through an endoscopic approach
-anterior wall of sphenoid sinus is exposed and resected, and site of CFS leak is delineated
-site of leakage then is grafted with fascia and coated with fibrin glue
304
Ear
-defects in tegmen can be exposed by a mastoidectomy or atticotomy
-leaks from posterior fossa dura into mastoid are approached through a mastoidectomy
-craniotomy usually is reserved for those with failures of various extracranial operations and for patients
with large or multiple defects
-material for dural repair:
-temporalis fascia, fascia lata, periosteum, perichondrium, homograft dura, and methyl
methacrylate
305
PEDIATRIC RHINOSINUSITIS
Physical Examination
-look for purulent discharge at middle meatus
-polyps are unusual except in CF or allergic fungal sinusitis
Diagnostic Aids
-plain films are unreliable: both under- and overestimate amount of sinus disease noted on CT scans
-imaging not necessary to confirm diagnosis of RS in children
-indications for CT scan:
-severe illness or toxic condition in a child
-acute RS that does not improve with medical therapy in 48-72 hours
-immunocompromised host
-presence of suppurative complication other than orbital cellulitis
ETIOLOGY
BACTERIOLOGY
-Acute RS:
-Streptococcus pneumoniae (30%)
-Moraxella catarrhalis
-Haemophilus influenzae
306
-Chronic RS:
-Aerobic bacteria
-Streptococcus pneumoniae
-Moraxella catarrhalis
-Haemophilus influenzae
-Staphylococcus aureus
-a-hemolytic Streptococcus
-Pseudomonas aeruginosa
-Anaerobic bacteria (~50%)
-Peptococcus
-Peptostreptococcus
-Bacteroides
MEDICAL MANAGEMENT
-saline irrigation
-treatment of allergy, immunodeficiency
-antibiotic treatment toward S. pneumoniae, M. catarrhalis, H. influenzae (70% of responsible organisms)
-nonsevere acute RS:
-no abx in previous 4-6 weeks: amoxicillin (45-90 mg/kg/d), cefpodoxime proxetil,
cefuroxime axetil
-previous abx: Clavulin, amoxicillin (80-90 mg/kg/d), cefpodoxime proxetil, cefuroxime
axetil
-if condition not improved in 72 hours, change to antibiotics effective against resistant
organisms
-severe acute RS:
-agent towards B-lactamase enzymes (eg. Clavulin, second-generation cephalosporin)
-severe or toxic condition with suppurative complications
-IV antibiotics against penicillin-resistant Streptococcus pneumoniae, B-lactamase-
producing H. influenzae and M. catarrhalis
-anaerobic infections generally susceptible to amoxicillin/clavulanate
-note: spontaneous resolution rate of acute bacterial RS is 49.6%
SURGICAL MANAGEMENT
-questionable efficacy
-tonsillectomy
-few advocate this procedure for RS
-adenoidectomy (unless there is hypertrophy causing obstruction)
-antral lavage
-rarely successful with one intervention
-inferior meatal antrostomy
-poor long-term patency and low likelihood of controlling sinus symptoms
-probable efficacy
-middle meatal antrostomy
-most physiologic method to ventilate maxillary sinus
-creating an accessory ostium can contribute to a recirculation phenomenon
-anterior or anterior and posterior ethmoidectomy
307
COMPLICATIONS AND EMERGENCIES
-orbital:
-orbital inflammation (preseptal)
-orbital cellulitis
-subperiosteal abscess
-orbital abscess
-cavernous sinus thrombosis
-blindness
-intracranial:
-meningitis
-epidural abscess
-subdural abscess
-acute, chronic brain abscess
Orbital complications
-young children frequently respond to medical treatment; older children often require surgery
-potential routes for expansion of infection from ethmoid to orbit:
-arterial
-direct expansion
-venous
-lymphatic seeding
-Chandler et al Classification:
308
Intracranial Complications
-meningitis, epidureal, subdural (most common), and acute or chronic brain abscess
-symptoms:
-fever, headache, behavioural changes, seizures, nuchal rigidity, focal neurologic signs,
photophobia
309
CONGENITAL MALFORMATIONS OF THE NOSE
NASAL EMBRYOLOGY
CHOANAL ATRESIA
-1/5000-8000 births
-50% have other associated congenital anomalies
-F:M = 2:1
-65-75% unilateral, the rest bilateral
-up to 75% of bilateral cases associated with CHARGE
-other anomalies associated with atresia:
-polydactyls, nasal-auricular and palatal deformities, Crouzon’s syndrome,
craniosynostosis, microencephaly, meningocele, meningoencephalocele, facial
asymmetry, hypoplasia of orbit and midface, cleft palate, hypertelorism
-30% pure bony; 70% mixed bony-membranous
-classically: 90% bony, 10% only membranous
-anatomic deformity:
-narrow nasal cavity
-lateral bony obstruction by lateral pterygoid plate
-medial obstruction caused by thickening of vomer
-membranous obstruction
-presentation:
-unilateral:
-may be asymptomatic; involved side has tenacious secretions
-bilateral:
-cyclic cyanosis relieved by crying
310
-if later in life: mouth breathing, bilateral thick nasal discharge, absence of taste or
smell, undernourishment, defective speech, chronic sinusitis, conductive hearing loss
-diagnosis:
-unable to pass small catheter (6 French) through nose into nasopharynx
-other: no fogging of mirror, no movement of cotton wisp when breathing
-endoscopy
-CT scanning (procedure of choice)
-repair:
-unilateral repair usually delayed for at least 1 year; reduced risk of postoperative stenosis
-bilateral:
-oropharyngeal airway or McGovern nipple used as temporizing measures
-transnasal:
-advantages:
-can be performed quickly with minimal blood loss
-no possible risk of palatal growth or occlusal abnormalities later in life
-disadvantages:
-limited by access to the posterior nasal cavity (eg. size, septal
deviations)
-associated with higher rate of restenosis and need for serial dilations
-transpalatal:
-advantages:
-superior visualization and access to bony regions involved in atresia
(ie. posterior vomer, posterior lateral wall)
-shorter stenting period
-higher success rate
-disadvantages:
-orthodontic growth and development may be interrupted d/t
interruption of palatal growth centers
-palatal wound breakdown
-potential injury to greater palatine vessels
-transantral:
-opening posterior choana into a common cavity with a maxillary sinus to
prevent restenosis in cases of recurrent stenosis
-transeptal: older pts with unilateral atresia
-endoscopic approaches
-post-op management:
-antibiotics
-anti-reflux medications: reduce incidence of granulations and restenosis
311
-CT:
-narrowed bony pyriform aperture
-may show nasolacrimal ducts encased in narrow pyriform aperture
-surgical correction in severe cases:
-transnasal or sublabial approach
-abnormal bone removed with drills and microscopic visualization
-stents placed for no longer than 1 week
-embryology:
-prenasal space lies between nasal and frontal bones and cartilaginous skeleton
-extends from nasal tip to brain
-fonticulus frontalis:
-space b/n frontal and nasal bones completely fuses in area of future cribriform plate with
foramen cecum, separating intracranial contents from extracranial structures and nose
-failure of closure herniation of intracranial contents
312
-neurosurgical consult mandatory
-lateral rhinotomy, transnasal approach, coronal flap approach for glabellar lesions
Nasal dermoids
-may contain skin, hair follicles, sebaceous glands and sweat glands
-contain only ectoderm and mesoderm
-most common midline nasal mass
-1-3% of all dermoids; 10% of dermoids in H+N region
-most often asymptomatic until later in life when they begin to drain
-pathogenesis:
-faulty closure of fonticulus frontalis invagination of dermal elements
-prenasal space theory:
-space b/n nasal bone and deeper cartilage - extends from dura, along midline and to tip
of nose
-during development, dura normally retracts up through foramen cecum which closes; a
dermoid may be present anywhere along prenasal space
-dura that remains in contact with skin as it retracts will result in a sinus or pit
-may present as midline pit or deformity anywhere along midline from nasal tip to glabella
-dermoids should not be manipulated or biopsied until attachment to CNS has been ruled out by radiologic
study
-CT or MRI needed in pre-op workup
-surgical excision:
-neurosurgical consultation for CNS connections
-elliptical incision made around fistula tract
-approaches:
-lateral rhinotomy
-open rhinoplasty
-inverted-U incision
-midline nasal dorsum incision
313
JUVENILE NASOPHARYNGEAL ANGIOFIBROMA
-Juvenile angiofibroma (JNA) is a benign tumour that tends to bleed and occurs in the nasopharynx of prepubertal
and adolescent males
Epidemiology:
-accounts for 0.05% of all head and neck tumours
-1:5,000-1:60,000 in otolaryngology patients has been reported
-occurs exclusively in males; females diagnosed with JNA should undergo genetic testing
-onset most commonly is in second decade; range is 7-19 years
-rare in patients older than 25 years
Etiology:
-originates in close proximity to posterior attachment of middle turbinate, near superior border of
sphenopalatine foramen
-hormonal theory suggested
-other theories:
-desmoplastic response of nasopharyngeal periosteum or embryonic fibrocartilage between
basiocciput and basisphenoid
-etiology from nonchromaffin paraganglionic cells of terminal branches of maxillary artery
Pathophysiology:
-tumour starts adjacent to sphenopalatine foramen
-bilobed or dumbbell-shaped, with one portion of tumour filling nasopharynx and other portion extending
to pterygopalatine fossa
-fills nasal cavity; septum deviates to other side
-superior growth is directed toward sphenoid sinus, which also may be eroded
-lateral spread directed toward pterygopalatine fossa, bowing posterior wall of maxillary sinus
-proptosis and optic nerve atrophy results if orbital fissures are encroached
Clinical:
-Symptoms:
-nasal obstruction (80-90%)
-epistaxis (45-60%)
-headache (25%)
-facial swelling (10-18%)
-other: unilateral rhinorrhea, anosmia, hyposmia, rhinolalia, deafness, otalgia, swelling of palate,
and deformity of cheek
-Signs:
-nasal mass (80%)
-orbital mass (15%)
-proptosis (10-15%)
-serous otitis due to eustachian tube blockage
-zygomatic swelling and trismus denote spread of tumour to infratemporal fossa
Differentials:
-nasal polyps, antrochoanal polyp, teratoma, encephalocele, dermoids, inverting papilloma,
rhabdomyosarcoma, squamous cell carcinoma
314
Imaging Studies:
-Plain x-ray
-view of sinuses may demonstrate nasopharyngeal polyp
-bowing of posterior wall of maxillary sinus and maxillary sinus opacification
-CT scan
-extension to sphenoid sinus, erosion of greater sphenoidal wing
-invasion of pterygomaxillary and infratemporal fossae (widening of pterygopalatine fissure)
-MRI is indicated to delineate and define extent of tumor
-angiography
-branches of external carotid system are primary feeders (94%)
-main supply comes from internal maxillary artery, but ascending pharyngeal or vidian arteries
may contribute
Histologic Findings:
-tumor usually sessile, lobulated, rubbery, and red-pink to tan-gray in
appearance
-encapsulated and composed of vascular tissue and fibrous stroma
with coarse or fine collagen fibers
-vessels are thin-walled, lack elastic fibers, have absent or incomplete
smooth muscle, and vary in appearance from stellate or staghorn to
barely conspicuous due to stromal compression
-immunostaining for vimentin
Staging:
Therapy:
-hormonal therapy
-testosterone receptor blocker flutamide was reported to reduce stage I and II tumours to 44%
-despite tumour reduction with hormones, this approach is not used routinely
-radiotherapy
-some centers have 80% cure rates with XRT
-adverse effects of XRT make this modality not very useful
315
-stereotactic radiotherapy (ie, Gamma knife)
-delivers a lower dose of radiation to surrounding tissues
-most authorities reserve XRT for intracranial disease or recurrent cases
-surgical therapy:
-lateral rhinotomy, transpalatal, transmaxillary, or sphenoethmoidal route is used for small
tumours (Fisch stage I or II)
-infratemporal fossa approach used when tumour has a large lateral extension
-midfacial degloving approach, with or without a LeFort osteotomy, improves posterior access to
tumour.
-facial translocation approach is combined with Weber-Ferguson incision and coronal extension
for a frontotemporal craniotomy with midface osteotomies for access
-extended anterior subcranial approach facilitates en bloc tumour removal, optic nerve
decompression, and exposure of cavernous sinus
-intranasal endoscopic surgery is reserved for tumours limited to nasal cavity and paranasal
sinuses
Preoperative details:
-preoperative embolization used to limit blood loss during surgery
Complications:
-excessive bleeding
-malignant transformation has been reported in 6 cases
-transient blindness has been reported as a result of embolization, but it is a rare occurrence
-osteoradionecrosis and/or blindness due to optic nerve damage may occur due to radiotherapy
-fistula of palate at junction of soft and hard palate may occur with transpalatal
-anaesthesia of cheek is a frequent occurrence with Weber-Ferguson incision
316
LEMIERRE SYNDROME
Definition
-an acute medical condition characterized by anaerobic oropharyngeal infection leading to septic
thrombophlebitis of the internal jugular vein
-often complicated by septic pulmonary emboli and distant metastatic infections
-since the advent of antibiotics, this syndrome has become rare and is likely frequently overlooked
Clinical Presentation
-swelling in the upper neck, with tenderness of the lateral aspect of the neck, parallel to the
sternocleidomastoid muscle
-trismus or pain when turning the head away from the side of the thrombus
-pleural effusions and occasionally thoracic empyemas, with symptoms of dyspnea and pleuritic pain
-diagnosis of Lemierre syndrome can be made if symptoms and signs of oropharyngeal infection are
followed by those of internal jugular vein thrombophlebitis
Microbiology
-Fusobacterium necrophorum most common bacteria
-others:
-Bacteroides melaninogenicus, Eikenella corrodens, and non-group A streptococcus
-Fusobacteria are gram-negative obligate anaerobes that can be found in the upper respiratory tract
and occasionally in the gastrointestinal tract and genitourinary tract
Treatment
-consists of IV antibiotic therapy and surgical drainage of purulent collections
-ligation and resection of the internal jugular vein thrombosis is usually unnecessary and should be
considered only in patients with refractory sepsis or severe respiratory compromise from repeated
pulmonary emboli
-initial antibiotic therapy should include antibiotics with good antianaerobic activity
-fusobacteria are typically sensitive to penicillins, clindamycin, metronidazole, and
chloramphenicol
-use of anticoagulation in Lemierre syndrome is controversial
-anticoagulation may expedite clinical improvement and should be considered in when
there are no contraindications
317
Medical Management of Acute Bacterial Sinusitis
(Ann Otol Rhinol Laryngol 109:2000)
CLASSIFICATION
-Acute: < 4 wks
-Subacute: 4 - 12 wks
-Chronic: > 12 wks
-Recurrent: 4 or more episodes in 1 year > 7 days
EMBRYOLOGY OF SINUSES
Ethmoid -> Maxillary -> Sphenoid -> Frontal
PREDISPOSING FACTORS
-prior URTI
-concurrent Group A strep infection
-allergic rhinitis
-environmental pollutants
-dental infections
-hormonal changes
-iatrogenic: mechanical ventilation, NG tubes, nasal packing
-anatomic variations: tonsillar/adenoid hypertrophy, deviated septum, nasal polyps, cleft palate
-swimming
-immunodeficiency
-secretory disturbances (CF)
-immotile cilia syndrome
-Kartagener’s syndrome
-bronchiectasis
-asthma/ASA/polyps
-immature immune system
PATHOGENS
-Streptococcus pneumonia (30-40%)
-Haemophilus influenzae (20-30%)
-Moraxella catarrhalis (12-20%)
-Streptococcus pyogenes (up to 3%)
-Others: streptococcus sp., staph. aureus, neisseria
-fungi: diabetic/immunocompromised
-anaerobes: chronic sinusitis, dental infections
ANTIBIOTIC RESISTANCE
-d/t overuse of antibiotics
-mostly d/t B-lactamase production
-penicillin-resistant pneumococci (33-55% isolates)
318
-ampicillin-resistant H.flu (~30-40% isolates)
-high rate (>75%) Moraxella resistance
DIAGNOSIS
-symptoms worsen after 5 days, persist for at least 10 days, are more severe than viral dz
-depends on presence of > 2 major factors or 1 major and 2 minor factors:
Major factors:
-facial pain or pressure
-facial congestion or fullness
-nasal obstruction
-nasal purulence or discoloured PND
-hyposmia or anosmia
-fever
Minor factors:
-headache
-halitosis
-fatigue
-dental pain
-couch
-ear pain, pressure, or fullness
-fever
ANTIMICROBIAL THERAPY
319
-gatifloxacin (Tequin) 400 mg qd
-moxifloxacin (Avelox) 400 mg qd
-clindamycin 140-450 mg tid/qid
DURATION OF THERAPY
-10 to 14 days
ADJUNCTIVE TREATMENTS
-promote ciliary function and decrease edema
-saline nasal sprays, humidifiers, warm aerosols, steam, aromatic vapours, hot soups etc..
Topical decongestants:
-phenylephrine HCL, oxymetazoline HCL
-stimulate mucosal alpha-adrenergic receptors
-shrinking edematous mucosa
-limit to 3 days to avoid rhinitis medicamentosa
-use of systemic decongestants not recommended in children
In children: ethmoid infundibulum and anterior ethmoid most common affected sites
CONCLUSION
-diagnosis largely made clinically
-lab tests rarely require
-treatment focussing on relieving obstruction, treating infection, thinning the mucous, opening the sinus
ostia
-antibiotic selected according to resistance patterns found in community
320
Overview
• Anatomy and Development
Mucoceles of the • Physiology and Pathophysiology
Paranasal Sinuses •
•
Epidemiology
Clinical Features
Francis T.K. Ling, MD BSc • Treatment
Department of Otolaryngology – Grand Rounds • Case Presentations
University of Ottawa
Wednesday, January 28th 2004
Introduction Introduction
• Definition: • Mucoceles known for > 100 years
• Epithelial lined mucous-containing sac completely filling a • 1725: Dezeimeris first described frontal mucoceles
paranasal sinus • 1818: Langenbeck commented on clinical complaints and
• Capable of expansion by virtue of bone resorption and new bone symptoms
formation • “hydatids”
• 1890: Rollett introduced the term “mucocele”
• Most common lesion causing expansion of paranasal
sinuses
321
1
Anatomy and Development Anatomy and Development
• Ethmoid Sinuses • Sphenoid sinus
• Located in superior half of • In body of sphenoid bone
lateral nasal wall
• No significant sinus at birth
• Development begins during 3rd-
4th month of fetal development • Development begins at 5 years
• Continue to grow through • Final volume attained by 12-15
childhood until age 12 years
• Average volume 15 ml • Average volume: 7.5 ml
• Drainage: • Drainage:
• Anterior: infundibulum or • Sphenoethmoidal recess
ethmoid bulla
• Posterior: superior meatus
Physiology Physiology
• Sinus lining: • Pattern of clearance:
• Ciliated, pseudostratified, • Maxillary: floor
columnar epithelium stellate pattern along walls
• Mucous glands and goblet to natural ostium
cells mucous blanket • Frontal: inward flow
• “sol-gel” phase medially superior
lateral floor frontal
recess
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2
Pathophysiology Pathophysiology
• Obstruction of sinus ostium or outflow tract • Bone resorption:
• Inflammation (ie. Chronic sinusitis) • Epithelium continues to secrete
causing expansion of the mucocele
• Trauma
• Increased pressure
• Iatrogenic (eg. FESS) devascularization of bone and
• Mass/Tumour (eg. Polyps, ostioma, malignancy, ostioma) osteolysis
• Obstruction of minor salivary gland located within lining • Local inflammation secretion of
cytokines
of paranasal sinus
• Fibroblasts PGE2 + IL-1
• Eg. Mucous retention cyst of maxillary sinus • Epithelial cells TNF alpha
• Cause osteoclastic bone
resorption
Epidemiology Epidemiology
• 3rd or 4th decade • Rombaux et al (Belgium, 2000):
• M:F ~ 7:1 • 178 mucoceles
• Primitive mucoceles: 35%
• 10-15 years to develop
• Post-traumatic: 2.1%
• Frontal > ethmoid > maxillary > sphenoid
• Post-operative: 62.9%
• Fronto-ethmoidal ~65%
• Incidence after FESS not known
• Maxillary ~ 20%
• Sphenoid ~1-8%
• Posterior ethmoid ~1-6%
• Uncommon locations: middle turbinate, pterygomaxillary space
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3
Fronto-
Fronto-ethmoidal Mucocele Fronto-
Fronto-ethmoidal Mucocele
• General: • Ocular:
• Frontal headache (common) and/or deep nasal pain • Proptosis (common)
• Frontal swelling +/- infection/draining fistula • Periorbital pain
• Nasal obstruction and rhinorrea unusual • Displacement of globe
downward and outward
direction
• Reduced ocular mobility
• Diplopia
Fronto-
Fronto-ethmoidal Mucocele Maxillary Mucocele
• Neurologic: • “mucous-retention” cyst
• Destruction of posterior frontal sinus wall • Incidental finding
• Decreased LOC • Rarely achieve sufficient size to cause bony erosion
• Confusion
• Rarely require specific therapy if asymptomatic
• Meningitis
• Spontaneous regression without therapy
• CSF leak
324
4
Investigations Investigations
• CT scan provides excellent anatomical information • MRI scan:
• Findings: • Allows differentiation of mucoceles from solid component of
neoplasms or meningoencephalocele
• Completely opacified sinus cavity
• Demarcates mucocels and soft-tissue structures in the event of
• Thinned and expanded sinus walls
intracranial or intraorbital growth
• Loss of normal scalloped margin
• Depression or erosion of supra-orbital ridge and extension of soft
• Findings:
frontal tissue mass across midline • Signal intensity vary depending on state of hydration and age
• Majority show hyperintense T2 and hypointense T1
• Increased dehydration T2 become hypointense and T1 become
hyperintense
325
5
External Frontoethmoidectomy External Frontoethmoidectomy
• Technique (Cont’d) • Killian procedure
• Periosteum elevated to fronto-ethmoid • For tall sinuses in which
suture
disease cannot be removed
• Anterior ethmoid artery divided through floor alone
• Lamina papyracea removed and
• Floor and anterior wall
ethmoidectomy performed
removed
• Frontal sinus opened in medial part of
floor • Supraorbital bony strut (10
• Diseased tissue within sinus is removed mm)
• Large chute from frontal sinus through
ethmoid cavity into the nose
• +/- stent placement
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6
Osteoplastic Flap Osteoplastic Flap
• Technique: • Technique:
• Skin-tissue flap raised, • Periosteum incised and lifted
preserving periosteum and off bone
supraorbital nerves • Bone cuts made to create
• Perimeter of frontal sinus osteoplastic flap
marked with template from
Caldwell-view radiograph
327
7
Osteoplastic Flap Osteoplastic Flap
• Cranialization • Complications:
• Indications: • Fat donor site:
• Large portions of posterior frontal sinus destroyed with • Seroma
substantial epidural spread of mucocele • Hematoma
• Intracranial complications present • Abscess
• Frontal craniotomy usually required • Cellulitis
• Intracranial:
• Extradural dead space remains for extensive mucoceles
• Dural tears
• Dead space obliterates by frontal brain over several weeks
• Frontal lobe injury
• Oblteration of dead space by abdominal fat used to achieve • CSF leaks
immediate closure and to avoid scarred adhesions
• Meningitis
• Brain abscess
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8
Endoscopic Approach Endoscopic Approach
• Contraindications (Rombaux et al, 2000) • Technique:
• Absolute: • Polyps or polypoid
• Mucocele not accessible to endoscope mucosa cleared
• Mucocele located in external part of frontal or maxillary sinus from frontal recess
• Cutaneous fistula
• Relative:
• Loss of anatomical landmarks
• Revision surgery for recurrence lateral to frontal recess after
previous external approach
• Frontal recess stenosis with hypertrophic bone occluding area
• Associated disease (ie. Malignancy, large benign tumour)
329
9
Endoscopic Approach Endoscopic Approach
• Technique (Cont’d) • Postoperative Care:
• Floor of frontal sinus anterior to outflow tract removed • Antibiotics and saline spray
• Mucocele identified, opened and drained • Irrigation of stent
• Lining not curetted or removed • Removal of stent 6-12 weeks after surgery
• +/- stent insertion
330
10
External vs. Endoscopic Approaches Follow-
Follow-up
• “small, well-positioned mucoceles may be attempted first • Mucoceles may recur many years after surgery
endoscopically, but in the setting of massive mucoceles • Recurrences may be as long as 49 years after initial surgery
with risk of imminent complications and instability of the (Moriyama)
facial skeleton, the more conservative approach may be the • Recurrences should be treated as early as possible
more aggressive open techniques”
• “endoscopic transnasal approach best choice for
intracranially extended mucoceles because it is the least
invasive and can provide an adequate surgical view for
wide marsupialization”
331
11
Case Presentation #2 Case Presentation #2
332
12
Case Presentation #3 Case Presentation #3
333
13
Case Presentation #3 Case Presentation #3
• Repeat MRI
334
14
Case Presentation #4 Summary
• Post-op • Mucoceles most common lesion causing expansion of
• Accumulation of CSF under right forehead scalp paranasal sinuses
• No rhinorrhea • Long asymptomatic progress
• Bed rest and aspiration of fluid
• When symptomatic, usually present with ocular symptoms
• Persistent leak lumbar drain
+/- neurologic symptoms depending on location of
• Resolution of CSF leak
expansion
• No infection
• Fronto-ethmoidal mucoceles most common
• Discharge home
• Follow-up • Caused by sinus obstruction secondary to chronic
infection, surgery or trauma
• Well with no recurrence
Summary
• Treatment is surgical
• Traditionally, complete removal advocated via external approach
• Trend towards endoscopic management
• External or combined approaches usually reserved for extensive
involvement or failed endoscopic attempt
• Push towards endoscopic management of large intracranial
mucoceles
• Long term follow-up required to monitor for recurrence
335
15
Radiation-Induced Sarcoma
Pathophysiology:
-threshold dose for PRS is not known, although in most published series, a dosage of 40-60 Gy is reported
-development of PRS also is influenced by other factors:
-genetic tendency
-influence of chemotherapeutic agents
-unknown factors
-ionizing radiation is thought to act via genetic alterations, including mutations of p53 and retinoblastoma
(Rb) genes
Mortality/Morbidity:
-reported 5-year survival rate for PRS has been extremely poor, ranging from 8.7-22%
-poor survival rate is thought to be due to a number of interrelated factors, as follows:
-Significant delay in diagnosis
-Large unresectable lesions
-Elderly patients
-Anaplastic nature of lesions
-Lack of effective adjuvant treatment
History:
-pain is the most common complaint and is abrupt and rapid in onset, relentless and progressive, constant,
and worse at night
-mass (soft tissue or bone), bleeding, and pathologic fracture also are reported
Diagnosis:
-MRI
-biopsy
Histologic Findings:
-usually is a high-grade lesion
-bone:
-osteosarcoma was the most common type, comprising 61.5% of all cases
-fibrosarcoma (23.7%), malignant fibrous histiocytoma (MFH, 9.6%), chondrosarcoma (3.7%),
and rare cases of angiosarcoma and Ewing sarcoma
-soft tissue:
-most common histological type is MFH (70%), followed by osteosarcoma, fibrosarcoma,
malignant peripheral nerve sheath tumor (MPNST), chondrosarcoma, and angiosarcoma
336
Treatment:
Medical Care:
-PRS is high grade and advanced stage or metastatic at the time of diagnosis, patients commonly are not
eligible for curative surgery, and the prognosis for these patients generally is poor
-chemotherapy is the most common treatment modality and typically is associated with poor response rates
Surgical Care:
-wide or radical resection
Consultations:
-multidisciplinary approach
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ANATOMY AND PHYSIOLOGY OF THE NOSE
(ENT Secrets)
“Danger Triangle”
-from nasion to lateral corners of mouth
-venous supply of nose drains intracranially
-angular vein inferior ophthalmic vein cavernous sinus
-provides cutaneous nasal infections with a potential rout to spread intracranially
Nasal innervation:
-muscles: CN VII
-skin: CN V1 and V2 - touch and chemosensation
-olfaction: CN I
-sympathetic: via superior cervical ganglion sphenopalatine ganglion
-parasympathetic: superior salivatory nucleus CN VII sphenopalatine ganglion posterior nasal nerve
Nasal Reflex:
-strong nasal stimuli cardiopulmonary responses (breathing cessation and bradycardia)
-mild stimuli sneezing
Nasal lymphatics:
-nose and paranasal sinuses retropharyngeal nodes
-anteriorly submandibular or upper deep cervical nodes
Kartagener syndrome:
-immotile cilia syndrome due to absence of dynein arm on peripheral ciliary microtubules
-chronic sinusitis, bronchiectasis and situs inversus
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RHINITIS
(Supplements from ENT Secrets)
Rhinitis:
-nasal hyperfunction and tissue inflammation which leads to nasal congestion, rhinorrhea, nasal
obstruction, pruritus and sneezing
Classification:
-allergic
-seasonal
-perennial
-non-allergic
Allergic rhinitis most often mediated by Gell and Coombs Type I hypersensitivity
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Retropharyngeal Space
Boundaries:
anterior: visceral division of middle layer of deep cervical fascia
posterior: alar division of deep layer of deep cervical fascia
superior: skull base
inferior: level of T1 or T2
Contents:
retropharyngeal nodes separated by midline raphe
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Danger Space
Boundaries:
anterior: alar division of deep layer of deep cervical fascia
posterior: prevertbral division of deep layer of deep cervical fascia
superior: skull base
inferior: diaphragm
Contents:
none
Prevertebral Space
Boundaries:
anterior: prevertebral division of deep layer of deep cervical fascia
posterior: vertebral bodies
superior: skull base
inferior: coccyx
Contents:
none
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Boundaries:
anterior: mandible
posterior: intrinsic muscles of base of tongue
superior: floor of mouth
inferior: superficial layer of deep cervical fascia; hyoid bone
lateral: mandible
Contents: (sublingual space)
sublingual gland
hypoglossal nerve
Wharton duct
Parotid Space
Boundaries:
invested by superficial layer of deep cervical fascia
Contents:
parotid gland
external carotid artery
posterior facial vein
facial nerve
M asticator Space
Boundaries:
posterior: pterygomaxillary space
superior: temporal space
Contents:
masseter
pterygoid
ramus and body of mandible
temporalis tendon
inferior alveolar vessels and nerves
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ANATOMY AND PHYSIOLOGY OF THE SALIVARY GLANDS
DEVELOPMENTAL ANATOMY
Parotid Gland
-acinar cells mainly serous (basophilic)
-Stensen duct arises from anterior border, 1.5 cm below zygoma
-follows along plane from external auditory canal to columella
-opens intraorally just opposite second upper molar
-deep layer of parotid fascia extends from fascia of posterior portion of digastric muscle and forms
stylomandibular membrane
-parotid tissue can herniate through a weakness in the stylomandibular membrane and lie in the
lateral pharyngeal wall
Facial Nerve
-three motor branches at stylomastoid foramen:
-stylohyoid muscle
-postauricular muscle
-posterior belly of digastric muscle
-location:
-6-8 mm anteroinferior to tympanomastoid suture
-10 mm anteroinferior and deep to tragal pointer
-branches at pes anserinus: upper temporofacial and lower cervicofacial division
-pes ~ 1.3 cm from stylomastoid foramen
-constant relationships:
-buccal branch follows course of parotid duct and lies either superior or inferior to duct
-temporal branch crosses zygomatic arch parallel with superficial temporal vessels
-marginal mandibular branch is superficial to posterior facial vein (retromandibular vein)
Auriculotemporal Nerve
-branch of V3
-innervate scalp
-also carries postganglionic parasympathetic fibers from otic ganglion to parotid gland
-aberrant innervation to skin can result in Frey syndrome
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Arterial Supply
-external carotid artery superficial temporal artery transverse facial artery parotid gland,
Stensen duct, masseter muscle
Venous Drainage
-posterior facial vein (deep to facial nerve)
-eventually drains into internal jugular system
Lymphatic Drainage
-two layers of nodes
-superficial layer lies between gland and capsule
-drains parotid gland, EAC, pinna, scalp, eyelids, lacrimal glands
-deep layer
-drains parotid gland, EAC, middle ear, nasopharynx and soft palate
Submandibular Gland
-comprises both mucous and serous cells
-submandibular duct (Wharton) lies inferior to lingual nerve and superior to hypoglossal nerve
-parasympathetic supply from chorda tympani
-sympathetic fibers originate from superior cervical ganglion and travel with lingual artery
-blood supply: facial artery
Sublingual Gland
-primarily mucous-secreting acinar cells
HISTOLOGY
-functions of saliva:
-lubricates and moistens foods to facilitate mastication
-cools hot foods
-buffers chemicals
-lavages oral cavity (antibacterial)
-lysozyme, secretory IgA
-aids in digestion
-dental protection
-modulation of taste
347
-composition of saliva:
-water (99%)
-salts: (CaPO4, CaCO3)
-amylase
-albumin
-lysozyme
-IgA
-ptyalin
Production of Saliva
Secretory Unit:
-acinus, secretory tubules (intercalated duct, striated duct, excretory duct), collecting duct
-myoepithelial cells contract to expel preformed secretions
Secretory Process:
-serous acinar cells produce secretory granules with amylase
-mucous cell granules contain mucin
-as fluid moves distally, ducts alter its composition by secretion of electrolytes, water and organic
solutes and by resorption of water and electrolytes
-net effect: decrease in sodium and increase in potassium concentrations
-abundant mitochondria in striated duct for metabolic demands of transport of ions and water
Autonomic Innervation
348
auriculotemporal nerve parotid gland
-submandibular/sublingual glands:
-superior salivatory nucleus nervus intermedius chorda tympani lingual nerve
(submandibular ganglion) postganglionic fibers to submandibular and sublingual
glands
-acetylcholine is the primary neurotransmitter
349
SALIVARY GLAND IMAGING
Plain-film radiography
-to evaluate calculi or detecting calcification in hemangiomas, lymph nodes or pleomorphic adenoma
Sialography
-CT and MRI have replaced sialography in evaluation of salivary gland or adjacent tumour masses
-still most useful modality to evaluate intrinsic structure of salivary ducts
-indications:
-chronic, recurrent and nonspecific sialoadenitis
-Sjogren syndrome, Mikulicz syndrome
-submandibular or parotid gland sialolithiasis
-posttraumatic or postoperative fistula, stricture or cyst
-contraindications:
-acute infections
Computed Tomography
-Hounsfield units:
-a unit of x-ray attenuation used for CTs
-air: -1000 HU
-water: 0
-bone: +1000 HU
-fat: -20 HU
-muscle: +20 HU
-enhanced parotid: +35 HU
-submandibular glands: +40 HU
Diagnostic Ultrasound
-differentiates solid vs cystic masses
-for U/S guided FNA
Nuclear Scintigraphy
-sodium pertechnetate Tc 99m
-most commonly used radioactive pharmaceutical
-uptake by normal salivary gland tissue
-tumours usually have no uptake filling defect
-Warthin’s tumour and oncocytoma readily take up pertechnetate “hot spot”
-gallium 67 citrate:
-used for studying inflammatory or neoplastic disease
-taken up by dividing cells - excessive accumulation observed in inflammatory or neoplastic
processes:
-sarcoidosis, melanoma, lymphoma
-anticarcinoembryonic antigen imaging has high negative predictive value (100%) in malignancy of the
salivary glands
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INFLAMMATORY DISEASE OF THE SALIVARY GLANDS
Sjogren Syndrome
-sialography:
-gland involvement tends to be bilateral
-parotid gland mild to markedly enlarged
-multiple punctate contrast collections
throughout gland can progress to become
larger collections that are more globular
-may have areas of tubular sialectasia or
strictures
-retention of contrast material
-CT:
-bilateral parotid enlargement with multiple
areas of low attenuation
-may have cyst formation with lymphoid
infiltration (pseudolymphoma)
-high incidence of non-Hodgkin lymphoma -
presents as intraglandular mass
Sialolithiasis
-can be diagnosed with plain-film radiography
-20% of calculi in submandibular and 20-40% in parotid gland are not visible on plain-film
-sialography: intraductal filling defects
351
-usually salivary gland neoplasm
-masticator space lesions:
-can be meningioma, neurolemma, sarcoma, SCC, dentigerous cyst or masseteric hypertrophy
-no salivary gland lesions
-four findings that indicate masticator space origin:
-location anterior and lateral to parapharyngeal fat
-limitation of tumour by boundaries of masticator space (ie, sphenoid bone, posterior
aspect of mandible, and zygomatic arch)
-obliteration of fat planes within masticator space
-tendency to spread through foramen ovale
-MRI:
-primary salivary gland tumours and minor salivary gland neoplasms displace internal carotid
artery
-schwannomas (vagus nerve) and paragangliomas arise posterior to ICA and displace it anteriorly
-similar signal characteristics:
-well-circumscribed lesion with intermediate signal on T1 and increasing signal on T2
-paragangliomas may have salt and pepper appearance d/t flow voids
Benign Neoplasms
Pleomorphic Adenoma
-CT:
-well-circumscribed mass with homogeneous or heterogeneous density
-contrast enhancement varies but tends to be mild
-calcifications may be evident
-MRI:
-predominantly heterogeneous well-circumscribed mass
-T1 intermediate to low signal intensity
-T2 increased signal
352
Warthin Tumour and Oncocytoma
-CT:
-homogeneous well-circumscribed mass
-hypodense or cystic areas
-calcification does not occur
-MRI:
-T1 intermediate to low signal intensity
-T2 increased signal
-both Warthin and oncocytoma are unique in that they accumulate technetium-99m pertechnetate
Lipoma
-may be intraparotid or paraparotid
-CT: low attenuation (-50 to -150 HU)
-MRI: high signal T1; intermediate signal T2
Malignant Neoplasms
Mucoepidermoid Carcinoma
-low-grade MEC has CT and MRI characteristics resembling benign lesions
-well circumscribed and regularly marinated without infiltration into adjacent soft tissues
-low to intermediate signal intensity on T1 with increasing intensity on T2
-high-grade MEC:
-more irregular appearance with irregular margination and infiltration into soft tissues
-signal intensity intermediate on T1 and T2
Lymphoma
-multiple, well-circumscribed, homogeneous masses withing parotid gland and in paraparotid region that
may enhance slightly with contrast
353
IMAGING PROCEDURES
Imaging Study Indications Comments
Plain films Calculus disease Limited value; may differentiate salivary gland disease from bony
abnormality
Sialography Sjogren syndrome, chronic Best means of imaging ductal system; of limited value other than in
inflammatory conditions evaluating the ductal system
CT Chronic inflammatory Excellent anatomic detail for intrinsic and extrinsic salivary gland
conditions and complications, tumours; best means of identifying calculi or calcification
intrinsic and extrinsic masses,
calculus disease
MRI Chronic inflammatory Excellent anatomic detail in tumour evaluation; may be better than CT
conditions and complications, for parapharyngeal space and intracranial extensions
intrinsic and extrinsic masses
US Abscess, cyst, intrinsic salivary Best means of determining solid vs cystic lesions, but limited
neoplasm (?) nasopharyngeal detail
Radionuclide imaging Warthin Tumour Sodium pertechnetate Tc 99m taken up by benign neoplasms; gallium
67 citrate and bone-scanning agents occasionally useful for
malignancies
354
NON-NEOPLASTIC DISEASES OF THE SALIVARY GLANDS
Mumps
-most common viral disorder involving salivary gland
-peak incidence: 4-6 ya
-pathogen: paramyxoviruses
-pain, swelling, generalized symptoms
-dx: antibodies to mumps S and V antigens and to hemagglutination antigen
-complications: sudden deafness, pancreatitis, meningitis, orchitis
-tx: self limiting; requires only supportive care, audiological evaluation, vaccine is available
355
CHRONIC INFLAMMATORY DISORDERS
-d/t lowered secretion rate with subsequent salivary stasis
-sialectasis, ductal ectasia, and progressive acinar destruction combined with a lymphocytic infiltrate
-IgG dominates in saliva rather than typical IgA
-permanent xerostomia in 80%
-tx:
-start with conservative measures
-progress to periodic ductal dilatation, ligation of duct, total gland irradiation, tympanic
neurectomy, and excision of gland
-recurrent parotitis of childhood:
-M>F
-sudden onset with no obvious underlying cause
-no xerostomia; child not generally ill
-disease may disappear at puberty or continue into adulthood
GRANULOMATOUS DISEASE
Animal-Scratch Disease
-does not involve salivary glands directly; may involve parotid by contiguous spread
-gram-negative bacillus sensitive to gentamicin
-disease is self-limiting; treatment is symptomatic
-Cat-scratch Disease:
-Bartonella henselae
-Medical Care:
-appropriate therapy in persons with CSD has not been well studied
-in most patients who are immunocompetent, CSD is self-limited
-Effective antibiotics include rifampin, ciprofloxacin, trimethoprim-sulfamethoxazole
(TMP-SMX), and gentamicin
-tx for 10-14 days. No specific dose recommendations are available
Sarcoidosis
-unknown etiology
-diagnosis of exclusion
-uveoparotid fever (Heerfordt syndrome): uveitis, parotid enlargement and facial paralysis
-involvement of minor salivary glands may occur labial or palate biopsy may establish dx
-tx: corticosteroids in acute phase
SJOGREN SYNDROME
-lymphocyte-mediated destruction of exocrine glands leading to xerostomia and keratoconjunctivitis
-second most common autoimmune disease after rheumatoid arthritis
-average age of onset: 50y
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-associated with Non-Hodgkin’s lymphoma
-two forms:
-Primary Sjogren:
-involves exocrine glands only
-may involve up to 3% of population
-80%: unilateral or bilateral salivary gland swelling occurs
-Secondary Sjogren:
-associated with definable autoimmune disease, most commonly RA
-30-40% salivary gland swelling
-laboratory:
-B-cell hyperactivity polyclonal hypergammaglobulinemia
-70-90% have rheumatoid factor
-55-70% have ANA
-specific autoantibodies:
-anti-Ro (SSA) and anti-La (SSB)
-detected in 40-60% of pts with primary Sjogren
-dx: -requires biopsy of labial mucosal glands or parotids
-aggregates of 50 or more lymphocytes and plasma cells
-tx: -artificial saliva, frequent small drinks, artificial tears, consider pilocarpine hydrochlorate drops
and oral corticosteroids for severe acute exacerbation
SIALOLITHIASIS
-calculi: 80% submandibular gland; <20% parotid; 1% sublingual
-calcium phosphate
-commonly occur in pts with chronic sialadenitis
-gout: only systemic disease causing salivary gland calculi (uric acid)
-x-rays:
-90% submandibular calculi are radiopaque; 90% parotid calculi are radiolucent
-all detectable by CT
-submandibular calculi within duct; parotid are at hilum or within parenchyma
-tx:
-gland massage, bimanual expression
-transoral excision if calculi near duct orifice
-complete gland excision if calculi near hilum
-complications:
-fistulas, acute suppurative sialadenitis, ductal strictures
CYSTIC LESIONS
-dermoid cyst
-congenital ductal cyst
-dx by sialography
-no treatment unless repeated infections
-first arch branchial cleft cysts
-tract intimately associated with facial nerve
-acquired cysts:
-benign lymphoepithelial lesion, trauma, parotitis, calculi, duct obstruction, mucus extravasation,
HIV infection
-mucoceles and mucous cysts:
-minor salivary glands, most commonly on the lips, buccal mucosa and ventral portion of tongue
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RADIATION INJURY
-often permanent if exposed to > 40-50 Gy
-serous cells exhibit marked degranulation and disruption
-continued irradiation leads to complete destruction of serous acini and subsequent atrophy in gland
-interstitial fibrosis seen on histology
-tx: symptomatic (pilocarpine drops, artificial saliva, frequent drinks), dental care
TRAUMA
-ductal injury:
-suspected if any penetrating injury posterior to anterior border of masseter muscle
-tx: end-to-end anastomosis over polyurethane catheter with 9-0 sutures
-if not possible, duct ligated or new duct created from buccal mucosa
-facial nerve injury:
-if wound anterior to vertical line from lateral canthus to mental foramen repair is probably
unnecessary (even with clear dysfunction) b/c recovery is likely
-injuries posterior to this line are repaired immediately
-no real advantages with delayed repair
OTHER DISORDERS
-pneumoparotitis glass blowers
-chelitis glandularis
-enlargement of labial salivary glands
-medications:
-isoproterernol, ethambutol, phenobutazone,
phenothiazine, iodine compounds and heavy
metals
-necrotizing sialometaplasia
-commonly on hard palate
-mucosal ulceration with
pseudoepitheliomatous hyperplasia, ischemic
lobular necrosis, and dissolution of acinar
walls with release of mucous
-self-healing and requires no treatment
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CONTROVERSIES IN SALIVARY GLAND DISEASE
GUSTATORY SWEATING
-recent study showed that after 1 year, 43% of pts were symptomatic and 96% had a positive starch iodide
test
-only 5-10% had severe symptoms
Diagnosis
-Minor’s starch iodide method
-infrared thermography
-mainly used for research purposes
Prevention
-temporoparietal flap transposed immediately after parotidectomy
-sternocleidomastoid flap
-flaps have decreased rates of GS - but may interfere with postoperative tumour surveillance
Treatment
-antiperspirants and scopolamine - only provide temporary effects
-botulinum toxin:
-binds presynaptic cholinergic terminals and prevents release of ACh
-tympanic neurectomy
PAROTID CYSTS
-may be true cysts, lymphoepithelial cysts, mucoceles, keratomas, or branchial cysts
-asymptomatic masses observed
-surgical resection effective, although cysts may recur in residual tissue
-tetracycline sclerosis by direct injection
-botulinum toxin A injection subcutaneously near mass after diagnostic aspiration
XEROSTOMIA
-mostly after XRT
-pilocarpine:
-muscarinic receptor agonist
-used to ameliorate xerostomia
-stimulates undamaged cells
PAROTID SURGERY
Preoperative Evaluation
-EnoG use in parotid surgery is uncommon
-studies found that significant decrease in preoperative EnoG response correlated with postoperative facial
dysfunction
-when reduced by more than 80%, all pts were found to have facial nerve involvement
-EnoG did not correlate with facial nerve function for benign tumours
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Benign Mixed Tumours
Extent of Resection
-arguments in favour of a limited resection include:
-potentially smaller incision
-less postoperative facial distortion
-shorter operative time
-lower incidence of Frey syndrome because less parotid is removed
-for malignant tumours, usually a total parotidectomy is performed, because of possibility of direct
extension or even intraparotid nodal metastases
Other Facts
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TASTE
Definitions
-hypogeusia: partial loss of taste
-ageusia: total loss of taste
-dysgeusia: abnormal taste in absence of obvious stimulus
-flavour: combined sensation of taste, smell, temperature, texture and pungency
Tongue
Taste Buds, Receptor Sites and Taste Stimuli, Taste Quality Coding
-globular cluster of cells arranged like segments of an orange
-tips taper to thin microvilli that project above into the taste pore
-taste receptor cells have limited lifespan measured in days
-salts and acids interact with ion channel on taste pore membrane
-more than one receptor type for sweetness and bitterness
-neural fiber types specific to each of four basic tastes
Taste Papillae
-filiform:
-most numerous
-no role in taste - helps sustain tastants on tongue
-in cats are shaped like rasps for licking
-located all over tongue
-fungiform:
-distributed on tip and edge of anterior 2/3 of tongue and lateral edge
-functions in taste
-foliate:
-located between adjacent folds on edges of base of tongue; posterior lateral edge
-circumvallate:
-raised circular structures on the rear of the tongue
-forms an inverted V
Tongue Map
-myth that certain tastes occur only on one area of the tongue
-four taste qualities can be perceived on all loci where there are taste buds
Peripheral Nerves
-glossopharyngeal nerve (IX):
-taste and sensation to posterior 1/3 of tongue
-lingual branches
-taste sensations from circumvallate papillae and foliate papillae from rear edge of tongue
-afferent neurons to mucous membrane of base of tongue
-terminate in nucleus solitarius (the gustatory nucleus)
-facial nerve (VII) - chorda tympani:
-taste information from fungiform papillae on anterior 2/3 of tongue
-may also receive information from foliate papillae as well
-terminates in tractus solitarius
-facial nerve (VII) - greater superficial petrosal nerve
-taste sensation through innervation of palate; buds located on margin b/n hard and soft palates
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-vagus nerve (X) - superior laryngeal nerve
-innervates taste buds on laryngeal surface of epiglottis
-role in everyday taste is unknown
Central Connections
-taste fibers from CN VII, IX, X compose part of solitary fasciculus terminate on rostral half of
nucleus solitarius in medulla
-second-order gustatory neurons ventroposteromedial nucleus in thalamus
-third order neurons cortex (circular sulcus that separates frontal operculum from insula)
Tongue
-substances that alter taste have effects on taste membrane
Venous Taste
-stimulation of receptor sites that are on the bottom of the taste cell (ie. below the microvilli)
Peripheral Nerves
-chorda tympani
-most commonly involved in taste disorders
-taste loss in anterior 2/3 of tongue
-most commonly from acute or chronic OM
-release of inhibition from chorda damage enhanced tastes from some stimuli
-other causes: Bell palsy, Ramsay Hunt syndrome
Nervus Intermedius
-neoplastic processes that cause nervus intermedius dysfunction: acoustic neuroma, meningioma,
or facial nerve neuroma
Glossopharyngeal Nerve
-trauma after tonsillectomy, UPPP or any insertion of deep mouth gag where base of tongue is
compressed and lateral pharyngeal wall is manipulated or stretched
-Vernet syndrome: jugular foramen lesions paralyse all nerves that traverse the jugular foramen
(IX, X and XI)
-Collet syndrome: extension of lesion to involve the CN XII unilateral tongue paralysis
-Villaret syndrome: sympathetic trunk compromise along with CN IX-XII involvement
CNS
-unilateral pontine haemorrhage
-unilateral damage to rostral insular cortex
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Phantoms from damage to peripheral structures
-chorda tympani: bitter and metallic phantoms
-nervus intermedius: salty phantoms
-glossopharyngeal nerve: bitter taste phantom that increases with topical anaesthesia
Capsaicin:
-stimulates oral pain
-can also desensitize pain receptors may be used as an analgesic
-acoustic neuroma
-Bell’s palsy
-Ramsay Hunt
-XRT/chemotx
-diabetes
-epilepsy
-hypothyroidism
-psychiatric disorders
-medications:
-ACE-inhibitors (captopril, enalapril)
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STOMATITIS
DDx Stomatitis
Infectious: Inflammatory:
-viral: -erythema multiforme
-herpes -pemphigus vulgaris
-varicella zoster -cicatricial pemphigoid
-bacterial: -bullous pemphigoid
-Vincent’s gingivitis -lichen planus
-actinomycosis -Behcets
-syphilis -SLE
-fungal: -Wegner’s
-candidiasis
Other:
Iatrogenic: -apthous ulcers
-radiation/chemotherapy induced
HERPES
Etiology
-HSV-I more commonly associated
-transmission through contact with infected body fluids
-incubation time 7 days (range 1-28 days)
-lies dormant in trigeminal ganglion until reactivation
Clinical Features
-primary herpetic gingivostomatitis:
-usually seen in seronegative children and
occasionally in adults
-small vesicles occur on any mucosal surface
-stomatitis and pharyngitis
-most frequent clinical manifestations
-may be accompanied by fever, arthralgia, malaise,
headache, cervical lymphadenopathy, oral ulcers,
and gingivitis
-secondary (recurrent) disease
-lesions are confined to hard palate and gingiva Herpes gingivostomatitis
-reactivation triggered by UV, stress, fever, cold,
fatigue, immunosuppression, trauma, menses, chapped lips
-lesions usually heal in 1-2 weeks without scarring
Histopathology
-vesicles located intraepidermally
-formed by ballooning degeneration of epithelial cells
-homogeneous and glassy nucleus with nuclear material pushed out to the perimeter of the cell
Differential
-minor aphthous ulcers, erythema multiforme, acute necrotizing ulcerative gingivitis
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Treatment
-immunocompetent:
-supportive care (analgesics, antipyretics, hydration)
-antibiotics for secondary bacterial infections
-antiviral agents:
-acyclovir 100-200 mg 5x/day
-famcyclovir, valacyclovir, foscarnet
-recurrent herpes labialis
-acyclovir cream 5% 5x/day
-immunocompromised:
-acyclovir 250 mg/m2 q8h or 400 mg po 5x/day
VARICELLA ZOSTER
Varicella (Chickenpox)
-inspiration of contaminated respiratory droplets
-incubation period 2 weeks
-rash develops into vesicular eruption over trunk, head and neck
-infection lasts 7-10 days
-vesicles may be present on oral mucosa, commonly buccal
-treatment: supportive
Zoster (Shingles)
-VZV reactivation along sensory nerves
-incidence increased in immunosuppresive states (eg. malignancy, trauma,
drug therapy, radiation, steroid treatment)
-pain and tenderness along course of involved nerve
-most common complication: postherpetic neuralgia
-treatment: Chickenpox soft palate
-immunocompetent: supportive
-postherpetic neuralgia:
-acyclovir 800 mg 5x/day for 7d
-famcyclovir 500-700 mg tid x 7d
-topical antivirals early in course of disease
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DESQUAMATIVE GINGIVITIS
-diffuse erythematous desquamation, ulceration and possible bullae formation affecting free and attached
gingiva
-manifestation of several diseases:
-lichen planus
-cicatricial pemphigoid
-bullous pemphigoid
-dermatitis herpetiformis
-drug reactions
-incisional biopsy usually required to make definitive diagnosis
-direct immunofluorescence used to detect antibody or complement bound to tissue samples
-pemphigus vulgaris: binding to epithelial intercellular substance
-cicatricial pemphigoid: binding to basement membrane
LUPUS ERYTHEMATOSUS
Clinical Features
-Discoid LE:
-least aggressive form of lupus
-most often affecting women in 3rd-5th decades
-usually asymptomatic without visceral organ involvement
-elevated erythematous plaques with hyperpigmented margins
-oral lesions in 25% of patients
-subepithelial clefting
-diagnosis:
-positive basement membrane with direct immunofluorescence; negative direct
immunofluorescence, negative serology
-treatment:
-topical steroids
-sunscreens
-SLE:
-multiple organ involvement
-“butterfly rash” of malar eminence and nose
-subepithelial clefting
-diagnosis:
-positive basement membrane with direct immunofluorescence
-positive ANA, SS-A, SS-B
-screening test is fluorescent test for ANA positive in 98% of pts
-treatment:
-anti-inflammatory medications (salicylates, NSAIDs)
-systemic steroids for severe inflammatory states (prednisone 10-200 mg/day)
-antimalarial (chloroquine 250-500 mg/day, hydroxychloroquine 200-400 mg/day)
-can cause ocular toxicity
-cytotoxic agents (azathioprine, cyclophosphamide, methotrexate)
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CICATRICIAL PEMPHIGOID
Etiology
-chronic blistering of mucous membranes
-autoimmune disease with antibodies to lamina lucida and occasionally to lamina densa of basement
membrane zone
Clinical Features
-mean age 66 years
-F:M = 2:1
-mucosal lesions with subepithelial clefting forming bullae that rupture
-leads to ulceration and scarring
-cutaneous surfaces rarely involved
-most commonly affected sites:
-attached gingiva, presenting as desquamative gingivitis with diffuse or patchy erythematous
appearance
-conjunctiva (second most common site) - 50-70% incidence
Histopathology
-subepithelial clefting
-positive direct immunofluorescence at basement membrane
-negative indirect immunofluorescence (localized involvement, antibodies not circulating in serum)
Treatment
-topical steroids
-systemic steroids (prednisone 20-60 mg/day) for severe cases
-immunosuppressant (azathioprine, cyclophosphamide, methotrexate) for advanced cases
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BULLOUS PEMPHIGOID
Etiology
-antibodies directed at basement membrane (lamina lucida)
Clinical Features
-affects those in 7th and 8th decades
-M=F
-usually a cutaneous presentation with up to 40% of pts with oral
lesions
-subepithelial clefting
-oral lesion very similar to cicatricial pemphigoid
Histopathology
-positive direct immunofluorescence at basement membrane
-positive indirect immunofluorescence titers do not correspond to
severity of disease
Bullous pemphigoid
Treatment
-topical steroids or intralesional steroids for localized disease
-systemic steroids (prednisone 50-100 mg/day) to suppress new blister formation
-immunosuppressive agents (azathioprine) for maintenance often with steroids
-intravenous gamma globulin for severe disease requiring high-dose steroids
PEMPHIGUS VULGARIS
Etiology
-mucocutaneous diseases characterized by intraepithelial vesicle formation
-autoimmune disease:
-antibodies against Ca++-dependent cell adhesion molecule involved in maintenance of epithelial
integrity
-autoantibodies against desmosome-monofilament complexes results in acantholysis (loss of
cellular adhesion
Clinical Features
-pts 40-50 ya
-mucocutaneous disease with equal sex distribution
-increased in Mediterranean populations (Ashkenazi Jews)
-positive Nikolsky sign
Histopathology
-intraepithelial clefting with Tzanck cells (spheric free squamous cells ) = acantholysis
-positive direct intracellular immunofluorescence strongest at parabasilar region with decreasing intensity
toward surface
-intraepithelial blistering
-positive indirect immunofluorescence with titer level corresponding to severity of disease
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Treatment
-long-term and high-dose steroids often needed
-initial control to heal 80% of lesions (60-120 mg/day)
-immunosuppressive agents (azathioprine 50 mg/kg/day, cyclophosphamide 50-150 mg/day, cyclosporine 5
mg/kg/day) plus steroids for more refractory patients
-intramuscular gold +/- steroids
-tetracycline 500 mg and niacinamide 500 mg tid
ERYTHEMA MULTIFORME
Etiology
-hypersensitivity reaction implicated antigen-antibody complex
deposits in small vessels of dermis and submucosa
-target lesions are pathognomonic
-multiple infectious triggers and medications have been implicated
Clinical Features
-rapid explosive onset of macules, papules, vesicles, bullae, or
plaques of hands, feet, arms, legs, face, neck involving skin, mucous
membranes, or both
-usually subepithelial clefting with occasional intraepithelial vesicles
-often precede by recurrent herpes labialis (HSV I and II - 50%)
Target lesion of erythema multiforme
Stevens-Johnson Syndrome
-severe form of EM
-high fever, malaise, photophobia
-most cases drug induced
Histopathology
-no specific histologic appearance
-direct and indirect immunofluorescence are non-specific
Treatment
-supportive care (fluids, analgesics) for mild cases
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-topical steroids for mild to moderate cases
-systemic steroids for severe (ie. Stevens-Johnson syndrome, toxic epidermal necrolysis)
-prednisone 40-60 mg/day
-pts with multiple recurrences often controlled with high doses of tetracycline and niacinamide or acyclovir
(600-800 mg/day)
LICHEN PLANUS
Etiology
-inflammatory disease in which basal cell layer is destroyed by activated lymphocytes
-may be familial; may be induced by medications
Clinical Features
-F > M
-cutaneous lesions:
-small violaceus, pruritic papules over flexor surfaces or extremities
-oral lesions with a variety of presentations
-reticular form:
-most common, with white interlacing striae (Wickham striae) in an annular or reticular
pattern
-plaque form:
-resembles leukoplakia, often on dorsum of tongue and buccal mucosa
-atrophic form:
-produces desquamative gingivitis with burning or pain
-erosive form:
-very painful, erythematous erosion covered by a fibrinous layer
-bullous form:
-rare bullae range from several mm to several cm, rapidly rupture leaving a raw, painful,
ulcer bed
Histopathology
-histologic presentation generally diagnostic:
-hyperkeratosis
-liquefactive degeneration of basal cell layer
-“saw-toothed” rete peg formation
-bandlike lymphocytic infiltration in lamina propria
-civatte bodies: degenerative eosinophil ovoid keratinocytes
Treatment
-often asymptomatic and does not require any treatment
-topical steroids or intralesional injections for control of more severe symptomatic lesions
-cyclosporine rise (500 mg/day) for 4-8 wk improves healing and reduces pain
-systemic steroids for painful erosive variety
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CANDIDIASIS
Etiology
-local factors:
-physical irritation, preexisting infection, nutritional deficits, poor oral hygiene, denture wearing,
smoking and individual sensitivity
-systemic factors:
-endocrine alterations, AIDS, malignancy, systemic broad-spectrum antibiotic therapy, systemic
and inhaled steroid therapy, immature immunologic states of infancy, radiation or chemotherapy,
altered phagocytosis, pregnancy, old age
Clinical Presentation
-pseudomembranous candidiasis (thrush):
-classic form, adherent, white, soft plaques easily wiped off the mucosal surface, leaving raw bed
-acute atrophic candidiasis:
-erythematous patch or diffuse lesion, patches and depapillation and dekeratinization with burning
symptoms
-may be caused by broad-spectrum antibiotic use
-chronic atrophic candidiasis:
-diffuse erythema with pebbly to velvety surface limited to denture-bearing mucosa
-angular cheilitis involve oral commissure within folds
-hyperplastic candidiasis:
-resembles leukoplakia
-cannot be rubbed off
-mucocutaneous candidiasis:
-pseudomembranous variety involving skin and nails
-median rhomboid glossitis:
-lesion appears as an asymptomatic diamond-shaped area of depapillation found anterior to the
circumvallate papillae
Treatment
-nystatin
-imidazoles (ketoconazole, clotrimazole)
-fluconazole
Etiology
-most common type of nontraumatic ulcer
-cause unknown
-several agents implicated:
-viral, bacterial (streptococcus sanguis), nutritional deficiencies (B12, folate iron), hormonal
alterations, stress, trauma, food allergies, immunologic abnormalities
Clinical Features
-white ulcers with erythematous halos
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-major aphthous ulcers:
-1-3 cm, on keratinized freely movable gingiva, tongue, palate, anterior faucial pillar
-persist from 6 wk to several months
-heal by scarring
-herpetiform ulcers:
-painful crop of 20-200 small (1-3 mm) ulcers on movable and attached gingiva, tongue, palate
Histopathology
-no microscopic features specific to aphthous ulcers
Treatment
-tetracycline oral suspension (200 mg/5 ml) q6h for 5-7 days
-fluocinonide (0.05%) plus Orabase applied to lesion 6-7 times/day
-topical steroids may shorten duration of symptoms; use with antifungal to prevent candidiasis
-systemic steroids for severe aphthae
MUCOSITIS
Etiology
-chemotherapy, radiation therapy, or immunosuppression for bone marrow transplant
-radiation-induced mucositis often appears by the second week of therapy and may persist for 2-3 weeks
after completion of XRT
-treatment:
-cleansing of oral mucosa, maintenance of moisture, relief of pain and inflammation
-numerous anaesthetic or analgesic mucosal agents used for symptomatic relief
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PHARYNGITIS
DDx Pharyngitis
Infectious: Inflammatory/Autoimmune:
-bacterial -Stevens-Johnson syndrome
-streptococcus -pemphigus
-staphylococcus -cicatricial pemphigoid
-diphtheria -bullous pemphigoid
-pertussis -epidermolysis bullosa
-gonorrhea -Wegener
-syphilis
-viral Iatrogenic:
-herpes -radiation
-measles -chemotherapy
-EBV
-varicella Other:
-CMV -reflux disease
-fungal
-candidiasis
Bacterial Infections
Streptococcal Infection
-most frequent: GABHS (Strep. pyogenes)
-in children with GABHS pharyngitis antibiotic tx to avoid serious complication of rheumatic
fever
-diagnosis:
-enzyme immunoassay rapid antigen test or optical immunoassay rapid antigen test
-if negative, then many recommend C+S
-however culture still remains the safest and most cost-effective treatment strategy
-treatment:
-penicillin
-erythromycin in pen allergic
-first-generation cephalosporins recommended for treatment failures
-complications:
-rheumatic fever, rheumatic heart disease
-acute, poststreptococcal glomerulonephritis (ie. Bright disease) (risk not reduced by antibiotics)
-Grisel syndrome
-subluxations of atlantoaxial joint d/t infectious inflammatory process of H+N
-Scarlet fever:
-acute streptococcal pharyngotonsillitis accompanied by rash and production of
erythrogenic toxin
-face, palms, soles spared by rash
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Staphylococcal Infection
-mucopurulent drainage, mucosal erythema and localized pustules
-tx: anti-staphylococcal penicillins, erythromycin or cephalosporins
Diphtheroid Infection
-C. diphtheria
-gram positive, nonfilamentous rods
-produces exotoxins that cause localized tissue necrosis and inflammation
-rarely seen d/t vaccinations
-diphtheria more common in children < 10ya
-antitoxin remains only specific method of treatment
-antibiotics useful as adjuvant therapy
Pertussis
-Bordetella pertussis
-nonmotile, pleomorphic, gram-negative coccobacillus
-highly communicable
-violent paroxysms of coughing accompanied by loud inspiratory sound (“whooping cough”)
-usually self-limiting; death rarely occurs
-antibiotics do not alter the course of disease
-eradicated by immunization
Gonorrhea
-Neisseria gonorrhea
-gram-negative diplococcus
-must be cultured on chocolate agar
-generally asymptomatic, but may present with sore throat, tonsillar hypertrophy or cervical adenopathy
-tx: penicillin, tetracycline, cephalosporins or quinolones
Syphillis
-Treponema pallidum
-primary stage:
-chancre: may affect tonsils
-histology:
-inflammatory infiltrate composed of plasma cells with scattered histiocytes, lymphocytes
and PMNs
-obliterative endarteritis
-identification: dark-field examination of smears, Warthin-Starry staining
-secondary stage:
-skin lesions and lymphadenopathy
-pharyngotonsillitis
-tertiary syphilis:
-CNS involvement
-gammas: granulomatous nonprogressive lesions
-investigations:
-VDRL (screening)
-FTA-ABS (confirmation)
-treatment: penicillin
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Viral Infections
Measles
-coryza and conjunctivitis followed by typical spotty exanthematous lesions on buccal mucosa (Koplik
spots) and generalized cutaneous erythematous rash
Epstein-Barr Virus
-infectious mononucleosis
-lymphadenopathy and splenomegaly (50%)
-diagnosis:
-absolute lymphocytosis with atypical lymphocytes
-mono-spot test
-therapy is supportive, including rest and fluids
Cytomegalovirus
-most infections are asymptomatic, except in immunocompromised pts
-may present as an infectious mononucleosis-like picture
Fungal Infections
Candidal Infections
-Candida albicans
-if immune system is compromised then invasion of mucosal surfaces can occur dysphagia
-treatment with topical nystatin or oral ketoconazole or fluconazole
-amphotericin B for systemic involvement
-if confronted with presumed infectious process unresponsive to empirical antibiotic therapy, appropriate
cultures and biopsy sampling of affected tissues are necessary
-rare cause of pharyngitis
-caused by bacteria, mycobacteria, fungi, syphilis, parasites, sarcoid, Wegener granulomatosis, Crohn
disease and neoplasms
Radiation Pharyngitis
-inevitable side effect of H+N XRT
-symptomatic treatment
-treatment of superinfections include topical antifungals or systemic antibiotics
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Integumetal Disorders
Stevens-Johnson Syndrome
-cause unknown, but onset may follow URTI or use of certain drugs, esp. sulfonamides, anticonvulsants,
and barbiturates
-angiitis producing erythematous vesicular skin lesion which may become bullous
-treatment: symptomatic with maintenance of fluid and electrolyte balance during acute phase
Pemphigus
-autoimmune disorder
-pemphigus vulgaris:
-rapid appearance of various-sized vesicles and bullae, often involving large surface areas
-histology: intraepithelial vesicles or bullae that produce distinctive suprabasilar split
-treatment: steroids, immunosuppressive agents and antibiotics for secondary infections
Cicatricial Pemphigoid
-vesiculobullous, probably autoimmune disease
-lesions typically occur on conjunctiva and upper airway mucosa
Bullous Pemphigoid
-dz of the elderly
-generalized non-specific rash that persists for varying periods of time before vesculobullous lesions
appear
Epidermolysis Bullosa
-bullae or vesicles affect skin and mucous membranes with various degrees of severity
-ruptures of bullae leave raw, painful surfaces that heal by scarring
Reflux Pharyngitis
-associated with hoarseness, sore throat, chronic cough, globus pharyngeus, halitosis, cervical dysphagia,
esophageal and laryngeal carcinoma
-most accurate diagnostic test is 24h pH monitoring with both proximal and distal sensors
-empiric therapy with PPI or H2-blockers acceptable
PFAPA
-periodic fever, apthous stomatitis, pharyngitis, cervical adenitis
-children ~3ya
-glucocorticoid effectively control symptoms, tonsillectomy and cimetidine may lead to remission
Idiopathic Pharyngitis
-dietary and personal habits may play a role
-medications and commercial mouth washes can irritate throat
-thermal injury
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ODONTOGENIC INFECTIONS
LOCALIZED INFECTIONS
-percussion tenderness, increased pain to heat, diminished or absent response to electrical vitality testing
-soft tissue infection: diffuse cellulitis or walled-off abscess cavity
-may cause enlargement of lip (macrocheilia)
-maxilla: root ends are close to labial and buccal plates almost always produces extension buccally
-mandible: dental roots closer to lingual cortex however most cases spread buccally
Canine Space
-clinically a firm or fluctuant mass appears along the lateral border of the nose adjacent to the medial
canthus of the eye
-treatment: intraoral or percutaneous drainage
Buccal Space
-bounded by:
-buccinator muscle and buccopharyngeal fascia medially
-cheek skin laterally
-lip muscles anteriorly
-pterygomandibular raphe posteriorly
-zygomatic arch superiorly
-lower aspect of mandible inferiorly
-tender swelling of cheek, extends medially to middle of upper lip and involves one third of lower lip
-posteriorly extends over ramous of mandible to border of parotid gland
-superiorly may close eye entirely by producing circumferential eyelid edema
-orbital contents are protected
-treatment: percutaneous drainage
Sublingual Space
-communicates freely with that of the opposite side
-also communicates anteriorly with submental space through dehiscence in mylohyoid
-infections from anterior teeth as well as bicuspids and first molar tooth remain above mylohyoid shelf into
sublingual space
-treatment: intraoral drainage
Submandibular Space
-contents: submandibular gland, Wharton duct, lingual and hypoglossal nerves, facial artery and some
lymph nodes and fat
-involvement from infections of second and third mandibular molar teeth
-root apices beneath mylohyoid muscle
-treatment: external excision placed well below marginal mandibular nerve
377
Submental Space
-source of infection by drainage from mandibular incisor teeth as well as their gingiva and central portion
of lower lip
-treatment: small upper cervical incision placed in the midline
Ludwig Angina
-refers to collective involvement of submandibular and sublingual spaces bilaterally and submental space
-cases of dental origin arise from infections of mandibular molar teeth
-clinically:
-brawny edema across entire upper anterolateral neck with elevation of floor of mouth
-potential for airway obstruction
-organisms: variety of aerobic and anaerobic gram-positive cocci and gram-negative rods
-management:
-elective tracheotomy under local anaesthesia
-nasotracheal fiberoptic intubation as an alternative to tracheotomy
-drainage through external cervical approach;
-intraoral drainage carries risk of aspiration in pts with severe edema of oral cavity and
oropharynx
-systemic antibiotics
Masticator Space
-infections tend to involve all muscles
-severe trismus with minimal external swelling
-source of infection from maxillary and mandibular molar teeth
-confirmation of diagnosis by CT
-treatment: intraoral drainage
Parapharyngeal Space
-prestyloid compartment:
-IMAX, inferior alveolar, lingual and auriculotemporal nerves
-poststyloid compartment:
-IJV, carotid artery, CN IX, X and XI, cervical sympathetic nerves
-clinically:
-intraoral bulge of tonsil and lateral pharyngeal wall and external swelling of soft tissues over
mandible and parotid region
-surgical exploration and drainage performed when pt does not improve within 24 hours or deteriorates
under observation
-drained by lateral cervical incision
-complications may be d/t infection within poststyoid compartment
-most dreaded complications:
-mycotic aneurysm of carotid artery from erosion of wall by purulent material within its sheath
angiography and balloon occlusion to determine risk of stroke
-eroded segment of artery requires ligation to prevent catastrophic event
Retropharyngeal Space
-extends from skull base to pretracheal space and ends in mediastinum at level of carina
-in front of danger space which extends to posterior mediastinum
-most common dental source is carious or periodontal involvement of mandibular third molar
-clinical:
-dyspnea and stridor, with a “hot potato” voice
-fullness and erythema of posterior pharyngeal wall often with central furrow produced by midline
raphe
378
-usually toxic with spiking fevers
-treatment:
-best drained from external approach; intraoral drainage carries risk of pulmonary complications
from aspiration
-intravenous antibiotics
-complications:
-spontaneous rupture aspiration or lung abscess
-descending mediastinitis:
-30-50% mortality rate; CT chest for early identification and drainage required
-tx: IV antibiotics, cervical drainage, thoracotomy
Organisms:
-usually mixed flora:
-aerobic: Streptococcus, Staphylococcus
-anaerobic: Bacteroides, Fusobacterium, Peptostreptococcus, Prprionobacterium
Therapy:
-antibiotic therapy
-clavulin, clindamycin or ciprofloxacin
-local drainage of abscess
-radiographs of osseous strictures; possible CT of soft tissue spaces
-extraction or endodontic therapy of involved tooth
-intraoral drainage of local space (canine, buccal, sublingual)
-extraoral drainage of deep spaces (submandibular, submental, masticator, parapharyngeal,
retropharyngeal)
-drainage of paranasal sinus extension, orbital extension, and mediastinal extension
-debridement of osteomyelitis bone
-tracheotomy, when necessary
OTHER INFECTIONS
-classified into:
c) necrotizing fasciitis
-severe gangrene of skin and superficial and deep fascia
-caused by staphylococci, hemolytic streptococci, and gram-negative rods
-mostly arise from massive trauma associated with fracture of mandible; may arise from
isolated dental infection
379
-usually critically ill with extensive involvement of multiple spaces
-rapid progression of disease
-radiographic studies:
-subcutaneous emphysema, gas and pockets of suppuration in deep tissues and visceral spaces
-anaerobic and aerobic cultures should be taken
-anaerobes:
-Bacteriodes, Fusobacterium, Propionibacterum, Peptostreptococcus, Eubacterium
-gram negative:
-coliform bacilli: Proteus, Klebsiella, Enterobacter, Pseudomonas
-treatment:
-aggressive: fasciotomy and radical debridement
-intravenous antibiotics: eg. clindamycin and ceftazidime
-consider adjunctive HBO
DENTAL-SINUS-ORBITAL INFECTIONS
-superficial (preseptal: periorbital cellulitis) and deep (postseptal: orbital cellulitis, subperiosteal abscess,
orbital abscess, retrobulbar abscess) infections can occur from a dental focus
-access via pterygopalatine and infratemporal fossae
-anterior teeth retrograde spread through valveless anterior facial, angular and ophthalmic veins
-via orbital floor from maxillary sinus
-preseptal infections:
-periorbital edema w/o evidence of ocular involvement
-postseptal infections:
-proptosis, chemosis, ophthalmoplegia
-carries risk for blindness from IOP or optic neuritis
-surgical drainage:
-external ethmoidectomy and orbital decompression with antrostomy of involved
maxillary sinus
Osteomyelitis
-infection within medullary portion of bone
-organism most commonly isolated: Staphylococcus aureus and hemolytic streptococci
-risk factors:
-regional XRT, trauma, systemic disease (diabetes), osteodystropies (Paget disease, osteopetrosis),
endosteal lesions (cementomas), dental implants, immunocompromised state
-diagnosis:
-CT scanning bone destruction
-radionuclide studies increased activity at suspected site (high false positive)
-radiographically (chronic osteomyelitis):
-irregular lytic lesions
-occasionally in association with sequestrum of nonviable bone
-treatment:
-IV antibiotics (eg. clindamycin and ceftazidime for 3 weeks)
-oral antibiotics for 6 weeks
-debridement of foreign bodies, sequestra or necrotic tissue
-reconstruction as necessary following resolution of infection
Actinomycosis
-anaerobic branching gram-positive filamentous organism Actinomyces israelii
-entry through extraction site in host with poor hygiene
380
-painful indurated swelling with areas of suppuration with fistulous tracts through skin
-can cross fascial planes
-microscopy: sulfur granules seen in exudate
-treatment: Penicillin x 1 year or tetracycline
381
TEMPOROMANDIBULAR JOINT DISORDERS
ANATOMY
EVALUATION
History:
-jaw pain
-may manifest as otalgia
-headaches
-toothache
-facial pain
-vertigo
-trsimus
-nocturnal bruxism
-recent trauma
Physical:
-evaluate occlusion and intra-incisor opening (normal 40-50 mm)
-palpate TMJ and jaw muscles
-examine for tenderness, warmth, crepitus, and joint clicking
382
Applied Neuroanatomy
DIFFERENTIAL DIAGNOSIS
383
-fibrous and bony ankylosis
IMAGING
-imaging is indicated for confirmation of disk pathology and bone status before surgery or to establish a
treatment baseline
-MRI: indicated if suspect disc displacement or dysmorphology
-CT: indicated if suspect degenerative joint disease, bony deformities, or ankylosis
-arthrotomogram: requires injection of contrast into joint space, can detect disc displacement
TREATMENT
Initial Management
-behaviour modification: soft diet, avoid
gum chewing
-physical therapy: repositioning, repetitive
jaw stretching, active and passive
mobilization
-medical management:
-analgesic and NSAIDS
-muscle relaxants
-warm compresses
-ultrasound
-may consider corticosteroid
injections
-dental management:
-consult for malocclusion, carious
teeth, poorly fitting dentures
Joint Disorders
-prolonged dental or occlusal therapy for
internal derangements are contraindicated
-non-painful clicking joints do not require
treatment
-painful early clicks can often be managed
with NSAIDs and soft diet
-painful late clicks or painful clicks with
locking are less likely to respond to nonsurgical therapy
Surgical Techniques
-controversial
-indicated for confirmed TMJ intracapsular derangements
-arthroscopy (closed )and arthrotomy (open)
-findings:
-disk is sound can be repositioned over condyle with plication of the retrodiskal tissue and
reattachments of the ligaments
-disk not salvageable excised
-articular cartilage damage reconstruction by autogenous auricular cartilage graft
-or rotation of pedicled temporalis fascia or pericranial temporalis flap into the joint
384
-total joint prosthesis
-complications: 10-20% failure rate, joint degeneration, malocclusion, osseous ankylosis, foreign-body
reaction (implants)
385
SNORING AND OBSTRUCTIVE SLEEP APNEA
EPIDEMIOLOGY
Snoring
-common problem
-prevalence increases with age
-~40% of people snore increasing to 84% (M) and 73% (F) in the seventh decade
-good objective tests for snoring exist
SLEEP PHYSIOLOGY
Normal Sleep
-average duration for young adult: 7.5-8.5 hours
-two stages:
a) non-REM (~80% of sleep)
-slow HR and RR and low BP
-“quiet” stage of sleep
b) REM (~20% of sleep)
-bursts of rapid conjugate eye movement
-increased autonomic activity with large fluctuations of HR, RR and BP
-dreaming
-decreased muscular activity (paralysed)
-sleep architecture:
-stage 1 NREM
-low arousal threshold
-short duration: few minutes
-theta waves
-stage 2 NREM
-sleep spindles or K complexes on EEG
-duration: 10-25 minutes
-stage 3 NREM
-high-voltage slow-wave activity
-delta waves (deep sleep)
-short duration: few minutes
-stage 4 NREM
-delta waves (deep sleep)
-lasts 20-40 minutes
-sleep lightens stage 2 stage 1 or REM
-REM initially short but then increases as sleep progresses
-stage 4 sleep decreases as one ages: by age 60, stage 3/4 NREM may no longer be present
-most obstructive events occur during NREM III, IV and REM
386
SLEEP DISORDERS
Snoring
-originates from collapsible portion of upper airway
-vibration of soft palate, uvula, tonsillar pillars or base of tongue
-histologically, palates of snorers and apneics had mucous gland hypertrophy, muscle bundle disruption,
atrophy of muscle fibers and edema of lamina propria with vascular dilation
-vibratory trauma to pharyngeal tissue is an etiologic factor in both apnea and snoring
387
PHYSIOLOGY OF UPPER AIRWAY OBSTRUCTION
Complications of OSA
-arrhythmia
-cor pulmonale
-congestive heart failure
-motor vehicle accidents
-nocturnal death
-growth delay, FTT
-hypertension
History
-nocturnal signs and symptoms:
-heroic snoring
-restless disturbed sleep
-observed apnea
-nocturnal sweating
-daytime signs and symptoms
-excessive daytime sleepiness
-cognitive impairment
-morning headaches
-impotence
-factors that exacerbate OSA:
-alcohol and sedatives
-nasal obstruction: rhinitis, URTI
-weight gain
-patient characteristics associated with OSA: male, advancing age, truncal obesity, large neck
circumference and hypertension
-spousal reports of apnea have be found to be unreliable in predicting the presence or severity of OSA
388
Physical examination
-vital signs and BMI
-complete head and neck examination
-tongue size, tonsil size and BMI have been shown to be significant predictors of OSA
-laryngeal, nasopharyngeal, and base-of-tongue tumours can present as new-onset snoring in a
petient who never snored
-fiberoptic endoscopy: Mueller maneuver
-scope at level of BOT just above velopharyngeal valve
-patient asked to inspire with nose and mouth closed
-examine level of collapse
-if hypopharynx and/or larynx collapse, then test is positive site of obstruction is below
level of soft palate and therefore patient would not benefit from UPPP
DIAGNOSTIC STUDIES
Sleep Scales:
-Epworth Sleepiness Scale
-Standford Sleepiness Scale
-do not predict apnea with great certainty
-no set group of symptoms or patient characteristics that can rule in or rule out sleep apnea with certainty
Oximetry
-has been used as screening device for OSA
-if percentage of time spent with SaO2 below 90% was < 1% of sleep time, clinically significant apnea is
practically excluded
Polysomnography
-standard overnight polysomnogram in sleep laboratory is the accepted diagnostic method for diagnosis of
OSA
-records:
a) EEG
b) electrooculogram
c) ECG
d) EMG (submental and anterior tibialis)
e) SaO2
f) nasal or oral airflow
g) thoracic/abdominal movement
h) sleep position
i) blood pressure
-report addresses:
-sleep latency
-sleep efficiency
-RDI
-types of respiratory disturbances as well as average and maximum length of each event type
-sleep architecture
-volume and presence of snoring
-effect of position on respiratory disturbances
-whether respiratory disturbances occur more often in particular sleep stages; number and severity
of oxygen desaturation events
389
-full-night vs split night studies
-sleep apnea worse during second half of the night
-but studies have shown RDI in first part of night is predictive of second half of night in most
patients
-can institute CPAP for second part of night
Cardiopulmonary Disease
-initiation of nasal CPAP will bring improvement in hypertension control, congestive heart failure, and
pulmonary hypertension
-HTN has been found in 50% of OSA pts, pulmonary HTN found in 10-20% and cardiac arrhythmias also
are frequently noted in this population
Obesity
-BMI > 27
-weight loss associated with improvement in apnea in most patients
390
Behavioural Treatment
-weight loss
-avoidance of alcohol and medications that cause sedation
-elimination of tobacco and caffeine
-many pts benefit from 1-3 month period of nasal CPAP therapy combined with weight loss or elimination
of exacerbating habits in preparation for a surgical procedure
Nonsurgical Treatment
-nasal CPAP
-most effective nonsurgical treatment of OSA
-long term compliance not obtained in as many as 75%
-oral appliances:
-mandibular advancement device
-tongue-retaining device
-other:
-efficacy not known
-positioning devices: T-shirt with ball
-nasal splints
Nasal surgery
391
-contraindications:
-velopharyngeal insufficiency
-submucous cleft palate
-patients with special voice or swallowing considerations
-complications:
-bleeding, VPI, voice change, FB sensation, nasopharyngeal stenosis, respiratory distress
-death
c) Transpalatal advancement pharygoplasty
-can be performed after UPPP failure
-advancement of soft palate at the junction of the hard and soft palates
-complications:
-oronasal fistula, flap necrosis, wound dehiscence
Maxillomandibular surgery
-two stage surgical protocol offering 97% success
-used after more conservative procedures have failed
-includes:
-mandibular advancement with genioglossus advancement (phase I)
-enlarge and stabilize retrolingual airway by advancing insertion of the genioglossus or
geniohyoid muscles without moving the entire mandible or teeth
-hyoid myotomy and suspension (phase I)
-advances hyoid bone anteriorly, which advances epiglottis as well as BOT
-maxillomandibular osteotomy and advancement
-bimaxillary surgery to advance maxilla and mandible as far anteriorly as possible
-phase II of protocol
Tracheotomy
-indications:
-morbid obesity
-significant cardiac arrhythmias associated with apneic events
-severe apnea with oxygen desaturation below 40-50%
-cor pulmonale
-disabling somnolence
-failure of CPAP
-reduces morbidity and mortality associated with OSA
-life-saving procedure and is necessary in certain pts with severe apnea
-severe apneics have more airway edema, may have mild congestive heart failure with fluid retention and a
greater tendency to develop postobstructive pulmonary edema because of acute relief of obstruction
-difficult airways due to anatomy
-avoid oversedation
-post-operative monitoring for 24h
392
DEEP NECK INFECTIONS:
RECOGNITION, EVALUATION, THERAPY
Terminology
-Fascial layers:
-superficial fascial layer
-deep fascial layer
-anterior layer - superficial investing
-middle layer - pretracheal
-posterior layer - deep
-alar layer
-prevertebral layer
-visceral layer - buccopharyngeal
-Fascial spaces:
-Suprahyoid:
-divided by anterior layer of deep fascia:
-body of mandible, submaxillary gland, masticator, and parotid
-Peripharyngeal spaces:
-lie deep to anterior layer of deep cervical fascia
-lateral pharyngeal space, retropharyngeal space, submandibular space
-Other:
-danger space:
-formed by separation of alar and prevertebral layers
-allows access into mediastinum
-prevertebral space
-carotid sheath
-pretracheal space
-peritonsillar space
Cervical Fascia
-Superficial fascia:
-no fascial spaces
-subcutaneous tissue of head and neck enclosing muscles of facial expression and platysma
-Deep fascia:
-Anterior layer:
-originates from vertebral spinous processes and ligamentum nuchae
-encircles entire neck
-splits to enclose trapezius, omohyoid, SCM
-extends from hyoid superiorly to mandible splits to enclose inner and outer table of mandible
-outer table zygoma and temporalis muscle
-splits to encompass parotid, masseter and internal pterygoid muscles
-between hyoid and mandible: forms floor of submandibular space
-Middle layer:
-originates from anterior layer at lateral border of strap muscles
-travels posterior to strap muscles and anterior to trachea and thyroid
393
-superior extent to hyoid
-inferior extent to fibrous pericardium
-Posterior layer:
-originates from vertebral spinous processes
-encircles the neck
-extends to base of skull superiorly, deep to trapezius; enclosing vertebral muscles
-splits at transverse processes of vertebrae:
-alar fascia (anterior)
-prevertebral fascia (posterior): covers longus colli muscle
-Visceral fascia:
-connective tissue surrounding esophagus, thyroid gland, trachea
-no spaces formed
Fascial Spaces
-Peripharyngeal spaces:
1. Retropharyngeal space:
-from base of skull to bifurcation of trachea
-lies behind pharynx and esophagus
-contains loose connective tissue, lymph nodes
2. Lateral pharyngeal (pharyngomaxillary, parapharyngeal) space:
-from base of skull, contiguous with retropharyngeal space
-“conical”: base at petrous portion of temporal bone, apex at hyoid
-divided by styloid process and associated musculature into anterior and posterior compartments:
-anterior (prestyloid or muscular):
-fat and connective tissue
-closely related to tonsillar fossa medially and internal pterygoid muscle laterally
-internal maxillary artery
-inferior alveolar, lingual and auriculotemporal nerves
-posterior (poststyloid or neurovascular):
-CN IX, X, XII
-cervical sympathetic
-internal jugular vein
-common carotid artery
3. Submandibular space:
-superiorly: lingual mucosa
-inferiorly: anterior layer of deep fascia
-divided by mylohyoid muscle:
-sublingual: sublingual gland submandibular duct, lingual nerve and artery, hypoglossal
nerve, genioglossus and geniohyoid muscles
394
-submaxillary portion: anterior belly of digastric
-Other spaces:
1. Danger space:
-between alar and prevertebral fascia
-extends from base of skull to diaphragm
-provides route of spread for infection to mediastinum
2. Pretracheal space:
-most anterior of fascial spaces below hyoid bone
-defined anteriorly by middle layer of deep fascia, posteriorly by esophagus
-superior to hyoid; inferior to T4 along arch of aorta
3. Carotid sheath:
-contributions from all three parts of deep cervical fascia
-anteromedially: anterior layer, deep to SCM
-posteriorly: lamina from anterior layer prior to dividing to form middle layer
-sympathetic chain posteromedial to carotid sheath but superficial to posterior fascial layer
4. Prevertebral space:
-longus colli muscle
5. Peritonsillar space:
-faucial tonsils
MICROBIOLOGY
395
Radiology:
-lateral neck film:
-critical to obtain during inspiration - high false positives if taken during expiration
-measure anterior aspect of vertebral column to air column of posterior pharyngeal wall
-at C-2 may be as wide as 7mm normally in children and adults
-at C-6 may normally extend to 14 mm in children and 22 mm in adults
-posterior pharyngeal swelling > 50% width of vertebral body
-ultrasound not very useful
-MRI: disadvantage is may require patient transport - potential hazard if patient quickly deteriorates
-CT: preferred
-CXR to assess complications from DNI
-mediastinal extension, lung abscess, pyopneumothorax, aspiration
Submandibular Space
-most common DNIs
-prototypic infection: Ludwig’s angina
-alpha-hemolytic streptococcus most commonly isolated
-etiology:
-usually odontogenic (70-85%)
-disruption of mucosal layer by laceration or mandibular fracture and by tumour
-sialadenitis
-lymphadenitis
-presentation:
-typically 20-40y; 60% male
-oral cavity pain, anterior-neck stiffness, sialorrhea, dysphagia
-external swelling limited by anterior layer of deep fascia
-anterior or posterior tongue displacement
-swollen, indurated, erythematous FOM
-woody induration in suprahyoid region
-trismus minimal
-aphonic, “hot potato voice”
-tachypnea and stridor
-complications:
-asphyxia: posterior displacement of tongue (common cause of death in Ludwig’s angina)
-extension through buccopharyngeal gap: point at which styloglossus muscle exits submandibular
space between middle and superior constrictor muscles
-may enter into lateral pharyngeal space
-tongue necrosis
-aspiration pneumonia
-lung abscess
-treatment:
-evaluation and possible stabilization of airway
-antibiotics:
-high-dose IV penicillin +/- metronidazole or clindamycin for anaerobes
-surgery:
-if failure to respond to antibiotics or rapid progression threatening airway
-intraoral drainage:
-when infection limited to sublingual compartment and is uncomplicated
-external drainage recommended for all other cases via horizontal submental incision
-may require tracheotomy to secure airway
396
Lateral Pharyngeal (Pharyngomaxillary, Parapharyngeal) Space
-etiologies:
-penetrating trauma
-extension of infection from another area:
-laterally from peritonsillar abscess (separation by superior constrictor muscle)
-posteriorly from submandibular space infection
-from masticator space (most common source of extension)
-presentation:
-anterior (prestyloid) compartment: “symptomatic”
-pain, trismus, dysphagia
-systemic signs
-typically antecedent pharyngitis or tonsillitis (~10days)
-classically: trismus, medial bulging of pharyngeal wall, swelling at angle of mandible,
systemic toxicity
-posterior (poststyloid) compartment: “asymptomatic”
-systemic signs
-difficult to see on examination
-vascular complications:
-involve carotid sheath
-suppurative IJ vein thrombosis (most common) - Lemierre Syndrome
-erosion of carotid artery:
-20-40% mortality rate
-internal > external > common
-signs of impending bleed:
-shock, prolonged course, Horner’s syndrome, hemorrhaging,
hematoma, neuropathies of CN IX-XII, persistent peritonsillar
swelling, bleeding from EAC
-treatment:
-control airway, antibiotics, surgical drainage
-airway easier to control than with submandibular space infections
-empiric Abx choice:
-penicillin and metronidazole or clidamycin (anaerobes found more frequently)
-surgery:
-discouraged in the initial cellulitic phase
-intraoral drainage avoided as carotid sheath difficult to control
-submaxillary (Batson) approach (if no vascular complications)
-anterior sternocleidomastoid (Mosher) approach if vascular complications suspected
Retropharyngeal Space
-etiologies:
-nose, adenoids, nasopharynx and paranasal sinus infections that drain to retropharyngeal nodes
-retropharyngeal lymphatic chains usually involute by age 5; infections therefore due to
suppurative lymphadenitis rare after this age
-if present in adults, then tends to be more aggressive than in children
-penetratring or blunt trauma
-instrumentation
-intubation
-passage of NG tube
-extension from other spaces
-presentation:
-difficult, especially in children
-trismus uncommon
397
-“hot potato voice” if swelling in supraglottic region
-mass may be seen on posterior pharyngeal wall if below the palate
-bulging of posterior wall to one side (d/t midline raphe in retropharyngeal space)
-significant respiratory symptoms unusual unless involvement of mediastinum
-anterior mediastinum via pretracheal space; posterior mediastinum accessed to level of
tracheal bifurcation through retropharyngeal space
-pyopneumothorax, mediastinitis (50% mortality), purulent pericarditis, bronchial erosion
-radiology:
-lateral x-ray:
-reversal of normal cervical contour
-air in prevertebral soft tissues
-tuberculous erosion of cervical vertebra
-fluid collection in retropharyngeal space
-treatment:
-ensure secure airway; tracheotomy rarely needed
-transoral drainage and IV antibiotics will resolve most uncomplicated infections
-external approach if lateral space involved
-infectious complications:
-carotid artery erosion and haemorrhage
-internal jugular thrombosis
-Lemierre syndrome: caused by anaerobe Fusobacterium necrophorum
-spiking fevers
-tenderness of SCM
-neck stiffness
-metastatic abscess to lungs
-tx: anticoagulation, ligation or excision of vein for persistent embolization and
sepsis
-cavernous sinus thrombosis - via retrograde thrombophlebitis
-neurologic deficits:
-Horner’s syndrome
-cranial nerves IX-XII
398
-osteomyelitis of the mandible
-osteomyelitis of the spine
-mediastinitis
-requires immediate surgery: cervical drainage and thoracotomy and drainage
-pulmonary edema
-pericarditis
-aspiration (spontaneous rupture)
-sepsis
-surgical complications
-damage to neurovascular structures
-wound infections
-septicaemia
-scarring
-aspiration (rupture from instrumentation)
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Neck
A. Skeleton
B. Muscles
C. Nerves
Cranial Nerves
Facial (VII )
marginal mandibular branch dips down into neck in fascia
overlying submandibular gland
also innervates platysma, stylohyoid and posterior belly of
digastric.
Vagus (X)
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Cervical Nerves
Cervical plexus - anterior roots of C1- 4
Ansa cervicalis - to strap muscles (some travel with XII)
Branches to phrenic nerve
Sensory
Phrenic nerve - C3- 5
Brachial Plexus - C5- T1
Posterior rami - to posterior muscles and skin
Cervical sympathetic chain - travels in carotid sheath
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Internal maxillary
Thyrocervical trunk
Suprascapular
Transverse cervical
Inferior thyroid
Vertebral artery
Internal jugular vein (within carotid sheath)
External jugular vein
F. Thyroid Gland
G. Parathyroid Glands
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A. Anterior triangle
B. Posterior triangle
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occipital triangle-
formed by inferior belly of omohyoid, trapezius, and SCM
I. Lymphatic drainage:
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Review of Anatomy: Salivary Glands Page 1 of 2
Salivary Glands
A. Parotid Gland
Located on side of face, anterior to mastoid tip and external auditory canal,
inferior to zygomatic arch, and superior to lower border of angle of
mandible. Anteriorly, it overlaps masseter muscle.
Stenson's duct enters oral cavity through buccal mucosa opposite upper
second molar.
Parasympathetic secretory afferents to parotid leave inferior salivary
nucleus with glossopharyngeal nerve and travel via Jacobson's plexus in
middle ear to synapse in otic ganglion. Post- synaptic fibers are distributed
to parotid by auriculotemporal nerve.
Facial nerve passes through this gland.
B. Submandibular Gland
C. Sublingual Glands
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emptying into submandibular duct, and others draining directly into floor of
mouth.
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OTOLARYNGOLOGIC MANIFESTATIONS OF AIDS
(ENT Secrets)
CD4 count:
-represents absolute helper T-lymphocytes
-1000 cells/mm3: normal
-<200 cells/mm3: higher incidence of progression to AIDS; many prophylactic regimens initiated
Kaposi’s sarcoma:
-most common malignant manifestation of AIDS
Parotid enlargement:
-lymphoepithelial cysts: exhibit reactive lymphocytes which infiltrate parotid tissue
-management options (controversial):
-parotidectomy, needle aspiration, intralesional tetracycline sclerosis, low-dose radiation
-other: Kaposi’s sarcoma, NHL
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Otolaryngology - Head and Neck Surgery Page 1 of 1
Dr. F. Ling's
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UPPER DIGESTIVE TRACT ANATOMY AND PHYSIOLOGY
-lips:
-provides a seal for generation of pressure in oral cavity
-reduces loss of food or saliva
-tongue:
-under volitional cortical control
-responsible for movement of food during chewing and oral preparation
-pharyngeal swallow:
-peripheral afferent input to cortex and brainstem swallowing centers (nucleus solitarius
and nucleus ambiguus)
-motor program output:
-base of tongue moves backward to contact inward moving posterior and lateral
pharyngeal walls
-soft palate contact to back of tongue:
-holds bolus before beginning oral stage of swallow
-soft palate actively pulled down by palatoglossus muscle to contact back of tongue
-prevents premature loss of food or liquid into pharynx and ensure breathing during chewing
-velopharyngeal port:
-closes during pharyngeal phase to prevent food or liquid into nasal cavity
-accomplished through:
-velar elevation (levator muscle) and retraction (palatopharyngeal muscle)
-anterior movement of posterior pharyngeal wall (superior pharyngeal constrictor -
Passavant pad)
-mesial movement of lateral pharyngeal walls (superior constrictor)
-larynx:
-true vocal cords close false vocal folds anterior tilting of arytenoid cartilage to contact base of
epiglottis epiglottis folds over top of airway
-during pharyngeal swallow, hyoid and larynx elevate and move forward epiglottis folded to
horizontal position
-cricopharyngeal valve:
-prevents air entry into esophagus during respiration
-musculoskeletal sphincter: cricopharyngeus muscle and cricoid cartilage
-UES opened by anterior movement of hyolaryngeal complex
PRESSURE GENERATION
-second major component of deglutition is generation of pressure on bolus to drive it from mouth, through
pharynx
-propulsion of food bolus by tongue and pharyngeal pressure generators
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COORDINATION OF OROPHARYNGEAL SWALLOW EVENTS
-oral preparation:
-manipulation/mastication of food bolus cohesive bolus
-oral phase:
-tongue elevates bolus against palate, rolling and squeezing it posteriorly toward oropharynx
-pharyngeal phase:
-CN IX afferents stimulated medullary swallow center activated
-if bolus passes into valleculae and pharyngeal swallow has not been elicited delayed
pharyngeal swallow risk of aspiration
1. Velopharyngeal closure:
-levator veli palatini lifts soft palate
-palatopharyngeous tightens and raises pharynx and narrows oropharyngeal inlet
-superior pharyngeal constrictor (Passavant’s pad) contracts to meet soft palate and
posterior pharyngeal walls
2. Base of tongue propels bolus past vallecula
3. Laryngeal elevation and closure
-cessation of respiration
-larynx elevates ~2cm
-three sphincter for laryngeal closure:
-laryngeal inlet: epiglottis, aryepiglottic folds, arytenoids
-false vocal fold
-true vocal fold (most effective)
4. Pharynx shortens
-pharynx shortens by ~2cm
-pharyngeal constrictors push bolus while epiglottis directs food to piriform sinus
posterior pharyngeal wall cricopharyngeal sphincter
5. Cricopharyngeal sphincter opens
-food bolus enters cervical esophagus
-esophageal phase:
-cricopharyngeal valve opens
411
EFFECTS OF POSTURE
-chin tucked: anterior wall of pharynx is pushed posteriorly and airway entrance is narrowed
-head rotated: one side of pharynx is closed off from passage of bolus
-lifting chin: decreases oral transit time by using gravity to empty food from mouth
RESPIRATORY-SWALLOW COORDINATION
-most frequent normal coordination involves interrupting exhalatory phase of respiration with the swallow
and briefly returning to exhalation after the swallow
-thought to increase safety exhalatory airflow may assist in clearing any residual food from
around the airway entrance
-older normal individuals and dysphagic patients swallow more often by interrupting the
inhalatory phase of the respiratory cycle less safe because of risk of aspiration
412
UPPER AIRWAY ANATOMY AND FUNCTION
413
Mucosal Cover of Vocal Fold
-squamous epithelium
-lamina propria:
-superficial (Reinke’s space - lowest concentration of
both elastic and collagneous fibers)
-intermediate (elastic fibers)
-deep (stiff - high concentration of collagen fibers)
-vocalis muscle (medial thyroarytenoid muscle)
414
RESPIRATORY PHYSIOLOGY
-functions:
-sphincter
-cough
-ejects mucous and foreign matter
-helps maintain patency of pulmonary alveoli
-three phases: inspiratory, compressive and expulsive (outflow ~ 6-10 L/s)
-valsalva manoeuvre
-regulation of airflow
-produces sudden alterations in resistance to airflow
-respiratory rate primarily controlled by varying rate of exhalation
-sensory input to respiratory control
-sensory organ that exert influences on breathing and cardiovascular function
-three types of receptors:
-negative pressure receptors
-maintains upper airway patency
-mediated by superior laryngeal nerve
-airflow (cold) receptors
-modulate central respiratory drive: stimulation can RR or cause
apnea
-“drive” receptors
-proprioceptors that respond to respiratory motion of larynx
-laryngospasm:
-forceful and prolonged closure of larynx
-can occur with URTI - sometimes a decreased threshold can persist for many months after
infection
CIRCULATORY REFLEXES
-stimulation of larynx can produce changes in heart rate and blood pressure
-OSA increased negative pressure can induce cardiac arrhythmia
-hypertension
-bradycardia hypotension
-pathways not clearly understood
-afferent limb: superior laryngeal nerve
SPEECH
-consists of three component processes:
-phonation: -vibration of vocal folds
-resonance: -induction of vibration of rest of vocal tract to modulate and amplify laryngeal
output
-articulation: -shaping of voice into words
Phonation
-five conditions required:
-appropriated vocal fold approximation
-adequate expiratory force
-sufficient vibratory capacity of vocal folds
-favourable vocal fold contour
-volitional control of vocal fold length and tension
415
-vocal cycle:
-vocal folds approximated exhalation rise in subglottic pressure
-separation of vocal folds rapid decrease in subglottic pressure
-vocal folds return to midline (d/t pressure, elastic forces in vocal fold, and Bernoulli effect)
-pressure builds and cycle is repeated
-forms the mucosal wave
-volume is influenced by the expiratory effort/pressure
-frequency is influenced by vocal fold length and tension
-ossification of thyroid cartilage with increasing age contributes to elevation of pitch
Resonance
-gives voice characteristic acoustic pattern
-amplifies voice
-controlled by altering shape and volume of pharynx, raising or lowering larynx, moving tongue or jaw
position, or by varying amount of sound transmission through nasopharynx and nose
Articulation
-controlled by lips, tongue, palate, and pharynx
416
UPPER DIGESTIVE TRACT EVALUATION AND IMAGING
CLINICAL EXAMINATION
COMMON DISEASES
417
-causes solid food dysphagia
-may form Zenker’s diverticulum
-esophagitis:
-opportunistic infection: (eg. Candida, herpes, CMV)
-chemical injury
-strictures:
-chemical or traumatic injury
-CVA:
-common cause of dysphagia
-may need tube alimentation
-cancer:
-contrast examination documents location and size of lesion and presence of fistulae
-CT typically done to assess deep tissue invasion and to look for mediastinal adenopathy
INVESTIGATIONS
MANAGEMENT
Medical Management
-address underlying disorder if possible
-consider alternative temporary route of nutrition
Swallowing Rehabilitation
-change food consistencies (pureed diet easier to tolerate initially)
-posturing techniques:
-chin tuck, head turn to poorer functioning side, palatal prosthesis, muscle strengthening exercises
-supraglottic swallow:
-patient voluntarily closes airway by holding breath before swallow
-voluntary cough after swallow
-follow with additional swallow for residual bolus in pharynx or piriform
-Mendelsohn manoeuver:
-voluntarily elevates and anteriorly displaces larynx to prolong upper esophageal sphincter
opening
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AIRWAY EVALUATION AND IMAGING
DIFFERENTIAL DIAGNOSIS
Above larynx -micrognathia -retropharyngeal -facial fracture -allergic rhinitis -JNA -altered mental
-macroglossia abscess -retropharyngeal -WG status
-choanal atresia haematoma
PHYSIOLOGIC TESTING
IMAGING
Plain-Film Radiography
-lateral films taken both inspiration and expiration
-“vallecular sign” - SENS and SPEC for epiglottitis
-to detect infection, foreign bodies etc..
Fluoroscopy
-dynamic study
-ball-valve effects of a bronchial foreign body can be demonstrated
-laryngomalacia can be revealed
-motion defects of each hemidiaphragm
419
Contrast Radiography
-barium swallow historically used to help localize extrinsic or intrinsic mass
-now used to demonstrate GERD, aspiration and TEF
Ultrasonography
-evaluation of solid or cystic nature of extrinsic cervical airway masses
-eg. thyroid masses, TGDC, branchial cysts, hemangioma, lymphangioma, laryngocele
Arteriography
-for JNA, glomus tumours
-+/- embolization
CT
-superior bony definition
-disadvantages:
-greater cost, higher radiation exposure, limitation to axial scans
MRI
-does not rely on ionizing radiation
-can demonstrate anatomic site in multiple planes
-excellent tissue differentiation
ENDOSCOPIC ASSESSMENT
Diagnostic Endoscopy
-flexible scopes offer greater diagnostic capabilities; can be used to visualize subsegmental bronchi and
upper lobe bronchi
-rigid scopes superior for biopsies, obtaining cultures, retrieval of foreign bodies and surgical intervention
Rigid Laryngoscopy
-Jackson laryngoscope: can be used as an aid in intubation
-anterior commissure scope
-operating laryngoscopes: Jako or Dedo
COMPLICATIONS
-damage to teeth
-perforation
-pneumothorax
-from perforation by bronchoscope
-from jet ventilation at high pressures
-laryngospasm negative pressure pulmonary edema
420
ESOPHAGEAL DISORDERS
Embryology
-epithelial proliferation obliterates the lumen
-recanalization occurs by 8th week (abnormal recanalization results in congenital stenosis)
Anatomy
-three regions of natural constriction:
-cricopharyngeus: narrowest point in entire GI tract (15 cm from incisors)
-point at which aorta and left mainstem bronchus cross anteriorly (20-25cm from incisors)
-lower esophageal sphincter (40-45cm from incisors)
-esophageal layers:
-outer muscular layer
-longitudinal muscle
-no serosa layer, therefore minimal barrier to infection and tumour infiltration
-middle submucosa
-inner circular muscle
-inner mucosal layer: epithelium, lamina propria, muscularis mucosa
-upper 1/3: striated muscle; lower 2/3: smooth muscle
-blood supply:
-segmented from inferior thyroid artery (upper 1/3)
-thoracic aorta (middle 1/3)
-left gastric and inferior phrenic arteries (lower 1/3)
-histology:
-stratified squamous epithelium except distal 1-3 cm which is columnar epithelium
-innervation:
-mixed somatic innervation from CN IX and CN X
-left vagus nerve passes anteriorly and right vagus nerve passes posteriorly to form
esophageal plexus
-Auerbach’s plexus: myenteric plexus between muscle layers, parasympathetic
-Meissner’s plexus: submucosal plexus
Physiology
-primary peristalsis:
-initial peristaltic wave as food is passed into esophagus
-secondary peristalsis:
-contractions that clears any remaining food and is initiated by esophageal distention or by GER
-tertiary contractions:
-non-peristaltic and occur spontaneously or after swallowing
-may propel bolus in a retrograde direction to proximal esophagus
421
-up to 80% with symptomatic reflux have hiatal hernia
-normal tone: 10-40 mmHg (achalasia: > 40; scleroderma < 10)
-increase LES pressure
-alpha-adrenergic neurotransmitters
-beta-adrenergic blockers
-protein meals
-acid
-gastrin
-vasopressin
-decrease LES pressure
-beta-adrenergic stimulation
-alpha-adrenergic blockers
-fatty meals, chocolate, ethanol, smoking, caffeine
-secretin, nitrates, calcium channel blockers, glucagon
Symptoms
-dysphagia and heartburn most common
-odynophagia: inflammatory changes of esophageal mucosa
Physical Examination
-vocal cord paralysis: compression or invasion of recurrent laryngeal nerves
-obstructive esophageal lesions may manifest as pooling of secretions in hypopharynx
Radiologic Studies
-barium swallow; videofluoroscopy; CT/MRI
Esophageal Manometry
-for esophageal motility disorders
pH Monitoring
-24h pH monitoring
-electrode placed exactly 5 cm above LES
-reflux = lowering the pH to 4.1 at a level 5 cm above LES
-normal total reflux time is less than 1 hour during a 24 hour period
Endoscopic Examination
-rigid:
-better visualization of pharynx and upper sphincter
-larger deeper biopsies
-easier removal of foreign bodies
-direct visualization during dilation permitted
-ability to use endoscopic laser techniques
-flexible:
-general anesthetic not needed
-allows concurrent examination of stomach, duodenum
-closer examination of mucosal lesions
-endoscopic photography and videotaping permitted
-more flexibility in difficult anatomic conditions
422
GASTROESOPHAGEAL REFLUX DISEASE
Evaluation
-GERD common: 1/3 with occasional sxs; 10% with daily sxs
-most common ENT manifestations:
-hoarseness (71%)
-cough (51%)
-globus pharyngeus (47%)
-throat clearing (42%)
-difficulty swallowing (35%)
-heartburn, dysphagia
-slowly progressive dysphagia for solids suggests development of peptic stricture
-dysphagia for both liquids and solids suggests GERD-related motility disorder
-smoking and high-fat meals delay gastric emptying and increase potential for reflux
-diagnostic tests should be limited to patients with atypical or recurrent symptoms (indications)
-uncertain diagnosis
-recurrent symptoms
-inadequate response to therapy
-atypical symptoms (chest pain, hoarseness, cough, asthma)
-symptoms associated with complications (GI hemorrhage, unexplained weight loss, dysphagia,
odynophagia)
Treatment
-lifestyle modifications:
-avoid lying down soon after meals
-HOB elevated
-weight reduction; avoidance of fatty foods; smaller meals
-decrease intake of chocolate, peppermint, cigarettes, caffeine (decrease LES pressure)
-avoid NSAIDs which may induce mucosal injury
-medical treatment: H2 antagonists and PPI
-PPI: 95% healing of esophagitis; H2 antagonists: 35-65%
-both increased and divided doses of PPIs commonly used to treat extraesophageal manifestations
of GERD
-surgery:
-failed medical management
-Nissen fundoplication
Complications of Reflux
-esophageal stricture
-esophageal ulceration
-aspiration chronic cough, bronchitis, aspiration pneumonia, bronchiectasis, nocturnal dyspnea, asthma
-Barrett’s esophagus adenocarcinoma in 10%
-hoarseness, frequent throat clearing, cough
-early: posterior laryngeal edema/erythema
-late: ulceration and hyperkeratosis in interarytenoid area
-contact ulcers, Reinke edema, and laryngeal granulomas all associated with GERD
423
ESOPHAGEAL MOTILITY DISORDERS
Achalasia
-neuromuscular disorder: degeneration of ganglion cells of Auerbach plexus
-features:
-peristalsis
-esophageal dilatation
-failure of LES to relax
-increased LES pressure (> 40 mmHg)
-progressive intermittent dysphagia with epigastric pain
-men > women; 30-70 years of age
-failure of LES to relax retention esophagitis
-“bird’s beak” sign on barium swallow
-esophagoscopy to r/o masses and esophagitis
-treatment:
-encourage small meals, liberal use of liquids to wash down food
-decreasing LES pressure: calcium channel blockers and long-acting
nitrates (eg. isosorbide)
-dilatations of LES: 50% recurrence of symptoms; risk of perforation
-surgery:
-repeated failed dilatations
-Heller myotomy
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CRICOPHARYNGEAL DYSFUNCTION
-Plummer-Vinson syndrome:
-predominantly in Scandinavian women
-features:
-dysphagia, hiatal hernia, atrophic gastritis, achlorhydria
-cervical esophageal webs
-iron deficiency anemia (microcystic hypochromatic anemia)
-glossitis
-cheilosis, koilonychia, splenomegaly
-increased incidence of carcinoma in postcricoid and upper esophageal region
-treatment of webs: endoscopic rupture of web and iron replacement
-Schatzki’s Ring:
-occurs at squamocolumnar junction
-asymptomatic rings identified in 6%-14% of barium studies
-cause unclear
-asymptomatic: no treatment; severe: treated with dilatation
425
DIVERTICULA
-Zenker diverticulum
-pharyngoesophageal pseudodiverticulum of the pulsion type
-herniation between inferior pharyngeal constrictor and cricopharyngeus muscle (Killian’s
Triangle)
-6th-9th decade; M:F = 3:1
-dysphagia, regurgitation of undigested foodstuffs
-diagnosis by barium swallow; pouch usually on the left (80-90%)
-treatment:
-observation for asymptomatic diverticula
-endoscopic management:
-Dohlman procedure: diathermy and a bivalved esophageal speculum
-one blade in esophagus and the other in the pouch, the common wall
was removed sequentially with diathermy instruments
-open approach:
-most popular
-options:
-cricopharyngeal myotomy alone sufficient for small pouches (< 2 cm)
-diverticulectomy with myotomy for larger pouches
-diverticulopexy
-esophagitis
-most common cause = GERD
-immunocompromised patients:
-Candida albicans most common organism infecting the esophagus
-herpes esophagitis:
-cytologic examination demonstrates multinucleated cells containing intranuclear
426
inclusion bodies
-radiation esophagitis occurs rarely
-scarring and stenosis may occur from 6-18 months after radiation therapy
-drug-induced esophagitis:
-typically punctate ulcerations
-tetracycline, doxycycline, quinidine, potassium
-prevent by taking meds with sufficient fluid
-bullous dermatoses:
-pemphigoid, epidermolysis bullosa, toxic epidermal necrolysis, Stevens-Johnson syndrome
-pemphigoid:
-subepithelial clefting and linear pattern of direct immunoglobulin G
immunofluorescence at the basement membrane
-chronic blistering
-epidermolysis bullosa:
-hereditary skin disorder
-loss of cohesion between epidermis and dermis blister formation
ESOPHAGEAL CARCINOMA
427
-low grade lesions antireflux therapy
-high grade lesions resection of affected portion
-others:
-adenoid cystic carcinoma, mucoepidermoid carcinoma, small-cell carcinoma, sarcoma
-tumours limited to epithelium and lamina propria have not been associated with lymph node metastasis
-spread to regional lymph nodes seen in 50% of pts with infiltration of submucosa
-surgery remains treatment of choice
-tumours limited to epithelium and lamina propria: endoscopic resection, endoscopic laser
photocoagulation or thoracoscopic resection
-advanced disease: transthoracic esophagectomy with gastric pull-up or esophagogastrectomy
-Boerhaave syndrome:
-spontaneous rupture of esophagus
-precipitated by vigorous coughing, weight lifting, straining
-usually associated with a left-sided, transmural rupture of distal esophagus
-thoracotomy or transcervical exploration may be indicated for adequate surgical drainage
Hemorrhage
-causes: esophageal varices, neoplasm, esophagitis with erosion, Mallory-Weiss syndrome, endoscopic
surgery
-treat hypovolemia, conservative measures; if refractory endoscopic laser treatment, angiographic
embolization, surgery
Mediastinitis
-causes: perforation with leakage or abscess formation, tumour erosion
-treatment: IV Abx; exploration and drainage
Obstruction
-causes: tumour, foreign body, stricture, achalasia
-treatment: removal of FB, dilatation, surgery, esophageal replacement, gastrostomy
428
TRACHEOTOMY AND INTUBATION
Techniques of Tracheotomy
Elective Tracheotomy
-in OR under controlled conditions
-Bjork flap:
-suturing an inferiorly based flap consisting of anterior portion of a single tracheal ring
-reduces incidence of accidental decannulation and eased reinsertion
-contraindicated in operations on children:
-can cause unacceptable rate of tracheal stenosis and persistent tracheocutaneous fistulae
Timely Tracheotomy
-must be performed in 5-10 minutes
-vertical incision that extends from cricoid cartilage to about 3.75 cm inferiorly
Emergency Tracheotomy
-anoxia causes death in about 4-5minutes; tracheotomy must be performed within 2-3 minutes
-better to perform elective tracheotomy under local anaesthesia
-best performed through vertical incision beginning at level of cricoid and extends inferiorly 1-1.5 inches
-avoids injury adjacent neck structures
Cricothyrotomy
-cricothyroid membrane near skin surface
429
-risk of damage to subglottic larynx
-relatively contraindicated in children < 12 years, patients with infection in the larynx and pts with
laryngeal trauma
Complications of Tracheotomy
-Intraoperative:
-damage to great vessels (most common intraoperative complication)
-damage to tracheoesophageal common wall
-pneumothorax
-pneumomediastinum
-Early postoperative
-tracheotomy tube obstruction (most common early postop complication)
-tracheotomy tube displacement
-pulmonary edema
-infection
-respiratory arrest from loss of hypoxic drive (in pts with long standing obstruction)
-Late
-tracheal stenosis (most common late postop complication)
-granulation tissue
-trachea-innominate artery fistula
-60% of cases of fistula occur within 2 weeks of tracheotomy
-73% mortality
-mx: overinflate tracheotomy cuff
-insert ETT below level of bleeding while attempting to compress innominate
artery anteriorly against sternum
-cuff pressure kept less than 25 cmH2O - pressure at which submucosal capillaries are occluded
430
Complications of Percutaneous Dilational Tracheotomy
-misplacement of dilator in a paratracheal position
-haemorrhage
-subcutaneous emphysema
-damage to posterior tracheal wall
-death
ENDOTRACHEAL INTUBATION
Techniques
Complications of Intubation
-acute pulmonary edema
-caused by sudden loss of highly negative intrathoracic pressure during inspiration and positive
pressure during expiration
-rapid increase in systemic venous return
-most commonly occurs in recovery room after extubation
-mx: mechanical ventilation and diuretics
-improper tube placement
-long-term intubation
-Laryngeal Stenosis: occurs at narrowest part of airway:
-children: subglottis
-adults: glottis
-Tracheoesophageal Fistula:
-rare complication
-Recurrent laryngeal Nerve Injury:
-nerve can be pinched by an ETT
-Sinusitis: nasotracheal intubation
431
F.Ling - Tracheotomy (4)
432
CONTROVERSIES IN UPPER AIRWAY OBSTRUCTION
Child Adult
Nonsurgical Management
-oxygen
-heliox - can improve ventilation temporarily until definitive control of airway can be obtained
-epinephrine aerosols to decrease soft tissue edema
-short duration
-can have a rebound effect
-steroids
-large doses of dexamethasone (1mg/kg)
Surgical Management
-direct neck trauma with progressive breathing difficulty
-intubation contraindicated because of possibility of laryngotracheal separation
-temporary tracheotomy if separation suspected
-postglottic stenosis: open repair
433
-bilateral vocal cord paralysis: consider tracheotomy, arytenoidectomy
-laryngeal papilloma: CO2 laser therapy
-foreign body: rigid bronchoscopy
-adenotonsillectomy:
-does not increase the likelihood of overwhelming infection
434
MANAGEMENT OF INTRACTABLE ASPIRATION
PHYSIOLOGY OF SWALLOWING
Oral Phase
-tongue and bolus pressed against faucial arches and palate
triggers reflex-driven, central programmed pharyngeal swallow
-defects in pharyngeal sensation, central neurologic disease or postsurgical changes in tongue or
palate can cause inability to initiate a reflexive pharyngeal swallow
Pharyngeal Swallow
-cessation of respiration
-palate elevation and closure of nasopharyngeal isthmus
-glottic closure
-laryngeal elevation
-pharyngeal peristalsis
-cricopharyngeal relaxation
-dilation of pharyngoesophageal segment
Esophageal Phase
-involuntary peristalsis
ETIOLOGY OF ASPIRATION
435
Glottic Closure
-aspiration often associated with vocal cord paralysis or inadequate glottic closure
-other abnormalities often occur before a patient with aspiration due to incompetence of the glottis has
substantial morbidity
Sensory Loss
-sensory loss correlates with risk of aspiration pneumonia among patients who have had a stroke
Identification of aspiration
-aspiration pneumonia
-recurrent pneumonia of unknown causation
-“bronchorrhea” after tracheotomy
-coughing, choking with eating
-dysphagia and prolonged time for eating
-weight loss
Clinical Evaluation
-history and physical
-endoscopic laryngeal evaluation:
-hypopharynx and larynx examined for anatomic and physiologic abnormalities
-pharynx can be rapidly assessed during swallowing to ascertain aspiration risk and alternative
feeding strategies
-dye test (for patients with tracheostomy)
-modified barium swallow
-swallowing scintigraphy
THERAPEUTIC OPTIONS
Initial Interactions
-nonsurgical:
-NPO, NG feeds, mx of respiratory failure, control of GER
-risk of aspiration pneumonia not eliminated with nonoral feeding
-tracheostomy tube may facilitate pulmonary toilet
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Other Nonsurgical Options
-through speech pathologist
-dietary modifications
-thickened feeds reduce aspiration for pts with inappropriate delay in initiation of swallow
-compensation techniques
-supraglottic swallow:
-for residue on glottis
-patient voluntarily closes airway by holding breath before swallow
-cough and second swallow before next inspiration
-turning head to side of unilateral pharyngeal weakness compresses piriform sinus to prevent
accumulation of residue
-chin tuck: flexing neck compresses vallecula
-Mendelsohn manoeuver:
-voluntary elevation and anterior displacement of larynx to prolong upper esophageal
sphincter opening
Surgical Options
Adjunctive:
-G-tube
-cuffed tracheotomy tube
-reduce saliva production
-bilateral chorda tympani section
-ligation of submandibular or parotid duct
Cricopharyngeal Myotomy:
-reduce obstruction at pharyngoesophageal segment
-considered when radiographic evidence of restriction at cricopharyngeus muscle is found
-Laryngeal stenting:
-aspiration likely for a finite period and recovery is expected
-stent for 2-3 months
-Laryngeal Suspension:
-indicated for severe aspiration from supraglottic and pharyngeal dysfunction
-suspends larynx anteriorly by positioning thyroid cartilage under mandible
-may improve voicing and swallowing
437
-Tracheoesophageal Diversion (Lindemann Procedure) and Laryngotracheal Separation:
-Lindemann procedure:
-trachea divided and proximal end anastomosed to anterior esophagus
-distal end of trachea brought to skin as it is in total laryngectomy
-Laryngotracheal separation:
-proximal tracheal stump closed in a pouch: theoretically reversible procedure
-standard procedure in most institutions for mx of intractable aspiration unresponsive to more conservative
measure or adjunctive surgical procedures
-Total Laryngectomy:
-gold standard
-intractable aspiration after partial laryngectomy or total glossectomy
-indicated for life-threatening complications
-unacceptable to pts with neurologic disease: risk of pharyngeal closure higher in debilitated pts
CONCLUSIONS
438
EVALUATION OF THE DYSPHONIC PATIENT
History
-character of dysphonia:
-onset and duration
-time course
-periodicity
-contributing factors:
-recent URTI, fever, sore throat, cough, congestion, history of voice, tobacco, alcohol abuse
-PMHx:
-peripheral nerve diseases and other neurological disorders, GERD, hypothyroidism,
psychological stressors
-previous laryngeal trauma, surgery or airway manipulation
-associated symptoms:
-odynophagia, dysphagia, aspiration, weight loss, hearing loss, heartburn
DDx
Congenital Infectious/Idiopa Trauma/Toxic Tumour Endocrine Neurologic Systemic
thic
439
-excessive airflow from a longer “open phase” or incomplete adduction
-glottal chink, bowed deformity secondary to vocal fold paralysis, presbylarynx, glottic lesions,
muscle-tension dysfunction, abductor spasmodic dysphonia, psychogenic
-arrest of phonation:
-sudden stops
-spasmodic dysphonia, load bearing vocal fold mass, muscle-tension disorders, psychogenic
-aphonia:
-often functional disorder
-stridorous:
-hypernasality or hyponasality
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Review of Anatomy: Oral Cavity and Pharynx Page 1 of 2
ORAL CAVITY
A. Boundaries
Anterior - lips
Posterior - anterior tonsillar pillars
Roof - hard and soft palate
Floor - mucosa overlying sublingual and submandibular glands.
Walls - buccal mucosa
B. Contents
PHARYNX
A. Nasopharynx
B. Oropharynx
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Review of Anatomy: Oral Cavity and Pharynx Page 2 of 2
constrictors
C. Palatine Tonsils
D. Hypopharynx
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Alaryngeal Speech
Electronic speech aid (Neck Type) -easy to learn to use -noisy electronic sound
-fits in pocket or purse -cannot be used with heavily scarred or
-volume and pitch controls erythematous neck
-adequate volume to be heard in noisy -moderate initial cost; occasional repair cost
places -requires clear articular skills
-intelligible speech
Electronic speech aid (Oral Type) -as for Neck Type -electronic sound
-less noisy than neck types -“clumsy” feeling initially to talk with tube
-can be used soon after surgery even in in mouth
presence of much scar tissue -moderate initial purchase cost; occasional
repair cost
-requires excellent articulation skill for easy
intelligibility
Tracheoesophageal speech -“natural” non-electronic sound -if not done as primary procedure, requires
-requires short learning period another surgical procedure
-smooth, fluent speech using long sentences -requires manual dexterity, visual acuity,
because of availability of pulmonary air and level of alertness to care for
-flexibility of loudness and pitch variations -requires use of finger to occlude stoma or
-sound of voice does not call attention to daily affixing of valve to peristomal area
itself -buildup of candida deposits requiring
-extended wear prosthesis types obviate frequent cleaning
need for frequent removal -puncture may stenose
-slight risk of aspiration if prosthesis
dislodged
PNEUMATIC DEVICES
Types
-DSP8 Speech Aid
-Tokyo Speech Aid
-ToneAire Artificial Larynx
ELECTRONIC DEVICES
Description:
-vibrator provides sound source
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Specific Types:
1. Cooper-Rand Electronic Speech Aid
2. Servox Inton
3. Romet Speech-Aid
4. SPKR
5. Denrick Speech Aid
6. TruTone Electonic Speech Aid
7. Nu-Vois Artificial Larynx
8. P.O. Vox (no longer available)
9. UltraVoice
10. SolaTone
11. Optivox Electrolarynx
ESOPHAGEAL SPEECH
Description:
-production of voice source within esophagus
-uses cricopharyngeal muscle
-air expelled through the narrowed segment (pharyngoesophageal or PE segment) vibrates and
produces sound
1. Injection method
-air injected from mouth into esophagus via tongue and pharynx
-“glossal press”; “glossopharyngeal press”
2. Inhalation method
-relax PE segment
-lower pressure within esophageal segment relative to atmospheric pressure
3. Swallowing
-not advantageous for creating an air supply for esophageal speech
-requires a trigger to initiate a swallow
-not possible to “dry swallow” quickly and repetitively as required for speech
-voluntary control of the air supply from the stomach may be impossible to achieve
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Indications for Use of Esophageal Speech:
-exceptions: extensive pharyngeal, esophageal, lingual, and/or mandibular resection; patients with
compromised medical status; significant hearing loss; no desire to learn esophageal speech
Description:
-surgical, endoscopic voice restoration preocedure
-small puncture made through tracheoesophageal wall into esophagus
-pulmonary air drives vibration of PE segment
-oral cavity articulates sound
-prosthesis with one way valve prevents aspiration, maintain patency of puncture, and allow flow
of air into esophagus for voice production
Surgical Procedure:
-primary of secondary puncture
-primary puncture for uncomplicated cases of total laryngectomy
-secondary usually delayed a minimum of 6 weeks after completion of post-op radiation therapy
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LARYNGITIS
DDx: Laryngitis
Infectious: Inflammatory/Autoimmune:
-viral: -Wegener’s
-croup (parainfluenza) -relapsing polychondritis
-rhinovirus, RSV, adenovirus -SLE
-bacterial: -epidermolysis bullosa
-H. influenzae, -cicatricial pemphigoid
pneumococcus, hemolytic
strep Iatrogenic/Trauma:
-epiglottitis -radiation laryngitis
-diphtheria -thermal injury
-tuberculosis -laryngopharyngeal reflux
-syphilis
-leprosy Idiopathic/Infiltrative:
-scleroma (Klebsiella) -amyloidosis
-fungal: -sarcoidosis
-histoplasmosis
-blastomycosis Allergic:
-candidiasis -angioedema
-aspergillosis
-coccidiomycosis
CHILDHOOD LARYNGITIS
Viral Laryngitis
-most common cause of laryngitis
-associated with URI
-rhinovirus, parainfluenza, RSV and adenovirus implicated
-self-limited
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-organisms usually responsible:
-Haemophilus influenzae, pneumococcus and hemolytic streptococci
Laryngeal Diphtheria
-uncommon
-Corynebacterium diphtheria
-exudative inflammatory response of mucous membranes thick, gray-green plaquelike membranous
exudate over tonsils, pharynx and larynx
-complications:
-nephritis, airway obstruction, death (secondary to neurological toxin)
-tx: diphtheria antitoxin, erythromycin or penicillin
Laryngopharyngeal Reflux
-associated with laryngomalacia, vocal nodules, polyps, granulomas, laryngeal and tracheal stenosis and
laryngospasm
Spasmodic Croup
-noninfectious form of laryngeal inflammation, possible related to allergy or LPR
-affects children 1-3 ya
-usually at night with nocturnal stridor and respiratory distress - asymptomatic during day
-humidification is all that is need to alleviate symptoms
ADULT LARYNGITIS
Viral Laryngitis
-viral URI - rhinoviruses most common agent
-voice breaks, episodic aphonia, hoarse cough, lowering of vocal pitch
-self-limited; humidification, voice rest, hydration, smoking cessation, cough suppressants, expectorants
Bacterial Laryngitis
-supraglottitis
-fever, sore throat, muffled voice, odynophagia and dyspnea
-Haemophilus influenzae most common organism; Streptococcus pneumoniae, Staphylococcus aureus, and
B-hemolytic streptococci also found
-tx: humidification, hydration, corticosteroids, IV antibiotics
-ampicillin, cefuroxime, ceftriaxone, aztreonam, chloramphenicol
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NON-INFECTIOUS LARYNGITIS IN ADULTS
Laryngopharyngeal Reflux
-implicated in development of granulomas, stenosis, recurrent laryngospasm, globus pharyngeus, cervical
dysphagia, asthma, laryngeal carcinoma, chronic cough
-pts often deny heartburn
-possible findings:
-red arytenoids with interarytenoid mucosal hypertrophy
-subglottic edema forming “pseudosulcus vocalis”
-diffuse edema, Reinke edema, or mucosal thickening w/o significant erythema
-gold standard for diagnosis: 24H pH double probe monitoring
Traumatic Laryngitis
-vocal abuse
-persistent coughing, muscle tension dysphonia, direct endolaryngeal injury
-treatment: voice conservation and humidification
Thermal Injury
-exposure of larynx to steam, smoke or very hot liquids or food supraglottic edema and erythema
Angioedema
-vascular dilation and increased vascular permeability
-cause:
-medications: ACE inhibitors
-foods, insect bites, transfusions and infections
-hereditary angioedema:
-AD deficiency of C1 esterases inhibitor recurrent attacks of mucocutaneous edema
-aggressive treatment:
-O2, epinephrine, corticosteroids, antihistamines, aminophylline
Allergic Laryngitis
-controversial
Relapsing Polychondritis
-inflammation and fibrosis with destruction of cartilage of ears, nose, larynx, tracheobronchial tree
-airway involvement leads to high mortality seen with this disease
-treatment: dapsone, corticosteroids, immunosuppresive drugs; tracheotomy
Amyloidosis
-diffuse mucosal thickening, submucosal nodules or polyploid lesions
-usually involves supraglottis
-biopsy amorphous Congo red-staining material
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CHRONIC GRANULOMATOUS LARYNGITIS
Tuberculosis
-most common granulomatous disease of larynx
-may resemble carcinoma
-areas of involvement:
-interarytenoid space (most common)
-false and true vocal cords
-epiglottis
Syphilis
-second stage: diffuse erythematous papules, edema and ulcers (painless) that mimic carcinoma along with
cervical lymphadenopathy
-tertiary stage: gumma formation
Leprosy
-rare
-commonly involves supraglottic larynx
Histoplasmosis
-systemic mycotic disease
-Histoplasma capsulatum
-nodular superficial granulomas that can ulcerate and become painful
-amphotericin B is treatment of choice
Blastomycosis
-Blastomyces dermatitidis
-usually have multiorgan involvement
-histology: caseous necrosis with acute inflammatory infiltrate, microabscesses, pseudoepitheliomatous
hyperplasia, giant cells
-treatment: long-term amphotericin B, ketoconazole, itraconazole
-may develop pharyngocutaneous fistula if left untreated
Scleroma
-Klebsiella rhinoscleromatis
-primarily involves nasal cavity but may involve larynx
-subglottis most commonly involved
-histology:
-foamy vacuolated histiocytes (Mikulixz cells)
-degenerated plasma cells (Russell bodies)
-tx: tetracycline, fluroquinolones, clofazimine
Sarcoidosis
-multisystem granulomatous disease
-noncaseating granulomas and pale diffuse edema of supraglottis
-diagnosis of exclusion
-treatment: steroids
Wegener Granulomatosis
-necrotizing granulomas with vasculitis involving respiratory tract and kidneys
-treatment: cyclophosphamide, corticosteroids, and optional TMP-SMX
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Immunocompromised Host
-at risk for developing laryngeal opportunistic infections and malignancies (Kaposi sarcoma, non-Hodgkin
lymphoma, SCCa)
Radiation Laryngitis
-erythematous, swollen larynx with exudate and crusting
-treatment: hydration, humidification and acid suppression with steroids and antibiotics occasionally
-ddx: recurrent cancer, LPR, radionecrosis, hypothyoidism
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HOARSENESS AND VOCAL CORD PARALYSIS
-posterior commissure defects causing aspiration, air leakage, and hoarseness are commonly seen after
prolonged intubation
VOICE GENERATION
Patient History
-SSx:
-hoarse-breathy dysphonia, aspiration, stridor, dysphagia, limited phonation time, vocal fatigue
-inspiratory or biphasic stridor, weak cry, aspiration, hoarseness
-contributing factors:
-URTI, fever, cough, postnasal drip
-alcohol/tobacco
-voice abuse
-GERD
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-previous neck trauma, toxin exposure
-previous surgery (cardiothoracic, thyroid)
-previous history of cancer, cardiopulmonary disease
-hypothyroidism, diabetes, neurological disorders
-medications: ACEi chronic cough induced changes
Ancillary Tests
-videostroboscopy
-demonstrates subtle mucosal motion abnormalities
-electromyography
-laryngeal EMG used to differentiate between vocal cord fixation d/t cricoarytenoid joint
disorders vs neuromuscular disease
-studies primarily thyroarytenoid and cricoarytenoid muscles
-loss of muscle function: normal frequency of firing but decrease in amplitude
-loss of nerve function: normal amplitude but decreased frequency
-provides most accurate diagnosis of SLN paralysis
-CXR
-CT scan: head, neck, thorax
-modified barium swallow test
-labs: CBC, FTZ-Abs, lyme titers, thyroid function, toxin screen (lead+arsenic levels)
-note:
- below are “classic findings” however position of vocal cord paralysis is not very predictive of
site of nerve involvement and vice versa
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VOCAL CORD PARALYSIS IN CHILDREN
Etiology
-neurologic disorders: DDx Vocal Cord Paralysis (Children
-Arnold-Chiari malformation: traction on vagal
rootlets producing neuropraxia or axonotemesis Congenital
-paralysis often temporary, but tracheotomy -idiopathic
needed for bilateral VCP Infectious
-earlier decompress may lead to faster -syphilis (rare)
recovery time of paralysis and may avoid
tracheotomy Iatrogenic/Trauma
-surgery
-congenital idiopathic VCP -patent ductus arteriosus repair
-usually unilateral -TEF repair
-recovery in 20% -mediastinal and neck surgeries
-birth trauma -birth trauma
-traction and stretching of laryngeal nerves Neurologic
-surgical trauma -Arnold-Chiari malformation
-patent ductus arteriosus repair, TEF repair,
mediastinal and neck surgeries
-congenital infections
-rare
-syphilis
Management
-establish secure airway
-unilateral paralysis
-rarely requires tracheotomy
-usually observation
-bilateral paralysis
-may require tracheotomy
-arytenoidectomy and lateralization procedures postponed a minimum of 6 months to await
functional recovery
-lateralization good airway at expense of voice and airway protection
-arytenoidectomy or arytenoidopexy are irreversible - may offer decannulation of pt
-left side paralysed more frequently because of longer and intrathoracic course
Etiology
-surgical trauma - most common cause of unilateral and bilateral VCP
-neoplastic causes - bronchogenic carcinoma, thyroid carcinoma, upper esophageal and laryngeal ca
-neurologic conditions - poliomyelitis, pseudobulbar palsy, ALS
-idiopathic
-other causes: infection (eg. TB), drugs (eg. cisplatin), NG tube, ETT
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DDx Vocal Cord Paralysis (Adults)
Management
Medical Management:
-treat underlying cause if possible
-voice therapy:
-for unilateral paralysis
-isometric manoeuvers to improve glottal competence
Surgical Management:
1. Injection Thyroplasty:
-can be done external or internal (indirect or endoscopic)
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-advantages:
-easy, immediate improvement, may be complete in office
-disadvantages:
-irreversible if Teflon used
-changes mucosal wave
-does not correct large posterior defects
-materials used:
-Gelfoam:
-augmentation for pts in whom recovery is expected but who require immediate
improvement
-resorption occurs in 6-8 weeks
-Teflon:
-permanent injectable material
-irreversible complications: interference with vocal cord vibration and
destructive Teflon granuloma
-risk of migration
-supplanted by safer, more efficacious treatments
-Collagen:
-autologous or bovine collagen (risk of host reaction
-effective for up to 3 years
-collagen eventually resorbed and replaced with host tissue
-Fat:
-autologous
-does not last long
-complications
-over or underinjection
-acute hypersensitivity
2. Thyroplasty Type I:
-placement of silicone block to push inward against
paraglottic tissues, medializing membranous true
vocal cord
-cartilage window dimensions:
-upper: ½ distance from thyroid notch to
insertion of cricothyroid
-lower: ½ distance from upper rectangle to
insertion of cricothyroid
-posterior: 1/3-1/2 distance from midline of
thyroid cartilage
Typical dimensions of silastic wedge for thyroplasty
-anterior: within 5-7 mm lateral to midline
of thyroid cartilage
-advantages:
-reversible
-preserves mucosal wave
-immediate results
-may be done under local anaesthesia
-disadvanges:
-requires neck incision
-possible extrusion of implant
-not adequate for posterior defects
-risk of airway compromise
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3. Arytenoid Adduction:
-permanent sutures to anchor muscular process of arytenoid in adducted position to medialize VC
and close posterior commissure
-may be used in conjunction with type I thyroplasty
4. Laryngeal Reinnervation:
-types:
-ansa hypoglossi to recurrent nerve anastomosis
-end-to-end anastomosis of RLN
-ansa cervicalis to neuromuscular pedicle (omohyoid) to thyroarytenoid muscle
-vagus, ansa, phrenic nerve fibers or motor endplate insertion into thyroarytenoid
-no laryngeal motion appreciated due to synkinesis of reinnervation, but excellent voice quality
was achieved
Bilateral Paralysis
-treatment directed toward lateralizing one or both cords to improve airway at expense of aspiration and
voice quality
1. Tracheotomy
2. Laser Cordectomy:
-endoscopic removal of one vocal cords to open a/w
-scarring may narrow airway
3. Laser Cordotomy:
-posterior gap created as posterior portion of VC is released from vocal process and resected with
laser
-risk of aspiration
4. Arytenoidectomy:
-Woodman: -arytenoid excised with exception of vocal process; suture passed through vocal
process and thyroid ala and tightened to proved adequate airway and usable
voice
-endoscopic laser or microlaryngeal removal of arytenoid opens posterior glottis
5. Arytenoidopexy:
-suture passed around vocal process of arytenoid cartilage and positioned laterally without
removing arytenoid cartilage
-for pts where bilateral VCP may not be permanent
6. Electrical Pacing:
-pacing posterior cricoarytenoid muscle to coincide with inspiration
-long term efficacy and reliability remains to be proven
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DDx Immobile Cord
Infectious Inflammatory/Autoimmune
-syphilis -Wegener’s
-tuberculosis -relapsing polychondritis
-scleroma -rheumatoid arthritis (joint
-fungal infections involvement)
Neoplastic Idiopathic/Infiltrative
-laryngeal carcinoma -idiopathic
-amyloid
Iatrogenic/Trauma -sarcoid
-dislocation of arytenoid
-laryngeal trauma Neurogenic:
-vocal cord paralysis (see DDx for
cord paralysis above)
-central
-peripheral
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BENIGN LESIONS OF THE LARYNX
Congenital Iatrogenic/Traumatic
-? sulcus vocalis -vocal cord nodules
-embryonal cyst -capillary ectasia
-laryngocele -vocal fold hemorrhage
-saccular cyst -vocal fold polyp
-intracordal cyst
Infectious -contact ulcer
-tuberculosis -intubation granuloma
-syphilis -reflux disease
-fungal infections
Idiopathic/Infiltrative:
Neoplastic -sarcoidosis
-laryngeal papillomatosis -amyloidosis
-laryngeal polyps
-granular cell tumour Systemic:
-chondroma -hypothyroidism (myxedema)
-subglottic hemangiomas
-rhabdomyoma Other:
-lipoma -bilateral diffuse polyposis
-benign mixed neoplasm (Reinke’s edema)
-neurofibroma
-neurilemmoma
NODULES
-usually bilateral
-involve anterior or middle third of true VC
-edema in submucosa (Reinke space) organized fibrous tissue (hyalinization)
-tx: voice therapy (at least 6 months) and voice rest
-sx if malignancy suspected
-unilateral or asymmetric nodules usually are intracordal cysts
POLYPS
-pedunculate or sessile lesions involving middle half, anterior half or entire VC
-most common benign lesions of adult larynx
-two types:
-mucoid
-inflammatory process in subepithelial layer of loose connective tissue
-translucent
-angiomatous
-vascular
-dark red, protuberant, multinodular
-women most commonly affected with bilateral vocal fold polyps or polyploid change
-d/t heavy smoking and vocal abuse
-tx: surgical removal
-treatment of GERD important to prevent irritation, inflammatory changes and poor healing
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CYSTS
-most common site is supraglottic larynx
-mucous retention cysts most common
-found in valleculae, BOT, epiglottis or A/E folds
-embryonal cysts:
-congenital; arise in aryepiglottic fold or lateral pharyngeal wall
-tx:
-supraglottic cysts: excised or marsupialized
-intracordal cysts: careful dissection for complete removal while maintaining mucosal flaps
(microflap technique)
GRANULOMA
-usually arise near vocal process or body of arytenoid
-hx of GERD or previous traumatic or prolonged endotracheal intubation
-hoarseness, chronic throat clearing
-airway obstruction: “ball valving”
-tx:
-remove irritation: voice therapy, antireflux management
-surgical treatment:
-CO2 laser excision
-adjunctive steroid injection post-surgical ablation
-post-op:
-voice rest x 1wk
-modified voice use
-systemic broad-spectrum antibiotics for 3-4 weeks
-inhalational steroids not routinely recommended
-botulinum toxin type A injection: prevent forceful closure of arytenoids during phonation and
coughing
LARYNGEAL PAPILLOMATOSIS
-most common benign laryngeal tumour
-more prevalent in children and less common in individuals over 30ya
-transmission of HPV to child occurs in birth canal (1:80-1:500 risk of transmission)
-histo:
-papillary projections and hypervascular fibroconnective
tissue covered by hyperplastic squamous epithelium
-HPV-6 correlated with extent and severity of disease (ie. spread of
papillomas into trachea and lungs)
-most common sites:
-vocal folds and subglottic larynx
-avoid tracheotomy if possible
-malignant degeneration rare; associated with rad tx, tobacco abuse
-tx:
-frequent excisions to avoid tracheotomy
-laser excision:
-power setting of 2-8 W, impact spot sizes of 0.3 to 0.8 mm, intermittent mode of 0.1-0.5
second exposure
-other techniques: microlaryngeal techniques, cryosurgery, microcauterization, microdebridement
-other tried therapies:
-vaccines, chemotherapy, hormonal therapy (unsuccessful)
-interferon and photodynamic therapy
-intralesional injections of cidofovir or indole-3-carbinol
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LYMPHATIC AND VENOUS MALFORMATIONS
-haemangiomas:
-lesions with increased mitotic activity
-rapid postnatal growth slow involution usually by age 7
-treatment may not be necessary
-associated with cutaneous haemangiomas
-other treatment options:
-systemic steroids and tracheotomy if symptomatic stridor
-CO2 laser ablation for smaller, solitary lesions
-may cause scarring and laryngeal stenosis for larger circumferential lesions
-Nd:YAG laser NOT RECOMMENDED for subglottic hemangiomas because these lesions are
not vascular high risk of stricture formation and tracheal perforation
-malformations:
-lesions that are inborn errors of vascular morphogenesis and grown proportionately with the child
-venous malformations rarely involve larynx
-Nd:YAG laser treatment highly effective
CHONDROMA
-rare
-originate from epiglottis, cricoid, arytenoid or thyroid cartilages
-composed mostly of hyaline cartilage
-tx: complete surgical excision
-thyrotomy or lateral pharyngotomy approach
-endoscopic removal only indicated for extremely small tumours
-total laryngectomy reserved for extremely large tumours or recurrent poorly defined growths
NEUROGENIC TUMOURS
-extremely rare
-schwannomas
-benign and slowly growing
-submucosal, smooth, located in aryepiglottic folds and extending into supraglottic space
-most common nerve of origin: internal branch of superior laryngeal nerve
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AMYLOIDOSIS
-uncommon problem
-larynx most common site of localized amyloid deposition in respiratory tract
-supraglottis involved most frequently > glottis > subglottis
-laryngeal amyloid almost always localized and rarely systemic
-histology:
-extracellular, amorphous pink material
-“apple-green birefringence” seen with Congo red stain under polarized light
-EM: linear, nonbranching fibrils in B-pleated sheets
-tx: conservative removal
-steroids and antimetabolites are not helpful
-surgical removal either endoscopic or via laryngofissure
SARCOIDOSIS
-larynx involved in 1-5% of pts with sarcoidosis
-epiglottis most common site aryepiglottic folds > arytenoids > false vocal cords > subglottis
-lab studies:
- LFTs
- ACE levels, cutaneous energy, ESR, eosinophilia, hypercalcemia, hypercalciuria,
hypergammaglobulinemia
-histology:
-small noncaseating granuloma
-tx:
-endoscopic excision of obstructing lesions
-steroids
SURGICAL TECHNIQUE
-Benninger: cold vs laser excision
-no statistical difference in voice quality after surgery with either method
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CONTROVERSIES IN LARYNGOLOGY
CONTROVERSIES IN DIAGNOSIS
Stroboscopy
-stroboscopy allows evaluation of mucosal waves of vocal folds
-not useful in differentiating functional from organic voice disorders
-not useful in evaluating neoplastic lesions that involve anterior commissure, vocal processes, or
posterior larynx
-principle indications:
-differentiate intracordal cysts from vocal nodules
-evaluate for vocal fold fibrosis/scarring (adynamic segments after trauma, surgery, or
inflammatory disease)
-demonstrate recovery of vocal fold function after vocal fold surgery or laryngoplastic
phonosurgery
-determine functional significance of vocal fold vascular lesions
-evaluate thickness of some free edge neoplastic lesions
Laryngeal Electromyography
-provides essential information about neuromuscular status of larynx that no other test can provide
-cricothyroid superior laryngeal nerve
-thyroarytenoid recurrent laryngeal nerve
-parameters evaluated:
-recruitment
-waveform morphology
-presence of spontaneous activity
-indicates ongoing neural degeneration
-helpful in directing site of lesion analysis
-may indicate prognosis in paresis/paralysis
-eg. good prognosis = plentiful, low-amplitude, polyphasic motor units
-eg. poor prognosis = markedly reduced recruitment and large-amplitude motor units
-differentiates paralysis from fixation
Laryngopharyngeal Reflux
-controversy surrounds diagnosis and treatment, and its role in causing or exacerbating laryngeal diseases
-reasons for underdiagnosis:
-most otolaryngology pts with LPR do not have esophagitis or heartburn because they have
upright (daytime) reflux with normal or near-normal esophageal acid clearance
-traditional diagnostic tests for reflux are essentially tests for esophagitis
-ambulatory double-probe pH monitoring gold standard
-therapeutic trials with low-dose PPIs often ineffective for LPR because of short treatment times
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-most common findings of LPR are effacement of the ventricles by swollen false and true vocal cords
(ventricular obliteration) and pseudosulcus vocalis (subglottic edema)
SURGICAL CONTROVERSIES
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Microlaryngeal Surgery
-use of lasers in phonosurgical treatment of benign lesions remains controversial
-some claim thermal damage created by laser impairs surgical result
-some suggest that differences in outcome may be related more to surgical technique and
experience than to instrumentation
Lipoinjection
-use of autologous fat for injection augmentation of vocal fold has become an accepted tool
-areas of concern: optimal technique for graft harvest and injection, relatively poor long-term yield, and
inability to control fat cell graft distribution in injected tissue
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LARYNX - ANATOMY
(Cummings Ch. 97)
Hyoid bone
-derived from mesodermal cells that form cartilaginous masses in the second
and third branchial arches
-lesser horn derived from second branchial arch
-body and greater horn derived from third branchial arch.
-proximal portion of second branchial arch forms stapes of middle ear, styloid
process, and stylohyoid ligament
-In adults, the styloid process, stylohyoid ligament, and lesser horn of the hyoid
bone symbolize the line of the second branchial arch cartilage.
Laryngeal cartilages
Thyroid cartilage
-important landmarks: paired superior and inferior horns, lateral
plates or laminae, and thyroid notch/laryngeal prominence
-important synovial joints: cricothyroid joints
-similar to other synovial joints of the body, are subject
to arthritis
-pts with cricothyroid arthritis frequently complain of
odynophonia
-impaired mobility loss of pitch range and vocal
fatigue
-physical findings: bilateral vocal fold bowing, inability to
lengthen vocal folds with attempts to elevate pitch, and loss
of normal laryngeal crepitance during manual manipulation
of the cricoid and thyroid cartilages.
Cricoid cartilage
-only complete skeletal ring for the airway
-signet ring with a broad arch located posteriorly
-thyroid and cricoid cartilages attached anteriorly in midline by
median cricothyroid ligament
Epiglottic cartilage
-composed primarily of elastic cartilage
-mucosa covering anterior surface: stratified squamous epithelium -
posteriorly, near the inlet of the larynx, the epithelium is
pseudostratified, ciliated, and columnar.
-anterior midportion attaches to tongue by median glossoepiglottic
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fold and the paired lateral glossoepiglottic folds
Arytenoid cartilages
-landmarks: concave articular base, the apex, a muscular process
projecting laterally, and vocal process projecting anteriorly
-corniculate cartilage, usually articulates with the apex of the
arytenoid and is located within the inferomedial part of the
aryepiglottic fold
-posterior commissure, a reference landmark during laryngoscopy
-on the lateral aspect of the corniculate cartilages, within the
aryepiglottic folds, are cuneiform cartilages
-during laryngoscopy, corniculate and cuneiform cartilages appear as
small, paired swellings in the aryepiglottic folds lying on either side
of the posterior commissure
The cricoarytenoid joint (a synovial joint) may also be involved with arthritis.
This process should be considered in adult patients with idiopathic
vocal fold motion impairment and in patients with impaired motion after
prolonged endotracheal intubation.
LARYNGEAL MEMBRANES
Quadrangular membrane
-begins at lateral border of epiglottic cartilage and spans space
between epiglottic and arytenoid cartilages
-superior border of membrane is free and has oblique course from
upper part of epiglottis to corniculate cartilage
-inferior border of the quadrangular membrane extends from
inferior point of attachment of the epiglottic cartilage on the
thyroid cartilage to vocal process of the arytenoid cartilage
-anterior and posterior borders are fixed; superior and inferior
borders are free
-upper free border aryepiglottic fold
-lower free border vestibular folds
Triangular membrane
-in lateral profile, has a narrow base, the midline,
attaching to the thyroid and cricoid cartilages,
projecting to an apex, which is the vocal process of
the arytenoid cartilage
-superior border begins at the thyroid cartilage,
extending posteriorly as a concave line to the vocal
process forms vocal ligament
-inferior border attached to the cricoid cartilage
Laryngeal mucosa
-essentially all of mucosa from trachea to aryepiglottic fold composed of a pseudostratified, ciliated,
columnar epithelium, except for covering of true vocal folds, which is stratified squamous epithelium
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-tubuloalveolar glands are abundant, particularly in region of ventricle
lubrication for vocal folds
-at aryepiglottic fold, mucosa becomes stratified squamous epithelium
and covers lateral surface of quadrangular membrane
-pear-shaped mucosal recess: piriform recess
Laryngocele
-laryngocele is a herniation of ventricular mucosa
-expands upward in the pathway of least resistance
-inferiorly, triangular membrane (conus elasticus) blocks the
way
LARYNGEAL MUSCULATURE
Intrinsic musculature
-associated with the quadrangular membrane:
-thyroarytenoid
-thyroepiglottic
-aryepiglottic muscles
-acting on arytenoid cartilage:
-posterior cricoarytenoid
-lateral cricoarytenoid
-arytenoid muscles
-vocalis muscle: longitudinally arranged group of muscle
fibers paralleling the vocal fold
Respiration
-during maximal inspiration, larynx is drawn downward by
the effect of sternothyroid and sternohyoid muscles and by
traction on the trachea. True and false vocal folds flatten
(unfold) against the lateral wall of the larynx to maximally
open the airway
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-cricothyroid contraction, by itself, results in elongation of the vocal fold and slight adduction
Phonation
-myoelastic-aerodynamic theory (Voice cycle):
-requires that a mass of subglottic air be compressed by thoracic respiratory muscles while the
vocal folds are adducted and tensed
-at the moment glottic resistance is overcome by the pressure of the compressed air column, the
folds open, allowing air to flow through the glottis and reduce subglottic pressure
-elastic recoil of the vocal folds reestablishes glottic resistance, and, as long as subglottic pressure
is maintained, a cyclic movement or horizontal oscillation of the vocal folds will continue
-frequency of vocal cord vibration and hence frequency of phonated tone are related
mathematically to subglottic air pressure, airflow, and glottic resistance
-neuromuscular theory:
-muscles vocal folds by adjusting their length, tension, and mass, thus regulating the glottic
resistance.
-increased glottic pressure and increased glottal resistance result in an increased fundamental frequency;
decreased cricothyroid muscle activity is probably a response to regulate the fundamental frequency
Effort closure
-important to increase intrathoracic and intraabdominal pressure
-recurrent laryngeal nerve axons arise from motoneuron cell bodies in the nucleus ambiguus
-axonal processes from the nucleus ambiguus contribute to the vagus nerve and the cranial portion of CN XI
-two laryngeal branches are given off:
-superior laryngeal nerve:
-external laryngeal nerve
-to cricothyroid muscle and to inferior constrictor muscle of the pharynx
-recurrent laryngeal nerve:
-enters the larynx at the cricoid cartilage between the muscle fibers of cricopharyngeus muscle
and the esophagus
-muscles innervated unilaterally from their respective vagus, with the exception of the
interarytenoid muscle, which is innervated from both vagi
-sensation of larynx:
-internal laryngeal nerve:
-laryngeal mucosa at level of false vocal cord and piriform sinus
-recurrent laryngeal nerve:
-mucosa of the true vocal fold, subglottic mucosa, and adjacent esophageal mucosa
AUTONOMIC INNERVATION
-larynx receives autonomic innervation—adrenergic and cholinergic—from superior cervical ganglia and
vagus nerve, respectively.
BLOOD SUPPLY
-superior laryngeal artery
-branch of the superior thyroid artery, derived from the external carotid artery
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-distribution of the vessel includes the piriform sinus and the medial surface of the quadrangular
membrane as far inferiorly as the false vocal fold.
-inferior laryngeal artery
-derived from the inferior thyroid artery, which originates from the thyrocervical trunk of the
subclavian artery
-enters the larynx, along with the recurrent laryngeal nerve, at the junction of the cricopharyngeal
and esophageal muscle fibers
-supplies the muscles attaching to the arytenoid cartilages and the laryngeal mucosa adjacent to
the false vocal fold and laryngeal ventricle
VENOUS DRAINAGE
-follows the same pattern as arterial supply
-superior laryngeal vein parallels the course of the superior laryngeal artery and eventually empties into the
internal jugular vein
-inferior laryngeal vein is a tributary of the thyrocervical trunk of the subclavian vein
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CHAPTER 98: LARYNGEAL AND PHARYNGEAL FUNCTION PART SIX:
ELECTROMYOGRAPHY OF LARYNGEAL AND PHARYNGEAL MUSCLES
-an electrical potential can be picked up and displayed or recorded as EMG signals if a pair of electrodes
are placed in the muscle tissue.
-cricothyroid:
-needle insertion: level of lower edge of cricoid cartilage and 5 mm lateral to midline
-needle directed toward inferior tuberculum of thyroid cartilage
-verification : subject raises pitch of his or her voice
-cricothyroid shows marked activity for a quick rise in voice
pitch
-thyroarytenoid:
-subject in a supine position and attempting sustained
phonation
-skin is pierced at midline at the level of cricothyroid space
-needle is advanced to pass through cricothyroid membrane,
and tip is directed submucosally laterally and upward to
reach muscle
-verification: subject asked to sustain low-frequency
phonation
-thyroarytenoid also shows marked activity during
swallowing and glottal attack
-lateral cricoarytenoid:
-point of insertion is almost same as for cricothyroid
-needle is then inserted laterally and slightly upward,
penetrating cricothyroid membrane at a point anterior to
inferior tuberculum of thyroid cartilage and deeply enough to reach lateral cricoarytenoid
-verification: patient hold his or her breath or attempt glottal stop production
Pharyngeal muscles
-perioral approach is always attempted with subject in a sitting or a supine position
-levator palatini:
-insertion is made into levator ‘‘dimple’’ on soft palate, approximately 1 cm from midline and 1
cm from posterior edge of hard palate
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-palatoglossus and palatopharyngeus:
-inserting an angulated needle into anterior and posterior pillars
-in general:
-complete relaxation of healthy muscles gives no EMG activity
-NMU activity is recorded as action potentials when muscles contract
-strength of contraction of abductor laryngeal muscle (posterior cricoarytenoid) increases during deep
inspiration, whereas that of adductors increases during phonation, coughing, and swallowing
-pharyngeal muscle activity also increases during swallowing
-EMG is now widely accepted as a routine procedure for examination of facial, pharyngeal, and laryngeal
paralysis
-useful in differentiating laryngeal paralysis from mechanical fixation of CAJ and in estimating degree and
prognosis of paralysis
-usually two innervation territories (i.e., thyroarytenoid innervated by recurrent laryngeal nerve and
cricothyroid innervated by superior laryngeal nerve) are examined bilaterally
Normal laryngeal EMG pattern of TA during phonation and A. Incomplete paralysis. B. Complete paralysis.
deglutition
-in B: type of discharge is termed a fibrillation potential; prognosis for paralysis is usually poor
-synkinesis:
-misdirected regeneration of nerves to abductor and adductor muscle groups
-volitional EMG activity is recorded months to years after onset of paralysis without any sign of a
recovery of vocal cord mobility
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LARYNGEAL AND PHARYNGEAL FUNCTION
PART ONE: BREATHING AND SPEECH
(Cummings - Chapter 98)
LARYNGEAL MOTION
-vocal folds move in three dimensions, and length and shape may be actively altered
Protection
-laryngeal closure reflex is sensitive in infants and may be elicited by a stimulus as weak as water
-reflex increases, then decreases, along a time course similar to that of the incidence of SIDS,
suggesting that laryngeal reflexes may play a role in its cause
Cough
-plays important role in cleaning the tracheobronchial tree and in maintaining patency of the lower
airways
-abnormal cough may be a serious clinical problem
Control of Ventilation
-larynx regulates airflow
Sensory receptors
-larynx location of variety of sensory receptors
-exert influences on breathing and cardiovascular function
-three major types of laryngeal respiratory receptors: negative pressure, airflow, and ‘‘drive”
Circulatory reflexes
-stimulation of larynx affects heart rate and blood pressure
-bradycardia and hypertension
-afferent limb: superior laryngeal nerve
FUNCTION IN SPEECH
-three fundamental components in the processes: phonation, resonance, and articulation
-phonation: generation of sound by vibration of the vocal folds
-resonance: induction of vibration in the rest of the vocal tract to modulate laryngeal output
-articulation: shaping of voice into words
Phonation
-requirements for phonation:
-adequate breath support
-approximation of vocal folds
-favorable vibratory properties
-favorable vocal fold shape
-control of length and tension
-voice cycle:
-exhalation causes subglottic pressure to increase until the vocal folds are displaced
laterally
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-produces sudden decrease in subglottic pressure
-forces that contribute to return of vocal folds to midline:
-pressure decrease
-elastic forces in the vocal fold
-Bernoulli effect of airflow
-vocal folds return to midline, pressure in trachea builds again, and cycle is repeated
Expiratory force
-breath support available for phonation becomes a clinical issue in two situations:
-functional dysphonia:
-insufficient prephonatory inspiration excessive glottic pressure required to
produce acceptable volume
-may lead to stress-induced injury of the vocal folds
-patient has an organic voice disorder and impaired pulmonary function limits capacity to
compensate for glottic defect
-eg. pt with laryngeal paralysis more symptomatic with coexisting emphysema
Pitch control
-changes in vocal fold length and tension are used to control the fundamental frequency of vocal
fold vibration to produce dynamic inflections of the voice
-size and physical properties of a larynx determine the range of pitch that may be produced
-age-related loss of elasticity and increasing ossification of the thyroid lamina result in an
elevation of pitch
Resonance
-phonated sound acquires the characteristics of a human voice because of resonance of chest,
upper airway, and skull
VOICE ANALYSIS
Self-assessment
-patients subjective assessment of their own voice
Perceptual Analysis
-perceptual analysis is an important component of voice evaluation because it is the only approach that
really addresses how the voice sounds to other humans
-a systematic perceptual assessment involves ranking voice according to a standard scale
-voice may be described in terms of pitch, loudness, and vocal quality
-most commonly used scales employ ordinal severity rankings of equal-appearing intervals, usually with
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scores of one to seven in a few judgment categories, such as breathiness or roughness
-GRABAS Scale, widely used
-G: Overall grade
-R: Roughness
-B: Breathiness
-A: Asthenic quality
-S: Strain
Rating system: 0 Normal; 1 Mild abnormality; 2 Moderate dysfunction; 3 Severe impairment
Performance Assessment
-graphic plot of the pitch and loudness ranges is termed the phonetogram = voice profile
-one limitation of the phonetogram is that it only measures pitch and loudness, and it is not sensitive to
changes in quality
-Phonation Quotient:
-MPT/vital capacity
-useful in sorting out contributions of pulmonary function and glottic competence when
equipment for aerodynamic testing is not available
Acoustic Analysis
-acoustic algorithms analyze the complex sound waves of the voice in the domains of frequency, intensity,
and time
-spectrographic analysis may be used to identify presence of noise or loss of harmonic components in a
sound and clearly documents voice or pitch breaks
-fundamental frequency:
-slowest component frequency in voice
-indicates the rate of glottal opening and closing
-one cycle of fundamental frequency corresponds to one glottal cycle
-males: ~128 Hz; females: ~256 Hz
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-harmonics to noise ratio: correlates with perception of voice roughness
-harmonics = frequencies that are integer multiples of fundamental frequency
-noise = frequencies that are not integer multiples of f0
-shimmer and jitter are referred to as perturbation measures; reflect instability of vocal fold
vibration
-shimmer = average cycle-to-cycle change in
amplitude (loudness)
-expressed as a percentage of the mean
amplitude
-normal = 0.50 dB
-jitter = average cycle-to-cycle difference
in duration of the cycle
(fundamental period)
-expressed in milliseconds or as a
percentage of cycle length
-normal = 0.40%
-perceptual correlate of increased levels of jitter and
shimmer is harshness
AERODYNAMIC ANALYSIS
-measurement of phonatory airflow, pressure, and volume provides information about respiratory support
and laryngeal valving
Subglottic pressure
-degree of expiratory effort and tightness of glottic closure determine subglottic pressure
-subglottic pressure correlates with loudness
-techniques to measure subglottic pressure:
-include direct measurement by tracheal puncture or by suspending a miniaturized solid state
pressure transducer with its connections passing through the glottis
-esophageal pressure may be monitored as an indicator of intrathoracic pressure by using an
esophageal balloon, a fluid-filled catheter, or solid state transducer
-indirect estimation:
-intraoral pressure is monitored during repetition of the syllable /pi/ at a rate of about 1.5
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syllables per second
-when the lips are sealed and the glottis opens for production of a plosive consonant (P),
the pressure in the mouth should be same as in the subglottis, which should be the same
as that sustained during the phonation of /i/
Laryngeal resistance
-ratio of subglottic pressure to mean phonatory airflow rate
-a calculated value; only as reliable as the values measured or estimated for flow and pressure
-reflects degree of glottic closure, force of adduction, and vocal fold stiffness
-increased in patients with disorders manifesting as tight glottal closure, such as in those with spasmodic
dysphonia, plica dysphonia ventricularis, or hyperfunctional dysphonia
-low when glottal closure is inadequate, as in patients with abductor spasmodic dysphonia, hysterical
aphonia, or vocal fold tissue deficits
-vocal efficiency
-calculated by dividing sound pressure level of voice by simultaneously determined laryngeal
resistance
-reflects the amount of effort involved in phonation.
-phonation threshold pressure
-minimum subglottic pressure that can support phonation
-videostroboscopy provides a slow motion image of vibration, but this is an average of motion over many
cycles and not a true account of motion
-glottographic techniques, including photoglottography (PGG) and electroglottography (EGG), offer
simpler alternatives
Electroglottography
-electroglottograph, also known as laryngograph, tracks changes in vocal fold contact during phonation by
measuring electrical impedance across larynx
-low-voltage, high-frequency (approximately 1 MHz) sinusoidal current is passed between two electrodes,
one over each side of the thyroid cartilage
-output is filtered to produce the ‘‘LX’’ waveform, which reflects the impedance between the two
electrodes
-current passes most easily (i.e., with lowest impedance) during the period in which there is greatest
surface area of contact between two vocal folds
-only provides information about closed phase of glottic cycle
-one useful application of EGG is to derive f0
-for this same reason, Lx is a useful signal for driving the stroboscope
Photoglottography
-makes use of light transmitted across the glottis to track vocal fold motion during phonation
-light usually is introduced above glottis via a fiberoptic scope or a flashlight in the mouth, with the
photosensor placed on the skin of neck over the upper trachea
-glottis behaves as a shutter, as the amount of light transmitted is proportional to the area of glottic
opening.
-PGG only provides information about the open phase of the glottic cycle and therefore is complimentary
to EGG
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-EGG and PGG permit calculation of:
-speed quotient = (opening time divided by the closing time)
-stiff vocal folds result in a low speed quotient because glottis opens slowly and snaps
shut quickly
-flaccid vocal folds result in a higher speed quotient because the vocal folds open easily
and quickly but drift back to midline more slowly
-open quotient = duration of opening time divided by glottal cycle
-shift quotient = time of peak opening over glottal cycle
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NEUROLOGIC EVALUATION OF THE LARYNX AND PHARYNX
(Cummings)
-Brainstem lesions
-Flaccid paralysis
-Never isolated
Myasthenia Gravis
-defect of the neuromuscular junction
-easy fatigue with muscle use
-symptoms:
-involvement of ocular muscles most common: ptosis, diplopia
-general fatigue
-difficulty speaking, breathing, or swallowing
-bulbar muscle weakness
-weakness of palatal muscles nasal twang to the voice and nasal regurgitation
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-signs:
-fatigue of larynx and pharynx as a result of repetitive movements
-tests:
-EMG
-edrophonium (Tensilon) test
-treatment:
-ACh-esterase inhibitors
-thymectomy
-corticosteroids
-azathioprine, cyclophosphamide, cyclosporine
-plasma exchange: for acute worsening symptoms
-IV Ig
-voice symptoms:
-monotonous and raspy voice with abnormal hypernasal resonance
-speech is dysarthric and labored
-dysarthria is related to tongue involvement -d/t weakness and slowed tongue
-velopharyngeal incompetence
-signs:
-visible fasciculation in tongue “bag of worms”
-weakness in palate, pharynx, and larynx
-inability to make rapid muscle adjustments or repetitive motions
-pooling of secretions in the hypopharynx
-ALS vs MG: extraocular motion is preserved in ALS
-treatment:
-supportive care
-palatal-lift prosthesis may improve speech intelligibility and decrease nasal regurgitation during
speech
-NG or PEG to prevent aspiration
-tracheostomy for airway protection and assisted ventilation
Multiple Sclerosis
-diffuse demyelination process
-signs and symptoms consist of relapsing and remitting sensory and motor deficits
-visual problems, numbness, and limb weakness are common
-ENT problems include vertigo, tremor, scanning speech, and dysphagia
Bulbar Poliomyelitis
-postpolio syndrome
-syndrome may be derived from natural loss of motor neurons during the aging process
-acute bulbar polio causes pharyngeal and laryngeal paresis, but spares the cricopharyngeus
-leads to hoarseness, dysphagia, and aspiration
-cricopharyngeal myotomy often is helpful in patients with recent onset of polio
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Palatal myoclonus
-uncommon disorder consisting of rhythmic contractions of the soft palate, pharynx, and larynx at a rate of
one to two contractions per second
-symptoms:
-unstable voice
-resulting speech sounds similar to that of spasmodic dysphonia
-caused by a specific lesion - infarction of central tegmental tract (CTT = pathway from the midbrain to the
inferior olive complex)
Parkinsonism
-hypokinetic dysarthria
-extrapyramidal syndrome caused by cell death in the substantia nigra
-symptoms: resting tremor, muscle rigidity, bradykinesia, and loss of postural reflexes, flat facial
expressions and abnormal posture
-speech:
-generalized bradykinesia sluggish articulation and monotone voice with decreased loudness
-vocal folds are adynamic and bowed
-tremor may affect voice
-less often, a predominant effect of rigidity on the larynx strained voice with frequent breaks
similar to voice of spasmodic dysphonia
Pseudobulbar Palsy
-spastic dysarthria
-bilateral lesions of corticobulbar tracts
-muscle spasticity and hyperreflexia of the pharynx, palate, lips, tongue, and larynx
-voice:
-harsh, strained, and strangled, and sounds somewhat like spasmodic dysphonia
-hypernasality and slow, labored articulation and emotional lability and subcortical cognitive
impairments
Essential Tremor
-common neurologic disorder affecting those in middle to late adulthood that causes 6 to 8 Hz shaking of
the hands, head titubation, and tremulous voice
-vocal symptoms related to tremor of muscles in the larynx, pharynx, and soft palate and, sometimes, in the
cervical strap muscles
-often responds to a local injection of botulinum toxin
Dystonia
-uncontrolled contractions of any voluntary muscle or group of muscles and results in a torsional posture or
repetitive movements
-Spasmodic dysphonia appears to be an idiopathic focal dystonia of the larynx
-Meige’s syndrome is a regional dystonia of the head and neck
-may be evident in those with blepharospasm, oromandibular dystonia, torticollis, or spasmodic
dysphonia
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-Laryngeal dystonia
-adductor dysphonia
-more common than abductor spasmodic dysphonia
-focal laryngeal dystonia, causes vocal fold hyper-adduction
-can be exacerbated by stress
-SSx:
-spasmodic closure of the vocal folds during speech strained and strangled
voice
-glottic stammering (phonation breaks)
-may be associated with other dystonia, tremors or difficulty in breathing
-tx:
-voice therapy
-botulinum toxin injections of thyroarytenoid and lateral cricoarytenoid muscles
-effective for an average of 3 months
-abductor dysphonia
-focal laryngeal dystonia(in fewer pts) intermittent or sustained opening of the larynx
during speech breathy voice breaks or a whispering voice
-tx:
-voice therapy
-botulinum toxin injections of posterior cricoarytenoid muscles
-Botox injections decrease the symptoms of patients with dystonia, particularly for patients with adductor
spasmodic
Oral cavity
-Observe lips, palate, and tongue for abnormal spontaneous movement
-spasmodic motions are characteristic of Meige’s syndrome
-involuntary, slow, athetoid movements of the tongue tardive dyskinesia
-quivering, ‘‘bag of worms’’ characteristic sign of ALS
-test palatal movements and strength of tongue
-rapid repetition of the syllable “Pa” shows lip function, “Ta” shows tongue function
-LMN lesion decreases strength of this action
-UMN lesion decreases rate at which the patient can repeat the syllable, but regular rhythm
should be preserved
-cerebellar rhythm is erratic
-MG results in fatigue with repetitive motion
Flexible laryngoscopy
-Soft palate
-observed for any tremor or spasmodic movement at rest
-assess symmetry and competence of velopharyngeal closure
-Larynx
-repetitive phonations fatigue in patients with MG
-to assess the cricothyroid muscle (SLN), perform a pitch glide, phonating from a low pitch to a
high pitch and back down pitch should rise as the vocal folds become longer and thinner
-assess for hyperfunctional dysphonia:
-compression of the glottis in the anterior-posterior dimension
-contraction of aryepiglottic folds
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-false vocal-fold adduction, which may be severe enough to totally obscure true vocal
folds
-pt elevate larynx and speak with a low lung volume
-amenable to voice therapy
-Stroboscopy:
-slowed motion allows the most accurate assessment of the mucosal wave, which may be impaired
by scarring, edema, or subtle defects in the mucosa
-subtle edema, vocal cord cysts, or early carcinoma adynamic segment of the vocal cord on
stroboscope.
-allows accurate evaluation of closing and opening pattern of the larynx
-vocalis muscle atrophy
-posterior laryngeal edema
-faulty vocal technique
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PHONOSURGICAL PROCEDURES
(Cumming’s)
Percutaneous injection
-through thyroid ala at level of vocal fold determined by
palpating thyroid notch and inferior border of thyroid ala
anteriorly
-an anterior approach may be used through cricothyroid
membrane, approaching the vocal folds from below
-needle angled superiorly and laterally under
direct visualization using a flexible fiberoptic
nasopharyngoscope.
Transoral injection
-indirect laryngoscopy
-injection performed using a curved laryngeal needle
Laryngoscopic injection
-usually under G/A
-arytenoid cartilages palpated to ensure mobility
-laryngeal needle inserted lateral to vocal fold 2 mm deep at the level of vocal process
-Polytef paste or absorbable gelatin sponge is injected at single click intervals
-complications:
-underinjection, requiring repeat procedures
-overinjection with airway compromise
-improper placement of polytef, causing subglottic extension and potential stenosis
-migration of polytef
-intrachordal injection of polytef, impairing vibratory capability
-granuloma formation
-management of overinjection: -incising the mucosa over the site of injection and removing
excess material by suction
-polytef granulomas also require surgical excision
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Medialization thyroplasty
-indications:
-management of vocal fold paralysis
-vocal fold bowing resulting from aging or cricothyroid joint fixation
-sulcus vocalis
-soft-tissue defects resulting from excision of pathologic tissue
Technique
-performed through window
in thyroid lamina at level of
vocal fold
-inner perichondrium remains
intact
-silactic or hydroxylapatite
implants used
-overmedialization is
supported by Isshiki and
others deterioration in
voice quality over time as
intraoperative edema resolved
in postoperative period
-complications:
-penetration of endolaryngeal
mucosa
-wound infection
-chondritis
-implant migration or
extrusion
-airway obstruction
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Arytenoid adduction
Technique
-same incision used for medialization thyroplasty is extended just beyond posterior aspect of
thyroid lamina
-pharyngeal constrictor muscle is incised at its attachment to the thyroid lamina, exposing the
posterior margin
-cricothyroid joint disarticulated to allow exposure and elevation of piriform sinus mucosa
-penetration of endolaryngeal mucosa requires termination of procedure
-muscular process of arytenoid is identified by palpation beginning at the cricothyroid joint and
moving obliquely up the cricoid cartilage
-cricoarytenoid joint is opened by incising posterior cricoarytenoid muscle posterior to the
muscular process, allowing identification of the articulating surface
-adduction performed by tying two 4-0 nylon sutures around the muscular process and passing the
ends out through the thyroid lamina in directions that simulate the pull of the thyroarytenoid and
lateral cricoarytenoid muscles
-each suture is then tied over the thyroid lamina
Reinnervation procedures
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BILATERAL VOCAL FOLD MOTION IMPAIRMENT
-procedures:
-endoscopic arytenoidectomy
-lateralization of the vocal cord by suture placement
-laser arytenoidectomy:
-only good for removing anterior 2/3 of vocal cord; posterior 1/3 represented by
arytenoid more difficult to remove successfully laser
-partial arytenoidectomy predisposes pt to a greater incidence of postoperative chondritis
-laser cordotomy:
-transverse incision is made with laser through vocal fold immediately anterior to vocal
process wedge-shaped widening of posterior glottis
-external arytenoidectomy
Management of bilateral vocal fold motion impairment with weak voice and aspiration
-bilateral adductor paralysis is an unusual condition characterized by weak voice and aspiration
-methods effective with unilateral adductor paralysis, specifically injection of polytef paste, surgical
medialization, or arytenoid adduction, are not effective in this setting
-narrow-field laryngectomy most effective method for prevention of aspiration; however, it results in
elimination of the larynx as an organ of communication
-Other surgical approaches:
-epiglottic sew-down procedure
-surgical approximation of vocal folds
-tracheal diversion procedures
Lower pitch
-Type III thyroplasty
-for mutational falsetto and gender transformation
may be considered only after 3 to 6 months of voice
therapy and, when indicated, psychologic evaluation
and therapy
-dysphonia resulting from increased vocal fold
stiffness associated with laryngeal trauma,
radiotherapy, chronic laryngitis, sulcus vocalis, and
vocal fold atrophy Type III thyroplasty: A, Location of cartilaginous incisions. B,
-pts present with high vocal pitch associated with a Cartilaginous strips are removed. C, Relaxation of the vocal
narrow glottal chink and small amplitude mucosal folds decreases tension and the size of the glottic aperture.
wave
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Elevated pitch
-lengthening the vocal folds elevating vocal pitch
-achieved by advancing anterior commissure or by cricothyroid approximation
-indications:
-vocal fold bowing resulting from aging or trauma
-postsurgical defects
-androphonia
-gender transformation
-other methods:
-decrease vocal fold mass increasing frequency of vibratory cycle
-by removing tissue with laser or by mechanically inactivating the vocalis muscl
-vocal fold stripping
-laser vaporization
-steroid injection
Lengthening procedures
-Cricothyroid approximation
-simulates contraction of the cricothyroid muscle
-nonabsorbable mattress sutures placed, first
through cricoid cartilage and then through
thyroid cartilage
-simplest and safest lengthening procedure
-disadvantages include greater risk of reversion to lower pitch and potential narrowing of pitch range
Sulcus vocalis
-congenital soft-tissue deficit or linear furrow running longitudinally along the free edge of true vocal fold
-furrow may vary in length and depth extreme cases the sulcus divides medial edge into an upper and
lower lip double vocal fold appears
-cause unknown
-symptoms related to incomplete glottal closure:
-decrease in phonation time
-breathy high-pitched turbulent airflow
-speech therapy not been successful in managing symptomatic patients, and surgery has been directed
toward correcting the incomplete glottal closure
-management:
-intrachordal injection with cartilage paste or paraffin or collagen
-lengthening and shortening procedures
-medialization thyroplasty has been used successfully in managing patients with sulcus vocalis
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BENIGN VOCAL FOLD MUCOSAL DISORDERS
(Cummings)
-“body-cover” concept:
-cover:
-epithelium and superficial layer of lamina propria
-transitional zone:
-intermediate and deep layer of lamina propria = superior free edge of conus elasticus = vocal
ligament
-vocal fold muscle = body
EVALUATION OF PATIENT
History
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GENERAL MANAGEMENT OPTIONS
-hydration
-sinonasal management
-when optimal laryngeal function is of concern, as in a vocal performer, nasal conditions should
be managed locally (topically) when possible
-management GERD
-avoiding caffeine, alcohol, and spicy foods
-eating the last meal of the day (preferably a light one) no fewer than 3 hours before retiring
-using bedblocks to place the bed on a mild head-to-foot slant
-taking at bedtime an antacid or H2 blocker, or proton pump inhibitor 1 hour before dinner
-systemic medicines that may affect the larynx
-e.g., antidepressants, decongestants, antihypertensives, diuretics may dry and thicken normal
secretions mucosa more vulnerable to the development of benign disorders
Vocal nodules
-term reserved for lesions of proven chronicity
-occur most commonly in boys and women: ‘‘vocal overdoers’’
-pathophysiology:
-only anterior 2/3 of vocal folds participates in
vibration
-localized vascular congestion with edema at the
midportion of the membranous (vibratory) portion of
the vocal folds, where shearing and collisional forces
are greatest submucosal swelling
-long-term voice abuse hyalinization of Reinke’s
potential space and possibly some thickening of the
overlying epithelium
-laryngeal examination:
-nodules can vary in size, contour, symmetry, and color
-do not occur unilaterally
-management:
-medical: -good laryngeal lubrication through general hydration, managing contributions
of allergy and reflux
-behavioural: -voice therapy should play a primary role initially
-surgical: -option when nodules persist and voice remains unacceptably impaired (from
the patient’s perspective) after an adequate trial of therapy (generally a
minimum of 6 months, usually much longer)
Capillary ectasia
-occurs most often with vocal overdoers
-dilated capillaries more frequent in women speculation of estrogen effect
-pathophysiology:
-repeated vibratory microtrauma may lead to capillary angiogenesis
-capillary ectasia predisposes to mucosal swelling, a small incidence of vocal fold hemorrhage,
and hemorrhagic polyp formation
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-diagnosis:
-most often in female singers who complain that they
become a little hoarse after relatively short periods of
singing (reduced vocal endurance)
-laryngeal examination:
-abnormal dilation of the long arcades of capillaries that
proceed mostly anterior to posterior
-capillary lake: confluent dilated capillaries that almost
resemble a chronic haemorrhage
-management:
-medical: -stop anticoagulant drugs; treat acid reflux
-behavioural: -usual behavioral changes, which are also appropriate for persons with nodules,
are advocated
-no sudden, explosive use of voice
-surgical: -spot-coagulation to interrupt blood flow every few millimetres
-pathophysiology :
-shearing forces acting on capillaries within the
mucosa during extreme vocal exertion lead to
capillary rupture
-diagnosis:
-abrupt onset of hoarseness during extreme vocal
effort
-laryngeal examination:
-largely unilateral lesion process in the node position, a contact reaction on the fold opposite the
polyp, or a nodule if the person is a longstanding overdoer
-treatment:
-medical: -stop anticoagulant medications
-behavioural: -short course of voice therapy is appropriate, mainly to instruct the patient in
voice care
-small, early hemorrhagic polyp will resorb completely with many months of
conservative measures
-surgical: -evacuation of blood through a tiny incision in a recent large haemorrhage
-long-standing polyp trimmed away superficially
Intracordal cysts
-history of vocal overuse
-histological classification:
-epidermoid inclusion cyst (EIC)
-contain accumulated keratin
-rupture of cyst leaving opening as large as cyst glottic sulcus
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-mucus retention cyst (MRC)
-arise when duct of a mucus gland becomes plugged and retains glandular secretions;
epidermoid cysts
-diagnosis:
-history of voice abuse factors
-MRC often cause less vocal limitation than anticipated
from laryngeal appearance; EIC often cause more
limitation than expected
-laryngeal examination:
-MRC mucus retention cysts often originate just below
the free margin of the fold with significant medial
projection from the fold
-EIC project less from the fold and are harder to
diagnose when small
-treatment:
-medical: -hydration, potential acid reflux management may be helpful
-behavioural: -postoperative voice therapy may facilitate healing
-not successful for treatment, requires surgical removal
-surgical: -careful dissection around the cyst free of the mucosa and vocal ligament
-postoperative recovery takes longer than for nodule or polyp surgery (many
months rather than a few weeks)
Glottic sulcus
-occurs exclusively in the vocal overdoer
-pathophysiology:
-“congenital” vs “acquired”
-an epithelium-lined pocket whose lips
parallel the free edge of folds may
represent an epidermoid cyst that has
spontaneously emptied, leaving the
collapsed pocket behind to form a sulcus
-mucosal bridge: result of two parallel
sulci arising from a single cyst
-diagnosis:
-voice overuse and complaints of chronic
hoarseness
-laryngeal examination:
-stroboscopic evaluation reveals a segment of reduced vibration
-microlaryngoscopy required for definitive diagnosis because the lips of the sulcus are only
occasionally faintly visible with inspiratory phonation during the office or voice laboratory
examination
-management:
-surgical: -removal is technically demanding; involves considerable disturbance of the
vocal fold mucosa
-cordal injection to make the sulcus lips spread and the sulcus more shallow and
491
to accomplish some hydrodissection
-circumcision of lips of sulcus and dissection of the invaginated mucosal pocket
from underlying fold without injuring the vocal ligament
-pathophysiology:
-chronic smoking and voice abuse edema, vascular congestion, and venous stasis diffuse
polypoid changes
-diagnosis:
-voice examination reveals lower pitch than would be
expected, often well into the masculine range for
women
-upper voice is lost
-laryngeal examination:
-pale, watery bags of fluid attached to the superior
surface and margins of the folds
-management:
-medical: -stop smoking
-thyroid function tests if hypothyroidism is suspected
-behavioural: -short-term voice therapy: may reduce the polyps’ turgidity, with a
corresponding modest improvement in vocal functioning.
-surgical: -polyp reduction with mucosal sparing
Postsurgical dysphonia
-vocal fold stripping or laser vaporization of mucosa that removed underlying fibrous tissue or even muscle
-pathophysiology:
-results from scarred stiff vocal fold cover, phonatory mismatch of the vocal fold margins, or both
-laryngeal examination:
-videostroboscopy is essential
-allows careful analysis of mass lesions, areas of asymmetry, and the mucosa’s vibratory pattern
-management:
-behavioural: -voice therapy voice building approach
-using voice will soften scar tissue
-goals are to strengthen the laryngeal musculature to compensate for the
damaged mucosa and to encourage the mucosa to oscillate more freely because
of this sort of ‘‘phonatory massage’’of the mucosa
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-pathophysiology:
-thin mucosa and perichondrium overlying the cartilaginous
glottis become inflamed
-acid reflux may also increase inflammation of the vocal
process area.
-traumatized area ulcerates or produces a heaped-up
granuloma
-laryngeal examination:
-depressed, ulcerated area with a whitish exudate clinging to it
or a bilobed, heaped-up lesion on the vocal process may be
noted
-management:
-empiric antireflux regimen
-maturation and resolution may occur spontaneously over 3 to 6 months
-surgery as last resort because postoperative recurrence of ulcer or granuloma is predictable
-microlaryngoscopy if after a several-month trial of management an uninflamed, pedunculated
lesion remains and is causing symptoms
-removal should be limited, leaving the base or pedicle undisturbed
Intubation granuloma
-pathophysiology:
-direct abrasion of the arytenoid perichondrium, a break in the mucosa covering it as a result of
coughing on ETT, or long-term pressure necrosis of the vocal process area
-laryngeal examination:
-often large and spherical with some pedunculation
-attached directly to vocal process and are frequently bilateral
-may be partial or complete fixation of one or both arytenoid cartilages
-interarytenoid synechium also may be noted on occasion
-management:
-with time intubation granulomas usually mature and ‘‘fall off’’
-persistent granuloma:
-surgery or a trial of indirect corticosteroid injection in the office may be an option
-any identifiable stalk should be left with patient to minimize size of the surgical wound
Epithelial tumours
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-types:
-juvenile form:
-papillomatosis usually presents in infancy or childhood as
hoarseness and stridor
-often aggressive and rapidly recurrent, requiring frequent
laryngoscopies for management
-tracheal and brochial involvement increased with history of
tracheotomy, a high number of endoscopic procedures, and a
long duration of the disease
-adult-onset:
-occasionally solitary or at least more localized than juvenile-onset ones
-less aggressive
-treatment:
-carbon dioxide laser remains the most widely accepted management for papillomas in the larynx
-laser preferred because of precision and hemostatic properties
-other possible treatments:
-interferon: papillomas tended to regrow on cessation of interferon
-indole-3-carbinol, a natural derivative of cruciferous vegetables such as cabbage and
broccoli
-methotrexate
-cis-reninoic acid
-intralesional (S)-1-(3-hydroxy-2-phosphonylmethoxypropyl) cytosine as potential
management for many deoxyribonucleic acid (DNA) viruses, including human
papillomavirus
-some medical management modalities hold promise; all need further investigation and validation
-optimal management is careful serial laser laryngoscopies with consideration of investigational
use of interferon, indole-3-carbinol, or hydroxy phosphonyl methoxypropyl cytosine for patients
with a particularly severe form of this disease
Vascular neoplasms
Laryngeal hemangiomas
-often have associated with cutaneous haemangiomas
-mucosa-covered mass with or without bluish coloration may be seen in the subglottis
-management:
-tracheotomy for airway protection
-gives hemangioma an opportunity to involute spontaneously
-carbon dioxide laser for small, symptomatic tumours
-adult hemangiomas usually found at or above the level of the vocal folds
-should be left alone if at all possible
-corticosteroid or radiotherapy used when necessary
-carbon dioxide laser is not generally advised for adult cavernous hemangioma because the
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diameter of the vascular spaces exceeds this laser’s coagulating ability
Muscle neoplasms
Rhabdomyoma
-can be confused with a granular cell tumour or a rhabdomyosarcoma
-complete local excision is curative
Lipoma
-most frequent site of origin: false vocal fold
-conservative excision with complete removal or enucleation because incompletely removed lipomas
regrow
Cartilaginous neoplasms
Chondroma
-‘‘obvious smooth rounded mass covered by mucous membrane in the subglottic region of the larynx,’’ and
in most cases this mass was situated posteriorly and laterally
-laryngofissure used most often for removal and total laryngectomy for high-grade malignant tumours
Neurofibroma
-most common site of origin was the arytenoid or aryepiglottic fold
Neurilemmoma
-less common than neurofibromas and usually involve the aryepiglottic fold and false vocal fold
-conservative but complete removal by an approach consistent with tumour size and location
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LASER SURGERY OF THE LARYNX
(Cummings)
BENIGN CONDITIONS
Nodules
-excision required when lesion is well organized or fibrotic or if there is suspicion about the nature of the
lesion
-careful low-power vaporization from medial to lateral is technique of choice
Polyps
-excision using carbon dioxide laser allows precise removal because of its hemostatic capability and
nontouch technique, which does not obscure the surgeon’s view
-postsurgical management includes complete voice rest for 48 hours, followed by soft vocalization for 10
days
Cysts
-managed with the carbon dioxide laser by unroofing the cyst, aspirating its content, and marsupializing it
completely
Granuloma
-best management is to remove the factor that is causing chronic inflammation
-if surgical management is required, the carbon dioxide laser is ideal for excision
-postoperative antibiotics and systemic corticosteroids for up to 1 month is usually necessary for complete
resolution and healing
Papillomatosis
-frequent excisions recommended in children to avoid a tracheotomy and to allow the child to develop
good phonation, preserving normal vocal cord anatomy as much as possible
-done at a power setting of 2 to 3 W (0.3 mm spot size), at a 0.5- to 1-second exposure
-lesions vaporized to level of mucosa; avoid entry into Reinke’s space and deeper vocal ligament
-anterior commissure should also be avoided, leaving at least 1 mm of mucosa unmanaged
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Arytenoidectomy
-for management of bilateral vocal cord paralysis
-carbon dioxide laser is coupled to an operating microscope with a 400-mm objective lens
-laser settings: 0.1-second pulse duration, in repeat intermittent mode, at the power of 10 W and a
focussed spot size of 0.8 mm (20 W/cm2)
-disadvantages:
-(1) inaccuracy in final placement of the vocal cord as compared with external procedures
-(2) learning curve associated with the laser
-complications:
-granuloma formation, posterior commissure strictures, complete or partial failure with
medialization of the cord, loss of good voice production, perichondritis, and aspiration through a
largely patent posterior commissure
Laryngeal stenosis
-scar tissue is excised using a carbon dioxide laser with a spot size of 0.3 mm at 2 watts of power
(irradiance, 21.1 W/mm2) directed by a micromanipulator
-ensure mucosa over arytenoids and uninvolved interarytenoideus muscle are not injured
-surgical wound after scar excision is covered with autologous fibrin glue
-mucosal buccal graft to cover the mucosal defect
LARYNGEAL CANCER
Excision
Glottic cancer
-excision of early tumours of true vocal cords
-lesions most suitable for transoral laser excisional biopsy
-hyperkeratosis, dysplasia, carcinoma in situ, and early invasive squamous cell carcinoma (T1
tumours)
-excellent cure rate for T1 squamous cell carcinoma using this approach, which is comparable with results
achieved with radiotherapy
-criteria for endoscopic excision:
-lesion should be minimally invasive
-localized to the mid to anterior portion of true vocal cord
-should not extend to anterior commissure, the vocal process of the arytenoid cartilage, or
supraglottic or subglottic larynx
-vocal cord mobility should be normal, which indicates minimal deep invasion of the carcinoma
-if the tumour extends into anterior commissure region recurrence is likely with an endoscopic technique
-advantage of using laser is noncontact microprecision in a bloodless field
-potential disadvantage: risk of thermal damage, which for superficial lesions (e.g., keratosis, dysplasia)
puts an extra burden on the clinician in regards to the need for meticulous technique
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-carcinoma in situ:
-deeper excision exposing the vocalis muscle is required, and a 2- to 3-mm margin around the
tumour is obtained
-if lesion is found to violate vocal ligament invasive carcinoma.
-T1 lesions:
-carbon dioxide laser offers a 90% cure rate which is comparable with that for radiotherapy
-offers one-session treatment versus the multiple treatment sessions required with radiotherapy
-associated with less morbidity, can be repeated in cases of failure, and can be done as a biopsy
procedure
-when lesion extends to anterior commissure or to arytenoid cartilage, carbon dioxide laser
excision is contraindicated.
-margin of at least 2 to 3 mm of healthy surrounding tissue
-6-8 W of energy are used in a pulsed 0.1-second exposure
Supraglottic carcinoma
-role of carbon dioxide laser excision for supraglottic carcinoma is limited
-rare situations, a small T1 epiglottic carcinoma involving the suprahyoid portion of the epiglottis, the rim
of the arytenoepiglottic fold, or both can be managed by endoscopic laser excisional techniques
-radiotherapy is management of choice for patients with these tumours because the primary cancer and
high-risk lymph nodes are managed simultaneously
-laser usually used for a patient who refuses radical management, a high-risk surgical candidate, a patient
requiring palliation of symptoms) used for staging and to secure an airway
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VOICE REHABILITATION AFTER LARYNGECTOMY
Artificial Larynx
-rapidly learned speech substitute
-placement on neck or tube adapter to direct sound to oral cavity
-advantages: low cost, availability, short learning time, loudness
-disadvantages: dependence on batteries, mechanical sound, conspicuous appearance, loss of hands-free
speech, hygiene of intraoral tubes or dental appliance
Esophageal Speech
-only 30% of laryngectomized population develop useful esophageal speech
-voice is low in fundamental frequency (~65 Hz)
-air trapped and stored in esophagus (80 ml) released by diaphragmatic action to produce speech
-disadvantages: low acquisition rate and prolonged learning period
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-anesthetic placed at level of prevertebral fascia - skin entered at level of C2-C3
immediately parapharyngeal and medial to carotid sheath
-typical appearance shows reduction in mass of constrictor muscles, including axial
length
-largest percentage are pts who reflexively elevate upper esophageal sphincter pressure during esophageal
distention above threshold for voice fluency
-using breath control and internal feedback reduce esophageal distention and resultant upper
esophageal sphincter tonicity
-open-tract test: voice prosthesis removed and patient voices
-demonstrates failure is result of mechanics of unfavourable voice prosthesis
-if voice retains strained quality after proper fit change to TEP with low-resistance
characteristics and larger diameter
MANAGEMENT
-candidiasis results in premature failure of prosthesis (usually valve degradation with aspiration of liquids
through the prosthesis)
-tx with oral Nystatin
-persistent pharyngoesophageal spasm after successful primary TEP
-pharyngeal constrictor myotomy
-pharyngeal constrictor neurectomy
-botulinum toxin A injection
RESULTS
500
-complications:
-tracheoesophageal puncture dilation
-aspiration
-esophageal prolapse
-tracheostoma prolapse
-tracheal granulation tissue
-leakage at TEP
-aspiration
EMERGENCIES
-aspiration of prosthesis
-airway obstruction
-tracheoesophageal necrosis
-voice prosthesis incompetence
-dilatation must be performed with as little resistance as possible because it its possible to dissect into the
tracheoesophageal common wall and enter the anterior mediastinum
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GLOTTIC AND SUBGLOTTIC STENOSIS
-pathophysiology:
-ETT causes pressure necrosis mucosal edema and ulceration
-mucociliary stasis and infection and perichondritis
-chondritis and cartilage necrosis
-healing by secondary intention granulation tissue proliferation and deposition of fibrous tissue
in submucosa
-risks:
-prolonged intubation: greater than 7-10 days
-use of oversized ETT
-repeated intubations
-coexistence of ETT and NG tubes
-poor general condition
Other causes:
-laryngeal surgery
-emergency cricothyroidotomy
-high tracheotomy
MANAGEMENT
Tracheotomy:
-for severe cases of stenosis and airway difficulty
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-with normal growth and development, decannulation usually within 2 years
Endoscopic management:
-dilatation for early stenosis
-use of corticosteroids controversial
-CO2 laser - useful for early lesions
Decannulation in Children
-endoscopy performed to ensure airway is clear
-removal of suprastomal granulation tissue if present
-plugging of tracheotomy in hospital with oxygen monitoring
-if no desaturation then remove trach tube and occlude stoma
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Otolaryngology - Head and Neck Surgery Page 1 of 5
Dr. F. Ling's
Laryngeal Development
early:
RP out-pouches to develop respiratory diverticulum (RD)
origin of RD is primitive pharyngeal floor (PPhF) ==> glottic
region
cephalic portion of RD ==> infraglottic region
pharyngeal floor (PF) at level of 4th pouch
area from PF to PPhF = primitive laryngopharynx (PL) ==>
supraglottic region
later:
bronchopulmonary buds (BPB) from RD ==> lower
respiratory tract
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Phase (VI I I )
Overview
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Review of Anatomy: The Larynx Page 1 of 3
Larynx
A. Skeleton
Hyoid Bone
attachment to epiglottis and strap muscles.
Thyroid Cartilage
anterior attachment of vocal folds. Posterior articulation with cricoid
cartilage.
Cricoid Cartilage
complete ring. Articulates with thyroid and arytenoid cartilages.
Arytenoids
two cartilages which glide along posterior cricoid and attach to
posterior ends of vocal folds.
B. Divisions
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Review of Anatomy: The Larynx Page 2 of 3
Glottis
true vocal folds attach to thyroid cartilage at anterior commissure
posterior commissure is mobile, as vocal folds attach to arytenoids
bulk of vocal fold is made up of muscle covered by mucosa
free edge is characterized by stratified squamous epithelium
vocal folds abduct for inspiration and adduct for phonation, cough,
and valsalva.
Subglottis
below vocal folds, extending to inferior border of cricoid cartilage.
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AURICULAR TRAUMA AND SALVAGE
-untreated open auricular injuries invariably result in infection, ensuing deformities, and further tissue loss
-venous drainage of posterior surface of auricle occurs principally via posterior auricular vein
SURGICAL THERAPY:
-defects less than 1 cm with intact cartilage and vascularized perichondrium can be left to heal by
secondary intention
-alternatively, FTSG from contralateral postauricular sulcus can be used to cover defect
Abrasions
-abraded areas must be cleaned and thoroughly irrigated
-covered with topical antibiotic impregnated gauze for 24 hours
-treated as open wounds
Blunt trauma
-commonly result in hematoma and seroma formation between cartilage and perichondrium on anterior
surface of ear
-acute treatment involves drainage of effusion via needle aspiration or incision followed by application of a
pressure dressing
Lacerations
-closed by primary closure
-composite grafts:
-reattachment of completely severed auricular portions of less than 1.5 cm in diameter as
composite grafts is successful in limited circumstances
-success rate usually has been poor
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-small or large avulsions:
-“pocket principle” is used in reattachment of small or large avulsions
-involves dermabrading avulsed ear segment, reattaching it in its correct anatomic position, and
burying it under a layer of postauricular skin in subcutaneous tissue
-additional blood supply to reattached segment while in "pocket" secondary to increased contact
surface with surrounding dermis results in improved survival of reattached tissue
-remove segment from pocket after 10-14 days with overlying skin covering
-cover postauricular defect with local tissue advancement or a skin graft
TPFF
-used to salvage a major auricle replantation by covering salvaged or harvested autologous cartilaginous
framework
-a flap up to 17 x 14 cm in area can be harvested and can be used as an ipsilateral turndown flap or as a
free flap from contralateral side
-dermabrade and inset amputated ear
-raise TPFF based on superficial temporal artery and turn it over to cover reattached cartilage
-harvest a full-thickness skin graft to cover TPFF flap
Microsurgical replantation
-when traumatic injury results in total or near total auricular avulsions, microsurgical replantation provides
an excellent reconstructive option
Complete reconstruction
-procedure involves up to 3 staged procedures starting with harvesting of autogenous rib cartilage from
sixth, seventh, and eighth costal cartilages
-first stage, implant sculpted framework and rotate remnant earlobe into position
-second stage involves creation of tragus and conchal cavity several months later
-final stage consists of elevation of implanted auricle with split-thickness skin graft placement
retroauricularly
Auricular prostheses
-auricular prosthetics provides a final option
-problems with prosthetics have included detachment, improper color match, patient psychologic
discomfort about having prosthetics detach at inopportune moments, and surrounding tissue irritation
secondary to adhesives
-development of osseointegrated implants, in which pure titanium implants are placed into mastoid bone
region and after a period of healing, load-bearing superstructures are connected to implants, has reduced
significance of these problems
Bites
-among most common injuries to auricle
-treatment should include debridement, copious irrigation, primary closure or split-thickness skin graft
closure, and oral antibiotics, followed by a 24-hour check
-if cartilage is involved, risk of infection is significantly greater, and intravenous antibiotics should be
instituted
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FACIAL TRAUMA
GENERAL
Emergency Care:
-ABC’s
-suction + tracheostomy
-direct pressure to wounds - no clamping necessary
-fluid resuscitation
-irrigation and debridement
FACIAL FRACTURES
General Principles:
-nasal and zygomatic malar area most commonly involved followed by mandibular area
-O/E look for:
1. Sources of cervicofacial hemorrhage
2. Soft-tissue injury (contusions, abrasions, lacerations, haematomas, edema)
3. Ecchymosis (subconjunctival, circumoral, intraoral, or post-auricular)
4. Subcutaneous emphysema
5. Cervical spine injury
6. Intracranial injury
7. Bone deformity
8. CSF rhinorrhea
9. Cranial nerve dysfunction
10. Epistaxis
11. Patency of nasal airway
12. Trismus
13. Malocclusion of teeth
14. Point tenderness and pain at fracture site
15. Evidence of compound fracture
16. Integrity of tympanic membrane and ear canal
17. Eye injury (central and peripheral vision, ocular motility, diplopia, displacement, and
papillary function)
-Inv:
-C-spine films (seen in 15-20% with facial injuries)
-facial bone series (Water’s, AP and lateral)
-+ CT head
-panorex for mandibular fractures
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Mandibular Fractures:
-ring structure of mandible 94% have associated second fractured area:
-condyle # assoc. /w symphysis + contralateral condyle
-body # assoc. /w contralateral angle
-fractures by area:
-condylar: 36%
-body: 21%
-angle: 20%
-symphysis: 14%
-alveolus, ramus, coronoid (3%, 3%, 2%)
-Sxs: malocclusion, pain, inability to close jaw
-Treatment:
-closed reduction (jaw wiring) for minimally displacement
-intermaxillary fixation: 4-6 weeks in adults
-open reduction - plating/wiring; better approximation
-Complications:
-delayed healing, mal-union malocclusion, non-union
Nasal Fractures:
Hx:
-anterior blow: comminuted # with flattening of bridge
-lateral blow: convex deformity on other side
Dx:
-epistaxis
-external displacement of nasal bones
-localized bone tenderness
-nasal airway obstruction
-septal edema or deformity
-septal haematoma
-Treatment:
-closed reduction in 3-4 days after edema
-drain septal haematomas
-stabilization with external splints and internal packs
-nasoethmoidal # tx with ORIF
-Complications:
-CSF rhinorrhea if roof of ethmoid sinus or cribiform plate involvement
-disruption of nasolacrimal apparatus and medial canthal tendon
”pseudohypertelorism” or traumatic telecanthus
-ethmoid sinus disruption interstitial periorbital emphysema
-septal haematoma - risk of necrosis saddle deformity; prompt drainage required.
-septal deformity nasal obstruction
-lacrimal apparatus injury
Orbital Fractures:
-Orbital floor blow out most common; may occur with midface and zygomatic fractures
-Sxs:
-exophthalmos
-diplopia ( EOM d/t muscle/nerve entrapment; muscle contusion, edema, temporary
515
neuropraxia)
-facial asymmetry
-sensory nerve injury (V2)
-ocular complication
-Inv: CT scan
-Exploration and stabilization required if:
-exophthalmos
-diplopia with EOM disturbance after resolution of edema
-facial deformity
-persistent anesthesia in V2
-Tx: orbital floor reparation with bone graft or prosthetic material
-Complications:
-retrobulbar haematoma, residual entrapment of orbital contents
-continued diplopia
-late exophthalmos 2o to atrophy of periorbital fat-Ophthalmology consult prn
-LeFort I:
-d/t central midline blow
-lower midfacial fracture which runs transversely through lower maxilla and into lower nasal
cavity
-involves teeth, portion of maxillary sinus, hard palate, lower segment of pterygoid plates
-Ssx: malocclusion and mobility of maxilla
-O/E:
-buccal vestibule ecchymosis
-maxillary crepitus
-false motion of lower maxilla with stability of upper nose and orbits
-possible assoc. /w: lengthening of face, septal deformities, V2 paresthesias
-Tx:
-fix mandibular injuries first
-IMF usually gives sufficient reduction and stabilization
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-Complications:
-malocclusion
-paresthesia
-septal deformities
-facial asymmetry
LeFort II:
-aka “pyramid fracture”
-fracture lines through nasal and lacrimal bones, floor of orbit, inferior orbital rim, across
upper portion of maxillary sinus and pterygoid plates to pterygomaxillary fossa
-Ssx:
-naso-orbital flattening
-mobility of nasal bridge
-epistaxis
-malocclusion
-step deformities along orbital rims and nasofrontal areas
-CSF rhinorrhea
-V2 paresthesia
-Tx: ORIF /w plate and screw + bone graft if comminution or bone loss
-Complications as per LeFort I
-greater incidence of orbital injuries, CSF leaks, nasal deformities, lacrimal damage
-LeFort III:
-aka craniofacial dissociation
-fracture line across suture line b/n nasal and frontal bones, along ethmoid junction bone,
across superior orbital fissure, lateral wall of orbit and frontomaxillary and
zygomaticomaxillary suture lines
-Sxs similar to LeFort II + basilar skull injuries
-Battle’s sign (mastoid ecchymosis), Raccoon eyes, CSF otorrhea, hemotympanum
-Inv: CT
-Tx: as per LeFort II: ORIF
-stabilization via frontozygomatic sutures and zygomatic arches
-Complications:
-as per LeFort II + cranial base injuries/ neurological damage
517
-diplopia (downward displacement of trochlear and superior oblique muscle)
-overlying facial laceration
-Dx: Water’s or Caldwell views
-Open reduction invariably required, internal fixation seldom necessary.
518
AURICULAR TRAUMA
HEMATOMA
-caused by shearing forces
-blood between skin-perichondrial layer and cartilage
-“cauliflower ear”
-accumulated subperichondrial blood causes formation of neocartilage
-evacuate haematoma through incision in helical sulcus or antihelical fold
-pressure dressing applied for 7-10 days
General Concepts
-usefulness of avulsed segment:
-avulsed segment bites should not be reused as simple composite graft
-condition of surrounding tissue can limit reconstructive possibilities
Total Avulsion
-microvascular reimplantation yields best results
-if reimplantation not possible:
-existing cartilage used as subsurface framework and covered by vascularized tissue:
-a) temporoparietal fascial flap with delayed skin grafting
-used if missing postauricular skin
-b) postauricular advancement flap
-c) posteromedial skin removed, cartilage fenestrated, segment reattached against raw
postauricular surface established by means of raising a postauricular flap
-d) pocket principle technique
Partial Avulsion
Helical Rim
-helical rim advancement
-for defects lest than 2 cm in area
-tube flap
-for larger defects
-made from postauricular skin and transferred to auricle in multistage procedure
519
Defects of Lower Third
-lobule involved:
-primary closure with available tissue
-Pardue’s adjacent flap technique for earring cleft injury
-total lobule reconstruction
520
LARYNGEAL TRAUMA
Blunt Trauma
-endolaryngeal mucosal tears, edema, or haematoma
-fractures of laryngeal cartilages and disruption of laryngeal ligaments
-subluxation or dislocation of arytenoid cartilage fixed vocal fold
-cricoarytenoid joint injury unilateral injury to RLN
-cornus of thyroid cartilage can lacerate pharyngeal mucosa; pharyngoesophageal tears
-“clothesline” injury:
-cricotracheal separation
-bilateral RLN injury
-child (compared to adult):
-larynx situated higher in neck and protected by mandible
-less laryngeal fractures because of elasticity of cartilages
-increased likelihood of soft tissue damage
-cricothyroid membrane narrower less likely to have laryngotracheal separation
Penetrating Trauma
-damage directly proportional to velocity and mass of wounding object
Symptoms
-hoarseness
-pain
-dyspnea
-dysphagia
Signs
-stridor
-hemoptysis
-subcutaneous emphysema
-laryngeal tenderness
-loss of thyroid cartilage prominence
-vocal fold immobility
-laryngeal haematoma
-laryngeal edema
-laryngeal lacerations
Radiology
-CT scan
-contraindicated when airway is unstable
-not needed when:
-pts with obvious fractures,
large endolaryngeal lacerations,
or severe penetrating trauma
-pts with minimal anterior neck
trauma and normal physical
findings
521
-used to:
-detect cartilage fractures that are not clinically apparent (hyoid, thyroid, cricoid)
-assess poorly visualized areas (subglottis, anterior commissure)
-identify cervical injuries
-arteriography
-cervical spine radiography
-contrast esophagography
-start with water soluble contrast to avoid barium induced mediastinitis if tear exists
MANAGEMENT
Emergency Care
-multisystem trauma:
-establish airway
-cardiac resuscitation
-control of haemorrhage
-stabilization of spinal injuries
-adult airway
-controversy:
-establishing airway in presence of laryngeal trauma
-intubation can cause iatrogenic injury or loss of an already precarious airway
-many advocate tracheotomy under local anaesthesia or rigid bronchoscopic intubation
-alternatively, endotracheal intubation only with:
-experienced personnel
-direct visualization; no endolaryngeal lacerations; stable laryngeal framework
-small-diameter endotracheal tube
-pediatric airway
-difficult of near impossible to do tracheotomy under local anaesthesia
-inhaled anaesthesia with spontaneous respirations
-rigid bronchoscopic intubation followed by tracheotomy
522
Medical Treatment
-observation for 24 h
-voice rest
-systemic steroids (no evidence)
-elevate head
-humidified air
-antibiotics
-antireflux measures
Surgical Treatment
-early vs. late exploration (controversial):
-early:
-offers complete assessment of injuries, lower postoperative infection rate, quicker
healing, less granulation tissue, less scarring
-late:
-3-5 days
-allows edema to resolve
-may become infected; presence of granulation tissue
-tracheotomy under local for unstable airway
-endoscopy:
-ascertains extent of injury:
-look for haematoma, edema, lacerations, exposed cartilage and range of motion of true
vocal cords
-reduction of dislocated arytenoid
-bronch: evaluate subglottis and trachea
-esophagoscopy: r/o unsuspected perforations
-exploration:
-via laryngofissure (thyrotomy)
-exposed cartilage is a source of fibrosis and granulation tissue and must be covered primarily
-lacerations meticulously re-approximated
-fractures fixed with wire, nonabsorbable suture, or miniplates
-anterior commissure reconstructed; keel placed to prevent webbing
Grafting
-to cover exposed cartilage
-mucous membrane, dermis and STSG suitable
Stents
-indications:
-controversial
-extensive lacerations involving anterior
commissure
-multiple cartilaginous fractures that
cannot be stabilized adequately with
open reduction
-stent fixed to larynx in such a way that it moves
with larynx during swallowing
-pass suture through stent and larynx at
level of laryngeal ventricle and at
cricothyroid membrane
-usually left in place for 10-14 days
-remove early to avoid granulation tissue formation
523
Cricotracheal Separation
-risks:
-precarious airway
-loss of cricoid support
-high risk of injury to RLN
-late development of subglottic stenosis
-trachea tends to retract substernally and the larynx tends to migrate superiorly
-high mortality
-tracheotomy under local anaesthesia
-intact cricoid:
-mucous membrane repaired directly with absorbable suture
-fractured cricoid:
-reconstitution +/- stenting preferable to extensive resection and thyrotracheal anastomosis
COMPLICATIONS
-granulation tissue
-prevent by covering all exposed cartilage
-avoid stents when possible; leaving stents for the minimum amount of time when necessary
-careful excision
-laryngeal stenosis
-excision with mucosal coverage
-stenting selected cases
-laryngotracheoplasty
-tracheal resection with reanastomosis
-vocal fold immobility
-observe
-vocal fold injection
-thyroplasty-type vocal fold medialization
-arytenoidectomy and vocal fold lateralization for bilateral paralysis
-displaced stents
-may occur during coughing
524
MANAGEMENT OF SOFT-TISSUE TRAUMA
ANATOMY OF SKIN
Epidermis
-stratum corneum: no nucleus, keratin in cytoplasm, loosens then
desquamates
-stratum granulosum: 3-5 layers thick, flattened, keratohyalin
granules
-stratum spinosum: basophilic cells
-stratum basale: single layer of cuboidal cells at basal lamina
Epidermal-Dermal Junction:
-rete pegs: epidermal projections into dermal layer
-papillae: dermal, vascularized projections into epidermal layer
Dermis:
-papillary dermis: collagen and elastin fibers
-reticular dermis: denser layer
Subcutaneous layer:
-contains fat and fibrous tissue
WOUND MANAGEMENT
EMERGENCIES
Lacerations
-greater blood supply in face wounds can be closed primarily up to 48 or even 72 hours after injury
-non-traumatic handling of tissue required to prevent necrosis of skin
-wound contamination most directly related to elapsed time since injury occurred
Avulsions
-full-thickness tissue loss severe cosmetic deformity
-small defects can be excised and closed primarily
-options: skin grafting vs healing by secondary intention
Scalp Wounds
-five layers: skin, subcutaneous tissue, muscle and aponeurosis, loos connective tissue, pericranium
-lacerations repaired by undermining subaponeurotic plane above pericranium and performing a layered
closure
-secondary tissue expansion and flap reconstruction can resurface as much as 50% of scalp
525
-local flaps for defects < 5cm
Lip Injuries
-may close primarily up to ½ the upper or lower lip
-reconstruct in 3 layers including the orbicularis oris muscle
-use absorbable suture in mucosal and muscular layers
-for larger defects consider local flaps
Complications
-hypertrophic or keloidal scarring
-trapdoor deformities
-scar contracture
-step-off or distortion of anatomic landmarks
-sialoceles or salivary fistulae
-facial nerve palsy
-auricular deformities
-ectropion or other deformities of the eyelids
BURNS
Ears
-prone to suppurative chondritis
-redness swelling and deep pain
-tx: incision, drainage and debridement
526
Mouth
-usually from electrical cord biting in children
-conservative treatment: can be complicated by haemorrhage form labial artery
-delayed surgical excision and grafting: allows demarcation of involved area
-long term complication: microstomia from contracture; may consider placing an oral stent
Eyes
-risks ectropion, lid contraction, keratitis, and cataracts (electrical burns)
-FTSG to lower lids and STSG to upper lids may be needed to protect the globe
Frostbite
-commonly involve ears, cheeks and nose
-local rewarming by immersing involved part in bath maintained at 37.8-42.3oC
-surgical debridement delayed until extent of injury can be assessed
527
MANDIBULAR FRACTURES
ANATOMY
-components:
-symphysis, parasymphysis, body, angle, ramus,
coronoid process, condyle, alveolus
-inherent sites of weakness:
-third molar area
-socket of canine tooth
-condylar neck
-anterior muscles
-mylohyoid, geniohyoid, genioglossus, platysma,
anterior digastric muscles
-depress and retracts mandible
-posterior muscles: (muscles of mastication_
-temporalis: raises and retracts mandible
-masseter: raises and retracts mandible
-medial pterygoid: attaches to medial ramus; raises mandible
-lateral pterygoid: attaches to condyle; protrudes and depresses mandible
-upper border of mandible muscles of mastication produce tension stress use thinner, monocortical
tension plate along superior border
-lower border of mandible muscles produce compression stress use rigid compression plates along
inferior border
528
Types of Fractures
-simple (closed wound, skin and mucosa intact) versus compound (open wound, exposed bone)
-fracture pattern: comminuted, oblique, transverse, spiral, greenstick
-pathologic: fractures secondary to bone disease
Dental Evaluation
-32 permanent (secondary teeth)
-8 incisors, 4 canines, 8 bicuspids or premolars, 12 molars
-20 primary deciduous teeth
-8 incisors, 4 canines, 8 molars
Angle’s Classification
-Class I: orthognathic;
-mesiobuccal cusp of maxillary first molar lines buccal groove of mandibular first molar
-Class II: retrognathic
-Class III: prognathic
History
-pain and malocclusion
Physical Examination
-haematoma in FOM
-laceration of attached gingiva
-fragment mobility
-trismus
-deviation toward side of fractured condyle
-anterior open bite contralateral to side of fractured condyle
-possible anaesthesia or paraesthesia of lower lip and chin
-bilaterally displaced fractures of condylar neck symmetric anterior open bite deformity
Radiographic Evaluation
-panoramic view the single best radiographic evaluation
MANAGEMENT (GENERAL)
Principles
-goals:
-restore occlusion
-establish bony union
-return of function
-avoid TMJ ankylosis
-repair within first week, delayed repair increases complications
-in general favourable fractures may only need closed reduction, open fractures ten to require open
reduction
-all fractures involving tooth-bearing part of mandible considered compounded into mouth Abx
prophylaxis started
529
Closed Reduction (Maxillo-Mandibular Fixation - MMF)
-indications:
-for most favourable fractures that are minimally displaced
-selected condylar fractures
-for initial stabilization of occlusion prior to exposure of the fracture
-methods:
-arch bars, interdental eyelet wires (Ivy loops), circumferential wiring of dentures or teeth
-duration of fixation:
-depends on age and type of injury:
-children: 3-4 weeks
-adults: 4-6 weeks
-elderly: > 8 weeks
-condylar fractures: 1-2 weeks
-body and angle fractures: 4-6 weeks
-complications:
-airway compromise
-dental injury
-weight loss
-loss of fixation (malunion, nonunion)
-TMJ dysfunction
-aspiration
Open Reduction
-indication for ORIF:
-anticipated fragment displacement despite closed reduction
-unfavourable and comminuted fractures
-elderly; edentulous patients
-poor pulmonary reserve (unable to endure MMF)
-noncompliant patients, alcoholics, seizure disorder, mental retardation, psychosis
-multiple fractures or injuries
-bilateral fractures
-displacement into middle cranial fossa
-seizure disorder
-relative contraindications:
-poor bone height
-pediatric mixed dentition that limits placement of fixation devices
-approaches:
-transoral
-avoids injury to marginal mandibular nerve
-no external scar
-easy access to symphyseal, parasymphyseal, and body regions
-external:
-indicated for more posterior fractures which cannot be accessed intraorally or severely
comminuted fractures
-materials:
-rigid (plates, lag screws etc..) vs. non-rigid (interosseous wires)
-sagittal and oblique fractures may be more amenable to repair with lag screw techniques
-hole drilled perpendicular to fracture line
-compression not used in cases of infection or comminution large reconstruction plates used
instead
530
MANAGEMENT BY TYPE OF FRACTURE
Displaced Fractures
Symphysis-Parasymphysis Area
-tend to be vertically unfavourable
-custom acrylic lingual splint in addition to IMF to resist scissorslike collapse of mandibular arch
-ORIF avoids use of splints
-lag screws
Body
-transoral application of compression plate
-external incision and compression plate
-multiple lag screw fixation
531
Angle
-associated with highest incidence of infection
-in general have the highest complication rate by site because of location posterior to dentition,
thin-walled bone, and vector forces from masseter muscle
Ramus
-fractures are naturally splinted by pterygomasseteric sling and are amenable to closed reduction
-early release of IMF for non-displaced fractures (3-4 weeks)
-ORIF may be considered for multiple fragments or marked displacement
-Absolute indications:
-displacement into middle cranial fossa
-impossibility of obtaining adequate occlusion by means of closed reduction
-lateral extracapsular displacement of condyle
-invasion by foreign body (eg. Gunshot wound)
-Relative indications:
-bilateral condylar fractures in edentulous patient when splinting is impossible
-unilateral or bilateral condylar fractures when splinting is not recommended for medical
reasons or adequate postoperative physiotherapy is impossible
-bilateral condylar fractures associated with comminuted midfacial fractures
-bilateral condylar fractures associated with marked preinjury malocclusion
-exercise sessions every 2 weeks allow a brief release form IMF to avoid intra- and periarticular fibrosis
and ankylosis
SPECIAL CONSIDERATIONS
Edentulous Fractures
-closed reduction with arch bars applied to pt’s dentures
-Gunning splints secured to maxilla and mandible with wires
-rigid techniques often are used to manage edentulous fractures without advance mandibular atrophy
Pediatric Fractures
-in general prefer conservative management
-usually can tolerate some malocclusion which adjusts with growth
-rigid techniques place developing tooth buds at risk and usually are avoided
532
-most dreaded complication is development of ankylosis of TMJ can alter jaw growth and produce a
severe facial deformity
-allow weekly mobilization of jaw with rapid return to normal jaw function
External Fixation
-indications:
-contaminated gunshot wounds resulting in loss of part of the mandible
-osteomyelitis
-elderly
-provides the advantage of fragment stability with neither IMF nor a foreign body in the wound
Removal of Hardware
-controversial
-probably unnecessary
COMPLICATIONS
-infection
-ostoomyelitis
-malocclusion
-malunion
-caused by inadequate immobilization, inaccurate reduction, infection, gross loss of bone,
compromised blood supply, malnutrition, osteogenesis imperfecta, osteopetrosis
-nonunion
-non-osteogenic matrix produced
-may require bone grafting
-plate exposure
-TMJ ankylosis
-TMJ dysfunction
-sensory disturbances of inferior alveolar nerve
-marginal mandibular nerve injury
-necrosis of condylar head
-dental injury
EMERGENCIES
-airway obstruction (bilateral fractures of mandibular body)
-condylar displacement into middle cranial fossa
-adjacent injury to internal carotid artery
-haemorrhage
533
MAXILLARY AND PERIORBITAL FRACTURES
MAXILLARY FRACTURES
ANATOMY
Buttress System
-vertical buttresses:
-nasamaxillary
-zygomaticomaxillary
-pterygomaxillary
-horizontal buttresses:
-frontal bar: superior orbital rims and glabellar area
-inferior: inferior orbital rims, maxillary alveolus
and palate, zygomatic processes, serrated edges of
greater wings of sphenoid bone
LeFort Classification
-LeFort I
-low maxillary; transverse maxillary fracture
-upper alveolus becomes separated from upper maxillary
-typically caused by a low anterior-to-posterior force
-involves anterior lateral maxillary wall, medial maxillary wall, pterygoid plates, septum at floor
of nose
-LeFort II
-pyramidal
-caused typically from a superiorly directed force against the maxilla or an anterior to posterior
blow along the Frankfort plane
-involves nasofrontal suture; orbital foramen, rim and floor; frontal process of lacrimal bone,
zygomaxillary suture; lamina papyracea of ethmoid, pterygoid plate; and high septum
-LeFort III
-craniofacial dysjunction
-separates facial skeleton from base of skull, typically caused by high velocity impacts, moto
vehicle accidents, oblique forces
-involves nasofrontal sure; medial and lateral orbital wall and floor; zygomaticofrontal suture;
zygoma and zygomatic arch; pterygoid plates and nasal septum
534
PATHOPHYSIOLOGY
PATIENT EVALUATION
Computed Tomography
-critical areas in CT evaluation:
-vertical buttresses
-zygomatic arch
-orbital walls
-bony palate
-mandibular condyles
-orbital injuries likely to produce exophthalmos are those in which disruption of orbital floor exceeds at
total area of 2 cm2, bone volume changes exceed 1.5 cm3, or considerable fat and soft tissue displacement
occur
Ophthalmologic Evaluation
-testing of visual acuity, pupillary function, ocular motility
-inspection for hyphema
-inspection of fundus for gross disruption
MANAGEMENT PHILOSOPHY
Immediate Reconstruction
-usually within 24-48 hours
-immediate reconstruction is usually less difficult and more successful than delayed reconstruction
-delayed reconstruction:
-risk of cicatricial contraction of facial soft tissues, scarring, bone resorption
-can allow up to 2 weeks for delayed repair
535
Stable Internal Fixation
-rigid internal fixation devices can obviate the need for IMF used to stabilize maxillary fractures
-pts still need to be on soft diet to reduce mechanical loading of buttresses
SURGICAL TECHNIQUES
Zygoma
-four sutures involved in zygomaticomaxillary complex fractures (“tripod fracture”)
-zygomaticofrontal
-zygomaticomaxillary
-zygomaticotemporal
-zygomaticosphenoid
-stabilization requires minimum of two point fixation:
-zygomaticofrontal suture
-inferior orbital rim
-lateral antral wall
-zygomatic arch
-procedures usually delayed 5-7 days to allow resolution of edema
-closed reduction:
-used if no comminution Gilles operation +/- transzygomatic Steinmann pin fixation
-open reduction:
-used if comminution of lateral antral wall sublabial incision with plating at
zygomaticomaxillary buttress
-tripod fracture add transconjuntival incision to access medial orbital rim and lateral brow
incision for zygomaticofrontal suture
-centrally displaced zygomatic arch approached via coronal, hemicoronal, or extended pretragal
incision
536
Maxilla
-restoration requires reestablishment of proper occlusion and stabilization of midfacial buttress system
-must first ensure proper alignment of mandibular condyles
-usually IMF done first then midfacial vertical dimension stabilized by ORIF
-if condylar height cannot be maintained, then midfacial buttress system reconstructed first to
establish vertical and horizontal positioning of the occlusal plane
-restoration of zygoma required
-palatal fractures:
-parasagittal splits reduced anteriorly at inferior rim of piriform (plates) aperture and posteriorly
(interossous wire)
-maxillary reduction usually starts with reattachment of zygomaticomaxillary buttress (usually has less
severe injury) to obtain vertical height
-panfacial fractures:
-work from stable base
-begin with MMF and associated mandibular fractures
-work lateral (zygoma and ZM buttress) to establish anterior projection
-work medial to restore buttress system
537
COMPLICATIONS
-lid damage
-meticulous closure of transconjunctival incision required to prevent ectropion
-lip distortion
-caused by sublabial approach
-hollowing of soft-tissue contours over canine fossa
-superior deviation of corner of mouth and lateral aspect of upper lip
-caused by collapse and contracture of buccal soft tissues into large anterior and anterolateral
antral wall defects
-vision loss
-from trauma
-occasionally an oversized implant causes acute increase in IOP and must be removed
-implant visibility
-malocclusion
-can be caused by plates that are not correctly adapted to bone tightening of screws can produce
torque causing movement of fragments
-malunion, nonunion
-plate exposure
-forehead/cheek hypesthesia
-osteomyelitis
-dental injury
ORBITAL FRACTURES
ANATOMY
CLINICAL PRESENTATION
SSx: enophthalmos (? 2-3 mm pathologic), hypopthalmos, exophthalmos, proptosis, entrapment diplopia,
hypesthesia of infraorbital nerve, psedoptosis
538
Theories of Orbital Floor Injury
-Hydraulic Theory:
-force to orbital region increases intraocular pressure fractures floor
-Buckling Theory:
-force on inferior rim directly fractures floor
MANAGEMENT
539
COMPLICATIONS
-postoperative blindness
-CSF leak
-persistent enophthalmos and diplopia
-ectropion
-ectropion
-epiphora
-cheek hypesthesia
-extrusion of grafts
-osteomyelitis
-palpable or observable plates
540
FRACTURES OF THE NASAL AND FRONTAL SINUSES
NASAL FRACTURES
Basic Anatomy
-sensory innervation:
-supratrochlear nerve
-infratrochlear nerve
-anterior ethmoidal nerve external nasal nerve
-infraorbital nerve
-most fractures occur in lower half of nasal bones (thin at inferior articulation with upper lateral cartilage)
-see Nasal Anatomy Notes
-medial canthal ligament
-extension of tarsal plates which attaches to medial orbital wall
-receives contributions from tendinous portion of preseptal and pretarsal parts of orbicularis oculi
muscle, superior suspensory ligament (Whitnall), and inferior suspensory ligament (Lockwood)
-lacrimal collecting system
-puncta: located a medial aspect of upper and lower eyelids
-canaliculi: upper and lower canaliculi form common canaliculus
-lacrimal sac: located in lacrimal fossa, insertions of MCL straddle the lacrimal sac and act as a
pump
-lacrimal duct: enters into medial maxilla and exits into inferior meatus
Pathophysiology
-factors:
-patients’ age (tissue flexibility)
-amount of force applied
-direction of force
-nature of striking object
-soft tissue injuries: lacerations, hematoma, ecchymosis
-skeletal injuries: fractures, dislocation, fracture-dislocation
-force required to produce nasal fracture: 25-75 lb/in2
-frontal force: injury varies from minor to marked flattening of external skeleton
-lateral force: depression of ipsilateral nasal bone +/- outfracture of contralateral nasal bone
-from below: septal fractures and dislocations
-can cause telescoping of fragments and shortening of nose or blockage of one side
Treatment
-goals:
-restore satisfactory appearance
-restore nasal airway patency
-replace septum in midline
-preserve nasal valve integrity
-prevent postoperative stenosis, septal perforation, columellar retraction, and saddle deformity
-avoid interference with growth
General
-best opportunity during first 3 hours after injury
-reduction usually performed within 3-7 days
-indications for closed reduction:
-unilateral or bilateral fracture of nasal bones
-fracture of nasal-septal complex with nasal deviation less than one half width of nasal bridge
541
-indications for open reduction:
-extensive fracture-dislocation of nasal bones
-nasal pyramid deviation exceeding one half width of nasal bridge
-fracture-dislocation of caudal septum
-open septal fractures
-persistent deformity after closed reduction
Anesthesia
-2% lidocaine with epinephrine spray
-injection of 2% lidocaine with 1:100000 epinephrine along dorsum of nose lateral to nasal pyramid and at
base of anterior septum
-alternative: EMLA and intranasal cocaine
Delayed Management
-surgery usually delayed 6 months or more from initial closed or open fracture reduction to allow fracture
lines to stabilize and fibrosis to mature
542
Nasal Fractures in Children
543
Nasofrontal-Ethmoidal Fractures
-force directed from inferior aspect to external nose
-associated injuries:
-injury to nasofrontal duct or cribriform plate
-detachment of medial canthal ligaments pseudohypertelorism
-CSF rhinorrhea , anosmia, ocular injury, interruption of lacrimal system, cerebral contusion
-management:
-open reduction and stabilization of bone fragments
-“open sky incision”: bilateral Lynch incision connected by transverse incision below glabella
-fragments stabilized with wiring or plates
-calvarial bone grafts for severe fractures for dorsonasal reconstruction
544
Complications
Early
-edema
-ecchymosis
-epistaxis
-haematoma
-suspected when any patient has persistent swelling and pain
-infection
-CSF leak
Late
-airway obstruction
-fibrosis, contracture
-secondary deformity
-synechiae
-saddle nose
-septal perforation
Emergencies
-severe bleeding cauterization, packing, vessel ligation
-septal fracture-dislocation causing nasal airway obstruction in neonate closed reduction with cotton
swabs; no nasal packing
-septal haematoma in child immediate I+D; tissue destruction begins within 48h
-CSF rhinorrhea neurosurgical consultation
-visual impairment immediate ophthalmologic consultation
Anatomy
-three sides: anterior, posterior, floor (thinnest)
-drains through frontal sinus
-course of frontonasal duct is posterior and caudal
Evaluation
-ABCs
-CT scan
-coronal scans provide good definition of floor of sinus, FND, cribriform plate
-presence of fractures through floor of frontal sinus or anterior ethmoidal fractures suggests
presence of injury to FND
545
-surgical access:
-bicoronal flap or extension of laceration
-bilateral sub-brow incision
-“open sky” incision
-wound debridement
-surgical approaches:
-obliteration of FND
-obliteration of frontal sinus
-cranialization
Antibiotic Prophylaxis
-prevention of sinusitis and intracranial sepsis
-ceftriaxone or ceftazidine, and metronidazole
-for compound fractures, antibiotic therapy maintained for at least 2 weeks
-no antibiotics for closed fractures and isolated nondisplaced anterior table fractures
Treatment
-prevention of intracranial sepsis
-prevention of frontal sinus disease
-cosmetically acceptable outcome
546
Frontonasal Drainage
-best evaluation of FND integrity and patency is made intraoperatively
-patency evaluated with fluorescin, benzylpenicillion solution or methylene blue dye
-obliterate cavity if obstruction of FND is found
-fat, fascia, muscle, pericranium, cancellous bone
Complications
-frontal sinus
-headache, fullness; sinusitis; mucocele
-intracranial
-CSF leak; meningitis; brain abscess; seizures
-cosmetic
-scar numbness; wound infection; forehead depression
-ophthalmic
-diplopia; eye pulsations
547
PENETRATING FACE AND NECK TRAUMA
Definition:
-penetrating neck/face injury = breach of platysma
-muzzle velocity:
-low velocity (<1000ft/s) tissue damage
-high velocity (>1000ft/s) tissue loss
-mechanisms of GSW injury:
-direct tissue injury
-temporary cavitation
-anatomic structures may be significantly damages without actually being penetrated by
the projectile
-transmission of shock waves
-projectile rotation
-projectile shatter and secondary projectiles
Shotgun Injuries
-I: long-range:
- >7 yards distance between weapon and victim
-subcutaneous or deep fascia injuries only
-II: medium range:
-3-7 yards
-injuries to structures deep to deep fascia
-III: close range:
-<3 yards
-massive tissue destruction
-zoning system not helpful in predicting injury pattern
-high incidence of ocular injury ophthalmology consult
Stab Wounds
-AP and lateral skull X-ray to evaluate depth of penetration if
weapon still in place
-angiography with weapon in place can control proximal
vessels with balloons if major vessel is involved
548
Gunshot Wounds
-midface wounds:
-high prevalence of vascular injury (20%), globe injury (20%), intracranial penetration (20%) and
facial fracture (35%)
-indications for angiograms:
-proximity to major vascular structure
-penetration posterior to mandibular angle plane (imaginary vertical coronal plane at
level of angle of mandible)
-mandible wounds:
-often require emergency management of airway (50%)
-deflection of bullets by mandible into neck or intracranial cavity
Complications
-facial injuries:
-blindness/visual loss/diplopia
-facial nerve paresis or paralysis
-CSF leak
-soft tissue loss
-bony malunion, malocclusion, trismus
-orbital/periorbital cellulitis, sinusitis, oroantral fistula
-nasal obstruction/stenosis, choanal stenosis
-neck injuries:
-airway obstruction
-pharyngocutaneous fistula
-neck abscess
-mediastinitis
-vocal cord paresis
-cervical spine osteomyelitis
549
-most common vascular structures injured:
-internal jugular vein (9%)
-internal and common carotids (7%)
-subclavian artery (2%)
-external carotid artery (2%)
-most commonly missed injury in the neck: pharyngoesophageal injury
-most common cause of death: exsanguinating hemorrhage
MANAGEMENT
Zone I Injuries
-high risk injury to great vessels, trachea and lungs
-symptomatic/asymptomatic: angiography, esophageal evaluation (esophagoscopy and contrast
esophagography increases specificity and sensitivity to 100%)
-up to 1/3 patients are asymptomatic
-esophageal injury silent: risk of mediastinitis and sepsis
Zone II Injuries
-high risk injury to carotid sheath and aerodigestive system
-symptomatic neck exploration
-asymptomatic:
-controversial management:
-exploration vs directed serial examination
-exploration:
-may discharge patients home earlier if negative findings
-more accurate than diagnostic tests
-up to 50-70% of elective neck explorations are negative
-mandatory surgical exploration:
-gunshot wounds that cross midline
-obvious serious injury (stridor, active hemorrhage, absent carotid pulse)
-active bleeding, air bubbling through wound
-arteriorgraphy not available
-directed examination:
-missed injuries, serial examinations required
-arteriography, esophagogram/esophagoscopy, laryngoscopy, bronchoscopy
550
Zone III Injuries:
-high risk injury to distal carotid artery, parotid and pharynx
-potential injury to major blood vessels and cranial nerves at or near skull base
-treatment may be managed by interventional radiologist (arteriography and balloon occlusion)
Carotid Injury
-associated with high mortality (10-20%)
-primary repair treatment of choice, otherwise may consider patch grafting, by-pass grafting or ligation
-ligation should not be considered if suspect a stroke to avoid haemorrhagic stroke with revascularizatoin
551
COMPLEX FACIAL TRAUMA WITH PLATING
Fracture Reduction
-re-establishment of anatomic position and continuity of bony buttresses is key to fracture reduction
-stable reference points are used for fixation
-intervening gaps in buttresses are bone grafted
-buttresses must ultimately transmit forces of mastication to skull base
-donor sites: calvaria, ilium, ribs
Occlusion
-normal molar occlusion in anterior-posterior dimension defined as intercuspation of mesial buccal cusp of
maxillary first molar with buccal groove of mandibular first molar
-normal transverse relationship: buccal cusps of mandibular molars are between buccal and palatal cusps of
maxillary molars
-normal anterior dental relationship: maxillary anterior dentition is 1-3 mm anterior to mandibular anterior
dentition with central incisa overlap of 1-3 mm
-wear facets are main occlusal guide
552
-superior circumvestibular incision:
-exposes inferior maxilla
-pitfalls: infraorbital nerve damage, nostril stenosis, leaving inadequate oral vestibular mucosa for
wound closure
-bicoronal incision:
-exposes upper face
-pitfalls: damage to frontalis innervation and inadequate closure of galea brow ptosis
-lower lid incision:
-exposes infraorbital rim and orbital floor
-brow incision:
-exposure of frontozygomatic region
Complications
-osseous:
-osteitis/osteomyelitis
-delayed union/nonunion/malunion/malocclusion
-fibrous union with poor function
-bone loss
-TMJ dysfunction
-soft tissue:
-deficiency
-scarring
-ptosis/lagophthalmos
-entropion/ectropion
-nasal obstruction
-neurosplanchnic:
-brain injury
-globe injury/malposition
-CSF leak
-meningocele/encephalocele
-CN dysfunction
-glandular dysfunction
553
-Most common cause of death for individuals between 1-44 years
-third most common caus of death for all ages
-100,000 deaths per year in US; MVA ~50%
! " #$ $"%
Nasotracheal intubation:
-only in patients breathing spontaneously
Orotracheal intubation:
-manual in-line cervical immobilization in patients with potential c-spine injuries
-advantages: ability to visualize cords, larger-diameter endotracheal tubes
-disadvantages: requires neuromuscular blockade or deep sedation
Cricothyroidotomy:
-failed intubation or extensive facial injuries
-disadvantage: ETT must be < 6 mm in diameter
-contraindicated in patients < 12 years damage to cricoid cartilage, risk of subglottic stenosis
Tension Pneumothorax:
-respiratory distress, tracheal deviation away from affected side, lack of or decreased breath
sounds on affected side, distended neck veins or systemic hypotension, subcutaneous emphysema
554
on affected side
-treat with large gauge needle in 2nd ICS MCL followed by CT thoracostomy
Open Pneumothorax:
-full-thickness loss of chest wall with free communication b/n pleural space and atmosphere
-if diameter of injury greater than narrowest portion of upper airway, air preferentially moves
through injury site rather than the trachea
-treat with occlusive dressing over wound taped on 3 sides prevents conversion to tension PTX
-definitive treatment: wound closure and CT thoracostomy
Flail Chest:
-four or more ribs are fractured in at least two locations
-paradoxical movement of free-floating segment
) * + %,"
-check pulses, if palpable then sBP is at least: 60 mmHg (carotid); 70 mmHg (femoral); 80 mmHg (radial)
-control external haemorrhage: compression and splints
-avoid blind clamping risk to injure nerves
-two large bore IVs (16 gauge or larger) in antecubital fossa
-Saphenous vein cutdowns: 1 cm anterior and 1 cm superior to medial malleolus
-pediatric patients < 6 years:
-percutaneous femoral vein cannulation contraindicated b/c of DVT risk
-interosseous cannulation an option: proximal tibia or distal femur
- " % + + . $/ /* % %,"
CNS status sl. anxious mild anxiety anxious and confused and
confused lethargic
555
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a. Nonresponders:
-usually cardiogenic
-look at CVP and neck veins:
-flat neck veins, CVP < 5, hypovolemic ongoing haemorrhage
-distendend neck veins, CVP > 15 cardiogenic shock
-Ddx cardiogenic shock: (1) tension PTX; (2) pericardial tamponade; (3) myocardial
contusion or infarction; (4) air embolism
Pericardial tamponade:
-decreased RV output and CVP
-with acute tamponade, as little as 100 cc of blood can produce life-threatening homodynamic
compromise
-Beck’s triad: hypotension, distended neck veins, muffled heart sounds
-increased pulsus paradoxus
-treat with pericardiocentesis
-done even if pt stabilizes with volume loading still risk of subclinical myocardial
ischemia sudden lethal arrhythmias
-if still hypotensive emergency thoracotomy
Myocardial contusions:
-ECG abnormalities: ventricular dysrhythmias, a-fi, sinus bardycardia, BBB
-early placement of Swan-Ganz, urgent echocardiogram (r/o septal or free wall rupture, valvular
disruption, or pericardial tamponade)
Air embolism:
-air accumulation in LV impedes diastolic filling; can disrupt coronary perfusion
-Trendelenberg position emergency thoracotomy cross-clamping of pulmonary hilum air
aspirated from LV with 18-gauge needle
b. Transient Responders:
-usually have some degree of active haemorrhage
-penetrating injuries OR for exploration
-blunt trauma: CT or angiography if hemodynamically stable
-traditional volume resuscitation of patients sustaining penetrating torso trauma (PTT) has been questioned:
-active bleeding increases as venous and arterial pressure increases
-no survival advanced in hypotensive patients sustaining PTT and required operative treatment
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-special attention to back, axillae, perineum (often overlooked)
-DRE sphincter tone, blood, perforation, high-riding prostate
-Foley catheter:
-stable pts at risk for urethral injury urethrography before catheterizaiton
-signs of urethral injury: blood at meatus, perineal or scrotal haematomas, high riding prostate
-NG tube: decrease risk of gastric aspiration
-X-rays: AP chest, pelvis, c-spine
556
-high vs. low velocity; close vs. long range
-blunt trauma: associated with multiple, widely distributed injuries
-high vs. low energy transfer
$ .
-lateralizing findings: eg. unilateral dilated pupil unreactive to light, asymmetric movement, unilateral
Babinski’s reflex suggest treatable intracranial mass lesion
-stroke syndromes search for carotid dissection or thrombosis with doppler or angiography
-basilar skull fractures: otorrhea, rhinorrhea, “raccoon eyes”, Battle’s sign (mastoid ecchymosis)
-risk of meningitis
-CT +/- plain films should be done
Epidural Hematoma:
-blood accumulates b/n skull and dura
-disruption of middle meningeal artery
Subdural Hematoma:
-occur b/n dura and cerebral cortex
-venous disruption or laceration of parenchyma of brain
Post-injury Hydocephalus:
-bleeding into ventricles
Diffuse Axonal Injury:
-from high-speed deceleration injury and represents direct axonal damage
-CT: blurring of grey matter with multiple, small, punctate haemorrhages
-associated with poor outcome
& $*5
557
-prognosis and recovery poor
-Brown-Sequard syndrome:
-penetrating injury causing hemisection of cord
-ipsilateral loss of motor function, proprioception, and vibration
-pain and temperature on contralateral side lost
-Management:
-Zone I:
-involvement of visceral and vascular injuries in the thoracic outlet
-angiography of great vessels, esophagram, esophagoscopy, bronchoscopy if stable
-surgical exploration if unstable
-Zone II:
-prompt exploration if airway compromise, expanding haematoma, significant external
haemorrhage
-local exploration in stable patients:
-no penetration of platysma close wound and d/c home
-penetration of platysma observation for 12 h
-Zone III:
-require carotid and vertebral angiography if evidence of arterial bleeding
1. exposure of distal internal carotid and vertebral arteries difficult
2. internal carotid my have to be ligated high risk of stroke
3. active haemorrhage can be controlled be selective embolization
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Aortic Tears:
-tear of descending thoracic aorta most threatening
-findings on CXR suggestive of aortic tear:
1. widened mediastinum
2. abnormal aortic contour
3. tracheal shift
4. NG tube shift
5. left apical cap
6. left or right paraspinal stripe thickening
7. depression of left main bronchus
8. obliteration of aorticopulmonary window
9. left pulmonary hilar hematoma
-most otfen seen in high-energy-transfer deceleration MVA with frontal or lateral impact
-tear usually distal to left subclavian artery, where aorta is tethered by ligamentum arteriosum
-CT and angiography required
- 6., $"
-presence of abdominal rigidity or gross distention in patient with truncal trauma indication for prompt
surgical exploration
Penetrating wounds:
-gunshot wounds mandatory laparotomy
-anterior and lateral stab wounds explore in ER and determine if peritoneum violated
-injuries that do not penetrate peritoneal cavity no further evaluation
558
-DPL: most sensitive test for determining presence of intraabdominal injury
-positive if:
1. More than 10 ml of free blood aspirated
2. RBC > 100,000/mm3; > 10,000/mm3 when evaluating for diaphragmatic injury
3. Detection of bile, fecal material or observation of effluent draining through CT, NG, or Foley
-diaphragm penetration laparotomy
0 $+2 /
-frequently produces complex fractures
-potential injury to bladder, rectum and vagina
7% $ %$/
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-restore blood volume with type O RBCs intravascular haemolysis ~ 0.05%
-hemolytic reactions due to irregular antibodies in pts plasma (eg. Kell, Duffy, Kidd etc..); usually
not as severe as ABO incompatibility
-correct any coagulopathy with FFP and platelets
& ,1( + 7 /
-all undergoing operation should receive preemptive antibiotic therapy
-first generation cephalosporins for most operations
-tetanus prophylaxis
-compressive pulsatile stockings DVT prophylaxis
-thermal protection - hypothermia impairs coagulation and myocardial contractility and increases
559
myocardial irritability
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-arteries for which repair should always be attempted:
aorta and carotid, innominate, branchial, superior mesenteric, proper hepatic, renal, iliac, femoral
and popliteal
-veins: SVC, IVC proximal to renal veins, portal vein
-options for treatment:
-pulsatile observation, ligation, lateral suture, end-to-end anastomosis, interposition grafts
(autogenous vein or artery, PTFE graft, Dacron), transpositions, extraanatomic bypass,
interventional radiology
-exogenous grafts less than 6 mm more prone to thrombosis
-ligation of SVC associated with sudden blindness from compression of optic nerve from venous
hypertension
-ligation of suprarenal IVC associated with acute renal failure from venous hypertension
- % #$. 1$ %,"/
-“Bloody Vicious Cycle”: coagulopathy, profound hypothermia, metabolic acidosis fatal arrhythmia
-heat loss appears to be the central event since neither of other components can be corrected until
core temperature is restored
-staged operations indicated when a coagulopathy develops and core temperature < 34oC
-unorthodox techniques used to expedite wound closure reoperation planned within 2-
24h allows for correction of hypothermia, coagulopathy and metabolic acidosis
-“Abdominal or Thoracic Compartment Syndrome”
-sources: blood and edema
-acute increase in intracavitary pressure
-decreased residual functional capacity hypoxia
- venous return CO
- venous resistance perfusion to intraabdominal organs acute renal failure
-life-threatening hypoxia and renal failure if IAP > 25 mmHg (measured with Foley)
-treatment: decompress abdominal cavity; volume expansion and inotropic support
< 15: normal
15-25: volume expansion, may need decompression
26-35: watch PaO2, SaO2, U/O, decompression likely
> 35: decompress in operating room
560
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Cervical Spine:
-axial traction to reduce subluxations external fixation with halo-vest (3-6 months)
-surgical fusion for:
-neurologic deficit
-angulation greater than 11 degrees on flexion and extension x-rays
-unstable after external fixation
Spinal Cord:
-complete injuries untreatable
-concussive injuries in 3% of pts presenting with flaccid quadriplegia recover
-significant improvement if methylprednisolone used within 8h of injury
Larynx:
-cricothyroidotomy or tracheotomy in severe fracture to protect airway
-larynx repaired with fine wires and sutures
Venous Injuries:
-thrombosis generally asymptomatic
-stent placement if ICP remains elevated
561
(, * * %+$%
Great Vessels:
-angiography desirable for planning incisions
-median sternotomy: exposure of innominate, proximal right carotid and subclavian, proximal left carotid
artery
-“trapdoor” thoracotomy for good exposure of proximal left subclavian artery
($/%
-most common life-threatening complications from blunt and penetrating thoracic injury are hemothorax,
pneumothorax or a combination of the two
-chest tubes are a definitive treatment
-sources of bleeding: intercostal vessels, internal thoracic artery, pulmonary parenchyma, heart
Thoracic Incisions:
-anterolateral thoracotomy exploratory thoracotomy for haemorrhage
-excision can be extended bilaterally
-posterolateral thoracotomies only for:
-injuries of posterior aspect of trachea
-main bronchi near carina
-tear of descending thoracic aorta
Lungs:
-pulmonary tractotomy:
-linear stapling devices inserted directly into injury tract and position to cause the least degree of
devascularization
-lobectomy or pneumonectomy rarely necessary
562
6., $"
Vascular Injuries:
-vascular injuries in blunt trauma less common; usually involve renal artery and veins
-left medial visceral rotation expose upper abdominal aorta
-right medial visceral rotation expose infrahepatic vena cava
-injuries at bifurcation of IVC hidden by right common iliac artery; this artery is divided for exposure and
must be repaired after venous injury treated
Liver:
-manual compression, clamp hepatic pedicle (Pringle manoeuver), and perihepatic packing
-tight packing can compress IVC and reduce cardiac filling, and decrease tidal volume and FRC
-resectional debridement: remove non-viable tissue; do not remove > 75%
-complications after significant hepatic trauma:
-haemorrhage, infection, fistulas
-bilomas: loculated collections of bile (may or may not be infected)
-sterile bilomas will eventually resort
-biliary fistulas (3%): usually close without treatment
Spleen:
-splenic repair (splenorrhaphy), partial splenectomy, resection, or non-operatively
-trend toward non-operative management
-overwhelming postsplenectomy infection (OPSI):
-encapsulated bacteria: S.pneumonia, H. influenze, N. meningitidis
-resistant to treatment
-occurs in young children and immunocomporomised adults
-hilar injuries or pulverized splenic parenchyma splenectomy
-pneumococcal vaccine routinely given after splenectomy
Diaphragm:
-injured on left 75% of cases
-blunt trauma tear in central tendon that may be large
-laceration closed with 1-0 monofilament permanent suture
Duodenum:
-duodenal haematoma:
-more common in children
-blood b/n seromscular and submucosa layer obstruction
-x-rays: “coiled-spring sign of obstruction”
-most managed non-operatively with NG and parenteral nutrition
-duodenal perforations:
-caused by both blunt and penetrating trauma
-often contained by retroperitoneum
-most treated by primary repair
563
Pancreas:
-blunt pancreatic transection at neck of pancreas pseudocyst or pancreatic ascites
-dx with CT
-ductal injury require treatment
-methods of identifying ducal injuries:
-operative pancreatography
-coronary artery dilatory into main duct via papilla and observe wound
-ERCP
-injuries to head of pancreas final option is to drain pancreas; if fistula or pseudocyst develops, diagnosis
is confirmed; most fistulas close spontaneously with only supportive care
-injuries to neck, body, tail distal pancreatectomy
-pancreatic injuries should be drained when there is a possible unidentified major ductal injury
Pancreaticoduodenal Injuries:
-risk of duodenal suture line dehiscence and development of lateral duodenal fistula
-repair duodenal injury and drain pancreatic injury
-pancreatoduodenectomy:
-transection of intrapancreatic bile duct and main pancreatic duct in head of pancreas
-avulsion of papilla of Vater from duodenum
-destruction of entire second portion of duodenum
Colon:
-primary repair: definitive treatment at initial operation, but risk of leakage
-colostomy: avoids unprotected suture line in abdomen, but second operation required to close colostomy
-exteriorized repairs:
-suspending repaired perforation or anastomosis on abdominal wall with appliance after the
fashion of loop colostomy; if suture line does not leak after 10 days, it can be returned to
abdominal cavity under local anesthesia
-no longer indicated
Rectum:
-often injured by gunshot wound, rarely by stab wound, and frequently by acts of autoeroticism and sexual
misadventure
-intraperitoneal portion treated as per colonic injuries
-extraperitoneal injuries drained via retroanal incision
Kidneys:
-CT, IVP, arteriography used to evaluate extent of injury
-95% of blunt injury treated non-operatively
-persistent gross hematuria embolization
-nephrectomy an option provided that opposite kidney normal
-all penetrating wounds to kidneys are explored
Ureters:
-injuries from external trauma are rare
-occur in a few patients with pelvic fracture
-can be repaired primarily
-nephrostomy for proximal urethral injuries when renal function mut be preserved and patient will not
tolerate surgery for the length of time required for ureteral repair
564
Bladder:
-diagnosed by cystography, CT or during laparotomy
-intraperitoneal injuries primary repair
-extraperitoneal injuries foley catheter; direct operative repair not necessary
Urethra:
-blunt disruption of posterior urethra managed by bridging defect with Foley catheter
-strictures repaired electively
-penetrating injuries treated by direct repair
Gynecologic Injuries:
-rare
-repair of transected fallopian tube unjustified suboptimal repair increases risk of tubal pregnancy
-blunt trauma can cause uterine rupture in pregnancy
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-can cause exsanguinating retroperitoneal haemorrhage
-branches of internal iliac vessels and lower lumbar arteries often responsible
-options to decrease hemorrhage:
-external fixation
-MAST
-angiography with embolization
-pelvic packing
-open pelvic fracture: risk of sepsis and osteomyelitis high
-reduce risk of infection with sigmoid colostomy
-wound manually derided and irrigated daily until granulation tissue covers the wound
7% $ %$/
Compartment Syndrome:
-acute increase in pressure in a closed space that impairs blood flow to the structures within
565
-causes: arterial haemorrhage into compartment, venous ligation or thrombosis, crush injuries, infections,
crotalid envenomation, ischemia/reperfusion
-presence or absence of pulse is unreliable in diagnosis
-pressures > 45 mmHg require operative intervention
-treatment: elevation, evacuation of haematomas, fasciotomy
' !
6 $/
-most domestic animal bites are provoked attacks; it this history is obtained, rabies vaccine usually can be withheld
if the animal appears healthy
-unprovoked attack by a domestic animal more likely to indicate animal is rabid
-fully vaccinated dog or cat unlikely to become infected with rabies
-animals who have bitten observed for symptoms of rabies for 10 days
-incubation period: 10 days 1 year (most w/n 20-90 days)
-post-exposure prophylaxis:
-human rabies immunoglobulin (HRIG): 20 IU/kg
-vaccine: human diploid cell rabies vaccine (HDCV) or rabies vaccine adsorbed (RVA)
-five doses of 1ml IM:
-post-exposure, then days 3, 7, 14, 28
-routine postvaccination serologic examination not necessary unless patient is known to be
immunosuppressed
-corticosteroids can interfere with development of active immunity after vaccination and may predispose
the patient to rabies
-pregnancy not a contraindication
566
-laryngospasm, dysphagia
-drooling, maniacal behaviour, convulsions death, coma, paralysis, and death
-respiratory supportive care only treatment
" 5$/
Pit Vipers:
-venoms known to have neurotoxic, haemorrhagic, thrombogenic, hemolytic, cytotoxic, antifibrinolytic and
anticoagulant effects
-contain hyaluronidase
Coral Snakes:
-contributes to only 3% of all bites and 1.5% of all deaths from poisonous snakes
-blurred vision, ptosis, drowsiness, increased salivation, and sweating
-death may occur from inadequate ventilation
$",1%$
-honeybee, bumblebee, wasp, yellow and black hornet, fire ant
-venom causes more deaths in US yearly than are caused by snakebites
-fatal cases may manifest glottal and laryngeal edema, pulmonary and cerebral edema, visceral congestion,
meningeal hypermia, and intraventricular haemorrhage
& %"# /
-treat with copious irrigation with water to wash out any toxin and fragments of the ray spine’s
integumetary sheath
-venom is inactive when exposed to heat place injured part in hot water
-complications: tissue necrosis with prolonged drainage and chronically infected wounds
) , % # $/$ ! " ,3 9
-application of a substance with high alcohol content, followed by drying agent (eg. flour, baking soda,
talc, or shaving cream)
-tentacles removed by shaving
-baking soda neutralizes acidic toxins
- 1 .$ /
-Black Widow Spider:
-Latrodectus mactans venom primarily neurotoxic and centers on spinal cord
-generalized muscle spasm most prominent physical finding
567
-priapism and ejaculation have been reported
-treatment:
-narcotics and muscle relaxant
-calcium gluconate relieves symptoms by depressing threshold for depolarization
-Brown Recluse Spider:
-Loxosceles recluse: body 7-12 mm
-initial bite may go unnoticed
-severe bites result in progression to necrosis and sloughing of skin with residual ulcer formation
-haemolysis and thrombocytopenia responsible for deaths
-conservative therapy usually is preferred treatment
0 *, 1 ,"/
-bark scorpion medically significant
-venom is neurotoxic release of neurotransmitters from autonomic nervous system and adrenal glands
-tap test: hyperesthesia persists at site intense pain with light tap
-anxiety, blurred vision or temporary blindness, wandering eye movement, dyspnea, wheezing, dysphagia,
involuntary urination and defecation, opisthotonos
-somatic symptoms
-treated with cold compresses
568
AIRWAY IMAGING IN CHILDREN
Supraglottic Obstruction
Acute epiglottitis:
-lateral neck: thickening of both epiglottis and
aryepiglottic folds
-beware of normal findings:
-“omega epiglottis”: areyepiglottic folds
will remain thin
-other causes of epiglottitic enlargement:
-angioneurotic edema, candidal infection,
burns from corrosive ingestion, laryngeal
sarcoidosis, neoplasms, lymphatic
malformation, allergic reactions,
aryepiglottic fold cysts
Laryngomalacia:
-downward and posterior bending of epiglottis and
anteroinferior buckling of aryepiglottic folds
during inspiration
-best seen with fluoroscopy or endoscopy
Glottic Obstruction
Croup:
-lateral view:
-inspiration: distension of hypopharynx and narrowing of subglottic area
-expiration: collapse of hypopharynx and re-expansion of subglottic trachea
-indistinct vocal cords
-AP view:
-steeple or funnel-shaped subglottis
Bacterial Tracheitis:
-irregularity of walls of subglottic trachea
Laryngeal papilloma:
-nodular thickening of vocal cord on lateral view
Subglottic Obstruction
Subglottic Stenosis:
-narrowing persists during both inspiration and expiration
-CT or MRI best for diagnosis
569
Tracheomalacia:
-hypercollapsibility of trachea on expiration due to weakness of supporting cartilage
Subglottic Hemangioma:
-occur on lateral or posterior walls of subglottic trachea
-eccentric narrowing seen
-ddx: granuloma, ectopic thyroid or thymus tissue, subglottic mucoceles, post-inflammatory
histiocytoma, tracheal cysts
Retropharyngeal Abscess:
-lateral view:
-convex anterior displacement of posterior pharyngeal airway
-loss of normal step-off at origin of esophagus
-false positive if x-ray taken in expiration (clue: anterior buckling of trachea)
-straightening or hyperflexion of cervical spine 2o muscle spasm
-+/- gas in soft tissues
-CT scan:
-focal hypodensity with rim contrast enhancement
-US: to evaluate drainable fluid collection
-MRI:
-T1: dark
-T2: increased signal
Choanal Atresia:
-most common cause of nasal obstruction in neonate
-axial CT scans:
-children < 2ya: choanal orifice < 0.37 cm
-children < 8ya: vomer exceeds 0.34 cm
-medial bowing and thickening of lateral walls of nasal cavity
-fusion of lateral walls with enlarged vomer
Nasal Polyp:
-most common nasal mass seen in children
-MRI: bright T2 (fluid)
Juvenile Angiofibroma:
-enhances with contrast
-MRI: bright T2, flow voids
570
PEDIATRIC SLEEP-DISORDERED BREATHING
PATHOPHYSIOLOGY
-anatomic and neuromuscular factors:
1. Hypertrophied lymphoid tissue (adenotonsillar hypertrophy most common cause)
2. Dysmorphic constricted craniofacial development:
-retrodisplaced/hypoplastic mandible: Pierre Robin sequence
-small nasopharynx: Treacher Collin, Apert, and Crouzon syndromes
3. Macroglossia
4. Low lying hyoid bone
5. Neuromuscular hypotonia: eg. Down syndrome, cerebral palsy
-sleep fragmentation and decreased REM sleep causes daytime symptoms of the disorder
-pediatric SDB typically related to adenotonsillar hyperplasia with varying degrees of other skeletal and
soft-tissue anatomic factors playing less common or less important roles
-hypercapnia and hypoxemia and resulting arousals often result in reduction in REM sleep associated
with a reduction in growth hormones
-sequelae:
-instead of excessive daytime sleepiness
-hyperactivity, attention deficit, aggression, and other behavioural disorders may be seen
-mouthbreathing and hyponasal speech with articulatory errors
-SDB shown to affect school performance intervention resulted in improved grades
-high prevalence of allergy in snorers
-nocturnal enuresis frequently reported in children with OSAS
-failure to thrive
-poor weight gain due to:
-decreased GH production
-increased energy expenditure with nocturnal movement and calorie expenditure
-difficulty smelling and tasting food
-pulmonary hypertension, arrhythmias, cor pulmonale
EVALUATION
History
-sleep history:
-typical bedtime, number of hours of sleep, abnormal sleep positions, parasomnias (nocturnal
enuresis), character of snoring, observed pauses in respiration and signs of respiratory distress,
problems after waking up (headache/fatigue), behavioural disorders, school performance,
hypersomnolence
Physical Examination
-look for mouth breathing
-assess dental malocclusion, pharyngeal soft tissue anatomy, lingual shape and size relative to
oropharyngeal airway, shape of hard and soft palates, size of uvula, velopharyngeal function, degree of
tonsillar enlargement
Laboratory Evaluations
-PSG remains the gold standard for diagnosis of OSAS
-criteria for abnormal study:
-apnea index > 1
-oxygen desaturation > 4% more than 3x/h or associated with > 25% change in HR
-oxygen desaturation < 92%
571
-elevation of end-tidal CO2 to > 50 mmHg for more than 8% total sleep time or 45 mmHg for
more than 60% of sleep time
-flexible endoscopy provides the best assessment of the nasopharynx and its soft tissues
TREATMENT
572
LARYNGEAL STENOSIS
PEDIATRIC ANATOMY
-other features:
-subglottis is narrowest part of airway in children
-stenosis present if cricoid area < 4mm
-hyoid over-rides superior larynx
-superior border of infant larynx is located at C1
-epiglottis:
-overlaps dorsal surface of soft palate
-omega shaped
-more acute angle b/n glottis easily falls into laryngeal inlet
-circumferential mucosal edema of 1 mm narrows subglottic space by > 60%
LARYNGEAL STENOSIS
573
Congenital Laryngeal Stenosis
Subglottic Stenosis
-cricoid lumen < 4 mm in diameter
-d/t failure of laryngeal lumen to recanalize (failure with autolysis GRADING SCALE FOR LARYNGEAL
of epithelial remnant of growing respiratory tract) STENOSIS
-varying degrees of respiratory problems Grade Laryngeal Lumen Obstruction
-types: I < 50%
-membranous stenosis II 51-70%
-circumferential, fibrous soft-tissue thickening III 71-99%
IV complete obstruction
-granulation tissue
-submucsal gland hyperplasia
-submucosal fibrosis
-cartilaginous stenosis
-cricoid cartilage deformity
-normal shape small for infant’s size
-abnormal shape
-large anterior or posterior lamina
-generalized thickening
-elliptical shape
-submucosal cleft
-trapped first tracheal ring
-combined stenosis
Atresia
-high frequency of other congenital anomalies
-high mortality
-complete failure to recanalize laryngeal lumen
-requires tracheotomy
Webs
-usually arise anteriorly; 90% located at level of glottis
-10% associated with congenital anomalies; strong association with VCFS
-represent failure to completely recanalize larynx
-thin webs easily lysed; thick webs require open reconstruction
Postintubation Stenosis
-incidence 1-8%
-more common than congenital stenosis in pediatric age group
-pathophysiology:
-pressure of tube causes ulceration and necrosis of cricoid mucosa
-infection and perichondritis/chondritis of underlying cartilage
-healing and fibrosis occurs stenosis
-risk factors:
-cricoid ring is narrowest portion or airway
-ischemic necrosis can be caused by ETT pressure
-superimposed respiratory tract infection
-length of time of intubation
-repeated intubations
574
-diagnosis:
DIFFERENTIAL DIAGNOSIS
-CT scan reconstructions: length of
stenosis Neonate
-bronchoscopy: size of stenosis -laryngomalacia
-vascular compression (eg. innominate artery, aberrant
subclavian vascular ring)
Postoperative Stenosis -vocal cord paralysis
-after high tracheotomies and -bilateral (eg. Arnold-Chiari deformity)
cricothyroidotomies -unilateral (eg. traumatic postductus ligation)
-hemangioma, subglottic
-failed laryngotracheoplasty -complete tracheal rings
-laryngeal cleft
-cri-du-chat syndrome
Infectious or Inflammatory Stenosis -laryngeal saccules, laryngoceles
Child
Granulomatous Disease -dermoids, saccular, epiglottic cysts
-tuberculosis of larynx: -lingual thyroid
-most common sites: -infections (eg. epiglottitis, croup, bacterial
laryngotracheitis)
-interarytenoid space, -foreign bodies
arytenoid cartilages, -papillomatosis
posterior surface of true
vocal cords, laryngeal Adult
-vocal cord paralysis
surface of epiglottis -viral, granulomatous, fungal laryngitis
-nodular lesions and ulceration of -Reinke edema
epithelium perichondritis and -laryngeal trauma, potintubation
chondritis extensive scarring and -hemangioma, supraglottic
-idiopathic
stenosis -neurologic (eg. ALS, MS)
-systemic treatment leads to -caustic ingestion
complete healing of larynx -systemic disease (eg. RA, polychondritis)
-sarcoidosis, rhinoscleroma, WG (rare in -Tracheal tumours or obstruction
children)
Trauma
-d/t foreign bodies and instrumentation
-anterior blunt trauma posterior supraglottic and glottic stenosis
Systemic Diseases
-lupus, gout, rheumatoid arthritis or juvenile rheumatoid arthritis (Still disease) fixation of cricoarytenoid
joint
-dx: laryngoscopy and palpation to differentiate from vocal cord paralysis
Thermal Injuries
-steam, laser airway fires
-three factors: direct thermal injury, toxic effects of combustion products, and prolonged intubation
Caustic Ingestions
-laryngeal stenosis rare
-fibrosis of posterior cricoarytenoid muscle
-supraglottic scarring and stenosis
575
Radiation Effects
-may cause pharyngeal or laryngeal edema and stenosis
MANAGEMENT
-fewer than half of patients with congenital laryngeal stenosis require tracheotomy
Medical Therapy
-prevention
-experienced intubation personnel
-correctly sized ETT
-supportive therapy:
-humidification, antibiotics, steroid therapy
-management of GERD
-PPI
Surgical Treatment
-Preoperative workup:
-secure airway, endoscopic evaluation of
FACTORS PREDISPOSING TO FAILURE IN
airway size TREATING SUBGLOTTIC STENOSIS WITH CO2
-cardiac and pulmonary function LASER
-gastric reflux assessment
-failure of previous endoscopic procedures
-radiographic studies -significant loss of cartilaginous framework
-combined laryngotracheal stenosis
-Grade I or II stenosis, unilateral lesions -circumferential cicatrical scarring
-no treatment (majority) -fibrotic scar tissue in interarytenoid area of posterior
commissure
-dilatation, cryosurgery, division, micro- -abundant scar tissue greater than 1 cm in vertical
trapdoor flaps dimension
-endoscopic resection with laser surgery -severe bacterial infection of trachea after tracheotomy
(CO2 or KTP laser excision with dilation) -exposure of perichondrium or cartilage during CO2 laser
excision predisposing to perichondritis and chondritis
-66-80% success) -concomitant tracheal disease
-contraindications: significant
cartilage loss, concurrent
laryngotracheal stenosis, posterior
commissure involvement, circumferential cicatricial scar or thick scar (> 1cm), infected
tissue (chondritis)
-Failed extubation stenosis
-anterior cricoid split (for neonate only)
-tracheotomy
-Grades II, III, and IV stenosis; circumferential lesions, thick webs, failed endoscopic therapy, loss of
cartilaginous framework
-anterior cricoid split
-posterior cricoid split
-laryngotracheal reconstruction
-via laryngofissure:
-anterior split with lumen augmentation
-posterior split with lumen augmentation
-anterior and posterior split with lumen augmentation
-segmental resection with end-to-end anastomosis, tracheal or cricotracheal
576
Anterior Cricoid Split
-used instead of tracheotomy in neonate
-*Criteria:
-two or more extubation failures secondary to laryngeal pathologic conditions
-weight > 1500 g
-no assisted ventilation for 10 days before evaluation
-O2 requirements < 30%
-no CHF for 1 month
-no acute upper or lower respiratory tract infection
-no antihypertensive medication for 10 days
-anterior laryngofissure should only extend to lower one third of thyroid cartilage
Laryngotracheal Reconstruction
Cricotracheal Resection
-reserved for severe (grade III or IV) subglottic stenosis
-technically challenging but higher chance of achieving decannulation
-contraindication: subglottic scarring within 3 mm of vocal cords
-advantages:
-glottic sparing
-avoidance of donor site morbidity
-near normal-appearing and mucosalized airway
-disadvantages:
-risk to RLN
-anastomotic dehiscence
Stenting Options
-T-tube (Montgomery or Hood)
-wired-in metal tracheotomy tube within a Teflon stent (Aboulker or Cotton Lorenz)
577
STRIDOR, ASPIRATION, AND COUGH
Stertor
-inspiratory low-pitched sound
-nasopharyngeal and oropharyngeal obstruction
Stridor
-inspiratory stridor with supraglottic and glottic obstructions
-expiratory stridor with intrathoracic lesions
-biphasic stridor with fixed subglottic laryngeal and cervical tracheal lesions
-infant larynx:
-vc length: 6-8 mm
-posterior glottis transverse length: 4 mm
-subglottic diameter: 5-7 mm
-tracheal length: 4 cm
Cough
-inspiratory, compressive, expiratory phases
Swallowing
-preparatory, oral, pharyngeal, esophageal phases
-anatomical differences in children:
-hard palate closer to skull base
-larynx higher in neck
-adenoid pad, tonsils, tongue relatively larger
-airway protection: 3 interlocking systems:
-first system: swallowing mechanism
-second system:
-level 1: epiglottis, aryepiglottic folds, arytenoids
-level 2: false cords
-level 3: true cords
-third system: mucociliary clearance and cough reflex
STRIDOR
Evaluation
History
-birth history
-age of onset
-severity
-progression
-posturing and position changes
-hoarseness, eating or feeding difficulties, sleep-disordered breathing
Physical Examination
-ABCs
-H+N exam, FNL
578
Radiology and Special Studies
-CXR - in/ex views
-barium esophagram: r/o vascular rings and TEF
-CT: choanal atresia/stenosis
Airway Endoscopy
-good communication with anaesthetist
-inspection of equipment before induction of anaesthesia
-Storz bronchoscope
-Hopkins rod-lens telescope
-inhalational anaesthesia, spontaneous ventilation maintained
-steroids +/- racemic epinephrine to limit postoperative edema
-choanal atresia or stenosis -nasal polyps -encephalocele -hypotonia, neurologic -foreign body
-piriform aperture stenosis -rhinitis -dermoids disease -haematoma
-glossoptosis / macroglossia -retropharyngeal abscess -glioma -vocal cord paralysis -laryngeal fracture
-lingual thyroid -adenoid hypertrophy -dermoids
-vallecular cyst -tonsil hypertrophy -hemangioma
-craniofacial anomalies -epiglottitis -lymphangioma
-laryngomalacia -angioneurotic edema -papilloma
-laryngocele / saccular cyst -laryngitis -granuloma
-glottic web / atresia -laryngeal spasm -mediastinal tumours
-subglottic stenosis -croup -thyroid
-subglottic cysts -bacterial tracheitis -thymus
-tracheal stenosis -bronchitis
-tracheomalacia -asthma
-vascular ring
-complete tracheal rings
-foreguts cysts
-TEF
-congenital etiology in 85% of children < 2.5 years presenting with stridor
Laryngomalacia
-most common cause of stridor in infancy
-typically resolve by 12-18 months
-low pitch stridor with fluttering quality; most prominent in supine position
-FNL: cyclical collapse of supraglottic larynx with inspiration
-Type A: inward movement of AE folds
-Type B: curling of epiglottis
-Type C: inward collapse of cuneiform cartilages
-Type D: inward collapse of arytenoid cartilages
-Type E: folding inward of epiglottis
-Type F: shortened aryepiglottic folds
-usually no surgical intervention required
-supraglottoplasty if:
-inability to feed orally
-cor pulmonale
-FTT
-life-threatening episodes of obstruction
579
-types of supraglottoplasty:
-excision of cuneiform cartilages and/or redundant mucosa
-excision of superior epiglottis
-incision/release of aryepiglottic folds
Laryngeal Stenosis
-congenital laryngotracheal stenosis second most common cause of stridor in infants
-see Ch 73
Subglottic Hemangioma
-2:1 female predominance
-1.5% of all congenital laryngeal anomalies
-50% have cutaneous hemangiomas present at time of diagnosis
-most resolve by 5 years
Laryngeal Papillomatosis
-HPV-6 and HPV-11
-squamociliary junction (vocal cords) areas of injury (tracheotomy site)
-rate of vaginal transmission low (1-3%)
-C-section not routinely recommended to patients with genital papilloma
-tx: CO2 laser or debrider debulking
-non-surgical modalities:
-interferon-a, indole compounds, antiviral therapy, phototherapy
-tracheotomy:
-50% rate of tracheal spread
Vascular Anomalies
-d/t tracheal compression by:
-vascular rings (double aortic arch)
-pulmonary slings
-aberrant right subclavian artery
-absolute indications for surgical repair:
-reflex apnea: reflexive respiratory arrest secondary to stimulation of vagal afferent nerve fibres
during swallowing
-failure of medical management of respiratory distress after 48h
-prolonged intubation
580
Laryngeal Dyskinesia, Exercise-induced Laryngomalacia, and Paroxysmal Vocal Fold Motion
-resulting from neuromuscular dysfunction
Laryngotracheobronchitis
-“croup”
-most common infectious cause of stridor (affecting 3-5% of children at least once)
-peak incidence 2ya
-cause: parainfluenza virus type 1
-other: parainfluenza virus types 2 and 3, RSV, and influenza virus A
-barking cough, inspiratory high pitched stridor
-CXR: “steeple sign” - symmetric narrowing of subglottic space
-treatment:
-humidified oxygen
-dexamethasone (0.6-1 mg/kg) for severe breathing difficulty
-nebulized racemic epinephrine (be wary of rebound edema)
-< 5% of hospitalized children will require intubation and ventilation
581
ASPIRATION
Radionuclide Scintigraphy
-calculates percentage of aspiration
Electromyography
-permits study of individual muscles during swallowing
-pharyngeal constrictors, thyroarytenoid and cricopharyngeal muscles
-patterns: tonic, phasic, or absent
-can distinguish upper from lower motorneuron lesions
Management
582
COUGH
Evaluation
-chronic coughing
-productive (tracheobronchial disease) vs non-productive (upper airway lesion or asthma)
-PND, GERD, smoking
Investigations
-CBC, CXR, sputum: cytology, bacteria, TB, fungus
-+/- CT sinuses, PFTs
-+/- endoscopy
583
CAUSTIC INGESTION AND FOREIGN BODIES
IN THE AERODIGESTIVE TRACT
Clinical Presentation
-most signs, symptoms, lab tests are not consistently predictive of gastroesophageal involvement
-presence of oral injuries cannot accurately predict presence or absence of more distal involvement
-severity of external and oropharyngeal injury does not correlate with extent of esophageal and gastric
injury
-dysphagia, retrosternal pain, or abdominal pain often indicates severe esophageal injuries
584
-assess severity of injury:
-grade 1: superficial injury
-grade 2: transmucosal injury
-grade 3: circumferential transmucosal injury
-grade 4: transmural injury
Second Degree whitish exudate, erythema, underlying ulceration that may extend into the muscularis
Third Degree dusky or blackened transmural tissue, deep ulcerations that may extend into periesophageal tissue, lumen may be
obliterated
Complications
-most common: stricture formation
-esophageal perforation
-tracheoesophageal fistula
-gastric perforation
585
-mediastinitis, peritonitis, pneumonia
-sepsis, death
-(esophageal carcinoma)
FB Aspirations
-types of objects:
-vegetable matter (70-80%)
-peanuts, watermelon seeds, pumpkin seeds
-plastic pieces (15%)
-SSx:
-choking, stridor, chest pain, wheezing, hoarseness, audible slap
-auscultation:
-decreased air entry to affected side
-wheezing
-CXR:
-25% may be normal
-inspiratory and expiratory films needed:
-expiratory view:
-mediastinal shift opposite side of FB
-air trapping on affected side
-left lateral decubitus film: dependent lung remains inflated if obstructed
-right mainstem bronchi most commonly involved:
-larger than left side
-steeper angle
-greater airflow
-position more towards center
-types of obstruction:
-air valve: air can pass in/out normal CXR
-check valve: air can pass out but not in atelectasis
-ball valve: air can pass in but not out hyperinflation, deviation of mediastinum
-stop valve: air cannot pass in/out
-Management:
-avoid digital manipulation, back slapping, Heimlich manoeuver (unless completely obstructed)
-obtain description of object
-anaesthesia consult
-IV corticosteroids for organic aspirations
-bronchoscopy:
-must rule out multiple foreign bodies
-patient should be spontaneously breathing (ie. no paralysis)
-organic ingestions: IV steroids to reduce inflammation
-if unable to retrieve object after 1 hour stop procedure and bring back to OR the next day
-thoracotomy for multiple failed attempts at FB retrieval
586
FB Ingestions
-may present with respiratory distress d/t extreme compliance of wall b/n esophagus and trachea and mass
effect of FB
-most common area: C6 or level of cricopharyngeal muscle
-most common objects:
-coins (75%)
-meat/vegetable, small round trinkets etc (20%)
-complications:
-esophageal perforation
-mediastinitis
-pneumomediastinum
-pneumothorax
-aspiration
587
CONGENITAL NECK MASSES AND CYSTS
Midline
-thyroglossal duct cyst
-thymic cyst
-dermoids cyst
-plunging ranula
-teratoma of the neck
Entire neck
-haemangioma
-lymphatic malformation
Branchial Anomalies
-development of branchial apparatus (BA) begins at 2 weeks GA
-4th week of embryonic development
-condensation of mesoderm
-separated by external ectodermal cleft and internal endodermal pouch
-thin epithelilial plate separates each cleft and pouch
-each arch composed of an artery, cartilaginous bar, muscles and nerve
-course of each BA is caudal to structures derived from its arch and dorsal to structures that develop from
the following arch
588
Arch Nerve Muscle Skeletal Structure Artery Pouch # and Derivative
I Trigeminal (V) Mastication muscles, Meckel cartilage, malleus, Maxillary 1. Eustachian tube, middle
(Mandibular) mylohyoid, anterior incus, anterior ligament of ear
digastric, tensor malleus, sphenomandibular
tympani, tensor velum ligament
palatini
III Glosso- Stylopharyngeus Greater cornu hyoid, lower Common and 3. Thymus and inferior
pharyngeal (XI) body hyoid internal parathyroid
carotid
Anomalies:
-Sinus: vestigial cleft (external sinus) or pouch (internal sinus)
-Fistula: persistence of both cleft and pouch with dissolution of intervening separation plate
-Cyst: trapped portion of cleft or pouch
589
Second Branchial Anomalies (most common type)
Laryngoceles
-external laryngocele
-air-filled herniation of saccule of laryngeal ventricle
Fourth BA
Pseudotumour of Infancy
-affects 0.4% of all newborns
-pathophysiology:
-intrauterine or birth trauma causing muscle injury, hematoma, and resultant fibrosis
-firm round mass within SCM 2-3 weeks after birth
-diagnosis made by US
-conservative treatment with 80-100% complete resolution by 1 ya
-physical therapy, observation and reassurance
590
MIDLINE NECK MASSES
Thymic Cysts
-thymus:
-third pharyngeal pouch derivative
-formed during sixth week of life
-remnants may persist as cords along path of migration from angle of mandible to midline of neck
Dermoid Cysts
-usually in submental region
-do not elevate with tongue protrusion
-formed along lines of embryologic fusion
-lined by epidermis, containing epidermal appendages
-treat with simple excision
Plunging Ranulas
-pseudocysts of the floor of mouth caused by mucous extravasation from blocked sublingual gland
-isolated submental mass or in association with visible sublingual ranula
Lymphatic Malformations
-benign, multiloculated, soft, painless, compressive masses
-incidence 1.2-2.8 per thousand
-more common in posterior triangle of neck
-pathophysiology:
-abnormal development or obstruction of jugular lymphatics
-cosmetic deformity; masses in anterior neck may cause respiratory compromise
-US and CT: thin walled multi-loculated cysts
591
-tx: surgical excision
-high recurrence rate: 25-50%
Hemangiomas
-most common head and neck neoplasms in children
-<1/3 present at birth
-present first few months and enlarge over next 12 months
-involution occurs in 90%
-conservative treatment for most, surgery for deep seated tumours
-steroids and laser useful adjuncts
592
CONGENITAL ANOMALIES OF THE NOSE
EMBRYOLOGY
-third week of gestation, midline neural groove develops along dorsal surface of embryo forms neural
tube
-neural tube closure starts in mid-portion of embryo and progresses both anteriorly and posteriorly, leaving
neuropores at each end
-neural crest cells in lateral portions of neural tube begin migrating between tube and surface ectoderm into
mesenchyme
-anterior neuropore region especially vulnerable to developmental errors; it represents most distal end of
closed neural tube and most distal point of neural crest cell migration
-once neural crest cells reach their destinations, mesenchyme begins organizing and condensing into
mesodermal elements at various centers, which later fuse with one another and ossify
-potential spaces:
-fonticulus nasofrontalis: space b/n frontal and nasal bones
-prenasal space: space b/n nasal bones and nasal capsule
-foramen cecum: space b/n frontal and ethmoid bones; continuous with prenasal space
-spaces normally obliterate during fetal development
Dermoid -fistulous tract on nasal dorsum, with or without cyst located -complete surgical -infection
from nasal tip to glabella excision -cosmetic deformity
-protruding hair, cheesy contents typical CT may show bifid -meningitis
septum or patent foramen cecum
Glioma -smooth, firm, intra- and/or extranasal mass not attached to -surgical excision -cosmetic deformity
skin -nasal obstruction
-meningitis
593
NASAL DERMOIDS
-range of nasal anomalies varying from short epithelium-lined tract on nasal dorsum to tracts extending
from nasal dorsal skin through septum to dura
-can contain epithelium and skin appendages such as hair, hair follicles, and sweat and sebaceous glands
Embryology
-theories suggests that dermoids represent clusters of epithelium that became trapped at time of fusion of
ectodermal process
-if skin maintains its attachment to fibrous tissues of nasal capsule in the prenasal space or at fonticulus,
epidermal elements can be drawn under developing bones, forming a tract
Clinical Presentation
-sinuses and cysts generally occur in nasal midline
-pit, fistulous tract, or mass anywhere from nasal tip to glabella
-deeper involvement may occur and extension intracranially has been noted in 25-30% of cases
Evaluation
-CT and MRI are important in studying extent of lesion and if there is intracranial involvement
-CT findings that suggest deep extracranial involvement:
-fusiform swelling or bifidity of bony nasal septum
-widening of nasal vault
-glabellar erosion
-patent foramen cecum
-bifid crista galli
-MRI used to image soft-tissue masses in the sagittal plane
Treatment
-craniofacial approach if intracranial extension exists
-most dermoids do not have intracranial communication and can be safely approached externally
-approaches:
-vertical midline incision on nasal dorsum most efficient approach to extracranial dermoids
-medial osteotomies and outfracturing of nasal bones for exposure may be necessary
-external rhinoplasty approach:
-excellent cosmesis but limited exposure
-bicoronal flap approach:
-may be useful for dermoids at root of nose
-presence of epithelium in the stalk at skull base warrants an intracranial approach to completely and safely
excise entire tract
-glioma are unencapsulated collections of glial cells in a connective tissue matrix that may retain
attachments to the dura
-encephaloceles are herniation of meninges with or without brain tissue through skull base and by
definition communicate with CSF-containing subarachnoid space
Embryology
-glioma and encephaloceles are developmentally related, with glioma representing pinched-off
encephaloceles
-theories of encephalocele formation:
594
-incomplete separation of closed neural tube from surface ectoderm, resulting in a mechanical
barrier to neural crest cell migration and resultant lack of bone formation in that area
-delay of migration of neural crest cells to their normal destinations failure of migration would
result in an area of mesenchyma devoid of neural crest cells necessary for normal bony formation,
leading to a defect in the cranium
Clinical Presentation
-glioma:
-firm noncompressible masses that do not expand with straining or crying and do not
transilluminate
-external masses most common:
-glabellar masses (60%) may present as a lateral nasal mass
-intranasal mass (30%)
-combined (10%) dumbbell-shaped, with a connecting band passing through junction of
upper lateral cartilage and nasal bone
-may connect with dura
-encephalocele:
-consist of tissues prolapsed through a defect in cranium and are in continuity with CNS
-sincipital encephaloceles:
-aka frontoethmoidal encephaloceles
-skull base defect always between frontal and ethmoid bones at foramen cecum
-types:
-nasofrontal:
-sac passes directly forward between frontal and nasal bones
-nasal bones normal but displaced downward
-lesions located at glabella
-nasoethmoidal:
-sac passes downward below nasal bones and above upper lateral
cartilages to present as mass on lateral nose
-nasoorbital:
-sac extends under frontal and nasal bones to protrude through defect
in medial orbital wall
595
-basal encephaloceles:
-types:
-transethmoidal:
-sac herniates through defect in cribriform plate into superior meatus
and extends medial to middle turbinate
-sphenoethmoidal:
-sac extends through a cranial defect b/n posterior ethmoidal cells and
sphenoid to present in nasopharynx
-transsphenoidal:
-sac protrudes through a patent craniopharyngeal canal to present in
nasopharynx
-sphenomaxillary:
-encephalocele herniates through superior orbital fissure and then
through inferior orbital fissure to present in sphenomaxillary fossa
-occipital (75%) > sincipital (15%) > basal
-pulsatile, expand with crying or straining or with compression of jugular veins (Furstenberg
test)
-intranasal encephaloceles may resemble polyps but, unlike polyps, are located medial to middle
turbinate and are intimately related to nasal septum rather than to lateral nose
Evaluation
-any child presenting with external or
internal nasal mass requires careful
radiologic evaluation
Treatment
-glioma completely excised whenever
possible to minimize cosmetic deformity
and risk of meningitis
-extranasal glioma can be
approached through standard
external incision, depending on
location of mass
-combined lesions or intranasal
masses can be approached through
a lateral rhinotomy
-management of encephaloceles and those
glioma suspected to have intracranial
communications is primarily neurosurgical,
with excision of extracranial components
performed secondarily
596
CLEFT LIP AND PALATE:
EVALUATION AND TREATMENT OF THE PRIMARY DEFORMITY
1 affected parent 2% 7%
1 affected sibling 4% 2%
2 affected siblings 9% 1%
ETIOLOGY
597
-submucous cleft:
-microform expression of cleft of secondary palate
-bifid uvula
-midline diastasis of levator muscles
-posterior hard palate notching due to loss of posterior nasal spine
Cleft Palate
-muscle fibers of the palate follow medial margin of cleft and insert into medial cleft edges and posterior
edge of lateral bony hard palate
Facial Growth
-collapse of alveolar arches, mid-face retrusion malocclusion
598
GENERAL TEAM MANAGEMENT APPROACH
Lip Adhesion
-goal: convert a complete cleft lip into incomplete cleft lip, allowing definitive lip repair to be performed
with less tension
-performed at 2-4 weeks of age
-definitive lip repair at 4-6 months of age
-criteria:
-wide unilateral complete cleft lip and palate where closure with conventional lip repair might
produce excessive tension on the incision
-symmetric wide bilateral complete cleft lip with very protruding premaxilla
-introduction of symmetry to asymmetric bilateral cleft lip
-disadvantage: introduction of scar tissue
599
-von Langenbeck technique
-Bardach two-flap technique
-flaps based on posterior descending palatine arteries
-complete two-layer mucosa closure of the entire cleft, with dissection, redirection, and suturing
of soft palate musculature (intravelar veloplasty)
-Furlow technique
-for narrow soft palate cleft and submucous cleft
-double-opposing Z-plasty
-advantage: lengthens soft palate with Z-plasty, and overlapping the mucomuscular flaps realigns
the levator sling
-disadvantage: increased operative time, dissection, and scarring within the soft palate, and
increased risk of fistula at junction of the hard and soft palates
-attention directed to approximation and repair of levator veli palatini
-most common postoperative complications:
-hypernasal speech: 30%
-oral-nasal fistulas: 10-20%
Velopharyngeal dysfunction:
-due to deficiencies in palatal and pharyngeal musculature and/or inadequate palatal length
-speech articulation difficulties; potential VPI
VPI:
-speech therapy when child is 6 months old
-dental prosthesis may improve palatal lift
-surgery:
-secondary palatal lengthening
-pharyngeal augmentation
-narrow the anteroposterior diameter of nasopharynx using soft tissue or implants
-pharyngeal flaps
-convert incompetent nasopharynx into two lateral “ports”
-require good lateral pharyngeal wall motion
600
TONSILLITIS, TONSILLECTOMY AND ADENOIDECTOMY
ANATOMY
Adenoids
-formed during 3rd-7th months of embryogenesis
-functional and mechanical obstruction of ET with adenoid inflammation play significant role in
development of middle ear disease
-blood supply:
-pharyngeal branches of external carotid artery
-minor branches from internal maxillary and facial arteries
-sensation: CN IX and X
-three types of surface epithelium:
-ciliated pseudostratified columnar
-stratified squamous
-transitional
Tonsils
-may extend down to hypopharynx
-hyperplasia:
-abnormal tongue position, tongue-thrust habit, aberrant speech patterns, altered orofacial growth
-blood supply:
-FAIL: facial, ascending pharyngeal, internal maxillary, lingual arteries
-upper pole:
-internal maxillary artery palatine branches ascending/descending palatine arteries
-ascending pharyngeal artery
-lower pole:
-facial artery tonsillar branch (most important)
-dorsal lingual artery
-ascending pharyngeal artery
-lymphatic drainage:
-superior deep cervical and jugular lymph nodes
-sensation: CN IX and branches of lesser palatine nerve via sphenopalatine ganglion
-no afferent lymphatics
-crypts lined by specialized antigen processing squamous epithelium
-histology:
-reticular cell epithelium
-squamous layer
-antigen presenting cells (M-cells)
-extrafollicular area
-T-cells
-lymphoid follicle
-Mantle zone (mature B-cells)
-germinal center (active B cells)
Microbiology
-acute tonsillitis:
-classically GABHS (strep. pyogenes)
-other aerobic and anaerobic bacteria and viruses also implicated
F.Ling - T+ A (1)
601
-H. influenzae, S. aureus, S. pneumoniae, polymicrobial infection, BLPO, anaerobes
-viruses:
-initiators of mucosal inflammation, crypt obstruction and ulceration with secondary bacterial
infection
Immunology
-tonsils and adenoids involved in both local immunity and in immune surveillance
-no specific adverse effects with T+A; but still provide immune function
-tonsils and adenoids should be removed only for clearly defined clinical disease
Adenoids
Acute Adenoiditis:
-purulent rhinorrhea, nasal obstruction, fever, +/- otitis media
-loud snoring after episode of acute infection
Recurrent Acute Adenoiditis:
-4 or more episodes during 6 month period
-prophylactic Abx controversial
-daily low-dose (one half to one third full dose) or episodic prophylaxis (short course
with onset of URI)
Chronic Adenoiditis:
-nasal discharge, malodorous breath, PND, chronic congestion
-? role of extraesophageal reflux
Obstructive Adenoid Hyperplasia:
-chronic nasal obstruction (snoring and obligate mouth breathing)
-rhinorrhea
-hyponasal voice
Tonsils
Acute Tonsillitis:
-sore throat, fever, dysphagia, tender cervical nodes
-erythematous tonsils with exudates
Recurrent Acute Tonsillitis:
-4-7 episodes in 1 year
-5 episodes/year for 2 consecutive years
-3 episodes/year for 3 consecutive years
Chronic Tonsillitis
-no true consensus on definition
-symptoms > 4 weeks
F.Ling - T+ A (2)
602
Obstructive Tonsillar Hyperplasia
-snoring, dysphagia, voice changes (muffling or hyponasality)
-unilateral tonsillar hyperplasia should raise suspicion of malignancy
CLINICAL EVALUATION
Adenoids
-when medical therapy fails, adenoidectomy is the first step in controlling infection in the
nose/nasopharynx; about 67% of children show resolution
-sinusitis may take 2-3 months to clear after adenoidectomy
-nasality of speech:
-sounds that emphasize nasal emission: milkman, Mickey Mouse
-loss of appropriate nasality further supports obstructive adenoid hyperplasia
-lateral x-rays of limited use
-allergy evaluation
-r/o reflux
-r/o occult or overt submucous cleft palate risk of VPI with surgery
-occult cleft:
-bifid uvula
-abnormal movement of palate
-midline diastasis of muscles
-history of fluid regurgitation through nose
-nasopharyngoscopy:
-loss of midline bulge signifies absence of musculus uvulae associated with
higher risk of development of VPI postoperatively
Tonsils
-significant rare complications of GABHS:
-poststreptococal glomerulonephritis
-rheumatic fever
-obstructive tonsillar hyperplasia:
-snoring, choking and coughing, frequent
awakenings, restless sleep, dysphagia,
daytime hypersomnolence, behavioural
changes
-FTT, CHF (rare)
-unless significant (+3 or +4) hyperplasia, tonsils
should be left in situ (if no history of recurrent or
chronic infection)
-polysomnography:
-important to measure peak end-tidal CO2
if elevated then hypoventilation is present
-used mostly in child where diagnosis is
unclear or who has an unusual risk for
surgery
F.Ling - T+ A (3)
603
MANAGEMENT OF DISEASES OF THE ADENOIDS AND TONSILS
Adenoids
-recurrent or chronic cases treated with antibiotics effective against B-lactamase-producing organisms
-hyperplasia 6-8 wk course of intranasal steroids
-indications for adenoidectomy:
-obstruction
-AH with chronic nasal obstruction or obligate mouth breathing
-OSA
-FTT
-cor pulmonale
-swallowing abnormalities
-speech abnormalities
-severe orofacial/dental abnormalities
-infection
-recurrent/chronic disease
-recurrent/chronic otitis media with effusion
-chronic otitis media
-neoplasia
-contraindications for adenoidectomy:
-overt or submucous cleft palate (relative contraindications)
-lateral or superior adenoidectomy may suffice if severe OSA present
-neurologic or neuromuscular abnormalities with impaired palatal function
-anemia
-disorders of hemostasis
-complications:
-nasopharyngeal stenosis
-bleeding
-torticollis (Grisel’s syndrome)
-C-spine subluxations from hyperextension
Tonsils
-acute tonsillitis:
-first line antibiotics: penicillin
-chronic tonsilitis:
-clavulin or clindamycin for 3-6 weeks obviates need for tonsillectomy in 15% of children
-indications for surgery:
-obstruction
-TH with chronic nasal obstruction
-OSA
-FTT
-cor pulmonale
-swallowing abnormalities
-speech abnormalities
-severe orofacial/dental abnormalities
-infection
-recurrent/chronic disease
-tonsilitis with: -peritonisllar abscess, abscessed cervical nodes, acute airway
obstruction, cardiac valve disease
-persistent tonsillitis with: persistent sore throat, tender cervical nodes, halitosis
-tonsilolithiasis
-recurrent/chronic otitis media
F.Ling - T+ A (4)
604
-neoplasia
-post-tonsillectomy:
-10-day course of amoxicillin to help reduce pain and malodorous breath
PERITONSILLAR ABSCESS
-secondary to infection of peritonsillar salivary gland (Weber gland) located between tonsil capsule and
muscles of tonsillar fossa
-tx: hydration, pain relief and antibiotics effective against Staph. aureus and oral anaerobes
LINGUAL TONSILS
-extraesophageal reflux is a prime contributor to chronic lingual tonsilitis
-surgical excision rarely necessary
F.Ling - T+ A (5)
605
CONTROVERSIES IN TONSILLECTOMY,
ADENOIDECTOMY, AND TYMPANOSTOMY TUBES
Adjuvant treatment
-perioperative antibiotics
-fewer episodes of fever, offensive odour
-improved oral intake
606
-less pain, fewer days to return to normal activity
-perioperative steroids
-decreased post-op emesis
-decreased post-op pulmonary distress, subglottic edema
-pain reduction
Complications
-death, anaesthetic complications, endotracheal tube injury
-pulmonary edema
-atlantoaxial subluxations
-hemorrhage:
-primary bleeding: < 24H
-secondary bleeding: 7-10 days post-op
-dehydration
-Grisel’s syndrome
-vertebral body decalcification and anterior transverse ligament laxity from infection/inflammation
-causes pain and torticollis
-nasopharyngeal stenosis
-chronic otitis media with effusion unresponsive to medical management for 3 or more months bilateral or
for 6 months or longer unilateral; earlier when significant hearing loss (eg. > 25 dB), speech/language
delay, severe retraction pocket, disequilibrium/vertigo, or tinnitus is present
-recurrent episodes of OME not meeting criteria for chronic disease, but cumulative duration excessive (eg
6 of 12 months)
-recurrent AOM, especially when ABx prophylaxis fails to reduce the frequency, severity and duration of
attacks; minimum frequency of three or more episodes in 6 months or four or more episodes in 12 months
with one being recent
-ETD, when persistent or recurrent signs and symptoms, disequilibrium/vertigo, tinnitus, or a severe
retraction pocket, unrelieved by medical treatment; patulous eustachian tube; and during hypobaric
treatment in patients with a prior history of otitis media/eustachian tube dysfunction, or when eustachian
tube dysfunction develops during treatments
607
RANDOMIZED CONTROL TRIALS FOR
TONSILLECTOMY, ADENOIDECTOMY AND TYMPANOSTOMY TUBES
-tonsillectomy in children who meet the frequency severity and characteristics of episodes will be more
effective than not performing this operation
-adenoidectomy can reduce the frequency of recurrent acute otitis media in children who had had
tympanostomy tubes previously inserted, but continued to experience recurrent attacks after the tubes had
extruded
-lack of efficacy of adenoidectomy, +/- tonsillectomy, for children who had never received tympanostomy
tubes in the past
-adenoidectomy is efficacious in children who had COME, whether or not tympanostomy tubes had been
previously placed
-tympanostomy tube placement without addition of adenoidectomy is effective in the management of both
COME and recurrent AOM
-peritonsillar abscess as an indication for tonsillectomy also has not been evaluated by a prospective
randomized clinical trial
-no prospective randomized clinical trails have demonstrated that adenoidectomy is effective in reducing
the morbidity of sinusitis in children. Benefit of adenoidectomy remains uncertain
-even though these studies are not available, adenoidectomy should still be considered on an
individualized basis for chronic sinusitis
608
CONGENITAL ANOMALIES OF THE AERODIGESTIVE TRACT
Choanal Atresia/Stenosis
-bony atresia: transpalatal approach
-membranous atresia: transnasal endoscopic approach
Laryngomalacia
-usually few symptoms at birth with gradual development of high-pitched inspiratory stridor and occasional
609
feeding difficulties
-usually self-limited; complete resolution may take as long as 18 months
-intervention rarely necessary: tracheotomy or supraglottoplasty
Neoplasms
-most common lesions are vascular malformations
Web
-due to incomplete recanalization at 8th week GA
-types:
-supraglottic (2%)
-glottic (75%)
-subglottic (7%)
-most commonly in anterior portion of glottis
->50% obstruction requires intervention
-may require lysis via external thyrotomy or internal endoscopic lysis
Hemangioma
-usually develops biphasic stridor towards third week of life
-50% have associated cutaneous hemangioma
-spontaneous regression often occurs after 12th to 18th month
-treatment options:
-observation
-steroids
-interferon-alpha
-CO2 laser
-tracheotomy
-surgery
610
ANOMALOUS CONDITIONS OF THE TRACHEA
Tracheal Agenesis
-survival rare
Tracheomalacia
-collapse of anterior tracheal wall against soft posterior component
-most cases self-limited
-tx:
-observation (typically resolves with growth)
-correct GERD if present
-rarely requires tracheotomy or intubation; stent may be required
Tracheoesophageal Fistula
-5 types:
-esophageal atresia (EA) with distal TEF (85%)
-isolated EA (10%)
-isolated TEF (4%) “H-type”
-EA with proximal TEF (0.5%)
-EA with double TEF (0.5%)
-associated with VATER complex (Vertebral, Anal, Tracheal-Esophageal, Radial limb or renal defects)
-management requires surgical correction
Vascular Anomalies
-anomalous subclavian artery (Bayford syndrome)
-aberrant right subclavian artery arising from left descending aorta
-passes behind esophagus and trachea
-“dysphagia lusoria”
-barium swallow: compression passing obliquely up and to the right on AP view
-associated with nonrecurrent right recurrent nerve, aortic and subclavian aneurysm, and
diverticuli
-tx: ligate and reanastomose to right common carotid for severe symptoms
611
-double aortic arch
-most common vascular anomaly to cause stridor
-vascular ring encircles esophagus and trachea
-treatment: division of one component
-right aortic arch
-similar to double arch
-anomalous left common carotid artery
-innominate artery compression
-high innominate artery may cause anterior compression of trachea
-pulmonary artery sling
-left pulmonary artery originates from right pulmonary artery, slings around right mainstem
bronchus, then between trachea and esophagus
Tracheal Stenosis
-usually secondary to complete tracheal rings
-treatment conservative: steroids and Abx for URTIs
Duplication
-foreguts cysts in superior or posterior mediastinum
-true duplications in lower 1/3 of esophagus
-mucosa contains acid-secreting cells bleeding and ulceration
-treatment: surgical removal
612
NEONATAL RESPIRATORY DISTRESS
NOSE
-ddx:
-nasal dermoid
-encephalocele, glioma
-craniofacial anomalies: Treacher Collins syndrome, Apert syndrome
-piriform aperture stenosis
-nasolacrimal duct cysts
-choanal atresia
-adenoid hypertrophy
-nasopharyngeal tumour
OROPHARYNX/HYPOPHARYNX
-ddx:
-macroglossia, glossoptosis
-neoplasm: lingual thyroid, dermoid, vallecular cyst
-hemangioma, lymphangioma
-laryngomalacia
LARYNX
-ddx:
-vocal cord paralysis
-laryngomalacia
-webs, atresia, neoplastic disorders, stenosis, clefts
-laryngospasm
TRACHEA/BRONCHI
-ddx:
-complete tracheal rings, transesophageal fistula, tracheal hemangioma
-vascular compression
-mediastinal cysts and neoplasms
613
RECURRENT RESPIRATORY PAPILLOMATOSIS
INTRODUCTION
ETIOLOGY
Human Papillomavirus
-specific viral types correlated with disease severity and clinical course:
-eg. HPV 11 more obstructive airway course early and greater need for tracheotomy
-adult-onset RP could reflect either activation of virus present since birth or an infection acquired in
adolescence or adult life
-HPV present in genital tract of as many as 25% all women of child-bearing age
EPIDEMIOLOGY
614
-adult-onset RRP (AORRP)
-peaks b/n 20-40 /w slightly higher male predominance
-solitary lesions
-airway obstruction less frequently observed
-recurrence less common
-risk factors:
-younger first time mothers (longer 2nd stage of delivery)
-lower socioeconomic status
-50% born from mother with condylomata acuminata
-oral sex; multiple sex partners
TRANSMISSION
CLINICAL FEATURES
Surgical Management
-no single modality consistently effective at eradication
-goal is to debulk as much disease as possible while preserving normal morphology and anatomy and
preventing complications of subglottic and glottic stenosis, web formation and diminished airway
-potential surgical modalities
-microlaryngoscopy with cup forceps removal
-microdebrider powerized resection
-CO2 laser
-KTP/ND:YAG laser
-Flash scan lasers
-avoid tracheotomy: may seed lower airway or stoma
-aim of therapy:
-reduce tumour burden
-decrease spread of disease
-create safe and patent airway
615
-improve voice quality
-increase time interval between surgical procedures
Laser Surgery:
-protective precautions*:
-eye protection, laser masks for OR personnel; warning signs outside OR door
-protection of pts eyes and face with wet cloth
-smallest possible laser-safe ETT used
-cuff of ETT filled with saline
-room set-up:
-full set of laryngoscopes
-two ventilating bronchoscopes
-pediatric tracheotomy set
-for lasering:
-laser not used until oxygen and mixture is between 26 and 30% - minimizes possibility
of laser-induced ETT fire
-moistened neuropatties placed in subglottis to decrease air lead and provide backstop for errant
laser shots
Jet Ventilation
-limitations/disadvantages/complications:
-possibility of transmission of HPV particles into distal airway
-pneumothorax
-pneumomediastinum
-inadequate ventilation
-excessive mucosal drying
-insufflation of air into stomach
-disseminating blood into tracheobronchial tree
1. alpha-interferon
-most commonly recommended
-dose: 2mU/m2 per day or 4 mU/m2 every other day for 6 months
-discontinue if no response
-continue for additional 6 months if partial response
-continue for 3 months after complete response
-side effects:
-acute reactions:
-fever and flulike symptoms: chills, headache, myalgia
-chronic reactions:
-decrease growth rate
-elevation of liver transaminase
-leukopenia
-spastic diplegia
-febrile seizures
616
2. indole-3-carbinol
3. photodynamic therapy
4. cidofovir
5. acyclovir
6. ribavarin: antiviral drug used to treat RSV pneumonia
7. retinoic acid
8. mumps vaccine
9. methotrexate
617
THE SYNDROMAL CHILD
DEFINITIONS
-Association:
-nonrandom occurrence in two or more individuals of multiple anomalies
-eg. CHARGE association
-Deformation:
-abnormal form, shape or position caused by mechanical forces
-eg. congenital torticollis and facial asymmetry from oligohydramnios
-Disruption:
-morphologic defect of organ resulting from extrinsic breakdown or interference of an originally
normal developmental process
-eg. facial clefting as a result of amniotic bands
-Dysplasia:
-abnormal organization of cells into tissues and its morphologic results
-eg. Hurler syndrome: coarse facies, corneal clouding, macroglossia, skeletal abnormalities
-Malformation:
-morphologic defect of organ resulting form intrinsically abnormal developmental process
-eg. isolated cleft lips and anencephaly
-Polytopic field defect:
-pattern of anomalies derived from disturbance of a single developmental field
-eg. velocardiofacial syndrome
-Sequence:
-pattern of multiple anomalies derived from a single known or presumed prior anomaly or
mechanical factor
-eg. Pierre Robin sequence - primary abnormality is micrognathia glossoptosis causes cleft
palate
-Syndrome:
-pattern of multiple anomalies pathogenetically related but not representing a single sequence or a
polytypic field defect
-autosomal dominant:
-eg. Waardenburg syndrome and Treacher Collins syndrome
-autosomal recessive:
-eg. Usher syndrome, cystic fibrosis
-directed history:
-parental consanguinity and ethnicity, maternal and paternal ages, possible teratogen exposure,
outcome of prior pregnancies
-laboratory tests and karyotyping
-DNA analysis: eg. velo-cardio-facial syndrome
-dysmorphology database; ~ 30% of syndromal children will have private syndromes
618
TERATOGENS
-may alter fetal development in a recognizable pattern
-eg. CMV 10% symptomatic children microcephaly, cerebral calcification and chorioretinitis
-eg. fetal alcohol syndrome
-mental retardation and developmental delay
-microcephaly, epicanthal folds, elongated and undefined philtrum and flattened nasal dorsum
Achondroplasia
-most common cause of short-limb dwarfism
-due to defect in FGF receptor-3
-autosomal-dominant
-shortened limbs, long narrow trunk, frontal bossing and mid-face hypoplasia, lumbar lordosis, limitation
of elbow extension, genu varum, trident hand
-obstructive sleep apnea common
-brainstem compression central ventilatory problems sudden death
Branchiootorenal Syndrome
-autosomal-dominant
-branchial cleft anomalies: cysts or fistulae
-otologic malformations: preauricular pits, malformed auricles, ossicular and cochlear malformations
-renal malformations: renal genesis, polycystic kidneys, duplicated ureter
Down Syndrome
-most common genetic disorder associated with mental retardation and developmental delay
-1/700-1000 live births
-trisomy 21
-increased maternal age a risk factor
-microcephaly, mid-face retrusion, upslanting palpebral fissures, epicanthal folds, macroglossia
-40% have congenital heart malformations
-delayed gross motor skills
-increased joint laxity (10-20%) atlantoaxial subluxations
Fragile X Syndrome
-X-linked
-second most common genetic cause of MR
-prominent ears, large jaw, long face
-high pitched, jocular speech
-hyperkinetic behaviour
-macroorchidism, joint hypermobility, flat feet, mitral valve prolapse
619
Goldenhar Syndrome
-oculoauriculovertebral spectrum
-facial asymmetry
-unilateral external and middle ear deformities:
-mildly deformed ears to complete anotia
-external canal atresias and ossicular deformities
-vertebral malformations
-most cases are sporadic
Neurofibromatosis Type 1
-prevalence of 1/3000-4000
-café au lait spots and cutaneous neurofibromas
-axillary freckling, optic glioma, Lisch nodules (iris hamartomas), sphenoid wing dysplasia
-cervicofacial plexiform neurofibromas resemble “bag of worms”
Neurofibromatosis Type 2
-central form of neurofibromatosis
-bilateral acoustic neuromas, meningiomas, spinal cord schwannomas
-mean age of presentation is 20 - unilateral or bilateral hearing loss common
-two types:
-Wishart type:
-early onset and rapid growth, with other fibromatous tumours other than AN
-Gardner type:
-slower rate of growth and onset and usually only bilateral acoustic neuromas
-autosomal dominant
Usher Syndrome
-SNHL and retinitis pigmentosa
-most common cause of combined deafness and blindness in the Western world
-three types:
-Ush 1: profound SNHL, vestibular dysfunction, retinitis pigmentosa
-Ush 2: mild to moderate SNHL, normal vestibular function, retinitis pigmentosa
-Ush 3: progressive SNHL, progressive vestibular dysfunction and retinitis pigmentosa
Velocardiofacial Syndrome
-almond shaped palpebral fissures, deficient nasal alae, tubular nose with bulbous nasal tip, small mouth
-variable degree of palatal clefting
-adenoidectomy VPI
Waardenburg Syndrome
-heterochromia irides, white eyelashes, white forelock and SNHL, dystopia canthorum
620
PEDIATRIC MALIGNANCIES
-lymphoma:
-lymphoproliferative disorder
-the most common pediatric malignancy of the head and neck (excluding retinoblastoma and
neoplasms of the CNS)
-risks:
-irradiation
-EBV (Burkitt’s lymphoma)
-HIV, immunosuppression
-organic toxins (phenols, benzene)
-immunological diseases (rheumatoid arthritis, celiac disease)
HODGKIN DISEASE
Epidemiology
-bimodal incidence:
-ages 15-34 years
-later adult years
-M:F = 2:1
-EBV associated in 40%
Clinical Presentation
-80% with cervical lymphadenopathy
-cervical mass most common presentation
-spreads via contiguous lymph nodes
-mediastinal involvement tracheal or SVC compression
-B symptoms present in 30-40%
Pathology/Classification
-Reed-Sternberg cell:
-two or more nuclei and two or more large nucleoli
(“owl’s eyes”)
-large binucleated cells diagnostic for Hodgkin disease
-eosinophilic inclusions
-Rye Classification:
-lymphocyte predominant (2-10%): -abundant normal-appearing lymphocytes with rare
RS cells and no fibrosis
-associated with better prognosis
-mixed cellularity (20-40%) -pleomorphic infiltrate of lymphocytes, other
inflammatory cells, and more numerous RS cells
-nodular sclerosis (40-80%) -nodules of lymphoid infiltrates separated by bands
of collagen, containing lacunar cell variants of RS
cells
-more common in women
-lymphocyte depleted (2-15%) -paucity of lymphocytes, diffuse fibrosis, and bizarre-
appearing RS cells
-associated with poorer prognosis
621
Diagnosis and Staging
-excisional open biopsy usually required to establish diagnosis
-fresh sample required for immunochemistry
-Ann Arbor system:
-I: Single lymph node region or extralymphatic site (IE)
-II: Two or more lymph node regions or extralymphatic sides (IIE) on same side of
diaphragm
-III: Nodal regions, extralymphatic sites (IIIE), or splenic involvement (IIIS) on both sides of
the diaphragm
-IV: Disseminated disease
Treatment
-stage I and IIA: external beam XRT; 10-year survival rate 90%
-advanced disease: combination chemotherapy; complete response rate 44-87%
-MOP(P): mecholorethamine, oncovin (vincristine), prednisone, procarbazine
-ABVD: adriamycin, bleomycin, vinblastine, DTIC
-in children low dose radiation and chemotherapy recommended to limit toxicities and morbidity
Prognosis
-dependent on staging; overall >75% 5 year survival
-better prognosis for lymphocytic predominance types
-worse prognosis with presence of Reed-Sternberg cells, class B symptoms and higher staging
NON-HODGKIN LYMPHOMA
Epidemiology
-incidence increases throughout life
-increased risk in immunodeficiency states
-EBV appears to have role in pathogenesis
-cells of origin:
-85% NHL arise from B-cells
-15% NHL arise from T-cells
Clinical Presentation
-rapidly growing extranodal disease primarily involving head and neck (29%) and mediastinum (26%)
-Waldeyer ring hypertrophy
-may present with respiratory distress or SVC syndrome
-hematogenous dissemination early
-CNS involvement: CN palsies, MS changes
Treatment
-tumour burden (clinical stage and serum LDH concentration) most important predictor of outcome
-primary treatment is systemic chemotherapy
-typically treated with CHOP: cytoxan, doxorubicin, vincristine, prednisone followed by radiation
to involved sites
-XRT limited to emergency situations involving airway, nervous, or vascular compromise
622
RHABDOMYOSARCOMA
Epidemiology
-incidence at least equal to that of all other sarcomas combined
-most frequent soft-tissue malignancy of childhood
-head and neck involvement (35-40%)
-50% occur in children < 5ya
-rare distant metastasis
Clinical Presentation
-orbit > nasopharynx > middle ear/mastoid > sinonasal cavity
-nasal obstruction, epistaxis, otorrhea, proptosis, cranial nerve palsies
-parameningeal sites:
-middle-ear-mastoid
-sinonasal
-nasopharyngeal
-infratemporal fossa
-may spread into meninges, less favourable prognosis
Pathology
-classified based on histopathology:
-Embryonal and botryoid variant (75%)
-most common types among infants and young children
-spindle-shaped cells containing abundant eosinophilic cytoplasm
-botryoid variant: forms condensed layer of cells immediately beneath mucosa and
produces a polyploid lesion
-Alveolar (20%)
-occurs predominantly in adolescents
-small, round cells separated into alveolar groupings by fibrous septa
-Pleomorphic
-usually in adults
-well differentiated, consists of spindle and “strap” cells
623
-Group staging system (Intergroup Classification)
Group I:
-13%
localized disease with complete surgical resection and no evidence of regional nodal
involvement
Group II:
-20%
-Group IIA: grossly resected disease with microscopic residual disease and no regional
involvement
-Group IIB: complete resection with no residual disease, but they do show regional
disease with involved nodes
-Group IIC: containing patients with microscopic residual disease and regional nodal
involvement.
Group III:
-48%
-incomplete resection or biopsy only; gross residual disease
Group IV:
-18%
-distant metastasis at the time of diagnosis
Risk classification
Low risk:
-Patients have embryonal RMS either (1) occurring at a favourable site (stage I), (2)
occurring at an unfavourable site with complete resection (group I), or (3) occurring at an
unfavourable site with microscopic residual disease (group II).
Intermediate risk:
-Patients have (1) embryonal RMS occurring at an unfavourable site with gross residual
disease (group III), (2) metastatic embryonal RMS and are younger than 10 years, or (3)
any nonmetastatic alveolar RMS at any site.
High risk:
-Those at high risk include any patient with metastatic disease unless he or she is younger
than 10 years and has embryonal metastasis.
Treatment
-complete resection has a large impact on survival
-increasing efficacy of chemotherapy and radiation therapy reduced indication for radical surgery
-combination surgery and chemoradiation therapy advocated
-long-term survival can approach 60-70%
624
THYROID CARCINOMA
Presentation
-asymptomatic firm anterior neck mass
-signs/symptoms suggestive of malignancy:
-rapid growth
-new-onset hoarseness
-odynophagia
-hemoptysis
-vocal cord paralysis
-fixation to surrounding tissues
-75% cervical lymphadenopathy
-5-10% pulmonary metastasis
Pathology
-usually papillary
-risk factors:
-radiation exposure
-Gardner syndrome (familial polyposis)
-Cowden syndrome (familial goiter and skin hamartomas)
Treatment
-controversial total vs hemi-thyroidectomy for papillary/follicular ca
-medullary ca:
-family screened - those positive undergo total thyroidectomy
-age 6 years for MEN type 2A
-shortly after birth for MEN 2B
NASOPHARYNGEAL CARCINOMA
-rare
-type I (keratinizing), type II (nonkeratinizing), type III (undifferentiated)
-type III most common in children
-most present with asymptomatic metastatic cervical disease
-XRT +/- chemotx for disseminated disease
-5-yr survival 40%
NEUROBLASTOMA
-newborns and children <10 ya; peak 2 ya - highest incidence in first 2 years of life
-most common malignancy in infants under 1 ya
-60% have metastatic disease
-signs/symptoms:
-painless cervical mass
-Horner syndrome
-heterochromia iridis
-pressure symptoms related to aerodigestive tract
-osseous metastasis:
-calvarium
-orbit
-ribs
-long bones
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-diagnosis:
-IVP
-CXR, abdominal US, skeletal survey, liver-spleen scan, bone marrow aspirate
-urine vanillylmandelic acid (VMA)
-treatment:
-surgical excision
-chemotherapy for residual disease
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OTITIS MEDIA WITH EFFUSION
EPIDEMIOLOGY
-if a child has not had OM before age of 3 years statistically unlikely to develop severe or recurrent OM
-overall highest incidence of AOM in the 6-11 month age group
-mean duration of OME after AOM is 40 days
-incidence of OME appears to peak during second year of life, most prevalent during winter
months, and is associated with URIs
-most children have resolution of asymptomatic MEE within a few months without medical or surgical
intervention
-a very high incidence of middle-ear infections reported in Native Americans and Inuit
-strong genetic pre-disposition to OM
-other risk factors:
-low socioeconomic class
-day-care
-decreased breast-feeding
-second-hand smoke
-seasonal variation: more common in winter, fall, spring (correlation with URI)
-cleft palate
-craniofacial disorders:
-Down’s syndrome, Apert syndrome, mucopolysaccharidoses
-congenital or acquired immunodeficiency
-hypogammaglobulinemia, IgA deficiency, DiGeorge syndrome, HIV, chemotherapy
-allergy, nasal obstruction, ciliary dysfunction, prolonged nasal intubation
-environmental:
-day-care attendance
-smoking in households
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PATHOPHYSIOLOGY
-abnormal function of ET
-ET in infants and children: shorter, more horizontal
-congestion of ET leads to increased negative middle-ear pressure influx of bacteria and viruses from
nasopharynx induces inflammatory response
-abnormalities of the palate and associated musculature (tensor veli palatini) may worsen ET function
MICROBIOLOGY
EVALUATION
History
-otalgia, irritability, fever, lethargy, otorrhea
-hearing loss
Physical Examination
-otorrhea
-pneumatic otoscopy
- mobility on both positive and negative pressure MEE
-movement only on negative pressure ET dysfunction
-colour of TM:
-yellow or blue MEE
-dark red trauma, haemorrhage
-red AOM or hyperaemia
Hearing Evaluation
-audiometric evaluation
-ABR in newborns
-behavioural observation audiometry (BOA) for infants 6 months to 1 year
-visual reinforcement audiometry (VRA) for 1-2 ya
628
-play audiometry for 2-5 ya
-standard audiometry > 5 ya
-immitance audiometry
-recurrent/frequent OM
-those who clear effusion between episodes
-Rx: -antibiotic treatment for each separate episode of AOM
-prolonged prophylactic antibiotic treatment (Amoxil and Septra)
-for those with 3-4 episodes in 6 months; 4-6 in 1 year
-risk of developing resistance
-BMT
-those with persistent effusion
-use of nasal steroids not established
-lack of evidence showing that decongestants (systemic and intranasal) effective in curing or preventing
middle ear disease
Prevention
-changes in environmental factors
-taking child out of daycare
-preventing exposure to second hand smoke
629
-negative middle-ear pressure with impending cholesteatoma
-intervention in presence of complications of OM
-other “soft” indications:
-recurrent OM (3-4 episodes in 6 months; 4-6 in 1 year)
-to improve quality of life but no real medical indication for this
-average time tubes remain in place and functional is 8-12 months
-complications:
-otorrhea
-persistent TM perforation (1-3%)
-tympanosclerosis
-plugging of tube
-formation of granulation tissue
-cholesteatoma
-extrusion into middle ear
-factors related to persistent perforation:
-tube retention beyond 36 months and multiple sets of tubes
COMPLICATIONS
-Intratemporal:
-hearing loss (conductive and sensorineural)
-if MEE > 3 months and bilateral hearing and communication skills should be evaluated
-TM perforation
-CSOM +/- cholesteatoma
-retraction pockets/atelectasis
-cholesteatoma
-adhesive otitis media
-tympanosclerosis
-ossicular discontinuity/fixation
-mastoiditis
-petrositis
-labyrinthitis
-facial paralysis
-cholesterol granuloma
-infectious eczematoid dermatitis
-Intracranial:
-meningitis
-subdural empyema
-brain abscess
-extradural abscess
-lateral sinus thrombosis
-otitic hydrocephalus
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GENETIC HEARING LOSS
-childhood SNHL:
-50% genetic factors
-75-80% autosomal recessive
-18-20% autosomal dominant
-X-linked ~2-4%
-mitochondrial < 1%
-20-25% identifiable environmental causes, prenatal, perineal or postnatal
-25-30% sporadic (“cryptogenic”)
Michel Aplasia
-autosomal dominant trait
-structures of inner ear do not develop
-arrest/insult in development before end of 3rd week GA (otic placode formation)
-presents with anacusis
-hearing aids and cochlear implantation NOT useful
Mondini Aplasia
-autosomal dominant
-developmental malformation of cochlea
-second most common abnormal X-ray finding in SNHL
-only basal coil clearly identified
-absence of interscalar septum, endolymphatic aqueduct typically enlarged
-arrest/insult ~ 6-7th week GA
-association with syndromal and non-syndromal conditions (eg. CM) described
-associated with an increased risk of perilymphatic gushers and meningitis from a dilated cochlear
aquaduct
Scheibe Aplasia
-most common form of inner ear aplasia
-result in partial or complete aplasia of the pars inferior (cochlea and saccule) and normal pars superior
(SCCs and utricle)
-associated with other diseases such as Usher syndrome and Waardenburg syndrome
-normal bony labyrinth; malformation of membranous labyrinth
-organ of Corti poorly differentiated
-tectorial membrane malformed
-stria vascularis degenerated
-scala media compromised by collapse of Reissner membrane
-hearing aids useful
Alexander Aplasia
-aplasia of cochlear duct
-audio: high-frequency hearing los with adequate residual hearing in low frequencies
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Semicircular Canals
-lateral SCC are last to develop and have longest period of susceptibility to teratogenic insults
Bing-Siebemann Dysplasia
-complete membranous labyrinth dysplasia
-rare
Waardenburg Syndrome
-variable expressivity
-features:
-unilateral or bilateral SNHL
-pigmentary anomalies:
-white forelock, heterochromia irides (two different coloured eyes), premature graying
and vitiligo
-craniofacial features:
-dystopia canthorum (laterally displaced medial canthi), broad nasal root, synophrys
-two clinical types
-WS1 (presence of dystopia canthorum)
-20% with HL
-WS2 (absence of dystopia canthorum)
->50% with HL
-other types
-WS3 (Klein-Waardenburg)
-includes features of WS1 and skeletal malformations particularly in hands and forearms
-WS4 (Waardenburg-Shah)
-autosomal recessive
-features of WS2 with Hirschsprung megacolon
Stickler Syndrome
-associated with mutations of type II collagen gene (COL2a1) on Chr 12
-features:
-Pierre-Robin sequence
-severe myopia associated with retinal detachment and cataracts
-hypermobility and enlargement of joints with early adult onset arthritis
-progressive SNHL in 15%
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Treacher Collins Syndrome (Mandibulofacial dysostosis)
-high penetrance; new mutation in 60%
-treacle protein function in early craniofacial development
-features:
-microtia, aural meatal atresia, conductive hearing loss from ossicular malformation (~30%)
-SNHL and vestibular dysfunction may be present
-bilateral malar hypoplasia, downward slanting palpebral fissures, coloboma of lower eyelids,
hypoplastic mandible
Goldenhar Syndrome
-oculoauriculovertebral spectrum
-facial asymmetry
-unilateral external and middle ear deformities:
-mildly deformed ears to complete anotia
-external canal atresias and ossicular deformities
-vertebral malformations
-most cases are sporadic
Neurofibromatosis
-NF2 (Central)
-central form of neurofibromatosis
-localized to defect in long arm of chromosome 22
-bilateral acoustic neuromas, meningiomas, spinal cord schwannomas
-mean age of presentation is 20 - unilateral or bilateral hearing loss common
Otosclerosis
-appears to be transmitted in an autosomal dominant pattern with decreased penetrance, so only 25% to
40% of gene carriers show the phenotype
-preponderance of affected females suggests a possible hormonal influence
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NONSYNDROMIC AUTOSOMAL DOMINANT HEARING LOSS
RECESSIVE DISORDERS
Usher Syndrome
-SNHL and retinitis pigmentosa
-~3-4 cases per 100,000 population
-most common cause of combined deafness and blindness in the Western world (affects one half of 16 000
deaf and blind persons in the US)
-three types:
-Ush 1: profound SNHL, vestibular dysfunction, retinitis pigmentosa (90%)
-Ush 2: mild to moderate SNHL, normal vestibular function, retinitis pigmentosa (10%)
-Ush 3: progressive SNHL, progressive vestibular dysfunction and retinitis pigmentosa
-ophthalmologic evaluation is integral to diagnosis (RP diagnosed with electro-retinography)
Pendred Syndrome
-due to mutations in SLC26A4/PDS (pendrin) gene
-defect in tyrosine iodination
-SNHL associated with abnormal iodine metabolism euthyroid goiter
-most patients have Mondini aplasia or enlarged vestibular aqueduct
-dx: abnormal perchlorate discharge test: abnormal organification of nonorganic iodine
-treat goiter with exogenous thyroid hormone
-three subtypes:
-congenital severe-to-profound
-CX26 (GJB2 or DFNB2) gene defect most common; accounts for ~50% of recessive
nonsyndromic hearing loss
-produces gap junction protein connexin 26
-congenital moderate
-early-onset
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SEX-LINKED DISORDERS
Otopalatodigital Syndrome
-hypertelorism
-craniofacial deformity involving supraorbital area, flat midface, small nose and cleft palate
-short broad fingers and toes
-conductive hearing loss caused by ossicular malformation
Wildervanck Syndrome
-suspected X-linked dominant
-features: fused cervical vertebrae, sensorineural or mixed hearing loss (related to bony malformation of
inner ear), paralysis of 6th cranial nerve
Alport Syndrome
-SNHL associated with renal disease of varying severity
-progressive HL
-nephritis hematuria “red diaper” syndrome
-early diagnosis essential to facilitate management of renal disease
-X-linked d/t mutation of type 4 collagen gene (COL4A5)
MITOCHONDRIAL INHERITANCE
Hearing x deaf 0 5%
1 40-50%
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PEDIATRIC AUDIOLOGY
HEARING SCREENING
Infant Screening
-endorses universal detection of infant hearing loss by 3 months of age and intervention by 6 months of age
-risk indicators:
-NICU admission
-syndrome associated with hearing loss: NF, osteopetrosis, Usher syndrome
-family history of hearing loss
-craniofacial anomalies
-in uteri infection: TORCH, syphilis
-parental concern of hearing or speech delay
-post-natal infections: meningitis
-hyperbilirubinemia requiring transfusions
-neurodegenerative disorder (eg. Hunter syndrome)
-head trauma
-recurrent or persistent otitis media with effusion for at least 3 months
-children with indicators of progressive or delayed-onset hearing loss should be examined minimum
q6months through 3 years of age
Test Battery
-Immittance Testing
-tests middle ear function
-limitations:
-children less than 4 months have:
-incomplete ossification of canal wall, which increases volume and compliance
-unresolved mesenchyme in middle ear which increases resistance
-Speech Testing
-speech stimulation provides reference for frequency-specific testing
-broadband speech more meaningful to child - will respond at lower thresholds
-speech awareness threshold obtained
-speech recognition not attempted until 3 years of age
-Pure-tone Testing
-warble tones (younger children tend to respond better to this type of stimulus) in sound field
-pure tones with earphones (for older children)
-initial test frequency is 2000 Hz then 500 Hz signal (commonly affected in CHL)
636
-responses are reported as minimal response levels and are not considered true thresholds
Standard Audiometry
->5 years of age
SPECIAL TESTS
Amplification
-critical range of hearing 0-15 dB for a young child
-unvoiced consonants: s, p, k, th, f, sh fall at or below normal adult hearing thresholds
-resonance frequency of infant ear canal much higher than adults (7200 Hz vs 2700 Hz)
-affect selection of gain and peak frequency responses
-therefore must monitor these effects to prevent discomfort or overamplification
-binaural amplification used to limit auditory deprivation in select cases
Assistive Devices
-FM systems used to decrease signal-to-noise ratio, reverberation and distance problems that degrade signal
received by hearing aid
-definition:
-deficit in information processing of audible signals not attributed to impaired peripheral hearing
sensitivity or intellectual impairment
637
-refers to limitations in ongoing transmission, analysis, organization, transformation, elaboration,
storage, retrieval, and use of information contained in audible signals
-signs:
-easy distraction
-delayed responses
-frequent requests for repetition
-symptoms of hearing loss
-frequent reversals
-difficulty following directions
-inconsistent academic performance
-unexplained behavioural difficulties
-management:
-environmental modifications: preferential seating, increased visual cues
-compensatory strategies: cueing, repetition, review, etc..
-amplification with personal or classroom style FM systems
638
PEDIATRIC FACIAL FRACTURES
-controversial problems:
-elevation of functional matrix off underlying facial architecture to gain exposure to the fractures
may alter development
EPIDEMIOLOGY
EMERGENCY MANAGEMENT
-ABCs - c-spine
-need for tracheotomy controversial for severe facial fractures
ETIOLOGY
-alterations of growth and remodelling d/t trauma can cause facial deformities
-condyle:
-important site of mandibular growth
-injuries to this area however can, but do not consistently cause facial asymmetry
-crush injuries to condylar head before 5 ya predispose child to ankylosis and growth disturbances
-extensive remodelling of condylar fracture between ages 3-11 results in normal anatomic
features:
-injuries before 3 ya severe deformities
-injuries after 6 ya moderate deformities
-injuries during adolescence mild deformities
-midface more susceptible to developmental deformities from even minor trauma
639
-theories:
-loss of stimulus to normal growth
-mechanical restriction produced by scarring and loss of motion
-altered muscular activity
-interruption of vascular supply to teeth
Rigid Fixation
-concern about impairment of facial growth
-most data from animal studies but no firm conclusions
-use of bone grafts to bridge defects become incorporated into growing face
-rib grafts
-cranial bone grafts
-bone loss of buttresses of > 5mm should be bridged rigidly with calvarial bone grafts
-rigid fixation usually reserved in cases where fractures cannot be restored by any means
-minimally displaced fractures often best left alone or managed with closed reduction
-use as small plates as possible and do not cross more than one suture line
Surgical Approaches
-nasal or zygomatic arch fractures managed with closed or limited open techniques
-five basic incisions:
-lower gingivolabial sulcus incision:
-arch of mandible #
-coronal incision:
-upper third of face (zygomatic arches, upper orbital rims, nasoethmoidal region) #
-subciliary/trans conjunctival incision:
-inferior orbital rim and orbital floor #
-upper gingivolabial sulcus incision:
-maxilla #
-external:
-mandibular angle and ramus #
Nasal Fractures
-nose in children is soft - energy is dissipated easily
-septum more likely to be fractured
-nasal bones have little projection; children over 6 years more susceptible to bony fractures
-usually greenstick type #
-management:
-initial evaluation:
-often limited by swelling
-r/o septal haematoma cartilage necrosis saddle nose deformity
-treatment:
-usually 5-7 days post injury when swelling has subsided
-closed reduction
Mandibular Fractures
-infants younger than 2 years:
-accurate alignment with acrylic splints (dentist)
-wired in place with circum-mandibular wires for 2-3 weeks
-IMF not necessary
-children 2-5 years:
-may use arch bars for IMF
-piriform aperture suspension or circummandibular wiring may be necessary
640
-children 6-12 years:
-arch bars for IMF
Condylar Fractures
-three types:
-intracapsular crush fracture of head
-high condylar fracture through neck above sigmoid notch
-low subcondylar fracture (most common, often greenstick)
-treatment mainly conservative closed approach
-unilateral #:
-with normal ROM and normal occlusion: soft diet and movement exercises
-deviation with normal occlusion: arch bars with use of guiding elastic bands
-open bite deformity: 2-3 weeks of IMF followed by 6-8 weeks of guiding elastics
Dentoalveolar Fractures
-incisors and canines most commonly injured
-avulsion of secondary tooth: survival depends on early reimplantation
Midfacial Fractures
-injury ranges from simple blowout fractures to highly comminuted injuries
-ophthalmology consult required
-more likely to cause problems with facial growth and development and to result in permanent deformities
if left uncorrected
641
-steps for management of traumatic telecanthus:
-bicoronal incision
-explore central fragment reosteotomize
-reestablish nasomaxillary buttress with microplates
-transnasal wiring to reduce intercanthal distance
Maxillary Fractures
-Lefort system useful in predicting difficulty of reconstruction - but anatomic classification inadequate to
describe severity of injury and complexity of reconstruction needed
-functional classification
-type I: minimally displaced, usually not comminuted
-main buttresses cracked
-type II: moderately displaced with some area of comminution
-fragments large enough to accept plates and screws
-type III: severely displaced with multiple comminution
-requires stabilization and use of bone grafts for reconstruction
-maxillary fractures uncommon among children
642
CONGENITAL VASCULAR LESIONS
Clinical
-usually absent at birth, 30% present as red macule -all present at birth; may not be evident
-rapid postnatal proliferation -commensurate growth; rapid growth possible with hormonal
-slow involution changes, trauma or infection
-F:M = 3:1 -no involution
-F:M = 1:1
Cellular
-plump endothelium, increased turnover -flat endothelium, slow turnover
-increased mast cell count -normal mast cell count
-multilaminated basement membrane -normal thin basement membrane
-capillary tubule formation in vitro -poor endothelial growth in vitro
Radiologic
-angiographic findings: well-circumscribed intense lobular- -angiographic findings: diffuse, no parenchyma
parenchyma staining with equatorial vessels -low flow: phleboliths, ectatic channels
-MRI: intermediate signal intensity on T1 that increases on T2; -high flow: enlarged, tortuous arteries with arteriovenous
flow voids present shunting
-MRI: does not enhance on T2 images
Skeletal
-infrequent mass effect on adjacent bone; rare hypertrophy -low flow: distortion, hypertrophy or hypoplasia
-high flow: destruction, distortion, or hypertrophy
HEMANGIOMAS
-Kasabach-Merritt Phenomenon:
-not real hemangioma
-platelet sequestration, ecchymosis, no female predominance
-actual lesion is either kaposiform hemangioendothelioma or tufted angioma
-supportive treatment; avoid used of blood products causes sequestration and produce rapid
tumour enlargement
643
Management of Hemangiomas
-indications for immediate treatment:
-affects swallowing or vision
-life threatening: associated with high output cardiac failure or respiratory difficulty
-primary objectives:
-limit tumour growth
-avoidance of complications
-primary medical treatment
-oral prednisone
-continue treatment until involution is well established
-steroid resistant lesions:
-intralesional steroids
-limited to smalls lesions
-avoid periorbital injections risk of retinal artery thrombosis
-interferon alpha-2a
-s/e: low-grade fever, LFTs, transient neutropenia, anemia, spastic diplegia
-surgery
-photocoagulation:
-used during early proliferative phase q4-6 weeks on superficial lesions
-ineffective for deep hemangioma
VASCULAR MALFORMATIONS
Lymphatic Malformations
-occur when lymphatic sacs fail to communicate with lymphatic vessels
-variable extent of involvement in the head and neck
-spontaneous regression not frequent
-MRI findings:
-low T1, high T2, no flow voids
644
-staging system:
-I: unilateral infrahyoid
-II: unilateral suprahyoid
-III: unilateral suprahyoid and infrahyoid
-IV: bilateral suprahyoid
-V: bilateral suprahyoid and infrahyoid
Venous Malformations
-dilated vascular channels lined by normal endothelium
-common on lips and cheek
-soft compressible
-low-flow phleboliths
-tx: sclerotherapy or surgery
Arteriovenous Malformations
-abnormal communications between arteries and veins that bypass the capillary bed
-characteristically associated with a thrill or bruit
-MRI:
-no enhancement on T2
-flow voids on both T1 and T2
-angiography:
-dilatation and lengthening of arteries with early shunting of enlarged veins
-tx: surgery with pre-op embolization if symptomatic
Associated Syndromes
-Sturge-Weber:
-facial capillary malformation involving CN V1 with ipsilateral vascular malformation of
leptomeninges and eye
-choroidal malformation in eye causes glaucoma among 30% of pts
-Klippel-Trenaunay:
-cutaneous capillary malformation with underlying venous and lymphatic malformation
-skeletal overgrowth of a limb and possible growth retardation
645
Embryology of the Face, Lips
and Palate Development of the Face and Lips
ENT Residents’ Academic Half-Day
May 9th 2003
Resident Coordinator: Francis Ling
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1
7th week GA 10th week GA
• Lateral and inferior expansion of • Ectoderm and mesoderm of
each fused medial nasal process frontal process and each medial
forms the intermaxillary process. nasal process proliferate,
• The tips of the maxillary forming a midline nasal septum.
swellings grow to meet this This divides the nasal cavity into
process and fuse with it. two nasal passages which open
• The intermaxillary process gives into the pharynx, behind the
rise to the bridge and septum of secondary palate, through the
the nose, and the philtrum on the definitive choana.
upper lip.
10th week GA
• The philtrum is now formed, and
the lateral portions of the
maxillary and mandibular Development of the Palate
swellings fuse to create the
cheeks and reduce the mouth to
its final width.
647
2
9th week GA 10th week GA
• The palatine shelves begin to • The ventral secondary palate
fuse ventrodorsally with becomes the bony hard
each other, the primary palate through mesenchymal
palate and the inferior nasal condensations (endochondral
septum. ossification).
• The dorsal secondary palate
becomes the soft palate
through myogenic
mesenchymal condensation.
Cleft Lip
• Underdevelopment of
mesenchyme of the
Abnormal Facial Development maxillary swelling, resulting
in inadequate contact with
the medial nasal process and
intermaxillary process. The
length and depth of the
resulting cleft can vary
considerably.
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3
Cleft Palate Cleft Palate
• Caused by inadequate • It may result from a wide
palatine shelf growth, range of congenital insults
incorrect shelf elevation, an and genetic errors.
excessively wide head, • Etiology is again
failure of shelves to fuse or multifactorial, with the same
rupture after fusion. teratogens as for cleft lip,
although an x-linked cleft
palate syndrome has been
described.
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4
Introduction
• “2% of livebirths have congenital anomalies”
ENT Problems in the • 70% congenital anomalies occur in head and neck region
and the hand
Syndromic Child • Several thousand distinct syndromic entities described
• Many have craniofacial and otolaryngologic components
Francis T.K. Ling MD (PGY-3)
University of Ottawa - Department of Otolaryngology • Frequent ENT consults
Grand Rounds • Syndromes search for suspected defects
Wednesday April 2, 2003
Introduction Introduction
• Minor anomalies • Multidisciplinary approach
• Defects without serious medical or surgical significance • ENT consulted to deal with problems that affect:
• Epicanthic folds, coloboma, small or protuberant ears, small nares, • Respiration
bifid uvula
• Swallowing
• Occur in 15% of the population
• Hearing
• Half of all known minor anomalies occur in the head and neck
region • Speech
• Three or more minor malformations Major malformation found • Facial appearance
in 90%
• Evaluate for cardiac, renal or vertebral defects
Definitions Definitions
• Malformation • Deformation
• Morphologic defect of an organ resulting • Abnormal form, shape or position of a body
from intrinsically abnormal developmental part caused by mechanical forces
process • Usually occurs late in development
• Three types: • Eg. Congential torticollis and facial
• Incomplete (eg. Cleft lip) asymmetry from oligohydramnios
• Redundant (eg. Ear tags)
• Aberrant (eg. Mediastinal thyroid)
• Initiated late in fetal development are
simple; those initiated early usually more
complex and severe
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1
Definitions Definitions
• Disruption • Sequence
• Morphologic defect of organ • Pattern of multiple anomalies derived from a single known or
resulting from extrinsic breakdown presumed prior anomaly or mechanical factor
or interference of an originally • Eg. Pierre Robin sequence
normal development process
• Syndrome
• Rare
• Greek: “running together”
• Eg. Facial clefting as a result of
amniotic bands • Pattern of multiple anomalies pathogenetically related but not
representing a single sequence
• Association
• Nonrandom occurrence in two or more individuals of multiple
anomalies not known to be a sequence or syndrome
• Eg. CHARGE association
Otolaryngologic Problems
• Hearing loss
• Speech disorders
• Airway obstruction
Otolaryngologic Problems
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2
Hearing Loss Hearing Loss
• Congenital
• Devastating effect on speech and intellectual development • Usually conductive
• High risk with craniofacial anomalies • External auditory meatus atresia
• Various degrees of obliteration of middle ear cleft
• Delayed detection • Ossicular deformity
• Assumed mental retardation rather than hearing loss • Ossicular fixation
• Acquired
• Usually conductive
• Most often consequence of eustachian tube dysfunction
• OME
• Hypernasality • Hyponasality
• Causes: • Severe posterior displacement of midface
• VPI after cleft palate repair most common • Persistent congenital atresia or stenosis
• Anatomical anomalies involving nasal cavity and nasopharynx • Iatrogenic velopharyngeal stenosis from palatopharngoplasty
• Reduced with speech therapy
• Hoarseness
• Palatopharyngoplasty at 5 years of age if speech therapy
• Vocal cord nodules present in 20% of children with VPI
unsuccessful
• Increased laryngeal activity to compensate for loss of vocal power
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3
Airway Obstruction Airway Obstruction
Neonatal Nasal Airway Obstruction Neonatal Nasal Airway Obstruction
• CT findings • Treatment
• Narrowing of posterior choanae < • Surgical
0.34 cm in children under 2 years old • Transpalatal
• Inward bowing of posterior maxilla • Transnasal
• Fusion or thickening of vomer • Endoscopic
• Presence of bone or soft-tissue
septum extending across posterior
choanae
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4
Airway Obstruction Airway Obstruction
Neonatal Oropharyngeal Obstruction - PRS Neonatal Oropharyngeal Obstruction - PRS
• Airway Obstruction • Two categories:
• Neuromuscular impairment of • Nonsyndromic (80%): potential for catch-up growth
genioglossus and other parapharyngeal • Syndromic (20%): usually intrinsic defect
muscles • Stickler syndrome
• Anatomic abnormalities include • Velocardiofacial syndrome
retroposition of mandible and diminished • Fetal alcohol syndrome
effectiveness of genioglossus in exerting
anterior traction on the tongue
Airway Obstruction
Chronic Nasal Obstruction
• Distortion of midfacial anatomy
• Enlarged adenoids Specific Syndromes and
• Palatal clefts Associations
• Reduce caliber of nasal airway
• Distortion of nasal soft tissue
• Nasal mucosa edema
• Septal deviation
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5
Specific Syndromes & Association Branchio-
Branchio-oto-
oto-renal Syndrome
• Branchio-oto-renal Syndrome • Autosomal dominant
• Goldenhar Syndrome • Branchial cleft anomalies
• Down Syndrome • Cysts
• Treacher-Collins Syndrome • Fistulae
• Velocardiofacial Syndrome • Family history of “fish parts” removed from neck
• CHARGE Association • Otologic malformations
• Craniofacial Syndromes • Preauricular pits (75-85%)
• Apert • Malformed auricles
• Crouzon • Ossicular and cochlear malformations
• Pfeiffer • Hearing loss highly variable
Branchio-
Branchio-oto-
oto-renal Syndrome Goldenhar Syndrome
• Renal malformations • Oculoauriculovertebral spectrum
• Renal agenesis • Facial asymmetry
• Polycystic kidneys • Hypoplastic mandibular ramus and condyle
• Duplicated ureters • Maxillary, malar and temporal bone smaller on
• Hydronephrosis one side
• Mastoid poorly pneumatized
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6
Down Syndrome Down Syndrome
• Microcephaly • Otologic Disease
• Flat nasal bridge • Congenital:
• Midface retrusion • Increased incidence of congenital temporal bone anomalies
• Conductive, sensorineural and mixed
• Upslanting palpebral fissures
• Acquired:
• Epicanthal folds
• External canal stenosis
• Macroglossia • Immature immunologic development
• Congenital heart malformations • Defective eustachian tube cartilage and musculature
(40%) • Chronic ear disease
• Delayed gross motor skills
• Hypotonia and increased joint laxity
656
7
Treacher-
Treacher-Collins Syndrome Treacher-
Treacher-Collins Syndrome
• 1/25000 to 1/50000 • Prominent nasal dorsum
• Retrusive mandible
• Mandibulofacial dystosis
• Zygomatic and mandibular
• Autosomal dominant hypoplasia
• Bilateral, symmetric • Downslanting palpebral fissures
• Lower lid colobomas
abnormalities of first and
• Cleft palate (Pierre Robin
second branchial arch sequence)
structures • External and middle ear
anomalies
• 50% with hearing impairment
from ossicular malformation or
EAC atresia
Treacher-
Treacher-Collins Syndrome Velocardiofacial Syndrome
• Airway Issues • Common multiple anomaly syndromes
• Size of nasopharynx 50% smaller than • 22q11 microdeletion
normal
• Maxillary hypoplasia with choanal
• AD with variable expressivity
stenosis • 186 reported clinical features
• Micrognathia and retropositioned • 50 ENT related
tongue • Many are minor anomalies
• Prone to OSA and SIDS
• Characterized by craniofacial anomalies, conotruncal heart
• Difficult intubation
defects, immune deficiencies, and learning disabilities
• May require tracheostomy
657
8
Velocardiofacial Syndrome Velocardiofacial Syndrome
• Speech Abnormalities • Airway Obstruction
• Palatal abnormalities • Generalized hypotonia
common (75%) • Pharyngeal hypotonia
• 20% overt clefts • Retrognathia
• 80% submucous clefts
• Laryngomalacia
• Classic bifid uvula or
notching of hard palate • Laryngeal web
• Occult • Vascular rings
• Adenoidectomy • Anomalous subclavians compressing trachea
significant VPI
• PRS
658
9
Craniofacial Syndromes Craniofacial Syndromes
• Common features • Major complications
• Craniosynostosis • CNS:
• Hypertelorism • Progressive hydrocephalus
• Exophthalmos • Cerebellar herniation
• Parrot-beaked nose • Increased intracranial pressures
659
10
Craniofacial Syndromes Craniofacial Syndromes
• Pfeiffer • Pfeiffer
• Craniosynostosis, midface • Craniosynostosis, midface
deficiency, broad thumbs, deficiency, broad thumbs,
broad toes, brachydactyly, broad toes, brachydactyly,
variable syndactyly, variable syndactyly,
radioulnar fusion radioulnar fusion
660
11
Craniofacial Syndromes Craniofacial Syndromes
• Tracheal Cartilaginous Sleeve (TCS) • Tracheal Cartilaginous Sleeve (TCS)
• Rare • Diagnosed by bronchoscopy
• Exclusively in CS syndromes • Associated with increased morbidity
• Fusion of tracheal rings solid and mortality
cartilaginous tube • Longer length sleeves seem to be
• Makes airway more susceptible to associated with shorter life
obstruction expectancies
• “kinking off” • Treatment: tracheal resection
• Ineffective cough and poor
mucociliary clearance
• Internal lining more susceptible to
granulation
661
12
Craniofacial Syndromes Summary
• Phase IV – 3-5 years • Syndromes = frequent ENT consults
• LeFort III Advancement • The usual problems
Osteotomy
• Improves facial • Hearing
appearance • Speech
• Corrects exorbitism by • Airway
enlarging orbital
cavities • Basic knowledge of common syndromes
• Expands epipharynx • Other hidden major anomalies
• Restores dental
occlusion • Reduce morbidity and mortality
• Reduces symptoms of • Pass some exam questions
OSA
662
13
MIDDLE EAR AERATION
OTITIS MEDIA PATHOPHYSIOLOGY
-function:
-pressure regulation
-protection from NP sound pressure and secretions
-clearance
663
-surface tension factors
-experiments using surfactants shown to enhance clearance of middle ear and its function
-compared to atmosphere, middle ear is relatively hypoxic and hypercarbic
-intact TM
-Valsalva, Politzer tests
-inflation of the eustachian tube and middle ear
from the nasopharynx end of the system by one
of these classic methods is an assessment of tubal
patency only and not function, and failure to
inflate the middle ear does not necessarily
indicate a lack of patency of the eustachian tube.
-Toynbee’s test
-closed nose swallowing
-if negative pressure (even transitory in the
absence of a patulous tube) develops in the
middle ear during closed-nose swallowing,
eustachian tube function can be considered most
likely to be normal
-9-step tympanometric test (see figure)
-non intact TM
-inflation/deflation test
-same principle as 9-step tympanometric test
except measures pressure changes within middle
ear cavity
664
OTITIS MEDIA
Classification
-effusions:
-serous
-mucoid
-purulent
-acute (0-3 weeks)
-subacute (3-12 weeks)
-chronic (> 12 weeks)
Epidemiology
-if a child has not had OM before the age of 3 years, he is statistically unlikely to develop severe or
recurrent OM
-highest incidence of AOM for both sexes was in the 6-11 month age group
-mean duration 40 days
-incidence of OME peaks during second year of life, is most prevalent during the winter months, and is
associated with URIs
-resolution of OME after first episode of AOM:
-8 weeks: 80% cleared middle ear
-12 weeks: 90% cleared middle ear
Risk Factors
-anatomic abnormalities (affecting ET function):
-craniofacial anomalies: cleft palate, Apert, Down, mucopolysaccharidoses
-congenital or acquired immunodeficiencies
-hypogammaglobulinemia, IgA deficiency, DiGeorge syndrome, HIV, drug-induced
immunodeficiency
-nasal conditions:
-allergy, nasal obstruction (sinusitis, adenoid hypertrophy, nasal/nasopharyngeal tumours), ciliary
dysfunction, prolonged nasal intubation
-host factors:
-immature/impaired immunology
-familial predisposition
-sex/race
-environmental factors
-day-care attendance
-smoking in households
-other:
-bottle feeding
-reflux
665
Microbiology
Bacterial:
-acute (adults)
-Streptococcus pneumoniae (30-50%)
-non-typable Hemophilus influenzae (20-30%)
-Moraxella catarrhalis (10-20%)
-group A streptococci (1-5%)
-acute (neonates and infants)
-Streptococcus pneumoniae (30-50%)
-non typable Hemophilus influenzae (20-30%)
-Staph. aureus, group B streptococci, gram negative enteric pathogens (up to 20%)
-chronic suppurative
-P.aeruginosa
-S.aureus
-corynebacterium
-Klebsiella pneumonia
-anaerobes: peptostrptococcus, fusobacterium, propionibacterium acnes, bacteroides
-persistent effusion
-S.pneumoniae, H.flu, M.catarrhalis, group A strp in 30-50%
-resistance:
-Beta lactamase:
-30% H.flu
-100% M.catarrhalis
-pneumococcal resistance
-chromosomal alterations lead to decrease in penicillin binding proteins and increasing
resistance to sulfa, chloramphenicol, tetracycline, and TMP
-risk factors to resistance:
-multiple and prolonged courses
-not taking entire prescribed course
-inappropriate administration
Viral
-RSV, rhinovirus, influenza, adenovirus, enterovirus, parainfluenza virus
-may potentiate possibility of nasopharyngeal colonization with bacteria
-found in 17% of AOM
-bacteria and viruses in 9%
Diagnosis
-audiometry:
-< 6 months: ABR
-6 months to 1 year: behavioural observation audiometry (BOA)
-1-2 years: visual reinforcement audiometry (VRA)
-2-5 years: Play audiometry
-over 5 years: conventional audiometry
-tympanometry
-tympanoscentesis (indications)
-neonate (< 4 weeks) with otitis media; fever of unknown origin
-immunocompromised
-failed medical management
-guide treatment in the presence of highly resistant organisms
-relief of acute pain not responding to analgesics
666
Management
-"watch and wait"
-treat with antibiotics if:
-< 24 months (increased risk for developing meningitis)
-immunocompromised
-systemic symptoms or complications
-TM perforation with otorrhea
-temperature > 38.5oC
-otherwise treat symptomatically with analgesia (tylenol) for 48-72 hours, providing adequate
follow-up assured
-treat with antibiotics after 48-72 hours if worse or not better
-recurrent OM:
a) those who clear fluid between each infection
-antibiotic treatment for each separated episode
-prolonged prophylactic antibiotic (falling out of favour because of resistance)
-M+T
b) those with persistent effusions: (see COME section)
-antibiotics, pneumococcal resistance
-amoxicillin first line agent for a first episode of OM
-10 day treatment with follow-up in 2-4 weeks
-tubes
-indications:
-treatment of recurrent AOM unresponsive to medical therapy
-chronic OM with bilateral persistent effusion greater than 3 months and conductive
hearing loss
-negative middle-ear pressure with impending cholesteatoma
-intervention in the presence of complications of OM
-complications:
-risk of TM perforation:
-1-2% first set
-2-3% second set
-in place for > 2 years risk is 8-10%
-adenoidectomy
-results of studies evaluating efficacy of adenoidectomy in preventing or decreasing middle-ear
disease vary widely
-Prevnar:
-heptavalent pneumococcal vaccine
-reduced otitis visits by 7.8% and antibiotic prescriptions by 5.7%
-10% reduction in OM in the risk of 3 visits within 6 month period
-26% reduction in the risk of 10 visits within 6 month period
-tube placements reduced by 24%
-lack of evidence for other strategies such as decongestants/antihistamines, mucolytics, allergy therapy, ET
inflation, xylitol chewing gum, Valsalva’s manoeuvre etc..
COME
-persistent MEE present for > 3 months, hearing evaluation and possible surgical intervention should be
considered
-medical/surgical management
-treatment if fluid present > 3 months and:
-disease is bilateral, very symptomatic and associated with significant conductive hearing
loss
667
-significant TM changes such as deep retraction pockets or middle-ear changes such as
adhesive otitis or ossicular involvement
Complications
-CHL
-perforation
-tympanosclerosis
-describe pathology
-Tympanosclerosis is thought to be a complication of otitis media in which acellular
hyalin and calcified deposits accumulate within the tympanic membrane and the
submucosa middle ear. In most patients, these plaques are clinically insignificant and
cause little or no hearing impairment. Tympanosclerotic plaques within the tympanic
membrane appear as a semicircular crescent or horseshoe-shaped white plaque within the
tympanic membrane
-cholesteatoma
-cholesterol granuloma
-adhesive OM
-labyrinthitis
-facial paralysis
-acute mastoiditis
-petrositits (Grandenigo’s syndrome)
-meningitis
-sigmoid sinus thrombosis
-extradural abscess
-brain abscess
-otic hydrocephalus
668
CLEFT PALATE REPAIR
-Goals:
-separation of the nasal and oral cavities
-construction of a watertight and airtight velopharyngeal valve
-preservation of facial growth
-development of aesthetic dentition and functional occlusion
-Timing:
-controversial
-advantages: providing normal speech; better result with velopharyngeal competence the earlier the repair
-disadvantages: surgical effect on facial growth and dental occlusion
-Palatoplasty techniques
-important to reconstruct muscular sling improves subsequent palatal and eustachian tube function
Schweckendiek’s technique
-primary veloplasty
-closure of only the soft palate cleft
-incisions are made in the soft palate, muscle bundles
are dissected, a levator sling is reconstructed, and the
soft palate is closed.
-usually performed at age 3 to 12 months
-delayed closure of the hard palate at a later date
-advantages:
-construction of a velopharyngeal valve at an
early age
-minimal disturbance in future facial growth
-disadvantages:
-necessity of an additional operative procedure
and hospitalization
-required dental prosthesis
-technique is rarely indicated.
669
V-Y push-back
-Oxford method
-creation of two posteriorly based unipedicle flaps
with single or double (depending on the extent of
the cleft),anteriorly based, unipedicle, palatal flaps
-anterior flaps are advanced or rotated medially,
and the posterior flaps are retrodisplaced ith a V to
Y technique
-increases length of the reconstructed palate
-advantages:
-lengthening of palate
-improved speech resulting in more extensive palatal clefts than those obtained by Von
Langenbeck’s method
-disadvantages:
-failure to provide mucosal coverage of the retrodisplaced palate’s nasal surface reduces the
palatal lengthening obtained in the final result secondary to scar contracture of the raw nasal
surface
-difficulty of closing the cleft’s alveolar portion
-fistulas in the thin mucoperiosteal membrane near the hard/soft palate junction
Furlow’s palatoplasty
-double reversing Z-plasty operation
A to E, Furlow palatoplasty.
A Two mirror-image Z-plasties are drawn with the cleft as their central limbs.
B The oral-side Z-plasty flaps are elevated with the levator-palatopharyngeus muscle in the posteriorly based flap. Only the
mucosa is elevated in the anteriorly based flap.
C The nasal flaps are elevated with the remaining muscle in the posteriorly based flap.
D, E Transposing the two sets of flaps overlaps the palatal muscles and lengthens the soft palate
Two-flap palatoplasty
-creation of two posteriorly unipedicle-based flaps that
extend to the alveolar portion of the cleft
-these flaps are rotated and advanced medially to
reconstruct the defect
-does not allow closure of the alveolar cleft or lengthen
the palate unless a Z-plasty is used in the soft palate
670
-technique:
-a single mucoperiosteal flap is elevated from each palatal shelf
-flap is based posteriorly on the descending palatine artery
-palate is closed in three layers:
-nasal layer by a vomer mucoperiosteal flap to a palatal mucoperiosteal flap and velar
mucosa posteriorly
-palatal muscles are carefully approximated
-oral mucosa into close approximation
Complications
-most common complication of palatoplasty is hypernasal speech
-up to 30% to 40% of cleft patients
-fistula formation reportedly occurred in up to 21% of patients after palatoplasty
-anteriorly on the lingual surface of the maxillary alveolus and posteriorly at the hard/soft palate
junction
671
NON-GENETIC HEARING LOSS
INFECTIONS
Congenital Toxoplasmosis
-cats are primary reservoirs
-HL occurs in ~25% of untreated cases
-diagnosis by detecting specific antibodies in serum, plasma, SSF and intraocular fluid
-intensive therapeutic intervention with primarily infected expectant mothers and postnatal treatment of
congenitally infected infants minimizes fetal damage and may prevent the emergence of sensory deficits
Congenital Syphillis
-classic picture:
-SNHL, interstitial keratitis, Hutchinson’s teeth (notched incisors), nasal septal perforation
-positive fistula test (Hennebert’s sign)
-Tullio’s phenomenon: disequilibrium in the presence of loud sounds
-otosyphilitic SNHL in children varies in severity and assumes bilateral flat configuration
-HL may be sudden in onset
-speech discrimination disproportionately impaired compared to pure tones
-dx: fluorescent treponema antibody absorption test; may remain positive after treatment
-tx:
-parenteral penicillin
-conjunctive steroids help stabilize or improve auditory acuity in ~50% of otosyphilitic patients
Rubella
-SNHL, congenital heart defects, ocular defects, microcephaly, HSM, thrombocytopenia, mental or motor
retardation, interstitial pneumonitis, encephalitis, low birth weight
-second-trimester rubella resulted in deafness
-midfrequency SNHL from moderate to severe
-25% demonstrated progressive loss over time
-immunization has eradicated rubella in developed world
672
Herpes Simplex Encephalitis
-primary maternal genital herpes infection during pregnancy may result in spontaneous abortion, premature
labor, CNS damage or IUGR
-fetal infection occurs transplancentally or via an ascending route from infected genitalia
-associated SNHL in encephalitis attributed to CNS mechanisms
-tx: intensive antiviral drugs for infant infected with herpes simplex virus
Bacterial Meningitis
-HL generally appears early in clinical course child with meningitis who exhibits a normal ABR after
first few days of antibiotic therapy is unlikely to develop SNHL later
Aminoglycosides
-vestibulotoxic: streptomycin
-cochleotoxic: amikacin, kanamycin, neomycin
-gentamicin: vestibulotoxic in 2/3; cochleotoxic in 1/3
-pathogenesis:
-cause outer hair cell degeneration initially, with later inner hair cell damage commencing at basal
cochlear coil an proceeding apically
-synergistic effect with loop diuretics
-in preterm infants, complicated perinatal course and prolonged or high-dose aminoglycoside treatment
enhances risk of ototoxicity
Loop diuretics
-used to treat bronchopulmonary dysplasia
-can have prolonged effects in low birth weight infants
-effects generally rapid in onset and quickly reversible with furosemide
Retinoids
-treatment of severe recalcitrant cystic acne
-cause malformations in embryos
Antimalarials
-quinine and chloroquinine have ototoxic potential
-varying degrees of severe to profound SNHL
Cisplatin
-produces high-frequency SNHL, tinnitus, peripheral neuropathy, and dose-related renal insufficiency
-careful audiologic monitoring is indicated when dosage levels of 400 mg/m2 or greater are reached
HYPERBILIRUBINEMIA
-elevated bilirubin crossing BBB deposits in basal ganglia (ie. ventrocochlear nucleus) SNHL
-treatment with fluorescent lighting or exchange transfusion
673
RECURRENT OTITIS MEDIA AND MASTOID DISEASE
PERILYMPHATIC FISTULA
-discontinuity in bony or membranous enclosure that normally surrounds perilymphatic spaces of inner ear
can produce fistula
-risk factors:
-ear surgery, head or ear trauma, noise trauma, barotrauma, significant physical exertion, cranial
or inner ear anomalies, ossicular or middle ear deformities
-symptoms:
-aural fullness, sudden fluctuating or progressive SNHL, fluctuating speech discrimination scores,
roaring tinnitus, balance disturbances
-exacerbated by nose blowing, straining, Valsalva manoeuver, ET dysfunction or physical exertion
-fistula test:
-apply negative and positive pressure to EAC while monitoring of nystagmus
-helpful if positive, but inconclusive if negative
-surgical exploration may not yield a definitive diagnosis
674
PEDIATRIC TRACHEOTOMY DECANNULATION
-adults and children with very short-duration tracheotomy (less than 1 month) can be decannulated by removing the
tube and covering the stoma with an occlusive dressing
-most children, are more difficult to decannulate because of many factors, including suprastomal collapse and
granulation, the relative size of the airway, and possibly psychologic attachment to the tracheotomy tube
-a more controlled process, ward decannulation, is used in these children
Ward Decannulation
-recent endoscopy with suprastomal granulation removal required
-suprastomal collapse should be excluded
-tracheotomy tube is downsized in a controlled stepwise manner, usually one size smaller each day
-child should be kept on the ward and carefully observed at night
-once smallest tracheotomy tube has been tolerated, tracheotomy tube can be blocked for 12 hours during
the day and for 24 hours the next day and night
-tube can be safely removed and stoma covered, although the child still needs to be kept on the ward for
observation for about 5 days
-it this approach fails, the child needs to undergo endoscopy again to exclude cord fixation, cord palsy,
stomal granuloma, stomal collapse, and tracheomalacia
Surgical Decannulation
-endoscopy before decannulation shows significant suprastomal collapse
-entails formal closure of the stoma, sometimes with additional support from cartilage, is followed by
intubation
-tracheocutaneous fistula is excised preserving the tracheal wall unless a cartilage graft is required
-if cartilage is not required (mild to moderate collapse only), the stoma is closed and sutured laterally to the
sternomastoid to prevent collapse of the repair
-if cartilage is required, it is harvested from a rib and carved to a boat shape as for laryngotracheal
reconstruction
-postoperatively, the patient is intubated for 24 to 48 hours
675
SENSORINEURAL HEARING LOSS
676
EVALUATION OF THE HEARING-IMPAIRED CHILD
-physical examination:
-ear examination
-search for subtle findings (e.g., preauricular or branchial pits, heterochromia irides, blue sclerae,
dystopia canthorum, facial asymmetry, café au lait spots)
-investigations:
-CBC: -acute myelogenous leukemia
-FT-Abs -syphilis
-thyroid function -Pendred
-lipid profile -hyperlipidemia
-glucose -diabetes
-urinalysis/BUN/Cr -Alports
-ECG -Jervell and Lange-Nielsen
-serologic tests -CMV, rubella, toxoplasmosis
-ESR, ANA, RF -autoimmune disease/vasculitis
-69-kD inner ear antigen -autoimmune disease
-CT temporal bones -EVA, Michel, Mondini
-ophthalmology -early detection of coexisting retinitis pigmentosa with
electroretinography
-Usher (RP)
-Cogan’s (IK)
-connexin 26, 30
-audiology:
determine the type of hearing loss (i.e., conductive, sensorineural, or mixed); degree of
loss (i.e., mild, moderate, severe, profound, and anacusic); the audiometric configuration
and symmetry of the impairment; and finally, with serial assessment, the stability or
progression of the loss.
A diligent search for etiology of SNHL in a child using state of the art techniques will prove inconclusive
in 30% to 40% of cases
677
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The first 8 weeks constitutes the period of greatest embryonic development of the
head and neck.
There are 5 arches (pharyngeal or branchial). Btw these arches are the clefts
externally and the pouches internally.
The adenoids are colonized with bacteria soon after birth, enlarge early and middle
childhood form antigenic challenges and should regress by early adulthood.
Hypertrophic tonsils are rare in adults and suggest chronic infection or lymphoma.
679
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The tonsil is nestled in a fossa formed by the muscular anterior and posterior
tonsillar pillars (palatoglossus and palatopharyngeus) and lying superficial to the
superior constrictor muscle; preservation of these muscular condensations and the
overlying mucosa is critical to maintaining physiologic function of the palate
postoperatively.
The tonsil is contiguous inferiorly with the lingual tonsil. The point of attachment
(plica triangularis) must be transected during tonsillectomy. In pts with marked
hypertrophy, this extension is freq quite large and can result in troublesome
bleeding at the pt of transection at the base of the tongue.
The adenoid is positioned in the midline of the posterior wall of the NP immediately
inferior to the rostrum of the sphenoid and extending laterally to but not onto the
lateral wall of the NP. It makes up the most rostral portion of the pharyngeal
lymphoid tissue termed Waldeyer’s ring. The space created lateral to the adenoid
and posteromedial to the ET orifice is termed the FOSSA of Rosenmuller.
Gerlach’s tonsil is lymphoid tissue within lip of the fossa of Rosenmuller; goes into
ET.
Inferiorly, the adenoid extends nearly to the superior margin of the superior
constrictor…Passavant’s ridge.
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Tonsillar branch of the facial artery is the main supply of the entire tonsil.
Facial artery:
• Tonsillar art
• Ascending palatine art
Lingual art
•dorsal lingual branch
IMA
• Desceding palatine
• Greater palatine
Ascending pharyngeal (ECA)
Venous drainage of the tonsil is thru lingual and pharyngeal veins which empty into
the IJ.
In most people the ICA lies 2cm posterolateral to the deep surface of the tonsil;
however in 1% of the population, it is found just deep to the superior constrictor.
Adenoids: Ascending palatine, ascending phayrngeal, pharyngeal br of IMA,
ascending cervical branch of thyrocervical trunk
681
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The luminal surface of the tonsil is covered by stratified squamous epithelium (E)
which deeply invaginates the tonsil; the base of the tonsil is separated from
underlying muscle by a dense collagenous hemi-capsule (Cap). The parenchyma
contains numerous lymphoid follicles (F) dispersed just beneath the epithelium of
the crypts.
The surface of the adenoids differs from the tonsils in that the adenoids have deep
folds and few crypts , while the tonsils have from 10-30 crypts and the surface of
the adenoids is composed of ciliated pseudostratified columnar epithelium which
functions in mucociliary clearance. With chronic infection, this layer is thinned,
resulting in stasis of secretions and increased exposure of the tissue to antigenic
stimuli. Deep to the surface epithelium lies a stratified squamous layer followed by
a transitional layer. The SS layer thickens with chronic infection. The transitional
layer is responsible for antigen processing.
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1. MC bacteria:
Beta streptoccoci, staphylococci, streptoccocus pneumoniae, hemophilus
2. Prevalence of beta-lactamase producing organisms is rising:
from 2 % in 1980 to 44% in 1989 (FIND STUDY)
3. Prevalence of anaerobic org is also rising
Asymptomatic streptococcal pharyngitis responsible for at least 1/3 of ARF in 3rd
world. Gold std is throat culture.
Blood agar plate with septra more sensitive than plain agar plate.
Culture both tonsils; if only one, may miss 25%.
Rapid streptococcal antigen test, 12 min.; highly specific but variable sensitivity;
must confirm negative result with a throat cx.
• Newer solid-phase enzyme immunoassay
• Older latex agglutination test
Treat with 10 day course of PCN if high clinical suspicion (augmentin, clinda, pcn +
rifampin for recurrence)
Post treatment culture: high risk RF, remain symptomatic, recurring symptoms; if
asymptomatic but positive cx, treat if h/o RF or if FH of RF
Suspect infectious mononucleosis if sore throat and malaise persist despite abx
treatment; order WBC and Paul-Bunnell. Characterized by white membrane
covering one or both tonsils and hypersensitivity to ampicillin. Look for atypical
mononuclear cells and positive Paul-Bunnell blood test.
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Core species do not always correlate with surface bacteria. 90% correlation with
H.influenza, 73% strept pyogenes
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Tonsilloliths are yellow gritty particles in crypts, more commonly seen in adults
with a h/o recurrent tonsillitis.
Elongated styloid process causes pain exacerbated during maximal deglutition and
deep breathing…. 2nd branchial arch derivitative, approx 2.5 cm long, located btw
internal and ECA just lateral to tonsillar fossa.
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Neoplastic:
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Lymphoma (usually non-Hodgkins B-cell) and squamous cell
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Von Willebrand’s disease is the most common inherited coagulopathy (AD with
variable expression) (1% population) and is caused by a deficiency in Factor
VIII:VW complex necessary in platelet activation. 3 types… type 1 is the most
common (80-90%) with subnormal levels of qualitatively normal vWF and most
will respond to desmopressin. Type 2 is a defect in the factor, type 3 is complete
absence of the factor.
DX elevated PTT, BT, decreased vWF antigen, factor VIII procoagulant activity,
ristocetin cofactor activity; measure response of levels to desmopressin
(0.3microg/kg IV)
RX give IV over 30 min preop (peak levels 45-60 min), 12 hr postop, then q am
until eschar completely sloughed and fossae completely healed; also give
aminocaproic acid or tranexamic acid preop and postop to decrease fibrinolysis (oral
cavity high conc of fibrinolytic enzymes); not useful type 2/3
adverse effects… Na <132 or tachyphylaxis, d/c desmopressin, give cryoprepipitate
or vWF-containing antihemophilic factor
ITP:
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Findings:
1. Histories of recurrent throat infections that are undocumented do not validly
predict recurrence; need documentation by physician before performing
tonsillectomy
2. Using the selection criteria, the incidence of throat infection during the first 2
years of f/u was significantly lower in the surgical groups
3. Many pts in the nonsurgical group had fewer than 3 episodes of infx, and most
cases were mild… therefore, treatment should be individualized, taking into
consideration pt/parental preference, anxieties, tolerance of illness, tolerance of
antimicrobial drugs, child’s school performance in relation to illness-related
absence, accessability of health-care services, out-of-pocket costs, nature of
available anesthetic and surgical services/facilities
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Acute infection
Anemia
Disorders of hemostasis
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VPI: usu transient; sig in 1 in 1500-3000; only 1/3 identified preop as increased risk;
> 2mo speech therapy; > 6-12mo pharyngeal flap
NP stenosis: circumferential contracture of pharynx Waldeyer’s ring, T AND A;
syphilis; increased risk with excessive mucosal excision; difficult to rx
AA subluxation.. Grisel’s syndrome vertebral body decalcification and laxity of
anterior transverse ligament secondary to infection in the nasopharynx… may cause
spontaneous subluxation 1 week postoperatively…pain and torticollis (traumatic
adenoidectomy or injection of local anesthestic into prevertebral space)
15-28% tonsil tags; 6% recurrent pharyngitis
adenoids may grow from adjacent lymphoid tissue… incomplete removal?
Laceration of ICA usu occurs medially and near the skull base.
Pseudoanerusym of ICA requires embolization and proximal ligation.
722
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ECA ligation via lateral neck incision, retraction of SCM posteriorly if unable to
stop bleeding.
723
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Paradise:
Parallel randomized and nonrandomized clinical trials of
213 children who developed recurrence of OM after extrusion of t-tubes;
In both trials, over a period of 2 years, 28-35% fewer episodes than controls.
Gates: 578 children with chronic middle ear effusion. Adenoidectomy combined
with myringotomy or with t tube placement proved to be more effective thatn
myringotomy or tube placement alone in preventing recurrences of OM over a 2
year period
* differences were small (31 vs 36 weeks as mean cumulative times with effusion in
2 treatment groups over 2 yr f/u).
TT surgery alone is assoc with higher rate of repeat surgeries, increased rate of
otorrhea, greater expense and human cost of illness than initial adenoidectomy and
myringotomy
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Contraindications:
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Neurologic or neuromuscular abnormalities with impaired palatal function
Anemia
Disorders of hemostasis
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59
Carotid Body Tumours
Introduction:
-Paraganglionic tissue of the head and neck:
-embryologically derived from the neural crest
-develops in the paravertebral region in association with arterial vessels and cranial nerves
-associated with the autonomic nervous system
-Glenner and Grimley classification (based on location):
-branchiomeric
-intravagal
-aorticosympathetic
-visceroautonomic
Epidemiology:
-incidence less than 0.02%
-same frequency in male and female patients
-occur in all ages
-primarily occur in the fifth decade of life (45 to 50 years)
-greater incidence of carotid body tumours in:
-people who live at high altitudes
-higher predilection for female patients (8.3:1 vs 2:1)
-chronic hypoxia
-two forms of the disease:
1. Sporadic (~90%):
-5% incidence of bilateral carotid tumours
2. Familial (~10%):
737
-autosomal-dominant pattern
-32% incidence of bilateral tumours
-often associated with other paragangliomas (ie. glomus jugulare, glomus vagile)
Other Associations:
-medullary carcinomas of the thyroid
-neurofibromatosis
-parathyroid adenomas and hyperplasia
-suggests that such an association may represent another variable expression of the MEN syndrome
-Carney’s triad:
-extra-adrenal paraganglioma, gastric leiomyosarcoma, pulmonary chondroma
-rare and occurs predominantly in young girls
Pathology:
-grossly tumours vary from 2.0 to 9.0 cm with most being approximately 4.0 cm
-composed of nests of epithelial cells arranged in clusters : Zellballen
-two receptor cell types:
1. Chief cells (type I, epithelioid cells)
-contain 60-300 catecholamine-bound neurosecretory granules
2. Sustentacular cells (type II, supporting cells)
-more concentrated on the peripheral aspect of cell clusters
-devoid of neurosecretory granules
-cell clusters encased in a network of myelinated nerve fibers mixed with a rich vascular plexus
-lack a true capsule
Clinical presentation:
-palpable neck mass:
-most common presenting symptom
-often asymptomatic
-long history: average of 2 to 8 years; some for as long as 47 years
-others (fewer than 30% in one series)
-due to size of mass:
-neck pain/discomfort, dysphagia, dyspnea
-due to involvement of cranial nerves
-hoarseness (vagus), dysphagia (vagus), tongue weakness (hypoglossal)
-dizziness and hearing loss have been reported
-Horner’s syndrome (sympathetic chain): rare
-few documented cases presenting with cerebral ischemia
-functional tumours: secretion of catecholamines
-only 12 cases of functional CBT reported in the literature
-can produce paroxysmal hypertension mimicking pheochromocytoma:
-palpitations, flushing, dizziness, syncope, hypertension, fever
-preoperative administration of alpha-blockers and the intraoperative use of propranolol for beta-adrenergic
blockade have been advocated in the prevention of cardiovascular complications during the induction of
anesthesia and surgery
-on examination:
-mass located below the angle of the jaw deep to SCM
-sign of Fontaine: laterally mobile but vertically fixed - not that helpful
-may be pulsatile - bruit is infrequent
Differential diagnosis:
-branchial cleft cyst, carotid artery aneurysm, primary or metastatic carcinoma, enlarge lymph node, parotid gland
tumour, thyroid tumour
738
Natural History:
-tend to grow relentlessly if not resected
-slow growth at a rate of ~ 0.5 cm per year (2.5 cm in five years)
-no cases of spontaneous resolution have ever been reported
-without resection, 75% asymptomatic patient will eventually develop symptoms
-inferiorly, the fascia of the carotid sheath tends to restrict growth
-superiorly, there is no restriction
-extension to skull base infiltration of CNS
-medially and anteriorly:
-displacement or encasement of vagus, hypoglossal, or sympathetic chain by tumour
-incidence of cranial nerve involvement up to 20% (usually vagal or hypoglossal nerves)
-death can occur either from metastatic disease or from progressive growth:
-from strangulation or through intracranial extension and cranial neuropathies
-some have reported a 30% mortality from untreated, or inadequately resected carotid body tumours
Malignancy:
-literature ranges from 2.6% to 50%
-overestimated rate:
-histological appearance (based on nuclear atypia, nuclear to cytoplasmic ratio) does not correlate with
growth behaviour
-only admissible criteria for malignancy is the presence of distant metastases
-rate considered to be approximately 2 to 5% - most likely less than 3%
-commonly to regional lymph nodes
-also to brachial plexus, cerebellum, lungs, bone, abdomen, pancreas, thyroid, kidney, breast
-long survivals with disseminated disease are seen
eg. patient with spinal metastasis living for decades
b) Contrast-enhanced CT
-well marginated, ovoid mass which splays the internal and external carotid arteries at the level of the
bifurcation and demonstrates intense homogeneous enhancement following the IV administration of
iodinated contrast.
-useful in demonstrating the lateral and medial extent of the tumour
-useful in accurately estimating size
739
c) Intravenous digital subtraction angiography
-safer than conventional angiography
-generally does not provide the same detail
e) MRI
-signal voids: “salt and pepper” appearance due to highly vascularized parts with a fast blood flow
-better show the relation of the tumor to the adjacent internal jugular vein and carotid artery
-avoidance of ionizing radiation and iodinated contrast media
d) MRA
-direct vascular imaging showing the displacement of the carotid arteries, the vessels afferent to the mass
and the highly vascular tumor
-no exogenous contrast is administered
-spatial resolution of MR angiography is typically less than that of conventional angiography
-only the larger, more rapidly flowing feeding vessels will be identified extending to the tumour
-the lack of “tumour blush” on MRA is the norm rather than the exception, and should not exclude the
diagnosis of carotid body tumour
-although angiography has been the gold standard to diagnosing CBTs, recent reports in the literature are
increasingly advocating the use of CT/MRI as well as duplex doppler as first line investigative modalities.
Other Investigations:
-functional tumours:
-urinary metanephrines and vanillylmandelic acid (VMA)
-metaiodobenzylguanidine I 131 (131I MIBG) scan can determine the source of catecholamine production
and/or functional state of the tumor
-Brain flow studies:
-reserved for extensive tumours that are intimately associated to the carotid artery
-tumours larger than 3 cm
-recurrent carotid body tumours
-history of antecedent carotid injury
-any vascular tumour that invades the cavernous sinus or involves the ICA circumferentially
-carotid balloon occlusion with Xenon CT scan or EEG monitoring
-transcranial doppler
-SPECT
Treatment:
-Historical perspective:
-1880 - Reigner first attempt at surgical extirpation - patient did not survive
-1886 - Maydl successfully removed a CBT, leaving the patient aphasic and hemiplegic
-1889 - Albert; 1891- Marchand; 1903 - Scudder: first successful removal with preservation of the carotid
artery complex
-1940 - Gordon-Taylor demonstrated that there was a safe subadventitial plane of dissection
-1953 - Morfit et al added arterial reconstruction techniques
740
-1971 - Shamblin et al grouped these tumours based on extent of encirclement of carotid arteries
-because of the rather slow growth rate, one controversy over the years has been whether or not these lesion need to
be removed.
-early complication rates:
-Early mortality rates from 5 to 15% and as high as 29%
-cerebrovascular sequelae in 8 to 20%
-incomplete excision up to 30%
-cranial nerve injuries 32 to 44%
-Advances in pre-operative diagnosis and localization, intra-operative management of the carotid and cerebral
circulation, along with better anaesthetic management lead to marked decreased mortality rates:
-Chambers and Mahoney (1968):
-37/38 tumours without mortality, significant complications or permanent CN palsies
-Williams et al (1986-1990):
-0.6% (1/177)operative death
-2.3% (4/177)strokes
-29% (51/177)cranial nerve dysfunction
-The major series reported in the literature from 1991 to 1995 show further reduction of the overall
incidence of morbidity to 24.2% (stroke in 1.9% and peripheral nerve palsy in 22.3% of patients) without
any mortality.
-Recognition of their tendency for relentless growth and improved technical aspects of their surgical resection
favour surgical removal in most cases.
-Davidge-Pitts and Pananowitz have correlated size with Shamblin class:
-tumours larger than 4 to 5 cm tend to have partial or complete encirclement of carotid arteries,
and operative complications are much more frequent
-significantly increased incidence of postoperative morbidity with tumours larger than 5 cm
-early removal of an asymptomatic tumour is advocated to minimize potential cranial nerve and
carotid artery injury
-surgery is the current mainstay of therapy for carotid body tumours
-indications for conservative approach:
-patient’s age and medical condition
-patient with bilateral CBT and previous resection with resulting vagus nerve injury
Surgical technique:
1. Oblique neck incision made anterior to SCM
-subplatysmal flap elevation to provide wide exposure of the carotid system
2. Limited selective neck dissection is performed
-sampling of regional nodes for metastasis
-spinal accessory nerve is identified
-hypoglossal nerve identified - with division of ansa cervicalis, CN XII can be retracted superiorly
-vagus nerve identified
3. Common, external and internal carotid arteries proximal and distal to the tumour are controlled
-if the external carotid is involved within the tumour, it can be sacrificed
4. Subadventitial dissection in the plane of Gordon-Taylor
-tumour is dissected away from the surface of the internal carotid
741
-excessive bleeding may be avoided by ligation of the small tumour-feeding vessels on the posterior aspect
of the carotid bifurcation
-the tumor freed from the bifurcation is retracted superiorly to allow dissection of the superior laryngeal
nerve away from the deep surface of the tumour
5. If more exposure is needed superiorly, the digastrics is taken down along with the stylohyoid muscle
6. If the carotid is involved with the tumour, it is sacrificed and replaced with either a venous or synthetic graft
Postoperative complications:
-Mainly cranial nerve injuries
-vagus and hypoglossal most commonly affected
Adjunctive treatment:
1. Preoperative embolization:
-embolization is performed by the introduction of polyvinyl alcohol beads into the microvasculature of the
paraganglioma and gelfoam into the arterial branch itself to obliterate the flow
-operation within 48 hours after embolization is recommended to minimize revascularization edema or
local inflammatory responses.
-risks: TIA, stroke
-benefits: reduce hemorrhage during surgery and provide a more visible operating field; reduce the need
for transfusion
-controversy:
-La Muraglia et al (J Vasc Surg 1992;33(4):454-6) 11/17 preoperative embolization, the
significant difference in the intraoperative blood loss (372+213 ml compared with 609+564ml of
patients that were not embolized). However operative times were equivalent in both groups (4.1 h
vs. 4.5 h)
-Berguer and Kieffer disagree because of the high risk of stroke during embolization. They have
not found that the dissection is any less demanding than in those cases who did not have
preoperative embolization
-Litle VR et al (annals of Vasuclar Surgery 1996;10(5):464-8)
11 embolized vs 11 non-embolized
-no differences in blood loss, number of blood transfusion, operative time or perioperative
morbidity
-overall hospital stay was similar but the EMB group had a significantly longer preoperative
stay compared to the N-EMB group
-concluded that preoperative embolization does not significantly improve outcome in patients
undergoing resection of carotid body tumours measuring 4 to 5 cm
-some authors suggest the use be limited to tumours greater than 5 cm in diameter
2. Radiation therapy:
-still much controversy as to the effectiveness of radiation therapy
-usually reserved for inoperable, bulky and recurrent tumours although CBTs have been considered radio-resistant
-a number of reports have indicated excellent control of these tumours; long term follow-up is not available
-it is accepted that radiation (40-50 Gy) produces fibrosis of the tumours, controlling the tumour growth
but not curing it
-complications:
-necrosis of mandible, carotid artery, and larynx
-should not be considered alternative, but complementary to surgery
Follow-up:
-yearly follow-up with ultrasound or CT scan to measure progression if conservative route taken
-recurrences are uncommon, occurring in approximately 10% os cases
742
HEMANGIOMAS AND VASCULAR ANOMALIES
OF THE HEAD AND NECK
(Cumming’s)
Objectives:
CLASSIFICATION
(1) hemangioma:
-a lesion that grows rapidly in early infancy
-characterized by endothelial proliferation and invariably undergoes slow regression
743
DISTINGUISHING CHARACTERISTICS: HEMANGIOMA VERSUS VASCULAR MALFORMATION
Clinical
-hemangioma
-usually not seen at birth
-rapid postnatal growth (proliferative phase) for first 8-12 months of life
-slow regression over 5 to 8 years (involutive phase)
-vascular malformations
-by definition, are present at birth
-grows proportionately with the child
Cellular
-hemangioma:
-proliferating phase: rapidly dividing endothelial cells forming syncytial masses with and without
lumina
-mast cells significantly increased in proliferating hemangioma and return to normal late in
involuting phase; their role angiogenesis is poorly understood
-during involutive phase, endothelial cell activity diminishes and cellular parenchyma is replaced
by fibrofatty tissue
-vascular malformations:
-no cellular proliferation but rather a progressive dilation of vessels of abnormal mural structure
-lined by flat, quiescent endothelium lying on a thin single laminar basement membrane
Radiographic
Hemangioma Soft-tissue mass, Lobulated soft-tissue Uniform intense High-flow vessels within
isointense or mass, enhancement and around soft-tissue
hypointense, flow voids increased signal, flow mass
voids
Venous Malformation Isointense to muscle, Septated soft tissue Diffuse or No high-flow vessels
possible high-signal mass, high signal, signal inhomogeneous
thrombi voids (pheleboliths) enhancement
Lymphatic Malformation Septated soft-tissue Soft-tissue mass, high Rim enhancement or no No high-flow vessels
mass, low signal signal, fluid/fluid levels enhancement
Skeletal
-hemangiomas only rarely cause bone or cartilaginous hypertrophy
-slow-flow vascular anomalies, specifically lymphatic, venous, or lymphatovenous types, can cause
significant hypertrophy and distortion of the craniofacial skeleton
-fast-flow anomalies typically cause interosseous destruction
744
HEMANGIOMA
-superficial:
-skin raised with a vivid bright-red colour
-well circumscribed
-deep:
-proliferate in lower dermis or subcutaneous tissue with little involvement of superficial or
capillary dermis
-overlying skin is smooth with a bluish hue
-mixed:
-both deep and superficial skin layers involved
-“capillary-cavernous hemangioma”
Radiologic imaging
-order of investigations: US (with Doppler flow study) > MRI (occ CT) > angiography
Complications
-Obstruction
-Visual
-can result in deprivation amblyopia and failure to develop binocular vision
-Subglottic hemangioma
-usually presents after first 6 weeks of life
-more than half of these infants have an associated cervicofacial cutaneous hemangioma
-biphasic stridor - insidious onset of respiratory distress
-lateral radiograph of neck or a fluoroscopic study of upper airway:
-smooth, usually posteriorly based round swelling in subglottic space
-dx: requires direct laryngoscopy: smooth, easily compressible mass in subglottic space
-biopsy of not necessary for diagnosis
Alarming complications
745
-profound thrombocytopenia (2000 to 40,000/mm3)
-purpura and life-threatening bleeding into the pharynx, gastrointestinal tract, and/or brain
-occurs in 1% of infants with hemangiomas
-mortality of 30% to 40%
Management
-complete resolution of hemangiomas occurs in over 50% by age of 5 years and in over 70% by age of 7
years
-skin exhibits mild atrophy after involution
-for small hemangioma in an inconspicuous location, nothing should be done
Subglottic hemangioma
-lesion occupying < 20% of airway: no treatment required; await involution
-classically for respiratory distress, tracheotomy for 2 years until sufficient involution
-corticosteroid therapy:
-60% respond to corticosteroids
-dose: prednisone (2 to 3 mg/kg/day); lower dosage or an alternate-day regimen may be continued
for 4 to 6 weeks or longer
-CO2 laser:
-failed corticosteroid therapy
-CO2 laser beam used in intermittent mode at a setting of 0.05 seconds at 20 watts
-circumferential subglottic hemangiomas removed in stages to prevent subglottic stenosis, or
tracheostomy may become necessary
-surgical resection:
-via laryngofissure approach
-shell out tumour sub-mucosally
Corticosteroid
-high-dose corticosteroids remain premier pharmacologic agent for control of endangering
hemangiomas
-dosage: oral prednisone (2 to 3 mg/kg/day); IV in infants with respiratory complications
-if no response in 7 days, lesion is considered steroid unresponsive drug discontinued
-steroid dosage usually lowered slowly over several weeks if responsive or patient can be
switched to alternate-day therapy
-intralesional corticosteroids for small protuberant hemangiomas on face (upper-eyelid and
nasal-tip lesions)
-dose of triamcinolone and betamethasone no more than 40 and 6 mg, respectively
-one to five injections are necessary, spaced 4 to 6 weeks apart
Interferon-a-2a
-used in infants with life-threatening hemangiomas that do not respond promptly to corticosteroids
-agent of choice for patients with Kasabach-Merritt syndrome
Surgical therapy
-excision for removal of fibrofatty residuum or skin laxity post-involution
-indications for earlier operative intervention:
-hemangioma causing visual problems and is unresponsive to corticosteroid therapy
-early excision of an obstructing subglottic hemangioma using a CO2 laser
-pedunculated and ulcerated lesions removed rather than waiting for involution to occur
746
-evidence of psychosocial problems d/t body or facial image (lip and nasal tip)
-if skin removal will be necessary in the future either because of colour, quality, or contour,
notwithstanding the final result of involution
VASCULAR MALFORMATIONS
Capillary malformation
Histology
-abnormally dilated capillaries or venule-sized vessels in superficial dermis
-lesion may become raised and nodular with progressive vascular ectasia
Clinical features
-Sturge-Weber syndrome:
-port-wine stain within V1 area at serious risk for choroidal and intracranial vascular anomalies
-cerebral angiography: capillary, venous, and arteriovenous anomalies of leptomeninges
-leads to progressive degeneration and atrophy of cerebral hemispheres
Management
Laser therapy
-management of choice; causes thermal thrombosis
-argon laser used for adult patients
-flashlamp pulsed tunable-dye laser preferred for young children, patients with light-coloured
port-wine stains, and those whose skin is sensitive to heat
Surgical excision
-used in selected cases
Venous malformation
Histology
-dilated or ectatic vascular channels lined by normal endothelium
-thrombosis common (phleboliths)
Clinical features
-soft, compressible nonpulsatile mass with rapid refilling
-expansion on compression of jugular vein or Valsalva’s manoeuver
-phlebothrombosis recurrent pain and tenderness
Management
Sclerotherapy
-sclerosing agents: 95% ethanol or sodium tetradecyl sulfate (1% or 2%) injected into epicenter
Surgery
-for large or symptomatic venous anomalies
-subtotal resection to reduce bulk and improve contour and function or relieve pain
747
Lymphatic malformation
-once transected, however, lymphatic malformation have tendency to proliferate into surgical scar
Histology
-multiple dilated lymphatic channels lined by a single layer of flattened endothelium
-walls of variable thickness and are fibromuscular, with both striated and smooth muscle components
Clinical features
-may have wide infiltration
-associated with hypertrophy of both bone and soft tissue
Management
-surgical resection is management of choice
-laser reserved for disease not readily resectable by sharp dissection
-oral cavity and tongue lesions
-supraglottic region
-intralesional injection of OK-432
Arteriovenous malformation
Histology
-arteriovenous shunts
-dysmorphic arteries are thick-walled and of irregular caliber
-fragmentation of internal elastic lamina and highly disorganized smooth muscle in the media
-veins: progressive reactive hypertrophy, intimal thickening, and sclerosis caused by increased blood
Clinical findings
-manifest during late childhood, adolescence, or early adulthood
-throbbing pain, buzzing, or pulsatile tinnitus
-involved skin has elevated temperature, and a thrill may be felt
Management
-MRI and angiography for evaluation
-angiography: superselective embolization (pre-op)
-total resection
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MALIGNANT LESIONS OF THE ORAL CAVITY
(Cummings)
ANATOMY
Lymphatic Drainage
Lips:
-lower lip:
-bilateral metastasis
-medial portion: submental lymph nodes
-lateral portion: submandibular lymph nodes
-upper lip:
-preauricular, infraparotid, submandibular, and submental lymph nodes
-no crossing of midline has been documented for mucosal lymphatics
-submental, submandibular, and periparotid areas drain into lymph nodes of upper and occasionally middle
jugular lymphatic chain
Buccal Mucosa:
-submental and submandibular triangle lymph nodes
Alveolar Ridges:
-buccal aspect of upper and lower alveolar ridges:
-submental and submandibular lymph nodes
-lingual aspect of upper and lower gingiva:
-chiefly to upper deep jugular and lateral retropharyngeal lymph nodes
-lingual surface of the lower alveolus also may end in submandibular nodes
749
Retromolar trigone:
-upper deep jugular chain of lymph nodes; some to subparotid and lateral retropharyngeal lymph nodes.
Hard palate:
-sparse
-upper deep jugular (subdigastric) or lateral retropharyngeal nodes
-primary palate: prevascular and retrovascular group of submandibular nodes
Floor of mouth:
-superficial mucosa
-ipsilateral and contralateral preglandular lymph nodes
-deep collecting
-ipsilateral preglandular nodes
-most anterior collecting vessels of the deep system cross the midline
-posterior portion drain directly into the jugulodigastric and jugulocarotid nodes
Tongue:
-all vessels drain ultimately into deep jugular
lymph nodes
-nearer the tip of the tongue the lymphatics arise,
the lower is the first-echelon node; and the
farther posterior, the higher the node
-anterior (apex) submental nodes
-lateral or marginal trunks submandibular
nodes
-central trunks deep jugular nodes
-tongue base jugulodigastric nodes
MANAGEMENT
Radiotherapy
750
Prophylactic neck irradiation
-radiotherapy of N0 neck with 50 to 55 Gy will control occult disease and prevent later occurrence of
cervical metastases
-although prophylactic neck irradiation appears to be at least as effective as elective neck dissection in the
management of occult neck disease, prospective randomized studies are needed for conclusive evidence in
support of one modality or the other
Surgery
Neck dissection
-N0 necks but extensive primary lesions (T2, T3, or T4) high probability of neck metastases
-supraomohyoid neck dissection (zone I, II and III) warranted
-if no metastases, no radiation
-if metastases improved regional control with addition of XRT
-N1, N2, or N3 require a comprehensive neck dissection for optimal disease control and should undergo
postop XRT
-midline lesions may cause bilateral metastases
-if both are clinically N0, bilateral extended supraomohyoid neck dissections can be performed as
staging procedures
Combined therapy
-combination of radiotherapy and surgery in treating advanced stage III and IV disease of the oral cavity in
hopes of reducing local recurrence and improving survival rates
-pre- or postoperative radiotherapy has been shown to reduce neck recurrence
-Preoperative irradiation:
-45 to 50 Gy delivered at 2.0 Gy per day
-surgery is initiated after a 4-week interval following radiotherapy
-theoretic advantages:
-tumor cells may have better oxygenation before surgery and thus be more sensitive to
irradiation
-malignant cells at periphery of neoplasm are destroyed
-tumor seeding at the time of resection may be decreased
-may be fewer and less viable cells intravascularly and within lymphatics at time of
surgery, which could lower frequency of distant metastases.
-disadvantages:
-wound healing problems, which increase as preoperative doses exceed 40 Gy
-increased incidence of tissue necrosis, wound infection, and fistula formation occurs
when surgery is performed in a radiated region
-reconstruction usually is more difficult because of fibrosis and inflammation and
reduced blood supply
751
-changes in size of neoplasm as well as general inflammatory responses elicited by the
radiotherapy may obscure tumor margins
-Postoperative radiotherapy:
-begun 3 to 4 weeks following surgery
-theoretic advantages:
-safer administration of a higher total dose of irradiation
-destruction of subclinical residual tumor, which may remain following surgery
-fewer wound infections
-distinct tumor margins facilitating more accurate and complete surgical removal
-ability to direct radiation to specific areas observed intraoperatively where tumor-free
surgical margins are questionable
-disadvantage:
-surgery may interrupt blood supply of remaining tumor cells and lessen their sensitivity
to radiotherapy
-wound breakdown or other operative complications may delay onset or prevent delivery
of radiotherapy
Chemotherapy
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PRINCIPLES OF CHEMOTHERAPY IN
THE MANAGEMENT OF HEAD AND NECK CANCER
TYPES OF CHEMOTHERAPEUTICS
-alkylating agents:
-cross-link DNA and interfere with DNA replication
-nitrogen mustard, cyclophosphamide, chlorambucil
-cisplatin, doxorubicin, bleomycin, mitomycin C
-antimetabolites:
-interfere with cellular metabolism
-methotrexate, 5-fluorouracil, hydroxyurea, gemcitabine
-microtubule disruption:
-vincristine, vinblastine, vinorelbine
-microtubule stabilizers:
-paclitaxel, docetaxol
-topoisomerase I inhibitors:
-prevent unwinding of DNA
-irinotecan, topotecan
CLINICAL TRIALS
-phase I:
-tolerance and pharmacologic properties of newly developed compounds are studied
-end point is determination of maximally tolerated dose
-phase II:
-determine therapeutic activity, or efficacy, of a new drug in a specific disease and stage
-end point is definition of activity measured as response rate, at an acceptable rate of toxicity
-phase III:
-new drug or combination is compared with current standard therapy
-1/3 pts with SCC present with early-stage lesions no chemotherapy needed
-for all other pts, chemotherapy may have a role
-metastatic disease and for those with locoregional recurrences that cannot be managed with
further surgery or radiation, chemotherapy has a palliative role
-advanced stage III and IV cancer:
-may improve survival and organ preservation
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STANDARD CHEMOTHERAPY FOR RECURRENT OR METASTATIC CANCER
-response rates of various drugs ~30% or less with responses that are almost exclusively partial and of
short duration
-primary goal is palliation of symptoms, including pain, disfigurement by a mass, or decreased organ
function d/t invasive cancer
Methotrexate
-antimetabolite: interferes with intracellular folate metabolism
-binds to dihydrofolate reductase
-prevents conversion of folic acid to tetrahydrofolate inhibition of DNA synthesis
-active only during S phase
-side effects minimized with leucovorin
-toxic reactions: myelosuppression, mucositis, dermatitis, nausea, vomiting, diarrhea and hepatic fibrosis
-produces partial response rate of ~10%
Cisplatin
-antitumor activity results from intracellular binding to form bifunctional covalent links that interfere with
normal DNA function
-side effects:
-renal toxicity common
-nausea and vomiting, peripheral neurotoxicity, ototoxicity, and cumulative myelosuppression
-partial response rates of ~15-30%
-analogues:
-Carboplatin: decreased nephrotoxicity and neurotoxicity
5-Fluorouracil
-S-phase-specific uracil analogue
-mechanism of action:
-sequential phosphorylation and incorporation into RNA
-activation to 5-fluorodeoxyuridine monophosphate, which blocks thymidylate synthase and
blocks conversion of uridine into thymidine compounds
-cells unable to synthesize DNA
-side effects:
-myelosuppression, mucositis, dermatitis, diarrhea, cardiac toxicity
COMBINATION CHEMOTHERAPY
-in the management of head and neck cancer, most combinations have been based on methotrexate or
cisplatin
-combinations produce statistically significantly higher response rates than do single agents, including
methotrexate
-cisplatin and infusional 5-FU produce higher response rates than do single agents or other combinations
-in no comparison group is survival time meaningfully lengthened
-toxicities of cisplatin and infusional 5-FU are significantly greater than those of single agents
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Summary:
-methotrexate in weekly low doses, cisplatin, infusional 5-FU, paclitaxel and docetaxel are most active
single agents
-response rate is 20-40% and response lasts for 1-6 months
-combination chemotherapy produces higher response rates, although long-term survival rarely is achieved
-unresectable locoregionally advanced cancer, chemoradiation therapy clearly better than radiation therapy
alone in most settings
-studies suggest that intensive chemoradiation therapy can be at least equivalent to surgery plus radiation
therapy for medically fit pts
Nasopharyngeal Cancer
-chemotherapy is important in management of NPC
-considered standard therapy
-metastatic undifferentiated carcinoma, or lymphoepithelioma (WHO III) of the nasopharynx is highly
sensitive to chemotherapy
-Phase III Intergroup Study 0099 showed increased survival benefit with chemoradiotherapy (cisplatin/5-
FU) over radiotherapy alone for stage III and stage IV nasopharyngeal cancer (J Clin Oncol 1998;
16:1310-1317)
-76% versus 46% 3-year survival, P <0.001
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Resectable Cancer of the Head and Neck
-use of chemoradiation in the management of resectable cancer of the head and neck has not yet gained
widespread acceptance
-although some studies suggest that results on locoregional control and survival are comparable to surgery
and radiation
-most extensively used and studied combination is a regimen of cisplatin and 5-FU
-general conclusions of studies:
-overall response rates exceeding 80% are frequently achieved
-complete response rates usually range from 20-50%, most trials showing approximately 30%
-toxicity usually is moderate to severe, but administration of subsequent standard local therapy is
not compromised
-pts achieving complete responses have a better prognosis, particularly if the responses are
confirmed histologically
-organ preservation is possible at least in laryngeal and hypopharyngeal carcinoma
-survival assessed in randomized studies, generally does not improve
-most pts died of complications of locoregional disease; therefore the decreased rate of distant
metastasis did not translate into a survival benefit
-Department of Veterans Affairs Laryngeal Cancer Study (N Engl J Med 1991; 324:1685-1690):
-advanced laryngeal cancer
-standard tx: sx + XRT
-study tx: three cycles of neoadjuvant cisplatin and 5-FU followed by XRT
-findings: overall survival rates were identical in two groups - 68% 2-year survival, P=0.98
-high rate of preservation of the larynx (64% of pts in chemotherapy arm had larynx
preserved)
-similar rate of disease-free survival with laryngeal preservation (28%) was achieved in another
study with similar design in which pts had hypopharyngeal cancer
-Piriform Sinus Cancer Organ Preservation (J Natl Cancer Inst. 1996; 88:890-899):
-Phase III European Organization for Research and treatment of Cancer (EORTC)
-showed no significant change in survival with induction chemotherapy (cisplatin/5-FU) followed
by adjuvant radiation therapy over surgical management for advanced hypopharyngeal cancer (30-
35% 5-year survival)
-approximately half of patients who were alive at 3 years in the induction chemotherapy arm
retained their larynx
-study shows that all pts with laryngeal or hypopharyngeal carcinoma should be offered organ
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preservation therapy
-neoadjuvant chemotherapy has not conclusively improved survival and therefore continues to be
investigational therapy for dz of sites other than larynx and hypopharynx
CHEMOTHERAPY EMERGENCIES
Complications
-nausea, vomiting -antiemetics, fluids, relaxation, support
-diarrhea -control of infection, antidiarrheal therapy
-alopecia -none
-mucositis -mouth care, narcotic therapy
-myelosuppression
-neutropenia -GCSF, IV Abx, hospitalization if pt has fever
-thrombocytopenia -platelet transfusion if count is 10-20/ul or bleeding at <50/ul
-anemia -control of bleeding, erythropoietin therapy, transfusions
-nephrotoxicity -hydration, support, dialysis
-electrolyte wasting -repletion
-neurotoxicity -mainly supportive
-allergic reaction -antihistamine, steroids, epinephrine
-pulmonary toxicity -support, steroids, management of specific cause
-hepatotoxicity -mainly supportive
Emergencies
-neutropenia fever
-fever, chills, symptoms of infection plus absolute neutrophil count < 500/ul
-hospitalization, antibiotics (broad spectrum antipseudomonals), with or without GCSF
-thrombocytopenia
-platelet count <10-20/ul, petechia, overt bleeding
-transfusion, determining source of bleeding, avoidance of ASA and NSAIDs
-allergic reaction
-esp to paclitaxel or bleomycin
-rash, hives, stridor, hypotension
-antihistamine, glucocorticoid, epinephrine
-extravasation
-eg. vincristine or doxorubicin can cause necrosis of skin
-redness, swelling, pain
-subcutaneous epinephrine or hyaluronidase
-overdose
-drug dependent
-supportive, antidote if available
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PRINCIPLES OF RADIATION ONCOLOGY
RADIATION PHYSICS
Terminology
-Rad (Radiation Absorbed Dose)
-amount of energy deposited by ionizing radiation per gram of tissue
1 rad = 1 erg/cm3
1 Gy = 100 rads
Brachytherapy
-radioactive sources are placed within or close to target volume
-interstitial therapy: source placed into tumour and surrounding tissues
-intracavitary: within body cavities
-surface molds: onto epithelial surfaces
-advantages:
-radiation confined to implant volume greater dose delivered with lesser dose to adjacent tissue
-continuous delivery of radiation at a low dose rate
-avoids morbidity of XRT to other tissue structures
-disadvantages:
-tumour must be accessible and relatively well demarcated
-cannot be used as only treatment if there is high risk of regional lymph node metastasis
-usual dose:
-70-80 Gy to target volume for 5-7 days
RADIOBIOLOGY
Cell Death
-radiation cell “kill” is expressed as a logarithmic cell survival curve
-radiation does not kill a certain number of cells but a percentage of cells
-cells are considered “killed” when they lose clonogenic survival
-direct effect: secondary electron interacts with DNA to produce damage
-when a critical number of double stranded and single stranded breaks occur, then the cell
undergoes necrotic cell death or apoptosis
-indirect effect: secondary electron interacts with molecule in vicinity to produce a free radical which
damages the cell
758
-oxygenated cells are more susceptible to radiation than hypoxic cells
-exophytic tumours are typically well vascularized and therefore more susceptible to radiation
injury, ulcerative and infiltrative tumours are less vascularized and therefore more resistant to
radiation
Repopulation
-if tumour cell population is reduced, malignant cells respond with accelerated repopulation
-accelerated treatment schedules with twice-daily fractionation and combined accelerated-hyperfractionated
schedules have been developed to diminish the opportunity for repopulation of rapidly proliferating
tumours
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LOCAL CONTROL AS A FUNCTION OF RADIATION DOSE AND SIZE OF TUMOUR
30-40 ~60-70%
60-65 90% tonsillar fossa 80% tonsillar fossa 50% tonsillar fossae
90% RMT, ATP 75% supraglottic larynx
100% supraglottic 55% glossopharyngeal
larynx sulcus
88% base of tongue
70 100% tonsillar fossae 90% RMT, ATP 65% tonsillar fossa 90% 70%
100% glossopharyngeal 80% glossopharyngeal
sulcus sulcus
Regression Rates
-tumour regression rate is related to cycling time of tumour cells
-lethally injured cells and surviving cells are morphologically indistinguishable:
-biopsy is of little value in early postirradiation period
-positive biopsy result usually not reliable indicator of persistent disease until about 3 months
after treatment
TREATMENT
Contraindications to XRT
-patients with collagen vascular disease
-pregnant women
-previous XRT to head and neck region
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Doses Required for SCCa to control disease in > 90% of patients
-subclinical disease (<106 cells): 4500-5000 cGy
-microscopic disease (>106 cells): 6000-6500 cGy
-clinically palpable tumours:
-T1: 6000 cGy
-T4: 7500-8000 cGy
761
Postoperative Radiation Therapy
-arguments in favour:
-anatomic extent of tumour can be determined surgically; easier to define treatment portals
-greater dose of irradiation can be given postoperatively than can be given preoperatively
-total dose given can be based on residual tumour burden after surgery
-surgical resection easier and healing is better in tissue that is not irradiated
-disadvantages:
-radiation may need to be postponed secondary to postoperative complications
-typical dose is 60-65 Gy in 6-7 weeks
-higher doses needed if residual disease or positive margins
-reduces risk of recurrence in surgical field
-results are poorer if postoperative radiation therapy is delayed more than 6 weeks
Fractionation Schemes
-Standard fractionation:
-usually 2 Gy per day x 25 days (5 days/week x 5 weeks)
-Hyperfractionation:
-increasing number of doses (BID dosing)
-decreasing intensity per dose (~1.0-1.2 Gy per fraction)
-higher total dose
-treatment time constant
-higher probability of tumour control without increasing the risk of late complications
-increased acute side effects
-Accelerated fractionation:
-multiple fractions of 1.5-2 Gy daily (higher daily dose)
-decreased overall treatment time
-decrease total dose ~10%
-increases acute side effects and decreases late side effects
-increases tumour cell kill (prevents tumour cell proliferation)
-Hypofractionation:
-smaller number of larger fractions
COMPLICATIONS
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-fibrosis
-principal dose-limiting factor of XRT
-ocular complications (cataracts, retinopathy, optic nerve injury, lacrimal gland injury)
-serous otitis media, SNHL
-spinal cord injury
-Lhermitte syndrome: transitory syndrome characterized by electric shock sensations triggered by
flexing the cervical spine
-radiation myelopathy
-transverse myelitis
-brain injury (somnolence syndrome: transient condition characterized by lethargy, nausea, headache,
cranial nerve palsy or ataxia, brain necrosis)
-rare
-radiation induced cancer:
-increased risk of thyroid, salivary gland cancer, leukemia, sarcomas (may have lag period of 20
years)
-post-radiation hypothyroidism
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CUTANEOUS MALIGNANCY
RISK FACTORS
-sun exposure:
-UV B - 280-320 nm range
-host factors:
-fair complexion
-light hair
-blue eyes
-inability to tan
-propensity to sunburn
-history of multiple or severe sunburns
-Celtic ancestry
-other factors:
-chronic chemical exposure: arsenic
-radiation therapy
-trauma: burns, ulcers and scars (ie. Marjolin’s ulcer)
-immunosuppression
-HPV
-genetic syndromes:
-xeroderma pigmentosum (AR)
-nevoid BCC syndrome (AD) - aka Gorlin’s syndrome
-BCC beginning in childhood
-jaw cysts (odontogenic keratocyst), bifid ribs, scoliosis, MR and frontal
bossing
Epidemiology
-most common malignancy in humans
-comprises approximately 65% of all epithelioid tumours
-20% of all cancers in men and 10-15% of all cancers in women
-86% of lesions occur initially in the head and neck, with 25% of all primary lesions occurring on the nose
-more common in men than in women
-most frequently between ages 40-60 years
-rare metastasis
Evaluation
-five clinical forms:
-nodular or noduloulcerative
-morphealike or sclerosing
-superficial multicentric
-pigmented
-fibroepithelioma
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-nodular (Noduloulcerative):
-most common
-discrete, raised, circular lesion, pink, waxy with visible capillary network (telangiectasias)
-“central ulceration with rolled border”
-superficial:
-scarring and atrophy with threadlike waxy border; scaly
-more common on trunk and extremities
-morphealike:
-most dangerous
-macular, whitish plaque
-indistinct margins makes excision difficult
-aggressive, higher rate of recurrence
-worst prognosis
-pigmented:
-less common
-may resemble nevus or melanoma
fibroepitheliomas:
-firm pedunculate lesions that resemble fibromas
Histopathology
-large, oval nucleus with relatively little cytoplasm
-resemble basal cells of epidermis
-peritumoral lacunae: proliferation of stroma oriented in parallel bundles around the tumour masses
-mucinous stroma
-four histologic patterns:
-solid:
-proliferation of basaloid cells that extend into the papillary dermis, peripheral columnar
cells arranged in palisades
-keratotic:
-differentiated to hair-like structures
-cystic:
-differentiated to sebaceous gland-like structures
-adenoid:
-differentiated to tubular structures, lace-like histological pattern
Treatment Options
-excisional curettage (small lesions < 2 cm)
-cryosurgery (small lesions < 1 cm)
-scalpel excision (4 mm margins)
-XRT
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SQUAMOUS CELL CARCINOMA
Evaluation
-accounts for 10% of skin malignancies
-related to chronic sun exposure
-erythematous, ulcerated, crusting lesion
-granular friable base
-hyperkeratotic patch or an area of crusting
-occasionally a nodular exophytic lesion
-1-4% to 30% metastatic potential
Histopathology
-features:
-hyperchromatism
-pleomorphism
-increased mitotic activity
-intercellular bridges
-irregular masses of epidermal cells that proliferate downward and invade dermis
-differentiated tumours: keratin pearls
-actinically induced: more benign course with low incidence of metastasis
-de novo lesions: more aggressive behaviour, greater potential for metastasis
-regional metastasis:
-Clarkes level IV or V associated with 20% regional metastasis rate
-histologic variations:
-generic
-adenoid
-bowenoid
-verrucous
-spindle-pleomorphic types (sarcomatoid)
Treatment Options
-surgical excision
-XRT
-Moh’s
-neck dissection and superficial parotidectomy for clinically positive nodes only
PREMALIGNANT LESIONS
Actinic Keratoses
-most common premalignant lesion of H+N
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-chance of malignant progression: 20%
-“sandpaper-like scale”
-atypical squamous cells extend past dermal-epidermal junction into papillary dermis
-tx: superficial shave excision, cryosurgery, topical 5FU, TCA peel
Bowens Disesase
-carcinoma in situ of the skin
-full-thickness dysplasia of epidermis without evidence of invasion
-common in pts with chronic arsenic ingestion
-metastasize in 20-35% of cases; 30% develop invasive SCCa
Keratoacanthoma
-benign usually self-limited epithelial tumour
-in males and older pts
-rapid growth 2-6 months
-involution usually within 2-6 months
-most common area affected: nose
-surgical excision recommended because of lack of predictability
PROGNOSIS
Tumour Behaviour
-see table
Predisposing factors
TNM CLASSIFICATION OF SKIN CARCINOMA -genetic predisposition or syndrome
-history of arsenic use
-tumour arising in burns or scars
Tx: unknown -tumours arising in area of radiodermatitis
T0: no evidence of primary
Tis: carcinoma in situ Other factors
-recurrent tumours
T1: < 2cm -immune status
T2: 2-5 cm -tumours with significant tissue invasion
T3: > 5 cm
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T4: tumour invades extradermal structures (cartilage, skeletal muscle, bone)
Stage:
I: T1 N0 M0
II: T2 N0 M0
T3 N0 M0
III: T4 N0 M0
Any T, N1 M0
IV: Any T, Any N, M1
MANAGEMENT
Cryosurgery
-for some basal lesions
768
-liquid nitrogen
-advantages:
-high cure rate, tissue-sparing capabilities, expedience
-disadvantages:
-prolonged healing phase and wound care
-hypopigmentation and scarring can occur
Radiation Therapy
-uses: -poor operative candidates, surgical adjunct or for palliation
-curative in select patients
-advantage:
-ability to treat wide field of tumour and avoidance of surgery
-disadvantage:
-protracted treatment course, expense, adjacent tissue effects, limited effectiveness if tumours
involve cartilage or bone, radiodermatitis, delayed carcinogenesis
Photodynamic Therapy
-photosensitizing drug that selectively localizes in tumours exposure to light preferential tumour
necrosis
-still investigational modality
-lack of predictability
Interferon-Alpha
-investigational:
-BCC (nodular and superficial) have excellent responses
-intralesional injection 3x/week
-associated with leukocytopenia and thrombocytopenia
Excisional Surgery
-93-95% successful
-small, primary, well-demarcated nodular BCC:
-3- to 5-mm margin usually sufficient
-multicentric, large, or recurrent tumours, aggressive growth pattern BCCs, and SCC:
-excisional margins should be greater (1-2 cm)
-advantages:
-tissue for diagnosis and to assess completeness of excision
-excellent cosmesis
-disadvantages:
-time consuming, inconvenient
Mohs’ Surgery
-indications:
-recurrence
-morphea type
-high risk of recurrence (H zone)
-cosmetic regions in which reconstruction is difficult
-chemical fixative applied to cancer, fixing it in situ and permitting careful serial excision with examination
of entire specimen histologically
-maps extension of residual tumour so that reexcision of these pockets of cancer were possible
-96-99% cure rates
-advantages:
-examine resection margins in their entirety
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-microscopic foci of tumour identified, mapped and reexcised
-highest cure rate in management of advanced, high-risk or recurrent lesions
-disadvantages:
-time consuming
-expertise required
-80-90% of metastases from cutaneous SCCs occur first to the regional nodes
-N0 neck:
-monitoring for clinical nodal disease
-prophylactic radiation to primary site and primary draining lymph nodes reserved for very
high-risk lesions or those with neurotropism
-prophylactic node dissection is usually not recommended for those with no clinical evidence of
regional metastases
-if extension to the parotid capsule elective superficial parotidectomy should be considered
-N+ neck:
-therapeutic options include radiotherapy, surgical lymphadenectomy, or a combination of lymph
node dissection and radiotherapy
RECONSTRUCTION
-if confronted with indistinct deep margins or a high probability of recurrence, consider skin grafting and
observation for 6-12 months
-if possible, place incisions in a facial crease, hair-bearing areas, junctions of facial units, and parallel to
relaxed skin tension lines
-always plan reconstruction from simple to more complex microvascular patterns: primary closure skin
770
graft > local flap > regional flap > free flap
-if using a local facial flap, consider the donor site defect and its effect on functional structures (eg. eyelid,
mouth)
771
MALIGNANT MELANOMA
EPIDEMIOLOGY
772
-differential diagnosis:
-seborrheic keratosis
-benign nevi
-haemangioma
-blue nevi
-pyogenic granuloma
-pigmented basal cell carcinoma
MUCOSAL MELANOMA
DESMOPLASTIC MELANOMA
Clark staging
Level I - All tumor cells above basement membrane (in situ)
Level II - Tumor extends into papillary dermis
Level III - Tumor extends to interface between papillary and reticular dermis
Level IV - Tumor extends between bundles of collagen of reticular dermis (extends into reticular dermis)
Level V - Tumor invasion of subcutaneous tissue
773
T classification (thickness)
T1a - 1 mm without ulceration and level II or III
T1b - 1 mm with ulceration or level IV or V
T2a - 1.01-2 mm without ulceration
T2b - 1.01-2 mm with ulceration
T3a - 2.01-4 mm without ulceration
T3b - 2.01-4 mm with ulceration
T4a - Greater than 4 mm without ulceration
T4b - Greater than 4 mm with ulceration
N classification
N1 - 1 node positive for metastasis
N1a - 1 node positive for micrometastasis
N1b - 1 node positive for macrometastasis
N2 - 2-3 nodes positive for metastasis
N2a - 2-3 nodes positive for micrometastasis
N2b - 2-3 nodes positive for macrometastasis
N2c - Intransit met(s) or satellite(s) without metastatic nodes
N3 - 4 or more metastatic nodes or matted nodes or intransit metastases or satellite(s) with
metastatic node(s).
M classification
M1a - Distant skin, subcutaneous, or nodal metastases, normal LDH level
M1b - Lung metastases, normal LDH level
M1c - All other visceral metastases or any distant metastases with an elevated LDH level
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-neck dissection usually functional
-radical neck dissection for clinically positive nodes
-no survival benefit seen in those with lesions > 4mm thick
-for lesions > 1 mm thick and for ulcerated lesions without regional metastasis, excision is offered along
with a procedure to assess the status of regional lymph nodes
-development of sentinel lymph node biopsy may enhance sensitivity and specificity of ELND
-lymphoscintigraphy may provide an adjunctive method of identifying sentinel lymph nodes and defining
routes of lymphathic spread, especially in patients with primary tumours located in the midline that have
predicted drainage basins that are ambiguous or include both parotid glands
TREATMENT
Treatment Overview
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Primary Excision
-surgical resection is the mainstay of therapy
-resection margins: -in situ: 0.5 cm
-1-2 mm: 1.0 cm
-2-4 mm: 2.0 cm
->4 mm: > 2.0 cm (3.0 cm)
-frozen sections of analysis for surgical margins had sensitivity and specificity of 100% and 90%
respectively
Regional Lymphadenectomy
-therapeutic neck dissection and parotidectomy
-neck dissection recommended for clinically positive nodes
-extent of neck dissection remains area of controversy
-type tailored to site of primary tumour:
eg. primary of face, ear and anterior scalp: parotidectomy and LND levels I-IV
postauricular and posterior scalp and neck: levels II-V
Radiotherapy
-traditionally thought that melanoma was radioresistant; but this can be overcome by increasing the
individual dose fraction (hypofractionation)
-XRT generally not recommended for primary treatment of melanoma
-exceptions:
-elderly pts who are poor candidates for surgical resection
-extensive facial LM melanoma that precludes adequate surgical resection
-XRT very effective in post-operative adjuvant setting in achieving high rates of local-regional control
-pts should be considered for XRT either to primary site and/or regional nodal basins whose
primary lesions measure 1.5 mm or greater or are ulcerated
-pts with regional metastasis should be offered radiotherapy after excision of primary tumour and
neck dissection
-dosages of 6 Gy are delivered twice weekly over 2.5 weeks to a total of 30 Gy
Systemic therapy
-indications:
-for adjuvant treatment for those completed local-regional therapy and have no evidence of local,
regional, or systemic disease but are at high risk for systemic relapse
-presence of distant metastasis
-high risk patient:
-primary lesions that are ulcerated
-primary lesions > 4 mm or Clark level IV
-pts with satellitosis
-pts with in transit disease
-pts with nodal disease
Interferon
-has yet to be shown unequivocally to improve overall survival
-used for deep primary (> 4mm) or regionally metastatic melanoma
-intensive daily IV dose x 1 month
-3x/week daily maintenance dose for next 48 weeks
-adverse effects:
-cardiac and hepatic toxicity
-constitutional symptoms
-myelosuppression
776
Tumour Vaccination
-strategies stimulate immune system to overcome immune tolerance to tumour antigens and enhance the
immune surveillance of tumour cells
SURVEILLANCE
777
NEOPLASMS OF THE NOSE AND PARANASAL SINUSES
EPIDEMIOLOGY
TUMOURS OF THE SINONASAL
-less than 1% of all malignancies TRACT
-risk factors:
Epithelial
-exposure to industrial fumes
-benign
-wood dust (hardwood only) -keratotic papilloma
-nickel-refining processes -fungiform papilloma
-leather tanning -inverted papilloma
-cylindrical papilloma
-mineral oils -adenoma
-chromium and chromium compounds -malignant
-isopropyl oils -squamous cell carcinoma
-lacquer paint -transitional cell carcinoma
-adenoid cystic carcinoma
-soldering and welding -adenocarcinoma
-radium dial painting -melanoma
-previous radiation -olfactory neuroblastoma
-chronic infection -undifferentiated carcinoma
-EBV Burkitt’s lymphoma Non-epithelial
-smoking not a significant etiologic factor -benign
-most common malignant nasal tumours: -fibroma
-SCCa -chondroma
-osteoma
-adenocarcinoma -neurilemoma
-adenoid cystic carcinoma -neurofibroma
-hemangioma
-malignant
-soft tissue sarcoma
EVALUATION -rhabdomyosarcoma
-leiomyosarcoma
Diagnosis -fibrosarcoma
-nasal obstruction, epistaxis, nasal discharge -liposarcoma
-angiosarcoma
-asymptomatic in 9-12% -myxosarcoma
-regional and distant metastases infrequent -hemangiopericytoma
-cervical metastases 1-26% (most series report <10%) -connective-tissue sarcoma
-infraorbital or supraorbital numbness suggests malignant -chondrosarcoma
-osteosarcoma
invasion -lymphoreticular tumours
-proptosis, chemosis, EOM impairment, mass effect in cheek, -lymphoma
loose dentition -plasmacytoma
-giant cell tumour
-CT or MRI for evaluation Metastatic carcinoma
-CT: -good for demonstrating bone erosion
-MRI: -differentiates adjacent tumour from soft
tissue
-differentiates secretions in an obstructed sinus from space-occupying lesion
-demonstrates perineural spread
-less artifact effect with dental fillings
-imaging in sagittal plane
-no ionizing radiation
778
PARANASAL SUBSITES
Paranasal Sinuses:
-maxillary sinus most common site involved
-ethmoid sinus second most common
-typically presents in an advanced stage
Nasal Cavity:
-less than 10% regional metastatic potential
-60% 5-year survivial
Pterygopalatine Fossa:
-pyramidal-shaped space below the apex of the orbit and between the posterior wall of the
maxillary sinus and pterygoid plates
-contains foramen rotundum, vidian nerve, sphenopalatine nerve, lesser and greater palatine
nerves, sphenopalatine ganglion, and internal maxillary artery
-invasion of this space carries a poor prognosis
Infratemporal Fossa:
-bounded anterior by the maxilla, postiorly by the glenoid fossa and mandible, and medially by the
lateral pterygoid plates
-roof contains the foramen ovale and spinosum
-also contains the pterygoid muscles
Orbital Cavity:
-invasion into bony orbit or orbital apex requires orbital exenteration
PATHOLOGY
Papilloma
-may extend beyond site of origin and destroy bone
-three types:
-fungiform (50%)
-septum
-HPV 6 and 11
-22-50% recurrence rate
-3-5% associated with malignancy
-inverted (47%)
-lateral wall
-27-73% recurrence rate
-13% (10-15%) associated with malignancy; degenerates to non-keratinizing
SCCa
-HPV 16 and 18 weakly associated with malignant degeneration
779
-cylindrical (3%)
-lateral wall
-25-25% recurrence rate
15% associated with malignancy
-treatment of inverted papilloma:
-resection via lateral rhinotomy-medial maxillectomy approach
-endoscopic resection
Adenoma:
-arise from septum
-recurrence rate low after complete removal
SCC:
-risk factor: nickel exposure
-most common tumour of sinonasal tract (~80%)
Adenocarcinomas
-risk factors: wood dusts, leather tanning
-4-8% of all sinonasal tumours
-originate at ethmoid sinuses
-high (higher incidence of metastasis) and low (tend to recur locally) grades
Melanoma
-primary (<1%) or metastatic
-early vascular and lymphatic invasion
-median survival 36 months
Olfactory neuroblastoma
-arises from olfactory epithelium
-bimodal frequent at 10-20 and 50-60 ya
-histopathology:
-homogenous small cells with uniform round-to-oval nuclei
-true rosettes (Flexner-Wintersteiner [FW]):
-ring of columnar cells circumscribing a central oval-to-round space, which
appears clear on traditional pathological sections
-pseudorosettes (Homer Wright [HW]) rosettes:
-looser arrangement and the presence of fibrillary material within the lumen
-immunohistochemistry:
-positive for S-100 protein and/or neuron-specific enolase
-negative for cytokeratin, desmin, vimentin, actin, glial fibrillary acidic protein,
UMB 45, and the common leukocytic antigen
780
-Kadish Staging System:
-A: confined to nasal cavity
-B: in nasal cavity extending to PNS
-C: extending to orbit, base of skull, cranial cavity or with cervical/distant
metastasis
-UCLA Staging System:
-T1: involving nasal cavity and/or PNS, sparing most superior ethmoidal air cells
-T2: involving nasal cavity and/or PNS with extension to or erosion of cribriform
plate
-T3: extending into orbit or protruding into anterior cranial fossa
-T4: involving brain
-treatment: craniofacial resection +/- post-op XRT
Fibroosseous lesions
-osteomas, fibromas, chondromas most common
Neurogenic sarcoma
-rare - most commonly associated with NF
Rhabdomyosarcoma
-embryonal, alveolar and pleomorphic types
-tumours involving PNS classified as nonorbital parameningeal - behave more aggressively
-treatment: usually radical surgery with intensive radiation and chemotherapy
Fibrosarcoma
-arises from fibroblasts
-etiologic factors: radiation and trauma
-treatment: wide surgical resection; XRT for positive margins or recurrent tumours
Hemangiopericytoma
-arises from pericytes of Zimmermann
-considered low grade malignancy
-vascular, rare
-treatment primarily surgical
Osteogenic sarcoma
-etiologic factors:
-ionizing radiation, fibrous dysplasia, trauma, Paget disease, gene associated with
retinoblastoma
-treatment: surgical excision
781
Chondrosarcoma
-slow-growing
-surgical removal with wide margins
-metastatic potential and oncologic outcome of sarcomas is variable, however local behaviour is similar
-sarcomas are infiltrative
-often incompletely resected
Lymphoma
-usually non-Hodgkin type
-treatment: XRT for localized lesions and chemotherapy for systemic involvement
Extramedullary plasmacytoma
-found in H+N 80-90% of cases, 40% in sinonasal tract
-prognosis unpredictable
-most lesions respond to XRT
STAGING
Maxillary Sinus
Ethmoid Sinus
Ohngren’s Line
-imaginary line drawn between medial canthus and angle of mandible
-tumours arising below this line have better prognosis than tumours arising above this line
782
PRINCIPLES OF TREATMENT
Concepts
Early stages:
-single modality primarily with surgical resection for early maxillary or nasal cavity tumours
(except for small cell carcinoma, lymphoma, rhabdomyosarcoma)
-primary radiation therapy
Advanced stages:
-multimodality treatment:
-primary surgery with postoperative XRT
-primary XRT with surgical salvage
-Unresectable/Nonoperable candidates;
-may consider primary radiation, chemotherapy, or combination radiochemotherapy
Surgery
-approaches:
-endoscopic excision:
-low morbidity, no external scar, limited to benign small lesions
-lateral rhinotomy
-incision begins at medial aspect of eyebrow, follows along lateral nasal wall, around alar
crease to the philtrum and a sublabial incision
-may extend incision to include the lip for exposure of hard palate
-midfacial degloving approach
-incisions:
-transfixion incision
-intercartilaginous incision
-gingivobuccal incision -from midline to maxillary tuberosities
-for lesions that are inferior and involve medial maxillary walls
-limited superior and posterior visualization
-avoids external incisions and allows bilateral exposure
-Weber-Ferguson incision:
-addition of subciliary incision and lip splitting incision to lateral rhinotomy incision
-transpalatal:
-for tumours involving floor of nose/inferior portion of maxilla
-infratemporal fossa approach:
-access obtained via a preauricular or postauricular incision with extension in a
hemicoronal and cervical fashion
-may gain additional exposure by retracting the TMJ
-Raveh approach - anterior craniotomy
-anterior craniofacial resection for anterior tumours
-resection types
-medial maxillectomy
-removes lateral nasal wall and medial maxilla
-standard resection for inverting papillomas
-partial maxillectomy
-tumours confined to floor of antrum inferior maxillectomy
-preservation of orbital floor
783
-total maxillectomy
-removal of entire maxillary bone
-radical maxillectomy
-total maxillectomy with orbital exenteration
-craniofacial resection
-en bloc removal of the anterior cranial base including the cribriform plate and ethmoid
sinuses
-may require dural excision
Radiation Therapy
-may be used as single modality, adjunct to surgery, or as palliative therapy
-usually for unresectable or lymphoreticular tumours, poor surgical candidates
Chemotherapy
-usually used for palliation; limited reports based on non-randomized studies
Combination Therapy
-for positive margins, perineural, perivascular invasion
-positive lymph nodes or recurrent tumour
Nasal Cavity
-usually detected earlier associated with better prognosis
-SCCa most common malignant tumour in this area
-tumours extending to PNS, larger than 2 cm, or positive margins: post-op radiation
-5-year survival > 60%
Maxillary Antrum
-most common site of origin for malignancies of the sinonasal tract
-usually diagnosed at advanced stages: combination therapy
-5-year survival 40-50%
Ethmoid Sinus
-earlier diagnosis and better prognosis
-combination therapy recommended
-5-year survival 50-60%
Sphenoid Sinus
-extremely rare
-gross total removal and postop XRT
-5-year survival 5-25%
Frontal Sinus
-rare
-managed by combination therapy
784
MANAGEMENT OF ADVANCED TUMOURS
Orbital Invasion
-pathways of invasion:
-direct bony erosion (eg. medial wall or floor)
-perivascular or perineural invasion (eg. infraorbital or ethmoidal NV bundles)
-preformed pathways (eg. infraorbital fissure, nasolacrimal duct)
-bone erosion does not constitute an absolute indication for orbital exenteration
-prognosis is dismal palliation
-meta-analysis: no statistically significant difference in survival rate of patients who had orbital
exenteration compared to those that did not
-resection of medial an inferior orbital walls produces severe exophthalmos and hypophthalmos
-rigid reconstruction of bony orbit using titanium mesh +/- calvarial bone grafts
Cervical Metastasis
-incidence: 3-16% (10%)
-poor prognostic indicator
-elective neck dissection or irradiation for N0 neck not justified
-cervical metastasis usually during first 48 months after initial treatment sign of tumour recurrence
Pterygopalatine Fossa
-incidence 10-20%
-presence of tumour in this area a risk factor for recurrence
-radical surgery and radiation therapy advised
RECONSTRUCTION OPTIONS
785
COMPLICATIONS
Orbital
Surgical
-epiphora
-from stenosis of lacrimal sac
-tx: DCR or cannulation of lacrimal canaliculi for 12 weeks
-diplopia
-from limitation of EOM
-may be secondary to entrapment in craniofacial osteotomies
-tx: observe, release EOM if entrapped
-blindness:
-from compression of optic nerve
-tx: high-dose steroids and emergent surgical decompression
-exophthalmos or hypophthalmos
-tx: support globe with bone grafts and/or titanium mesh
Radiation Therapy
-full eye irradiation:
-dry eye will decompensate rapidly, leading to severe keratitis, panophthalmitis and
blindness within 1 year enucleation recommended
-100% of eyes receiving 5800 rad will develop severe panophthalmopathy and severe
corneal ulceration
-post-radiation retinopathy or optic neuropathy
Wound
-bleeding: packing, arterial ligation, or embolization
-infection: antibiotics/debridement
-loss of reconstructive flaps or skin grafts: debridement
Skull Base
-CSF leak
-observation, bed rest
-reconstructive flap for persistent leak
-meningitis
-antibiotics, correct CSF leak
-pneumocephalus
-aspiration if at tension and diversion of nasal airway with use of ETT, nasal trumpets or a
tracheotomy
-osteomyelitis: antibiotics, debridement, HBO
-frontal lobe syndrome: changes in patient’s affect
-cranial nerve injuries
Bleeding
-tx: -cauterization/packing
-arterial ligation/embolization in case of massive tumour where packing is impossible
-transoral ligation of internal maxillary artery and transorbital ligation of ethmoidal
arteries
786
Visual Impairment
-blindness d/t compression or stretching of optic nerve, its arterial supply or its venous drainage
-decompression of orbit or optic nerve
-radiation for lymphoreticular tumours
Infection
-acute bacterial sinusitis and possible orbital and intracranial complications
-treat with antibiotics and debridement
787
ORBITAL TUMOURS
-primary tumours
-hemangioma, NHL, inflammatory tumours, meningioma, optic nerve glioma
-secondary tumours
-invasion from other structures
-12% of orbital lesions; 33-45% of orbital neoplasms
-mucoceles, SCCa, meningioma, vascular malformations, BCC
-metastatic disease
-adenocarcinoma of lung and breast
-2-8% of orbital tumours
-pediatric group
-most are benign
-orbital dermoids, vascular tumours, optic nerve glioma, and inflammatory tumours
-10-30% malignant
-most common is rhabdomyosarcoma
-metastatic neuroblastoma, leukemic orbital involvement, Ewing sarcoma, extension of
retinoblastoma
VASCULAR TUMOURS
Cavernous Hemangioma
-most common primary intraconal orbital neoplasm found in adults
-slowly progressive, painless, unilateral proptosis over many years
-CT/MRI for diagnosis
-discrete round or oval mass without associated inflammation or infiltration
-usually enhances with IV contrast
-tx: complete surgical excision with excellent prognosis
Capillary Hemangioma
-most common vascular tumour of orbit and periocular tissue in infancy and childhood
-upper eyelid most common periocular location
-usually first noted during first month of life and grows to maximum size by 12-18 months of age
-spontaneous involution by age 4-8 years
-50% at 5years; 90% at 7 years
-complications:
-have potential to cause derivational and anisometropic amblyopia
-cosmetic cutaneous deformities
-proptosis and corneal exposure
-bony malformations
-CT/MRI:
-diffusely infiltrating nonencapsulated mass
-conformation to surrounding orbital structures
-enhances with contrast
788
-treatment for:
-amblyopia, proptosis with corneal exposure, optic nerve compression, bony deformities
-intralesional injections of corticosteroids, systemic steroids or careful debulking surgeries
Lymphangioma
-arise from pluripotent mesodermal tissue of the orbit and surrounding structures
-multiple, variably sized, thin-walled, endothelial-lined vascular channels
-superficial, deep, or both
-superficial:
-more common: involve conjunctiva and eyelids
-enlargement from bleeding, URTI
-CT: multiple, contiguous, dilated cystic spaces within orbit
-may be confused with a varix (dilated orbital vessel)
-varix is connected with normal circulation: enhances with contrast and enlarges with Valsalva
-resection difficult d/t infiltrative nature
-surgical debulking and cyst drainage are mainstays of treatment
HEMATOPOIETIC TUMOURS
Lymphoid Tumours
-represent 4-13% of all orbital tumours
-development of systemic lymphoma:
-20% with lymphoid tumours of conjunctiva
-35% with orbital tumours
-67% with eyelid disease
-orbital lymphoid lesions:
-almost exclusively in adults
-slowly progressive painless proptosis over several weeks to months
-CT:
-“putty-like” molding of tumour around other orbital structures
-no bony destruction
-most extraconal
-superior orbit most common location
-lacrimal gland involved in 40% cases
-biopsy needed for diagnosis
-most lymphomas are of monoclonal B-cell origin
-most reactive orbital lymphoid lesions are composed of a majority of T cells and polyclonal B
cells
Leukemia
-orbit can harbour malignant leukemic cells
-more common in children and often bilateral
-may resemble orbital cellulitis
-granulocytic sarcoma:
-collection of immature myeloid cells forming a mass in the orbit
-more common in children and may be seen in both acute and chronic myelogenous leukemia
-poor prognosis
-radiotherapy often used to treat orbital lesions
789
Langerhans Cell (Histiocytosis X)
-Langerhans cell is a macrophage that normally resides in epidermis of skin
-dz characterized by one or more destructive bone lesions of skull, ribs, sternum, long bones, vertebrae or
pelvis
-orbit rarely affected
-frontal and zygomatic bones most commonly involved orbital structures
-CT: circumscribed lytic bone lesion without sclerosis
-excision of isolated orbital bone lesions often curative
NEURAL TUMOURS
Schwannoma (Neurilemmoma)
-accounts for ~1% of all orbital tumours
-progressive visual loss or RAPD may be cause by tumours located in orbital apex
-more commonly located in intraconal space
-CT:
-well-circumscribed elongated ovoid mass that displaces surrounding structures
-may have areas of cystic degeneration and calcification
-small degree of enhancement after intravenous contrast injection
-MRI:
-hypointense on T1
-hyperintense on T2
-histology:
-schwann cells with characteristic patterns:
-Antoni A: orderly palisading arrangement of elongated spindle-shaped cells
-Antoni B: loose myxoid arrangement of ovoid or stellate cells
-tx: complete surgical excision
Orbital Meningiomas
-arise from optic nerve
-3% of all orbital tumours
-75% are female; 4th-7th decade; rare in children
790
-presentation:
-proptosis and visual complaints
-optic disk pallor, optic nerve head edema, diplopia, headaches, optociliary shunt vessels, ptosis
-CT:
-focal exophytic mass at any point along optic nerve
-may have calcification of tumour in subarachnoid space along optic nerve tissue “railroad
track” appearance
-cannot be removed from surface of optic nerve without causing severe vision loss
-tumours usually followed in elderly patients
-radiotherapy and hormone therapy used in some patients
MESENCHYMAL TUMOURS
Rhabdomyosarcoma
-most common primary malignant tumour of orbit in children
-most common soft-tissue malignancy of childhood
-presentation:
-progressive, painless, unilateral proptosis
-ptosis and palpable mass
-conjunctival chemosis, ophthalmoplegia, choroidal folds, optic disk edema, dilated retinal vessels
-CT:
-poorly defined homogeneous orbital mass
-25% intraconal
-bone destruction and sinus invasion present
-types:
-2/3 are embryonal
-alveolar most malignant and has predilection for inferior orbit
-pleomorphic most well-differentiated and carries best prognosis
Fibroosseous Tumours
Fibrous Dysplasia
-replacement of normal cortical bone with a cellular fibrous stroma containing multiple nests of immature
woven bone
-orbital and facial bone involvement more typical of monostotic form
-orbital roof most common site of orbital involvement
-presentation:
-proptosis, globe and orbit displacement, facial asymmetry
-CT:
-involved bone appears thickened and deformed
-multiple areas of lucent-appearing lytic spaces and “ground glass”-appearing sclerotic zones
-treatment:
-usually observation
-surgical removal if causing significant cosmetic deformity or vision loss secondary to
compressive optic neuropathy
-debulking the only option for some large tumours
791
Osteoma
-1% of all orbital tumours
-known to arise from bones of paranasal sinuses
-most originate from frontal bone
-unilateral solitary lesions
-r/o Gardner syndrome:
-familial condition associated with soft-tissue tumours and colon carcinoma
-CT: smooth rounded or lobulated mass with density similar to normal bone
-small tumours observed; larger tumours resected
-excellent prognosis
Osteosarcoma
-more commonly affects long bones
-rare orbital involvement
-gene responsible of osteosarcoma and retinoblastoma discovered on chromosome 13
-presentation: orbital pain, numbness and vision loss
-extremely poor prognosis
-surgical resection and systemic chemotherapy
792
INFLAMMATORY TUMOURS
CYSTS
-most common primary: dermoids
-most common secondary: mucocele
-dermoid cysts:
-arise from bits of embryonic ectoderm trapped within suture lines between orbital bones
-superficial dermoids: frontozygomatic, frontoethmoid, or frontolacrimal sutures
-subcutaneous mass at lateral portion of eyebrow
-deep orbital dermoids: sphenozygomatic or sphenoethmoid suture
-present with painless progressive proptosis and globe displacement
-CT:
-round, well-defined, thin-walled structure with non-enhancing lumen
-may have dumbbell shape as they extend through suture into temporalis fossa, sinuses or
cranial vault
-histology:
-stratified squamous epithelium with presence of dermal appendages
-treatment: surgical resection if symptomatic
SECONDARY TUMOURS
793
-BCC, sebaceous cell carcinomas, SCCa: most common eyelid neoplasm
-BCC: most common eyelid malignancy
-usually involving lower eyelid and medial canthus
-orbital exenteration and postop XRT advocated for orbital invasion
-SCCa and melanoma:
-most common lesions of conjunctiva
-choroidal melanoma:
-most common intraocular tumour
-retinoblastoma:
-malignant neoplasm of sensory retina
-most common intraocular tumour in children
-treatment combination of surgical excision, radiotherapy and chemotherapy
METASTATIC TUMOURS
794
SALIVARY GLAND NEOPLASMS
Multicellular Theory:
-neoplastic cells originate
from their secretory unit
counterparts
-eg. oncocytic tumours
from striated ducts,
acinic cell carcinoma
from acinar cells
Bicellular Theory:
-all neoplastic cells
differentiate from basal
(reserve) cells in
excretory and
intercalated
-Adults:
-80% parotid; 80% benign
-10-15% submandibular; 50% benign
-5-10% sublingual and minor salivary
glands; < 40% benign
-95% salivary gland neoplasms in adults
-Children:
-68% benign; 32% malignant
-most common benign mesenchymal
tumour: haemangioma
-most common benign epithelial tumour:
pleomorphic adenoma
-most common malignant: mucoepidermoid
carcinoma
795
BENIGN NEOPLASMS
Pleomorphic Adenoma
-65% of all salivary gland neoplasms
-parotid > submandibular > minor salivary glands
-smooth, lobular
-histology:
-myoepithelial component:
-spindle shaped with hyperchromatic nuclei
-epithelial (ductal luminal) component:
-varied growth patterns
-stromal component
-products of myoepithelial cells
-myxoid, chondroid, fibroid, or osteoid
components
-incomplete encapsulation and transcapsular growth with pseudopod extensions high rate of recurrence
after surgical enucleation
Warthin’s Tumor
-papillary cystadenoma lymphomatosum
-second most common benign neoplasm of parotid gland
-6-10% of all parotid tumours
-men, 4th-7th decades
-10% bilateral; malignant tumours rare
-histology:
-multiple cystic spaces with thick mucinous material
-epithelial component:
-papillary epithelium
-double layer of oxyphilic granular cells
-inner or luminal cells, non-ciliated, tall
columnar nuclei at luminal aspect
-outer or basal cells are round, cuboidal with vesicular nuclei
-lymphoid component:
-lymphoid stroma projecting into cystic spaces
-treatment: surgical excision; recurrence uncommon
Oncocytoma
-only in parotid gland
-<1% of all salivary gland neoplasms
-M=F; 6th decade of life
-histology:
-granular eosinophilic cells with small indented nuclei
-granularity from abundant mitochondria
-EM: mitochondria-filled cytoplasm
-tx: superficial parotidectomy
Monomorphic Adenoma
-benign, non-aggressive tumours
-basal cell adenoma (most common), clear cell adenoma, glycogen-rich adenoma
-well-circumscribed and encapsulated
-histology:
-rows of peripheral palisading cells with thick basement membrane
796
MALIGNANT NEOPLASMS
Mucoepidermoid Carcinoma
-most common malignant tumour of parotid (adults and children)
-second most common of submandibular
-60-70% located in parotid gland; palate next most frequent site
-low-grade:
-higher ratio of mucous cells to epidermoid cells
-behave like benign neoplasms
-small and partially encapsulated
-histology:
-aggregates of mucoid cells separated by
strands of epidermal cells
-macrocystic tumour foci
-intraluminal papillary projections
-positive keratin and mucin staining
-tx: superficial parotidectomy
-high-grade:
-higher proportion of epidermoid cells; may resemble SCCa
-aggressive neoplasms
-larger and locally invasive
-histology:
-few mucoid elements; very few cystic foci
-more solid nests of cells
-isolated foci of squamous keratinocytes and mucous secreting cells
-prominent clear cell may be present
-positive keratin and mucin staining
-tx: parotidecotmy with selective neck dissection (N0), radical neck dissection (N+), +/-
postoperative XRT
797
-local recurrence and persistence:
-70% 5-year survival
-40% 15-year survival
Adenocarcinoma
-commonly occurs in minor salivary glands
-aggressive; likely metastasize
-histology:
-no clear histomorphologic features diagnosis of exclusion
-cylindric cells of variable height form papillae, acini, or solid masses
-mucinous staining; differentiate from MEC by lack of keratin staining
-grading based on degree of glandular formation
798
Carcinoma Ex-Pleomorphic Adenoma
-tumour arising from pre-existing pleomorphic adenoma
-2-5% of salivary gland tumours
-slowly growing mass that suddenly increases in size; usually been present for 10-15 years
-histology:
-characteristics of a mixed tumour
-malignant portion may appear as an adenocarcinoma, SCC, undifferentiated carcinoma, or some
other form of malignancy
-local and distant metastasis common
-poor prognosis
-overall 5-year survival is 40%
-tx: combination surgery and radiation recommended
Undifferentiated Carcinoma
-rare
-M=F; 7th decade
-Greenlandic Eskimos: high incidence related to EBV
-aggressive with early metastasis and low survival rates
Sarcoma
-rare
-rhabdomysarcomas and fibrosarcomas most common histopathologic types
Lymphoma
-primary lymphoma rare (no known extrasalivary lymphoma)
-arises from intraglandular lymphoid tissue that occurs during embryonic development
-prognosis generally good
799
ASSESSMENT AND DIAGNOSIS
Etiologic Factors
-smoking not associated with most salivary neoplasms
-associated with development of Warthin’s tumour
-radiation-induced
-latency ~15-20 years
-most important etiologic factor
-most commonly pleomorphic adenoma
-most common malignancy is mucoepidermoid carcinoma
-occupational exposure to wood and furniture industries linked to minor salivary gland neoplasms
(adenocarcinoma of nasal cavity and paranasal sinuses)
History
-asymptomatic masses common
-pain associated with neural invasion
Physical Examination
-head and neck exam
-facial nerve function
-multiple masses, invasion of surrounding tissue, and associated cervical lymphadenopathy should raise the
suspicion of malignancy
Radiology
-CT/MRI useful for assessment of tumours involving parapharyngeal space
Diagnostic Surgery
-excisional biopsy and enucleation is associated with high rates of tumour recurrence
-proper approach is parotidectomy with preservation of facial nerve
Differential Diagnosis
-normal anatomic structures mimicking neoplasm:
-masseter, transverse process of atlas, processes of mandible
-inflammatory diseases; chronic sialadenitis
-nutritional deficiencies
-infections
-cystic lymphoepithelial lesions (HIV)
-metastasis: melanoma and SCC
-necrotizing sialometaplasia: benign but mimics SCC
800
MANAGEMENT
Surgery
-superficial parotidectomy
-tumour removed with a cuff of normal tissue
-also curative for low-grade malignancies
-eg. low-grade MEC, acinic cell carcinoma
-management of tumours involving the facial nerve (controversial):
-facial nerve resection if involved with tumour followed by immediate nerve grafting
-if facial nerve is functioning and able to sharply dissect tumour off, then try to save nerve
-modified neck dissection performed for histologically positive nodes
-no neck dissection for adenoid cystic carcinoma because no nodal metastasis
Radiation Therapy
-in combination with surgery improves locoregional control and survival
-neutron beam XRT appears to be better than conventional photon therapy for adenoid cystic carcinoma
-radiation therapy is recommended postoperatively for all pts with malignant salivary gland tumours
(especially if residual disease and high grade tumour)
-exceptions: T1 or T2N0 disease with low-grade histology and negative resection margins
Chemotherapy
-currently no proven benefit of adjuvant chemotherapy in improving locoregional tumour control or
survival for malignant tumours
-current role is palliation of symptomatic unrespectable recurrent disease after XRT
-pain relief in ~50% of pts
801
COMPLICATIONS
Early complications:
-facial nerve paralysis
-temporary paresis in 10-30%
-permanent paralysis in < 3%
-marginal mandibular branch the most at risk for injury
-(passes over facial artery at anterior border of masseter)
-haemorrhage or haematoma
-infection
-skin flap necrosis
-trismus
-fibrosis and scarring of masseter muscle
-improves with jaw-opening exercises
-salivary fistula or sialocele
-common
-self-limited; treated with pressure dressings +/- aspiration
-seroma
Long-term complications:
-Frey’s syndrome
-reported in 30-60% of pts; only 10% have symptomatic Frey’s syndrome
-gustatory sweating
-related to aberrant regeneration of nerve fibers from post-ganglionic secretomotor
parasympathetic innervation of parotid gland to severed postganglionic sympathetic fibers that
supply sweat glands of skin of face and auriculotemporal region
-tx:
-antiperspirant
-topical anticholinergics: eg. 1% glycopyrrolate
-botox injection
-Jacobson neurectomy
-surgery SCM/fascia flap
-recurrent tumour
-cosmetic deformity
-soft-tissue deficit
-hypertrophic scar/keloid
PROGNOSTIC FACTORS
802
Histopathology
-survival rates continue to decrease after 5 years for all tumour types except low-grade malignancies, acinic
cell carcinoma, and low-grade mucoepidermoid carcinoma
Tumour Size
-major prognostic indicator
-larger size related to poor prognosis, decreased survival and high rates of regional, distant metastasis and
recurrence
Skin Involvement
-associated with decreased survival
-requires excision of involved structures
Distant Metastasis
-occurs in ~20% of parotid malignancies
-occurs most frequently in adenoid cystic and undifferentiated carcinoma
-lung > bone > brain
Recurrence
-diminished survival rate
803
Pain
-6.5% of malignant tumours
-ominous sign
Gender
-men have poorer outcomes
Location
-no difference in survival based on location
-parapharyngeal space involvement associated with a poor prognosis
-for adenoid cystic carcinoma, major salivary gland tumours have better prognosis than minor tumours
804
LIP CANCER
FUNCTIONAL ANATOMY
-functions:
-maintaining oral competence
-speech articulation
-contribute to appearance and facial expression
-sensory innervation:
-upper lip: CN V2
-oral commissure: buccal branch of CN V3
-lower lip: mental branch of CN V3
-motor innervation: CN VII
-blood supply:
-superior and inferior labial arteries from facial arteries
-located just between submucosa and orbicularis oris at vermillion cutaneous junction
-lymphatics:
-upper lip:
-drainage to ipsilateral preauricular, infraparotid, submandibular and submental lymph
nodes
-no contralateral drainage because of embryonic fusion plane of central frontonasal
process separates lateral maxillary processes and their associated neurovascular and
lymphatic connections
-lower lip:
-drainage to submental and submandibular nodes
-drainage is bilateral
-upper deep jugular nodes (level II)
-middle deep jugular nodes (level III)
CLINICAL EVALUATION
DIFFERENTIAL DIAGNOSIS
805
-most commonly pleomorphic adenoma (67%)
-17% are malignant
-keratoacanthoma:
-benign self-limiting epithelial neoplasm
-initial rapid growth phase then spontaneous regression over weeks to months
-incisional biopsy
-premalignant lesions:
-chronic actinic changes: hyperkeratosis, leukoplakia, angular cheilitis
-associated with SCC 46%
-ulcerative inflammatory lesions:
-viral stomatitis
-primary syphilis
-other:
-melanoma
-microcystic adnexal carcinoma
-Merkel cell carcinoma
-malignant fibrous histiocytoma
-malignant granular cell tumours
Prognostic Factors
-poor indicators:
-large primary tumour (> 3cm)
-cervical node metastasis
-recurrent tumours
-perineural invasion
-poorly differentiated histology
-mandibular invasion
-commissure lesions (?)
-size:
-<2cm: 5yr-sr 90%
->3cm: 5yr-sr 64%
-mandibular involvement: 5y-sr <50%
-tumour thickness:
->5mm associated with significantly higher rate of cervical lymph node metastasis
-cervical nodes positive: survival is 25-50%
-grade:
-well-differentiated: 86-95% survival rates
-poorly differentiated: 38-71%
-recurrence: 5yr-sr decreases by 50%
-location: poorer prognosis associated with upper lip and commissure involvement
806
TREATMENT
LIP RECONSTRUCTION
807
-Abbe-Estlander flaps
-transfer full-thickness tissue from one lip to the opposite lip
-second stage procedure usually required
-width of flap should be half width of tissue excised
-Abbe flap originally designed to close medial defects
-can be medially or laterally based
-Estlander flap originally deigned to reconstruct defects near corner of mouth
808
-repair with distant flaps for defects involving entire lip
-RFFF with use of palmaris longus tendon for structural support
-others:
-pectoralis major myocutaneous flap
-radial forearm or fibular osseocutaneous flap for anterior mandible and lip defects
-iliac crest or scapular osseomyocutaneous flap for larger defects including floor of
mouth, tongue or cheek
809
COMPLICATIONS
Surgical
-wound infection and dehiscence
-incompetent oral sphincter
-microstomia
-poor cosmetic result
Radiation
-whistle deformity
-osteoradionecrosis
810
NEOPLASMS OF THE ORAL CAVITY
ANATOMY
-incisive foramina:
-house palatine nerves (V2) and nasopalatine arteries
-lie posterior to maxillary incisors
-provide route for tumour spread from palate into anterior nose
-palatine foramina:
-house greater palatine vessels and nerves
-potential routes for spread for hard palate neoplasm through the pterygopalatine fossa to skull
base
-primary routes of lymphatic spread deep jugular and/or lateral pharyngeal nodes
-primary palate drains to submandibular nodes
-referred otalgia results from innervation of V3, the lesser palatine nerve and the glossopharyngeal nerve
-lymph drainage:
-tip of tongue submental nodes
-lateral two thirds of tongue submandibular and jugulodigastric nodes
-medial tongue jugulomyohyoid nodes
-unlike base of tongue, oral tongue does not have bilateral lymphatic drainage
Epidemiology
-95% of malignancies are SCCa
-4% of cancers in males; 2% of cancers in females
-average age 60 years
-with continued smoking, pts cured of first primary carcinoma have 40% chance of developing second
H+N cancer or recurrence
-75% of cases SCCa involve only 10% mucosal surface of mouth
-mainly floor of mouth where flow and pooling of carcinogen-contaminated saliva occurs
-risk factors:
-alcohol and tobacco
-reverse smoking: carcinomas of the hard palate
-HPV subtype 16 estimated to be present in up to 22% of cases of oral carcinoma
-betel-nut chewing
-tobacco chewing
-poor dental hygiene
-chronic irritation; oral leukoplakia and erythroplakia
-Plummer-Vinson syndrome
811
Evaluation
-onset, duration and progression of lesion; painful
-contributing factors:
-trauma or caustic ingestion; risk factors for malignancy (weight loss, smoker, alcohol abuse,
family history, etc); history of connective tissue diseases, autoimmune disorders,
immunodeficiency, diabetes, radiation therapy, other malignancies
-associated symptoms:
-taste disturbances, persistent sore throat (>3weeks), odynophagia, dysphagia, halitosis,
hoarseness, trismus, fever, malaise, persistent otalgia
-biopsy of primary
-all chronic leukoplakia or ulcerative lesions that fail to heal after 1-2 weeks should undergo
excisional biopsy
-FNA of possible neck metastasis
-imaging studies
-CXR
-CT/MRI
-Panorex
-barium swallow
-laboratory tests: baseline LFTs
-consultations:
-radiation therapy - for adjuvant or definitive therapy considerations
-dental - pre-radiation dental treatment and posttherapy cases
-panendoscopy
812
Differential diagnosis of Benign Pigmented Oral Lesions
-generalized pale mucosa: -anemia, thalassemia
-black/brown discolouration: -bismuth and arsenic intoxication
-blue-gray gingival margin (Burton’s line) -lead intoxication
-generalized redness -polycythemia vera, hepatic insufficiency
-perioral melanotic macules -Puetz-Jeghers syndrome (GI hamartomatous polyps)
-small yellow spots -Fordyce’s disease (sebaceous gland histology)
-black-hair tongue -elongated (hyperplastic) filiform papillae
-telangiectasia -Osler-Wever-Rendu
-diffuse hyperpigmentation of mucosa -Addison’s disease
PATHOLOGY
Gross Pathology
-four forms of SCCa:
-exophytic
-ulcerative (most common)
-infiltrative
-verrucous
MANAGEMENT
Prognostic Factors
-size of lesion
-extent of nodal disease
-regional metastases portend a worse prognosis
-5-year survival rate ~50% lower than that in patients without clinical evidence of
metastases
-prognosis worse with multiple cervical metastases
-extracapsular spread = lower rate of survival; reduces survival rate by further 50%
-tumour thickness:
-depth of penetration
-significant correlation with treatment failure
-FOM tumours 2-3 mm thick better prognosis than thicker ones
813
-oral cavity tumours > 5mm significant metastatic rates
-perineural, perivascular and intralymphatic invasion
-DNA ploidy: nondiploid tumours worse prognosis
-overexpression of c-erbB-2 correlated with nodal dz and metastasis
-verrucous carcinoma better prognosis; tends not to metastasize
Radiation Treatment
-XRT = surgery for controlling small T1 lesions
-provides better functional result with speech and swallowing
-disadvantages: taste, xerostomia, protracted nature of treatment course
BUCCAL CANCER
-relatively uncommon
-ulcerative lesions penetrate early
-tumours <6mm have significantly better survival rates
-risk of metastasis:
-regional metastasis: 50% for all stages
-occult neck metastasis ~10%
-T1 lesions: surgery or XRT
-3-yr survival: 80%
-T2 lesions:
-3-yr survival: 60%
-Stage III and IV: surgery plus XRT
-3-yr survival (surgery or XRT alone): 41% (III); 15% (IV)
-3-yr survival (surgery and XRT): 60% (III); 35% (IV)
Verrucous Carcinoma
-predilection for buccal mucosa
-extension of lesion into underlying connective tissue deep to normal epithelium (“pushing margins”)
-treatment: surgical excision
-rarely metastasizes, therefore no neck dissection needed
814
HARD PALATE NEOPLASMS
-uncommon
-SCCa = salivary gland malignancies (1:1)
-India: incidence (40%) d/t reverse smoking
-incidence of nodal metastases is low (10%) - unnecessary for prophylactic neck dissection
-T4 lesions: 25% incidence of nodal metastasis - prophylactic neck irradiation can be considered
-tx: -XRT as effective as surgery for T1 and T2 lesions
-surgery preferred
-combination surgery (total or partial maxillectomy) and XRT for T3 and T4 lesions
-prognosis (5-yr survival): T1: 85%; T4: 30%
-composed of mucosa and periosteum over posterior and ascending ramus of mandible
-underlying mandible should be included in specimen
-often presents at an advanced stage
-regional metastasis ~10-20% at early stage
-treatment:
-T1 lesions: surgery or XRT
-T2 lesions: includes resection of soft palate swallowing problems
-XRT often treatment of choice
-T3 and T4 lesions: combined therapy
-composite resection (incl. partial mandibulectomy and neck dissection
-pre- or postoperative XRT
ALVEOLUS CARCINOMA
-excluding lip cancer, oral tongue is the most common site of oral cancer
-T1 and T2: surgery or XRT
-most are treated with surgery (partial glossectomy) because of morbidity of XRT
-control rates of 86% (T1) and 75% (T2) with XRT alone
-surgical management of a T2 primary must also include elective treatment of the ipsilateral N0
neck (treat levels I-IV)
815
-T3 and T4: combination therapy
-surgery with post-operative radiation
-overall survival rates: 30-35%
-controversy still exists for prophylactic neck therapy for T1 lesions
-no clear indicators exist
-significantly increased risk of neck metastases with tumour thicknesses of > 2-5 mm
-measurement of tumour thickness can be made with frozen-section analysis and can be used to
guide elective therapy of the N0 neck
-perineural invasion at primary site increases recurrence and mortality
-reconstruction:
-tongue flaps provide worst functional reconstructive results; should be avoided
-STSG provides good functional results
-myocutaneous or free flap
-T1 lesions:
-surgery alone; 5-yr survival 70%
-XRT alone; 3-yr dz free survival 85%
-T2 lesions: XRT or surgery +/- neck dissection
-high rate of occulte nodal disease: 23-50%
-highest complication rate if XRT used for cure
-3-yr dz free survival 64%
-40% occult metastatic rate
-Stage III and IV:
-T3: 70% occult metastases
-combination therapy
-survival rates: 30-35% (III) and 20-25% (IV)
816
F.Ling - Oral Cavity Neoplasms (7)
817
ODONTOGENIC CYSTS, TUMOURS,
AND RELATED JAW LESIONS
ODONTOGENIC CYSTS
Inflammatory Cysts:
818
Developmental Cysts:
NON-ODONTOGENIC CYSTS
-incisive canal cyst (nasopalatine duct cyst, median anterior maxillary cyst)
-most common developmental jaw cyst
-Stafne bone cyst (lingual salivary gland depression):
-not a true cyst but an anatomic depression of the lingual aspect of the posteroinferior body of the
mandible that contains normal salivary gland tissue
-traumatic bone cyst:
-not a true cyst; represents an empty cavity within cancellous bone
819
-surgical ciliated cyst of the maxilla
-iatrogenic lesion
-entrapment of sinus epithelium during a previous Caldwell-Luc procedure
ODONTOGENIC TUMOURS
-classified into three groups based on germ cell layer of origin: epithelial, mesenchymal, and mixed
-ameloblastoma:
-most common epithelial odontogenic tumours
-rare: ~1% of all tumours/cysts of jaws
-arise from odontogenic epithelium or enamel organ
-benign but locally invasive
-thought of as the oral counterpart to basal cell carcinoma
-peak occurrence 3rd to 4th decade (mean 40 years)
-large expansile multilocular or soap-bubble radiolucency
-posterior mandible (80%)
-immature adnexal neoplasm with infiltrative growth and limited metastatic potential
-cause cortical thinning and perforation, pathological fracture, and soft-tissue penetration
-types:
-central: arise in bone (intraosseous)
-plexiform unicystic:
-more aggressive central variant, occurs in the lining of follicular cysts or
impacted teeth
-peripheral:
-arise in soft tissue around
alveolar bone, much less
aggressive, may be treated
with local excision
-histology:
-tall columnar cells with reversed
nuclear polarity
-types: -follicular
-basal cell
-granular cell
-plexiform
-acanthomatous
-desmoplastic
820
-may contain amyloid with concentric calcifications or psammoma-like bodies
(Liesegang rings)
-odontogenic myxoma:
-benign slow-growing, expansile tumour
-arise from periodontal ligament, dental papilla or dental follicle
-gelatinous solid tumour
-recurrence rate 25%
-malignant transformation not expected
-cementomas:
-class of benign tumours that secrete cementum
-types:
-periapical cemental dysplasia
-more common in black females, multiple lesions, develops through varying
stages (osteolytic, cementoblastic, and maturation)
-cementoblastoma:
-true benign tumour of cementoblasts of the tooth root, usually form first
mandibular tooth
-cementifying fibroma:
-similar to ossifying fibroma
-unicystic ameloblastoma:
-expansile clinically non-infiltrative cystic neoplasm
-presents as an expansile well-demarcated unilocular radiolucency resembling a large dentigerous
cyst
-treated by curettage 15% recurrence
-may progress to infiltrative ameloblastoma if not treated
-ameloblastic fibroma:
-uncommon benign neoplasm
-odontoma:
-mature histodifferentiation but disorganized morphodifferentiation
-production of enamel, dentin, cementum and pulp haphazardly admixed within a collagenous
capsule
821
RELATED JAW LESIONS
Fibroosseous Lesion
-fibrous dysplasia:
-affects maxilla more frequently than mandible
-developmental disturbance of bone formation that may be confined to one bone or multiple
skeletal sites
-formation of dysplastic bone that is unresponsive to physiologic demands
-fusiform swelling with indistinct blending borders that incorporate cortical bone
-ossifying fibroma:
-true neoplasm of the medullary portion of the jaws
-rapid growing bony hard mandibular swelling
-well-demarcated radiolucent or mixed lesion that diverges dental roots and displaces anatomic
structures at its expanding periphery
822
MANAGEMENT
Evaluation
-slow-growing tumours compensatory changes in alveolar processes occlusion maintained
-fast-growing tumours can produce significant malocclusion
-dysethesia neural compression or invasion suggests malignancy
-appearance patterns on Panorex:
-well-demarcated lesions outlined by thin sclerotic borders suggest slow growth
-expansion, root displacement and/or resorption, and cortical thinning suggest rapid growth
-FNA to rule out vascular lesion
-open biopsy:
-excisional enucleation for smaller cysts
-incisional procedure for larger lesions
Treatment
Dentigerous Cysts
-minimal recurrence potential
-removed by conservative enucleation and curettage (E&C) of cystic lining from osseous defect
-other lesions amenable to E&C:
-lateral periodontal cyst, residual cyst, gingival cyst, paradental cyst, COC (Gorlin cyst), traumatic
bone cyst, surgical ciliated cyst of the maxilla
-AOT, ameloblastic fibroma, central odontogenic fibroma
Odontogenic Keratocysts
-association with impacted tooth requires removal of both cyst and tooth
-must remove any tiny shards of cystic lining that may persist after cyst removal
-resection of overlying mucosa, rotary burr reduction of osseous walls of cyst cavity, and
intracavitary destructive measures:
-chemical tissue fixation with Carnoy solution
-intracavitary cryotherapy with liquid nitrogen
-if mandibular defect > 4cm, immediate transoral bone grafting recommended to avoid pathologic
fractures
-may require marginal or segmental mandibulectomy for larger lesions
-other lesions with similar treatment approaches:
-glandular odontogenic cyst, small localized odontogenic myxomas and Pindborg tumours
Amelobastoma
-mandibular resection with adequate zone of radiographically normal-appearing trabecular bone around
main tumour mass
-1-1.5cm margin of adjacent radiographically uninvolved bone
-soft tissue extension requires resection - neck dissection not needed
-postoperative follow-up critical - 50% recurrences found within first 5 years
-treatment principles also apply to:
-odonotameloblastoma, larger or recurrent Pindborg tumours (CEOT), odontogenic myxoma
-unicystic variant of ameloblastoma:
-satellite lesions at cyst periphery or extension of intramural ameloblastoma through
823
fibrous wall of cyst
Malignant Ameloblastoma
-resection of primary tumour
-neck dissection for demonstrable metastasis
-aggressive resection of pulmonary metastasis
Ameloblastic Carcinoma
-radical surgical resection as for SCC with neck dissection reserved for demonstrable lymphadenopathy
Fibrous Dysplasia
-total resection and reconstruction
Ossifying Fibroma
-complete removal required
COMPLICATIONS
824
NECK DISSECTION
ANATOMY
825
-marginal mandibular branch of facial nerve:
-1 cm in front of and below the angle of mandible
-overlies facial artery and vein
-spinal accessory nerve:
-medial to digastric and lateral or immediately posterior to IJV
-usually within 1cm above Erb’s point (posterior border of SCM where greater auricular nerve
turns around it)
DIAGNOSTIC EVALUATION
-error rate in assessing presence or absence of cervical lymph node metastasis by palpation ranges from 20-
50%
-CT/MRI have higher sensitivity and specificity in detecting mets in nodes > 1-1.5 cm
-33% of all mets from SCC of H+N in nodes < 1 cm
-circular enlarged nodes more likely to be malignant
-if tumour involvement of common or internal carotid artery is suspected angiography to determine status
of contralateral intracerebral circulation
-most malignancies in the neck are from metastasis (~85%)
-primary neck cancers in the neck are less common (~15%) - usually from salivary tumours, thyoird
cancers or lymphoma
Fine-Needle Aspiration
-specificity: 94-100%
-sensitivity: 92-98%
826
STAGING
Nodal Levels
I: -submental and submandibular triangles
II: -upper third (superior to hyoid bone or carotid bifurcation to base of skull); contain upper jugular
lymph nodes; upper limit is digastric muscle
III: -middle third (superior to omohyoid muscle to hyoid bone); contain middle jugular lymph nodes
IV: -lower third (superior to clavicle to omohyoid muscle); lower limit is transverse cervical vessels
V: -posterior triangle
VI: anterior neck between carotid sheaths
AJCC Staging
N0: -no regional lymph nodes
N1: -single ipsilateral lymph node < 3 cm
N2a: -ipsilateral lymph node between 3 and 6 cm
N2b: -multiple ipsilateral lymph nodes < 6 cm
N2c: -bilateral or contralateral lymph node; < 6 cm
N3: -lymph node > 6 cm
Radical
Modified radical (I, II, III)
Selective
-lateral
-anterolateral (supramylohyoid or supraomohyoid)
-posterolateral
-anterior
Extended
827
-combined use of RND and XRT can decrease recurrences in the ipsilateral side of the neck and
prevent recurrence in the contralateral side in pts with cervical lymph node metastasis who have
combinations of poor prognostic factors
828
Indications:
-supraomohyoid ND:
-SCC of oral cavity staged T2-T4N0 or TxN1 when palpable node is < 3cm, clearly
mobile and located in levels I or II
-bilateral if anterior tongue and floor mouth malignancy
-SCC of lip or skin of midportion of face associated with clinically discrete single
metastasis to submental or submandibular nodes
-in conjunction with parotidectomy in pts with SCC, Merkel cell carcinoma, selected
stage I melanomas (thickness b/n 1.5-3.00 mm) in cheek and zygomatic regions of the
face
-lateral ND:
-tumours of larynx, oropharynx and hypopharynx staged T2N0, selected T3N0 and TxN1
when palpable node is located in levels I or II
-usually bilateral
-posterolateral ND:
-melanomas, SCC or other skin tumours that originate in posterior and posterolateral
aspects of the neck and occipital scalp
-anterior neck dissection:
-differentiated thyroid cancer
-esophageal and tracheal tumours and in laryngeal cancers with subglottic extension
Results:
-supraomohyoid and lateral ND:
-recurrence rate:
-negative nodes: 3.4% at 2 years
-positive nodes: 12.5% at 2 years (multiple nodes, extracapsular spread)
-important to dissect nodes in level IV in pts with cancer of oral tongue: “skip metastasis” in
15.8% to level IV or III
-important to dissect nodes out of retro-accessory triangle
829
COMPLICATIONS OF NECK DISSECTION
Air Leaks
-circulation of air through a wound drain
Flap Necrosis
-from poorly planned incision that compromises vascular supply, wound infection, fistulas
Bleeding
-haematoma:
-early milking of drains may evacuate accumulation of blood
-may require evacuation in OR
-failure to evacuate haematoma may predispose patient to wound infection
Chylous Fistula
-attempt to ligate intraoperatively
-post-op chylous fistula occurs after 1-2% of neck dissections
-adverse sequelae:
-electrolyte abnormalities
-malnutrition
-immune dysfunction
-treatment:
-conservative management unlikely successful if > 600 ml drains in 24h
-amount of output: Fistulas with higher output that cause more physiologic derangements
may require earlier aggressive therapies.
-conservative management:
-closed wound drainage
-pressure dressings
-low-fat nutritional support (medium chain fatty acids)
-correct electrolyte abnormalities
-nutritional therapy:
-enteral diets with fat restriction or the use of medium chain triglycerides:
-medium-chain triglycerides are absorbed directly from the gut into the portal
venous circulation.
-TPN affords full caloric and nitrogenous support while allowing bowel rest
-bowel rest achieves a decrease in chyle flow, allowing healing to occur
830
-surgical therapy:
-surgical ligation of the leaking lymphatic vessels
-other forms of therapy to plug the leak have included fibrin glue or the use of chemical
irritants such as tetracycline
Blindness
-rare
-intraorbital optic nerve infarction
Apnea
-carotid body denervation after bilateral neck dissection
-phrenic nerve injury
EMERGENCIES
831
TREATMENT PLANNING DECISIONS
-Areas of controversy:
-superiority of elective treatment over observation and treatment only when lymph node metastasis become
clinically apparent
-indications for elective treatment
-extent of cervical lymph node dissection
-selection of elective surgical treatment versus elective neck irradiation
Indications
-based on the likelihood of occult lymph node metastasis associated with a given primary tumour
-elective neck dissection if:
-primary tumour associated with high risk of occult metastasis
-neck is entered for reasons of surgical approach
-possibility of occult lymph node metastasis is 20% or higher
Site of Origin
-overall incidence of nodal metastasis
-SCC of oropharynx > oral cavity
-lower lip and buccal mucosa < floor of mouth and oral tongue
-supraglottic >> glottic
Tumour Angiogenesis
-immunostaining of endothelial cells for factor VIII-related antigen (marker for angiogenesis) was
strongly related to probability of metastasis
832
Extent of Elective Cervical Lymph Node Dissection
-MRND, Type III or selective ND are currently preferred operations for elective surgical treatment of the
N0 Neck
-removal of SCM, IJV or posterior triangle of neck not done unless obviously involved by tumour
Surgical Treatment
-may require removal of hypoglossal nerve, carotid, and overlying skin if involved with tumour
-preservation of adjacent structures should be pursued only when clearly identifiable plane exists between
tumour and such structure
-results of selective ND and MRND appear comparable to those of RND
833
CONTROVERSIES IN MANAGEMENT OF N0 NECK IN SQUAMOUS CELL
CARCINOMA OF THE UPPER AERODIGESTIVE TRACT
-three options:
-close observation
-elective radiation therapy
-elective neck dissection
-controversy stems partly from uncertainty about actual risk or occult adenopathy and accessibility of at-
risk lymphatics for any particular tumour
-no biologic marker currently available to identify involved nodes
-theoretic benefit of elective neck treatment must be weighed against morbidity of treating pts who do not
have metastasis
-micrometastasis can occur in small lymph nodes
834
Option 3: Elective Neck Dissection
-proponents believe the prognostic information gained and potential for increased regional disease control
and survival justify the small amount of added operative time and low morbidity of the procedure
-several END studies demonstrated a high incidence of occult metastasis
-MD Anderson:
-overall occult metastasis rate of 25% in N0 necks
-6% had extracapsular spread of tumour in nodes
-several studies suggest that number and size of positive nodes are significant prognostic factors and that
ECS is an independent prognostic variable
Decision Analysis
-Weiss:
-suggested that elective treatment should be considered if probability of occult cervical metastasis
was greater than 20%
-relative utility of surgery over radiation became apparent if probability was greater than 50%
-recommended the choice of radiation versus surgery should be predicated on treatment of the
primary
835
SPECIAL CONSIDERATIONS IN MANAGEMENT OF THE N0 NECK FOR SPECIFIC PRIMARY
SITES
Oral Cavity
-supraomohyoid neck dissection (I-III) frequently used
-skip metastases occur in more than 15% some advocate including level IV in the dissection
-it has been observed that 33% of oral tongue and 40% of FOM failures occurred in contralateral
undissected neck
-ASHNS clinical practice guidelines:
-T1 and T2 oral cancers:
-unilateral neck dissection should be performed for clearly unilateral lesions, and
bilateral neck dissections should be performed for lesions at tip of tongue approaching or
crossing midline
-T3 and T4 tumours:
-ipsilateral or bilateral neck dissection or ENI recommended (5000 rads)
-neck not electively treated in T1 and T2 lesions of the lower lip
-bilateral neck dissection (regions I-III) appropriate for anterior tongue and floor of mouth cancer
-region V included if suspicious nodes are present
-unilateral neck dissection recommended for RMT lesions > T2
-early lip, buccal mucosa, and hard palate cancers do not require neck dissections because of low
metastatic rate
Oropharynx
-region II most commonly involved
-Shah: recommended elective dissection of regions II-IV
-cancers of base of tongue and pharyngeal wall had occult metastatic rates of 33% and 46% respectively
-bilateral modified neck dissection removing regions 1-V in base of tongue cancers with N0 necks is
appropriate
-clinical practice guidelines recommend with the exception of early tonsil cancer, radiation
Hypopharynx
-have high incidence of nodal metastasis
-regions II and III at highest risk
-pts with cancer of medial pyriform, midline hypopharyngeal wall, and postcricoid region are at high risk
for bilateral involvement
-guidelines recommend that all pts be treated with END or ENI but are not more specific
-bilateral SND (II-V) recommended for these pts
-pts with tumours involving only the lateral hypopharynx can be treated with unilateral neck dissection if
ipsilateral neck does not have suspicious nodes
-elective region I dissection can be considered optional in hypopharyngeal cancer
Larynx
Supraglottic Cancer
-regions II, III and IV are at high risk for occult metastasis from laryngeal cancers
-clinical practice guidelines recommend bilateral neck dissection unless radiation is given
-region VI dissection and ipsilateral thyroid lobectomy should be considered when supraglottic cancer
becomes transglottic
Glottic Cancer
-clinical practice guidelines indicate that T1 and T2 lesions should have delphian node treatment in the
narrow field laryngeal radiation portal
836
-no indication for END
-T3 and T4 not specifically addressed in the guidelines
Subglottic Cancer
-SND of regions II, III, IV and VI bilaterally is appropriate for primary subglottic cancer
-involves subtotal thyroidectomy
Nasopharynx
-clinical practice guidelines currently favour radiation therapy for treatment of nasopharyngeal carcinoma
-chemotherapy improved survival (72% 5-year-sr cf 54% with XRT alone)
-radiation field should include levels II-V and retropharyngeal nodes bilaterally
-clinical practice guidelines for all sites tend to agree that all T4 cancers require postop irradiation
-T1-T3 indications:
-multiple levels of lymph node involvement
-more than two or three positive nodes
-ECS
-intravascular or perineural invasion
-positive margins
837
HYPOPHARYNGEAL CANCER
Diagnosis
-rich lymphatic network in submucosal tissue surrounding the hypopharynx allows early spread to regional
lymph nodes and direct extension into adjacent soft tissues
-risk of occult nodal metastasis: 30-40%
-78% of patients have palpable cervical metastases at presentation
-most patients with hypopharyngeal cancers (70%) manifest stage III disease
ANATOMY OF HYPOPHARYNX
-three subsites:
-piriform fossa
-posterior pharyngeal wall
-postcricoid area
-lymphatics:
-rich submucosal lymphatic network exits through
thyrohyoid membrane superior and middle jugular lymph
nodes
-inferiorly paratracheal lymph nodes and low jugular nodes
-metastasis to retropharyngeal nodes, paratracheal nodes,
paraesophageal nodes, and parapharyngeal space nodes
occurs
838
-nerve supply:
-superior and middle constrictor muscles:
-superior laryngeal nerve and pharyngeal plexus (including pharyngeal branches of vagus
and glossopharyngeal nerves and contributions from superior cervical ganglion)
-inferior constrictor muscles:
-branches from external and recurrent laryngeal branches of vagus nerve
-piriform sinus:
-internal branch of superior laryngeal nerve
DIAGNOSIS
-history of heavy alcohol ingestion; heavy smoking; and persistent dysphagia, persistent sore throat, or a
FB sensation in throat
-average duration of symptoms before presentation: 2-4 months
-referred otalgia via Arnold’s nerve, a division of CN X
-suggests malignancy hypopharynx, base of tongue, or supraglottic larynx
-20% have an asymptomatic neck mass: jugulodigastric or midjugular lymph node
-associated symptoms: weight loss, hemoptysis and hoarseness
-FNL: ulcerative lesion, pooling of secretions, fixation of vocal cords if advanced
PROGNOSIS
-pathologically positive cervical adenopathy related to tumor size:
-tumours < 4 cm 50% incidence of positive nodes
-tumours > 4 cm 85% incidence of positive nodes
-management modalities:
-full-course XRT with surgical salvage
-surgery alone
-combination pre- or post-XRT with surgery
-chemotherapy preceding or during surgery or radiotherapy
839
Surgery
-indications for nonresectability:
-involvement of carotid artery
-fixation of posterior pharyngeal wall (prevertebral fascia invasion)
-evidence of distant metastatic disease
-causes of surgical failure:
-tumor extension into thyroid gland, paratracheal nodes, and upper mediastinal lymph nodes
-submucosal extension inferiorly into cervical esophagus
Primary radiotherapy
-used for:
-(1) patients who have early malignancies, often confined to medial wall of piriform sinus,
particularly exophytic tumors without extension into piriform apex
-(2) patients who have primary malignancy of posterior pharyngeal wall
-(3) those who refuse surgical resection or are too ill to undergo resection
-(4) palliation to reduce bulk of extensive nonresectable malignancies and alleviate pain
-local control rate:
-T1 lesions: 79%
-T2 and T3 lesions: 56%
Results
-XRT alone insufficient management for patients with cervical metastases:
-5-year survival rate: 8%
-pts with T2 lesions: 69% had positive node findings at presentation
-survival decreased by 50%
-Pingree et al:
-5-year survival:
-surgery alone: 41%
-radiation alone: 21%
-combined surgery and XRT: 33%
-5-year survival for stage I and II hypopharyngeal cancer:
-surgery alone: 48%
-combined surgery and XRT: 40%
-Spector et al:
-69% of patients presented with positive metastatic disease
-87% of patients presented with stage III or IV disease
-overall incidence of distant metastases was 17.7%, and 6.2% of patients developed a second
primary cancer
Surgical/Reconstruction Options
-lateral pharyngotomy for a limited posterolateral pharyngeal wall lesion or medial piriform sinus lesion
-supracricoid hemilaryngopharyngectomy
-total laryngopharyngectomy:
-Pectoralis major myocutaneous flap
-Deltopectoral flap
-Radial forearm free flap
-Free jejunal graft
-Gastric pull-up
-mortality is 8%-15%, complication rate is 26-50%
-Colon transposition
840
MANAGEMENT OF THE NECK
-N0 neck:
-must address and manage zones II, III and IV
-usually via modified or anterior neck dissection
-eg. piriform sinus tumours: levels II and III primarily involved
-N+ neck:
-comprehensive neck dissection (levels I-V)
-most studies support use of postoperative XRT for local control, although increased survival has not been
shown, for patients with N1 and N2 cervical disease
-radiation control:
-N0 neck: minimum dosage of 5000 rad
-N1 neck: minimum dosage of 6500 rad
-presence of contralateral node 4x greater in pts with palpable ipsilateral adenopathy
-control of contralateral neck: 6000 rad
-contralateral neck dissection is reserved for patients who have palpable nodal disease or if tumor
extends across midline
-need to administer postoperative radiotherapy within 8 weeks of surgery has been a major argument of
advocates of preoperative radiotherapy
-El-Badawi et al:
-surgery-only group: 25% survival rate
-combined surgery and post-op XRT: 40% survival
-recurrence above clavicle:
-T1-2: 18%
-T3-4: 33%
-distant metastasis after treatment:
-N0-1: 16%
-N2-3: 28%
-Garden et al:
-primary XRT:
-local control:
-89% of T1 and 77% of T2 lesions
-surgical salvage only successful in 6 of 19 primary recurrences
-5-year survival rates:
-68% for T1 lesions and 46% for T2 lesions
-protocol: twice-daily hyperfractionation
841
LYMPHOMAS OF THE HEAD AND NECK
(Non-Hodgkin)
-risk factors:
-congenital immunodeficiency disease
-acquired immunodeficiency
-HIV/AIDS
-immunosuppression from organ transplantation
-autoimmune disorders
-Hashimoto thyroiditis
-Sjogren lymphoma of salivary glands
-rheumatoid arthritis
-celiac disease
-EBV nasal lymphoma, Burkitt’s lymphoma
-organic toxins (phenol, benzenes)
Site Symptoms
Thyroid Mass
842
-Working Formulation (separates lymphomas according to natural histories):
-architectural pattern (follicular or diffuse)
-predominant cell type (large cell, small cleaved cell, mixed small and large cell, small
noncleaved cell, lymphoblastic)
-low- (12%), intermediate- (72%), high-grade (16%)
-with time, lymphomas can transform from low- to intermediate-grade type
-WHO classification takes into account immunophenotypic characteristics
-not useful in guiding treatment or predicting clinical behaviour
Low grade
-small lymphocytic (consistent with CLL) -B-cell small lymphocytic or extranodal marginal zone
-follicular small cleaved cell -follicular lymphoma, grade 1
-follicular mixed -follicular lymphoma, grade 2
Intermediate grade
-follicular large cell -follicular lymphoma, grade 3
-diffuse small cleaved cell -mantle cell, lymphoplasmacytic
-diffuse mixed -diffuse large B cell, peripheral T cell
-extranodal NK/T cell
-diffuse large cell -diffuse large B cell, peripheral T cell
(rapidly fatal; most common NHL type in the -extranodal NK/T cell
head and neck)
High grade
-immunoblastic -diffuse large B cell, peripheral T cell
-extranodal NK/T cell
-lymphoblastic (usually T-cell origin) -lymphoblastic
-small noncleaved cell (EBV + HIV associated) -Burkitt lymphoma/Burkitt-like
Clinical Assessment
-staging tests:
-biopsy and pathologic review (open)
-complete physical examination
-indirect laryngoscopy
-CBC
-LFT
-HIV
-CXR hilar adenopathy
-CT/MRI head and neck
-upper GI series with small bowel follow-through
-association of Waldeyer ring and GI tract in 3-11%
-CT abdomen
-lymphangiogram (if available)
-lumbar puncture
-paranasal sinus higher propensity for CNS involvement
-bone marrow biopsy
-18% of pts with extranodal H+N lymphomas have BM involvement at presentation
Staging System
-Ann Arbor staging system (see Pediatric Malignancies)
-found more useful in predicting disease-free survival
843
MANAGEMENT
Low-grade
Stage I or II
-involved-field or extended-field radiation therapy
-5-y: -65% disease free
-75% alive
-10-y sr: 60-65%
Stage III or IV
-CVP or chlorambucil
-complete response in 60-80%
-most eventually relapse
-fludarabine (purine analogue) for relapses
-Rituximab (minimally toxic monoclonal antibody directed against CD20 B-cell)
-interferon-alpha
-observation until patients become symptomatic with bulky disease
Intermediate-grade
Stage I or II
-age, performance status, stage, bulk of disease, number of extranodal sites, and serum LDH
influence prognosis
-CHOPx3 XRT CHOPx3
-CHOPx3 XRT
-5-y: -disease free: 80-100% (I); 75-80% (II)
-overall survival: 75-90% (I and II)
-poor outcome for pts with lymphoma of PNS or with NK phenotypes
Stage III or IV
-chemotherapy is the primary treatment
-usually CHOP or other combination chemotherapy
-complete response rate: 50-85%
-5-y: -disease-free: 30-60%
-overall survival: 35-70%
-XRT used to consolidate areas of bulky disease or for urgent treatment of airway obstruction
844
High-grade
-lymphoblastic lymphoma
-intensive combination chemotherapy
-60% can be cured
-small noncleaved cell lymphoma
-combination chemotherapy with escalated doses of cyclophosphamide, doxorubicin, vincristine,
prednisone, methotrexate, etopsoside, cytarabine, and intrathecal methotrexate
-at risk for tumour lysis syndrome
-65% are alive at 2 years
Thyroid Lymphomas
-XRT primary treatment of stage IE and IIE
-poor prognostic factors:
-bulky tumour, extracapsular extension, fixation and retrosternal involvement
-add CHOPx3-6 with radiation
-chemotherapy mainly for stage III and IV disease
Orbital Lymphomas
-low grade: XRT alone @ 30-35 Gy
-70% disease-free survival
-intermediate grade: XRT @ 36-40 Gy +/- chemotherapy
-high grade: XRT + chemotx
-advanced stage: combination chemotx
HIV-associated Lymphomas
-typically intermediate- or high-grade with advanced stage and frequent extranodal involvement
-common sites: gingiva, oral mucosa, parotid gland, conjunctiva
-overall survival generally poor
COMPLICATIONS OF THERAPY
Radiation Therapy
-major acute toxic effect is mucositis mouthwash
-xerostomia sialogogues, oral pilocarpine
-hypothyroidism thyroid replacement
Chemotherapy
-myelosuppression
-neutropenia or thrombocytopenia
-alopecia
-nausea and vomiting
-haemorrhagic cystitis (cyclophosphamide)
-cardiac arrhythmias/dysfunction (doxorubicin)
-neurologic (vincristine):
-neuropathy, constipation, ileus, hoarseness
-pulmonary fibrosis (bleomycin)
845
EMERGENCIES
-oropharyngeal/laryngeal lymphoma
-airway obstruction
-tumour lysis syndrome
-hyperuracemia, hyperkalemia, hyperphosphatemia, hypocalcemia
-cardiac arrhythmia, renal failure, death
-tx: allopurinol, IV hydration, alkalinization of urine
-febrile neutropenia
-sepsis, shock, death
-leptomeningeal lymphoma
-cord compression, confusion, cranial neuropathies
-paralysis, coma
846
THYROID DISEASE AND SURGERY
EMBRYOLOGY
ANATOMY
PHYSIOLOGIC CONSIDERATIONS
847
Thyroid Hormone Effects
-elevates metabolic rate (thermogenesis, increases oxygen consumption)
-essential for normal neural and skeletal development (stimulates chondrocytes, bone reabsorption, growth
of neuronal tissue)
-increases sympathetic activity (increases heart rate and contractility)
-releases steroid hormones
-stimulates erythropoiesis
PATHOLOGY
Benign Lesions
-F:M = 5:1
-~1% of women develop disorders of thyroid function
-nodules very common: 3-7% of population with palpable nodules 5% of these nodules are malignant
-categories:
-nontoxic
-diffuse and multinodular goitre
-toxic
-toxic multinodular goitre, solitary toxic adenoma, diffuse toxic goiter (Graves disease)
-inflammatory
-acute, subacute, chronic thyroiditis
-most common benign neoplasm: follicular adenoma
-malignancy usually cannot be determined by cytology or intraoperative frozen sections requires
evidence of capsular invasion, blood vessel invasion or metastatic disease
Thyroid Cysts:
-typically arises from degenerated nodules, may result from cystic degeneration of malignancy
-may observe for regression, FNA relieves pain and acquires cells for cytology
-may consider lobectomy for recurrent cysts that are recalcitrant to drainage or bloody aspirates
Multinodular Goiter:
-more common in women
-pathophysiology:
-iodine deficiency TSH hypersecretion stimulates chronic thyroid hyperplasia and
involution multinodularity
-toxic nodular goiter: variation of diffuse colloid goiter in which one nodule is hyperfunctional
resulting in hyperthyroidism
-dx: FNA of a prominent nodule, TFT to confirm euthyroid sate (may be hypothyroid)
-tx: iodine replacement (reverses goiter), hormonal suppression (controversial), radioactive iodine
therapy or surgical excision (considered for cosmesis, decompression, concern for malignancy, or
toxicosis)
Malignant Tumours
-thyroid cancers account for 1.5% of all cancers
-death rate low: 1200 pts in US die annually
Papillary Adenocarcinoma
-most common type: 80% of all thyroid ca
-occurs earlier in life - peak in 3rd and 4th decade
-F > M ~ 3x
-4-10% have history of prior neck irradiation
848
-histologic features:
-papillary structures
-follicles
-Psammoma bodies - present in 40-50%
-presence in lymph nodes strongly
suggestive of PTC
-intranuclear vacuoles - “Orphan Annie-eyed” or
ground glass nuclei
-internuclear clefting, nuclear groove
-multicentric
-subtypes:
Papillary thyroid carcinoma with Psammoma body
-usual papillary (70%) (arrow). Note papillary structure and cells with “Orphan
-encapsulated (10%) Annie-eyed” nuclei.
-follicular (10%)
-tall cell (10%) - more aggressive variant
-diffuse sclerosis (3%)
-oxyphilic (2%)
-others (1%): columnar cell, clear cell, insular, lipomatous, trabecular
-clinical behaviour similar amongst various subtypes
-multicentric: both lobes affected in 80% of cases
-lymphatic spread
-locoregional metastasis high: 37-65%; micrometastasis in 90% lymph nodes
-impact on prognosis controversial: increases risk of recurrence but only slightly
increases mortality rate
-angioinvasion and distant metastases occur less frequently (2-17% of cases)
-prognosis:
-70-95% 5-year survival
-additional mortality rate of 10-20% over a 10-20 year period
-excellent prognosis for occult papillary carcinoma (<1.5cm) and papillary microcarcinomas
(<1.0cm)
Follicular Carcinoma
-10% of all thyroid cancers; occur almost exclusively in pts > 40 ya
-F > M ~ 3x
-requires open biopsy for diagnosis:
-capsular invasion or angioinvasion must be
demonstrated for diagnosis of FTC
-unifocal; multicentricity uncommon
-factors related to poor prognosis:
-increased degree of angioinvasion
-older age of onset
-distant metastasis at time of diagnosis
-metastasis:
-lymph node metastasis not a prevalent feature
(occur in < 20%)
-distant metastasis in 65%
-prognosis:
-70% 5-year survival; 40% at 10 years
-20% if distant metastasis at initial diagnosis
-50-60% of pts with FTC die of their dz
849
Hurthle Cell Tumours
-type of follicular tumour composed predominantly of
Hurthle cells
-large polygonal
-indistinct borders
-large pleomorphic hyperchromatic nuclei
-granular, eosinophilic/oxyphilic
-may be malignant (carcinoma) or benign (adenoma)
-capsular invasion and solid pattern of growth predict a
more aggressive behaviour carcinoma
-more aggressive variant of follicular carcinoma
with poorer prognosis
-at presentation: Hurthle cells demonstrating oxyphilic cytoplasm
-intrathyroidal (70%)
-cervical lymph node metastasis (20%)
-distant metastasis (10%)
-tx:
-hemithyroidectomy for Hurthle cell tumours lacking histologic criteria of malignancy
-total thyroidectomy with postoperative ablation for malignant lesions
-post-operative suppressive therapy recommended for all pts with Hurthle cell carcinoma because
they usually produce thyroglobulin and have TSH receptors
Medullary Carcinoma
-5-7% of thyroid carcinomas
-M=F
-types:
-Sporadic: 60-80% (usually unilateral, unilateral, worse prognosis)
-Familial: 10-40% (usually bilateral) - better prognosis than sporadic
-MEN type IIA: MTC, pheochromocytoma, hyperparathyroidism
-MEN type IIB: MTC, pheochromocytoma, neurofibromatosis
-originate from C-cells (derived from neural crest)
- produce calcitonin and carcinoembryonic antigen (CEA)
-also secrete gastrin, ACTH, substance P
-histology:
-nests of small, round cells
-amyloid production
-dense, irregular areas of calcification
-metastasis:
-early cervical lymph node metastasis in 50%
-involve central, paratracheal, and
jugular nodes
-distant metastasis to mediastinum, liver, lung
and bone in 8%
-diagnosis:
-measurement of calcitonins levels, with aid of Medullary thyroid carcinoma with amyloid stroma
pentagastrin stimulation used to:
-determine therapeutic success
-indicate recurrence
-screen family members for disease
-CEA a less sensitive marker for MTC
-screening with RET proto-oncogene
-can exclude 50% family members from further testing
850
-false negative rate 5%
-if positive >90% will develop MTC within first 2 decades of life
-monitoring for recurrence:
-persistently elevated calcitonin
-CT scan to look for lymph node metastasis
-octreotide scanning if unable to visualize nodes on CT
-PET scan (future)
-treatment:
-prophylactic treatment:
-total thyroidectomy in children with RET mutation by age of 5-6 years
-total thyroidectomy and cervical lymph node dissection
-prophylactic ipsilateral neck dissection for MTC > 2cm (nodal metastasis > 50%)
-neck dissection for persistently elevated calcitonins levels curative in 10-20%
-not sensitive to radioactive iodine
-prognosis:
-50-80% 5- and 10- year survival
-46% 10- year survival if cervical lymph node metastasis present
Anaplastic Carcinoma
-1-5% of all thyroid carcinoma
-mainly affects pts > 65 years
-usually present as large, fixed masses with vocal cord paralysis, compression of trachea or esophagus and
distant metastasis
-histology:
-giant and spindle cells in various proportions
-often represents the transformation of well-
differentiated carcinoma that was present for
many years
-small cell type responsive to radiation
-prognosis:
-10% 1-year survival
-average survival after diagnosis: 3-6 months
-effective treatment rarely feasible
-surgical debulking of tumour (controversial)
-most patients treated by combinations of
irradiation with surgery or chemotherapy
-multimodal treatment incl. doxorubicin Anaplastic thyroid carcinoma
and actinomycin D
Lymphoma
-associated with chronic lymphocytic thyroiditis and
Hashimoto’s thyroiditis
-dx: difficult to distinguish lymphoma from chronic
lymphocytic thyroiditis by FNA alone, therefore a
confirmational open biopsy is required along with
lymphoma staging work-up
-treatment:
-radiotherapy to neck and superior mediastinum
-surgical excision considered if tumour is
confined to the thyroid
851
EVALUATION
Clinical Parameters
-strong suspicion of malignancy
-firm or hard nodules
-homolateral vocal cord paralysis
-obvious metastatic disease
-other factors:
-history of irradiation early in life (40% risk of malignancy)
-presence of other endocrine tumours
-genetic syndromes (eg. Cowden disease and Gardner syndrome)
-coexisting thyroid disease
-FHx thyroid carcinoma
-solitary nodule: 4-33% malignant
-50% malignant in children; 85% with ca will have cervical adenopathy
-likelihood of malignancy within a solitary nodule is higher in male than female
-thyroid suppression strategies
-decreased volume of thyroid nodules by at least 50% in as many as 40% of pts
-goal to maintain TSH levels between 0.1 and 0.5 mIU/L with 0.125 and 0.15 mg thyroxine OD
-failure to respond to suppression is an indication for further investigations or surgery of the
nodule
-FNA and imaging investigation must be accomplished as a prerequisite
Radioisotope Scanning
-evaluates function of nodule
-also to identify ectopic thyroid tissue (including retrosternal goiter, lingual thyroid and metastasis)
-hot nodules identified in 26% of thyroid cancers
-sensitivity and specificity low
Ultrasonography
-most sensitive in defining thyroid lesions
-identifying and monitoring nodules
-differentiates cystic from solid nodules in more than 80% of cases
-7% malignant in cystic lesions
-12% malignant in solid-cystic lesions
852
Computed Tomography
-not routinely used
-mainly to evaluate substernal goiter
-to evaluate cervical lymphadenopathy, airway and vascular displacement, tumour invasion
TREATMENT
Issues of Controversy
-selection of procedure: hemi- vs total thyroidectomy
-no prospective study to examine treatment outcome
-various recommendations, but no consensus:
-Hay et al: higher risk of locoregional recurrence - therefore total thyroidectomy in pts
with AMES low-risk PTC
-Wanebo et al: total thyroidectomy in high-risk pts showed no benefit over partial
thyroidecomy
853
-management of cervical nodes
-should a procedure be performed?
-occurs predominantly on right side
-found in < 1% of pts
Risk Factors
-Age
-one of most significant factors
-F<50 and M<40 have better survival rates than older pts
-mortality rates:
-<20ya: 2%
-20-40 ya: 5%
-40-50 ya: 8%
->50 ya: 34%
-Size of Primary
-lesions > 5cm have significantly poorer prognosis
-Unifocal or Multifocal Disease (PTC)
-microscopic foci of papillary carcinoma may remain clinically unapparent for a lifetime
-incidence of recurrence in opposite lobe has been shown to be low
-none of patients with recurrent disease in opposite lobe died of dz
-Extrathyroidal extension
-unfavourable prognostic sign
-associated with increased recurrence (local, regional and distant)
-Cervical Metastases
-increased risk of cervical recurrence without any increase in mortality
-Distant Metastases
-greatly increases risk of mortality
-AMES:
-age, metastasis, extent of disease, size of lesion
-classified as low- or high-risk
-low-risk:
-7.7% recurrence rate, 1.8% mortality rate
-high-risk:
-59.1% recurrence rate, 46% mortality rate
854
-other classification systems:
-AGES (Mayo Clinic): age, histologic grade, extent, size
-MACIS: metastasis, age, completeness of surgical resection, extrathyroidal invasion, size
Low-Risk Patients
-mortality rates due to tumour are same regardless of extent of resection
-hemithyroidectomy appropriate for low-risk pts but restricted to those with lesions < 1.5 cm
High-Risk Patients
-more aggressive surgery
-total thyroidectomy reduces recurrence and increases survival
-tumour mortality rates as high as 42% out weigh increased morbidity associated with total
thyroidectomy:
-incidence hypoparathyroidism: 3-32%
-permanent RLN injury 1-11%
Radioiodine Therapy
-total thyroidectomy is often followed by ablation of residual thyroid tissue with 131I
-less than 10% of thyroid tissue should remain for ablative treatment
-pts in higher risk groups treated with postop ablative tx lower recurrence and overall mortality
-risks of therapy:
-dose dependent (but rare)
-acute myelogenous leukemia
-cancer of the bladder and female breast
-neonatal genetic and chromosomal abnormalities
-pre-iodine ablation treatment:
-no thyroid replacement for 6 weeks then RAI therapy
-alternatively, replace with T3 (cytomel) for 4 weeks and stop 2 weeks before RAI therapy
COMPLICATIONS OF THERAPY
855
HYPERTHYROIDISM
-Graves disease:
-3rd or 4th decade
-F>M ~7x
-diffusely enlarged thyroid gland; hyperplasia, increased colloid material
-autoantibodies detectable:
-thyroid stimulating antibodies: thyroid receptor autoantibody (IgG)
-extrathyroidal manifestations: exophthalmos, pretibial myxedema, thyroid acropachy
-dx: thyroid stimulating antibodies, elevated T3, T4, RAIU and thyroglobulin; decreased TSH
Treatment of Hyperthyroidism
Suppressive Therapy
-first line in attempt, non-destructive
-thionamides: PTU, methimazole, carbimazole
-inhibits T3 conversion and the oxidation and organification of iodine
-may cause hepatitis, agranulocytosis, parotitis
-iodides: KI, Lugol’s solution
-excess iodine inhibits thyroid hormone (Wolff-Chaikoff Effect)
-lithium:
-inhibits thyroid hormone release
-contraindicated in renal failure and cardiovascular disease
-beta-adrenergic blockers: propranolol, nadolol
-used to control peripheral manifestations of sympathetic overactivy
Surgery
-indications:
-failure of non-surgical management
-massive goiter with or without local symptoms
-florid disease
-desire for rapid control of toxic process
-patient bias
-pharmacologic intolerance
-suspicion of malignancy
856
-Preoperative preparation
-must establish euthyroid function and prevent thyroid storm in postoperative period
-thyroid storm: massive outpouring of T4 and adrenergic hormones that may prove fatal
-most regimens:
-thionamide antithyroid agents thyroid function is restored, followed by -
iodine solution administered for 10-14 days before surgery
-beta-adrenergic blocking agent effective for rapid preoperative preparation
-Surgical Approach:
-Graves disease: subtotal thyroidectomy
-unilateral toxic nodular goiter: lobectomy
-bilateral goiter: subtotal thyroidectomy
THYROIDITIS
Subacute Thyroiditis
-pathophysiology:
-viral (mumps, coxsackievirus) decreased iodine uptake
-painful enlarged thyroid, self limiting, malaise, associated URI
-treatment:
-symptomatic therapy, observation
857
TSH), FNA only for prominent nodules suspicious of carcinoma or lymphoma that do not resolve
-treatment:
-long term thyroxine therapy with TFT monitoring
-surgical excision for compressive symptoms, suspicious nonfunctioning nodule
Riedel’s Thyroiditis
-thyroid fibrosis of unknown origin
-“rock hard” thyroid
-produces local pressure and hypothyroidism
-treatment: hormone replacement, may consider surgical release at isthmus
858
PARATHYROID DISEASE AND SURGERY
-aberrant sites:
-anterior mediastinum, usually in thymus (3rd arch derivative)
-posterior mediastinum (4th arch derivative)
-aorta pulmonary window (3rd or 4th)
-retroesophagus, prevertebral
-tracheoesophageal site
-intrathyroidal site
-carotid bifurcation
CALCIUM PHYSIOLOGY
-Parathyroid Hormone:
-increases serum calcium and decreases serum phosphate
-stimulates osteoclastic resorption of bone
-increased calcium absorption and phosphate excretion by kidney
-increases rate of conversion of 25-hydroxyvitamin D3 to 1,25-dihydroxyvitamin D3 in kidney
-increases gastrointestinal absorption of calcium by enhancing vitamin D synthesis
-Vitamin D:
-stimulates calcium and phosphate absorption in the intestine
-promotes bone osteoclast activity
-promotes retention of calcium by the kidneys
-Calcitonin:
-inhibits calcium resorption by osteoclasts
-increases kidney clearance of calcium and phosphate
859
-hyperparathyroidism:
-primary:
-caused by adenoma or hyperplasia
of parathyroid glands
-other causes:
-parathyroid carcinoma
-familial hypocalciuric
hypercalcemia
-secondary:
-glands that are hyperplastic
because of malfunction of another
organ system
-causes:
-chronic renal failure
-Paget’s disease
-osteogenesis imperfecta
-multiple myeloma
-pituitary adenoma
-bone metastasis
-tertiary:
-occurs when PTH production is
irrepressible in patients with
normal or low serum calcium
levels
-persistent hyperfunction despite correction
PREOPERATIVE EVALUATION
History
-low-dose radiation exposure implicated
-Lasix increases urinary excretion of calcium hypocalcemia and hyperplastic parathyroid glands
-?FHx of MEN syndromes
860
Laboratory Evaluation
-electrolytes:
-serum calcium levels should be elevated on at least three occasions
-magnesium (usually low)
-chloride (usually elevated from PTH induced bicarburia)
-phosphate (usually low)
-if serum albumin is abnormal, calcium level should be adjusted to it
-measure ionized calcium levels and PTH
-others:
-ALP: suggests bone disease
-BUN/creatinine: renal function
-urine calcium:
-elevated in primary hyperparathyroidism
-low levels in familial hypocalciuric hypercalcemia
-thyroid function tests
-ACE levels: sarcoidosis
-serum prolactin and gastrin and urine catecholamines and metabolites: evaluate for MEN
syndromes
861
-glucocorticoid: inhibit calcium intestinal absorption, may be effect for hypercalcemia secondary to
malignancy
-gallium nitrate: inhibits bone resorption, used for parathyroid carcinoma
-hemodialysis: indicated for life-threatening conditions
-the longer the pathologic process of hyperparathyroidism are unchecked, the more severe demineralization
of the skeleton, nephrocalcinosis, and other symptoms will become
-if ALP is elevated, pt may need calcium supplementation during postoperative period while bone
metabolism equilibrates
-be prepared to resect from 1 to 3.5 glands or perform total parathyroidectomy and autotransplantation of
20 mg of tissue into a muscle bed
-superior parathyroid are more constant in their position:
-posterior aspect of thyroid lobe at point where recurrent laryngeal nerve passes under the
cricothyroid muscle
-inferior parathyroid usually found within 1-2 cm of inferior thyroid artery
Treatment Options:
-removal of adenoma and identification of other glands with biopsy of one normal gland
-subtotal parathyroidectomy with or without autotransplantation
-total parathyroidectomy with autotransplantation
-cryopreservation of parathyroid tissue and later transplantation
Operative technique
-if one enlarged gland is found frozen section adenoma one other gland is sampled
if normal, surgery is completed
if hyperplasia then assume parathyroid hyperplasia and perform subtotal parathyroidectomy
3.5 glands are removed
-measuring intra-operative PTH
-half-life of PTH is 4 minutes
-baseline PTH level measured preop
-after gland removed, rapid assay PTH measured after 10 minutes
-if more than 50% decrease in level, it is assumed that the pathologic gland has been
removed
-primary hyperparathyroidism in pregnancy:
-uncommon
-neonatal tetany may occur d/t precipitous drop in calcium postnasally
-pregnant women should undergo surgery during second trimester to avoid miscarriage
862
Surgery for parathyroid carcinoma
-carcinoma rare
-0.5% to 4% among pts with primary hyperparathyroidism
-wide excision required; local recurrence rate = 30%; regional and distant metastasis ~25-30% of these
patients
-structures needed to be excised:
-parathyroid gland, ipsilateral thyroid lobe
-skeletonization of tracheoesophageal groove, excision of paratracheal lymph nodes
-radical neck dissection reserved for palpable nodes
-primary radiation inadequate
COMPLICATIONS
863
NASOPHARYNGEAL CANCER
ANATOMY
-boundaries of nasopharynx
-superior: base of skull; basisphenoid and basiocciput
-posterior: bodies of atlas and axis
-anterior: choanal
-inferior: soft palate
-lateral: pharyngobasilar fascia and superior pharyngeal constrictors
-anatomic subsites:
-lateral wall:
-eustachian tube
-fossa of Rosenmuller (pharyngeal recess) - located posterosuperiorly to ET
-superior:
-foramen lacerum internal carotid artery cavernous sinus
-anterior:
-CN V3 crosses skull base through foramen ovale
-posterior:
-1.5 cm from jugular foramen (CN IX-XI)
-lies at apex of parapharyngeal space; at convergence of fascial planes that
separate space into three compartments:
-prestyloid compartment:
-maxillary artery and lingual and inferior alveolar nerves
-retrostyloid compartment:
-carotid sheath contents
-retropharyngeal compartment:
-nodes of Rouviere
-access to nodes of the opposite neck
-path of least resistance for cancer spread
864
-posterosuperior wall:
-rectangular region between Rosenmuller’s fossa
-anterior wall:
-narrow region of tissue bordering posterior choanae
-mucosa:
-at birth: pseudostratified columnar epithelium (PSCE)
-eventually replaced by squamous epithelium (SE); lateral walls, small patches of PSCE remain
-transitional epithelium:
-contains globular or cuboidal cells
-located where PSCE and SE meet
-lymphoid tissue and minor salivary glands
-nasopharyngeal carcinoma:
-85-95% of malignancies in nasopharynx
-remainder are lymphomas
-amplification of c-erbB-2 gene associated with poor prognosis
HISTOPATHOLOGY
EPIDEMIOLOGY
-combination of genetic and environmental factors responsible for increased susceptibility to NPC
-NPC susceptibility genes linked to HLA region on chromosome 6
-dietary factors:
-salt-preserved foods; dried salted fish
-cigarette smoking (not a strong association)
865
-EBV:
-80-90% of non-keratinizing SCCa have abnormally increased antibody titers to EBV
viral capsid antigen (VCA) and early antigen (EA)
CLINICAL EVALUATION
Examination
-fiberoptic examination:
-friable exophytic, frankly malignant-appearing mass
-smooth submucosal bulge
-no abnormality seen (6%)
-smooth, submucosal and midline masses usually represent
embryologic remnants:
-eg. Tornwaldt cysts, pharyngeal bursa remnants
-FNAB of neck masses valuable
-CT scan with contrast the imaging study of choice
Laboratory Tests
-serologic testing may help establish diagnosis of NPC in pt with
unknown primary
Friable exophytic mass in nasopharynx
-those with occult or early (stage I) WHO type II or III NPC:
-86% positive EA (IgG) titers
-82% positive VCA (IgA) titers
-EBV titers in type I NPC not significantly increased
-screening in high-risk Chinese populations are valuable
-antibody-dependent cellular cytotoxicity (ADCC assay)
-provides prognostic information (except for type I); high titers associated with good prognosis
-EA and VCA have not shown to have prognostic value
866
Diagnostic Surgery
-biopsy
Staging
-shortcoming of various staging systems:
-eg. AJCC system: 80% of all pts placed into stage IV at presentation
-precise extent of NPC primary often difficult clinically because submucosal spread beneath
normal-appearing mucosa is common
-cervical metastasis:
-Ho et al:
-no significant difference in survival of patients with upper neck nodes compared with
pts whose disease is limited to nasopharynx
-Ho’s line:
-defines a line that begins at lateral border of trapezius insertion into occiput and
extends diagonally to sternal head of clavicle effectively separating levels I, II
and III from areas IV and V
-disease below line markedly worse prognosis; significantly increased risk of
distant metastasis
-Neel et al
-presence of unilateral compared with bilateral nodal disease had no prognostic
significance
MANAGEMENT
TNM Staging
T1 -limited to nasopharynx
T2a -extension to nasal cavity or oropharynx; no parapharyngeal space involvement
T2b -extension to nasal cavity or oropharynx; with parapharyngeal space involvement
T3 -bony and/or paranasal sinus involvement
T4 -cranial nerve, intracranial, orbital, infratemporal fossa, hypopharyngeal involvement
Stage I: T1 N0
Stage II:
A: T2a N0
B: T2b or N1
Stage III: T3 or N2
Stage IV:
A: T4 B: N3 C: M1
867
Radiation Therapy
TREATMENT OF NASOPHARYNGEAL CANCER
-cobalt 60 or 4-6 MeV photons
-4500 cGy in 180-200 cGy fractions Radiation therapy
via paired lateral apposed fields -External beam supervoltage radiation
-primary treatment mode: field includes primary tumour,
covering nasopharynx and neck
first echelon lymph nodes, and all clinically involved
bilaterally nodes plus prophylactic radiation of supraclavicular
-lateral apposed boost fields are lymph nodes
directed at primary tumour site -Intracavitary brachytherapy
-may supplement external irradiation as part of primary
-critical to successful eradication of
treatment or for management of residual recurrent
primary tumour is ensuring that tumour
entire volume receives 6000 to 7000
cGy of 60Co-equivalent photon Surgical treatment
-plays limited role in management
energy
-surgical procedures (infratemporal fossa approach,
-brachytherapy used for recurrent NPC to transparotid temporal bone approach, transpalatal approach)
avoid overdose of adjacent normal tissues may be preferable to radiation for local recurrence
-high activity gold 198 or iridium
Other treatment
192 seeds via endotracheal tube -chemotherapy
-permanent implants of high-activity -proven efficacy regarding survival
iodine 125 into tumour bed via large -may help palliate intractable pain
spinal needle -immunotherapy
-impact on long-term survival obscure
-chemotherapy an adjunct to radiation therapy -vaccines
-combined-modality results in a -future potential development of vaccines for EBV-
significant decrease in distant related diseases
metastasis but little or no
improvement in local control or
disease-free survival* (new evidence suggests otherwise)
-drawback is toxicity that may lead to breaks in radiation treatment
-split-course XRT results in decreased survival compared with continuous course XRT
-cisplatinum-containing regimens (hematologic toxicity) does not overlap with radiation therapy
(mucosal damage)
-combined therapy yields slightly higher absolute survival rates
-chemotherapy already has been well established as a valuable modality for palliation of
unresectable disease
Surgical Treatment
-most frequently indicated surgical procedure:
-neck dissection to remove clinically positive cervical disease that has not been eradicated by full-
course radiation therapy
-surgical approaches for recurrent or residual disease:
-transparotid temporal bone approach
-infratemporal fossa approach
-maxillary swing procedure
-transpalatal approach
868
PROGNOSIS
COMPLICATIONS
-xerostomia
-salivary tissue cannot tolerate > 3500 cGy of radiation
-tx: artificial saliva, water, Pilocarpine
-dental caries
-eustachian tube dysfunction: d/t postradiation fibrosis in nasopharynx
-serous otitis media resistant to conservative measures
-trismus, discomfort, induration of neck and entrapment neuropathy of CN IX, X, XI, and XII
-inappropriate shielding
-hypopituitarism, hypothyroidism, optic neuritis, radiation retinopathy
-temporal lobe necrosis, transverse myelitis
-chemotx related:
-5-FU: acute toxic response in mucosa is exacerbated
-bleomycin: aggravates soft-tissue fibrosis in irradiated areas
-cisplatin: SNHL (~30% of patients)
869
OROPHARYNGEAL CANCER
-relatively uncommon
-<1% of all new cancers
-peak incidence 6th-7th decade; M>F
->90% SCCa
ANATOMY
-boundaries:
-anterior: circumvallate papillae (base of tongue), anterior tonsillar pillars, junction of hard and
soft palates
-lateral: tonsillar regions
-posterior: posterior pharyngeal wall
-superior: soft palate
-inferior: pharyngoepiglottic folds
-anatomic subsites:
-base of tongue
-tonsils
-tonsillar pillars
-soft palate and uvula
-posterior and lateral pharyngeal walls
-glossotonsillar sulci
-sensory and motor supply:
-CN IX (glossopharyngeal nerve) and CN X (vagus nerve)
-motor and most sensory innervation to soft palate: CN V2 and V3
-blood supply: branches of external carotid artery
-lymphatic drainage:
-levels II and III
-central structures (BOT, soft palate, posterior pharyngeal wall) drain bilaterally
-tonsillar region and posterior pharyngeal wall retropharyngeal nodes upper level II nodes
-parapharyngeal space:
-divided by layer of fascia running from tensor veli palatini muscle to styloid into two
compartments:
-prestyloid compartment:
-fat, variable portions of deep lobe of parotid, small branch of trigeminal nerve
to tensor veli palatini
-poststyloid compartment:
-carotid artery, jugular vein, cranial nerves IX to XII, sympathetic chain, lymph
nodes
-vagus and glossopharyngeal nerves have tympanic and auricular branches (Jacobson and Arnold nerves)
referred otalgia
PHYSIOLOGY
870
ETIOLOGY
HISTOPATHOLOGY
NATURAL HISTORY
DIAGNOSIS
History
-alcohol and tobacco abuse
-pain (most common presenting symptom)
-dysphagia
Physical
-nodal enlargement (primary symptom in 30%)
-trismus
-cranial nerve deficits
871
Imaging studies
-CXR
-CT scan/ MRI
-assessment of advanced stage tumours or when involvement of mandible, parapharyngeal space,
prevertebral fascia, neck nodes, or retropharyngeal nodes is suspected
-Panorex
Laboratory studies
-CBC and chemistry
-LFTs
-ECG
TREATMENT
RADIATION
-6000 to 7000 cGy through external-beam shrinking field to primary lesion and necks over 6-7 weeks
872
SURGERY
Primary Tumour
-tumour becomes unresectable after extension into poststyloid parapharyngeal compartment, prevertebral
fascia, or involvement of carotid artery
-resection margins: 1-2 cm
-frozen section required because of submucosal spread
Surgical Approaches
Transoral Approaches:
-Oral:
-no external excisions
-limited exposure
-for small (T1), superficial or exophytic cancers (eg. on soft palate, anterior tonsillar pillar,
posterior wall, uvula)
Transpharyngeal Approaches:
-Suprahyoid Pharyngotomy
-lesions at base of tongue and pharyngeal walls
-pharynx entered through vallecula
-visualization of superior margin in large tumours is inadequate
-risk of cutting into cancer if extensive involvement of tongue base or vallecula
-Lateral Pharyngotomy
-small lesion of base of tongue and pharyngeal walls
-pharynx entered posterior to thyroid ala on least affected side
-limited superior visualization and risk of damage to hypoglossal and superior laryngeal nerves
Transmandibular Approaches:
873
involvement that is not amenable to marginal resection
-Mandibulectomy
-for advanced cancers with overt bony invasion
-entire mental canal must be resected if there is overt mandibular canal invasion
-disadvantage: functional and cosmetic deficits
NECK
RECONSTRUCTION
-limited to restoration of integrity, bulk and sensation, but complex motor functions or the oropharynx
cannot be duplicated at present
Soft-Tissue Reconstruction:
-small defects of pharyngeal walls up to 3 cm and those less than 1/3 the volume of tongue base can be
closed, primarily by STSG or left to granulate if not open into neck
-free fasciocutaneous flaps are required for larger defects to prevent tongue tethering or pharyngeal
stenosis
COMPLICATIONS OF TREATMENT
FOLLOW-UP
Radiation
-1st year: 1-3 mo
-mucositis
-2nd year: 2-4 mo -xerostomia
-3rd year: 3-6 mo -taste dysfunction
-4th and 5th: 4-6 mo -dysphagia
-fibrosis
-after 5th: 12 mo
-ulceration and tissue necrosis
-osteoradionecrosis of mandible
-hypoglossal palsy
PROGNOSIS
Surgical
-5-year survival: -approach related:
-stage 1: 67% -damage to teeth
-stage 2: 46% -damage to nerves
-stage 3: 31% -cerebral embolism and carotid artery
thrombosis
-stage 4: 32% -resection and reconstruction related
-haemorrhage
-wound infection and dehiscence
-positive resection margin
-pharyngocutaneous fistula
-aspiration
-dysphagia
-poor speech
-VPI
-ET dysfunction
-nonunion and osteomyelitis of mandible
-malocclusion and TMJ dysfunction
874
HYPOPHARYNGEAL CANCER
BASIC SCIENCE
Anatomy
-superior limit: pharyngoepiglottic fold (level of hyoid bone)
-inferior limit: inferior border of cricoid
-three anatomic sites:
-piriform fossa
-postcricoid region
-posterior pharyngeal wall
-innervation:
-sensation: glossopharyngeal nerve and internal
branches of superior laryngeal nerve
-motor: inferior constrictor and cricopharyngeus via
pharyngeal plexus
-lymphatic drainage:
-upper deep cervical lymph nodes
-retropharyngeal nodes (superior)
-jugulo-omohyoid nodes (lateral)
-paratracheal, paraesophageal, thyroid nodes (inferior)
875
Physiology
-important component of both respiration and deglutition
-obstruction d/t edema secondary to lymphatic invasion or infection
-invasion of arytenoid or RLN a/w obstruction and aspiration
DIAGNOSIS
History
-treated for pharyngitis
-tobacco and ethanol abuse
-weight loss, dehydration
-odynophagia, dysphagia
-hoarseness, dyspnea
-otalgia
-neck mass
-airway obstruction
Physical
-weight loss or cachexia, decreased skin turgor
-hyporesonant voice (“hot potato”), hoarseness, stridor
-status of dentition
-indirect examination with mirror: pooled secretions, vocal cord paralysis, other lesions
-flexible fiberoptic laryngoscopy
-full neck examination
Radiology
-CXR
-barium swallow
-to evaluate swallowing mechanism and dynamic effects of tumour on swallowing
-detect GERD
-CT and/or MRI of neck
Laboratory
-complete chemistries
Pathology
-95% epidermoid carcinomas; 5% adenocarcinomas arising from glandular structures
876
-sites of involvement:
-piriform fossa: 64%
-posterior wall: 30%
-postcricoid: 4%
-submucosal spread common; may have “skip areas”
-adequate margins:
-superior: 2-3 cm of mucosa from gross tumour edge
-inferior: 4-6 cm if tumour involves cervical esophagus
-lymph node metastasis
-palpable nodes present in 75%
-bilateral disease in 10%
-if N0 then risk of occult nodes is high (30-40%) - therefore
must treat all necks
-risk at presentation of distant metastasis: 20%
PROGNOSIS
MANAGEMENT
Preoperative Treatment
-nutritional support
-enteral feeds
-improving pulmonary status (ie. antibiotics for COPD)
Treatment Options
-early:
-T1: -XRT to primary and bilateral necks
-surgical salvage
-T2: -XRT to primary and bilateral necks
-consider chemotherapy
-consider hyperfractionated XRT
-late:
-T3: -chemoradiation (organ preservation approach -
induction chemotherapy followed by adjuvant
XRT) with surgical salvage
-surgery and neck dissection with postoperative
XRT
-T4: -surgery (laryngectomy/pharyngectomy) and neck dissection with postoperative XRT
877
Surgery TREATMENT OF
HYPOPHARYNGEAL CANCER
-neck dissection performed in most patients - bilateral
recommended in pts with medial wall piriform sinus disease Surgery
-suprahyoid pharyngotomy
-partial laryngopharyngectomy
Posterior Hypopharyngeal Wall Cancer -laryngectomy
-often remain localized and present opportunity for wide excision -pharyngectomy
with uncomplicated reconstruction -partial cervical esophagectomy
-skin graft
-approached via suprahyoid pharyngotomy -free flap
-incision into posterior hypopharyngeal wall carried down to -gastric interposition
prevertebral fascia -feeding tube
-posterior wall defects reconstructed with STSG secured with -neck dissection
-superior mediastinal dissection
bolster Radiotherapy
-bolster removed transorally 5-10 days post-op -T1, some T2
-reconstruction of posterior or posterolateral hypopharyngeal wall -postsurgical
should not extend below level of corniculata cartilages with larynx Chemotherapy
Chemoradiation
in place marked interference with swallowing High-dose Intraarterial chemotherapy and
radiotherapy
Piriform Fossa Cancers Must treat necks even in pts w/o palpable
metastases
T1 Cancers
-indications:
-must be < 2 cm and located in superior aspect of piriform fossa
-no impairment of vocal cord movement
-1.5-cm margin between inferior aspect of tumour and piriform fossa apex
-good pulmonary function
-partial laryngopharyngectomy
Postcricoid Cancer
-total laryngectomy, partial pharyngectomy and cervical esophagectomy
-total esophagectomy if inferior line of resection is below mediastinal inlet
-paraesophageal and paratracheal lymph node resection with hemithyroidectomy also essential - might also
require mediastinal dissection
Reconstruction
-enough pharynx primary closure
-not enough pharynx RFFF, pectoralis major flap
-no pharynx jejunal free flap, RFFF, pectoralis major flap, colonic flap
-laryngopharyngoesophageal defect gastric pull up
Radiation therapy
-primary radiation for curative treatment is preferable for T1 lesions
-debate for T2 lesions: XRT with surgery for salvage
878
Chemotherapy
-currently under investigation
COMPLICATIONS
EMERGENCIES (pretreatment)
-Obstruction
-airway
-tracheotomy
-laser debulking
-esophagus
-feeding tube
-fluid resuscitation
-disimpaction
-Hemorrhage
-isolate source
-angiography
-embolization
-surgical ligation
879
CERVICAL ESOPHAGEAL CANCER
ANATOMY
-cervical esophagus:
-superior limit: cricopharyngeus
-inferior limit: suprasternal notch
-layers:
-mucosa: stratified squamous epithelium
-submucosal or areolar layer
-muscular layer (striated muscle)
-outer longitudinal layer
-inner circumferential layer
-blood supply:
-arterial: thyroid branch of thyrocervical trunk
-venous: inferior thyroid vein
-nerve supply:
-vagus
-lymphatic drainage:
-paratracheal nodes
superiorly to lymphatics of pharynx IJ nodes
OR inferiorly to superior mediastinum
PHYSIOLOGY
EPIDEMIOLOGY
-80x more common in Middle East, southern and eastern Africa, and northern China
-alcohol and tobacco major risk factor
-other risk factors:
-nitrosamines
-most common malignancy: SCCa
-other tumours:
-adenocarcinoma:
-arises from gastric mucosa near GE junction
-associated with Barrett’s esophagus
-5% with GERD Barrett’s 5% adenocarcinoma
-Tylosis:
-AD trait: marked thickening of palms and soles
-associated with high risk of esophageal carcinoma by age 65
-increased risk of developing second primary in upper aerodigestive tract
880
EVALUATION
Clinical Presentation
-solid food dysphagia and weight loss
-most common abnormal finding: neck mass (21%)
-pooling of secretions in hypopharynx
-vocal cord paralysis
-associated diseases: achalasia, Plummer-Vinson syndrome, prior H+N cancer
Laboratory tests
-barium swallow routinely used to evaluate patients with cervical dysphagia
-probably superior to CT or MRI in delineating cephalocaudal extent of mucosal involvement
-CT/MRI used to define depth of invasion and to identify liver, pulmonary or mediastinal metastasis
DIAGNOSTIC SURGERY
STAGING
MANAGEMENT
-summary:
-extension to postcricoid area mandates laryngectomy
-involvement of thoracic esophagus mandates total esophagectomy
-gastric pull-up is preferred reconstruction
-chemotherapy and radiation are used for palliation of patients with advanced carcinoma
-complicating factors:
-obstruction aspiration pneumonia
-malnutrition
-intractable aspiration:
-laryngotracheal separation (Lindeman):
-proximal trachea is oversewn - suture line reinforced with muscle flap developed from
adjacent SCM
-esophagectomy or laryngopharyngoesophagectomy for incurable carcinoma rarely indicated
881
Nonoperative Management of Cervical Esophageal Cancer
-survival rate of patients requiring total cervical esophageal reconstruction for advanced carcinoma of the
hypopharynx and cervical esophagus:
-2 year disease-free survival rates are poor (9-39%)
-reconstructive options:
-tubed pedicle flaps (eg. pectoralis major, latisimus dorsi)
-disadvantages: bulkiness, wound breakdown and fistula common, post-op stenosis
-colonic interposition
-mobilization on superior mesenteric artery
-significant incidence of postoperative infection
-not first-choice reconstructive alternative
882
COMPLICATIONS
EMERGENCIES
883
EARLY GLOTTIC CARCINOMA
Vertical Partial Laryngectomy and Laryngoplasty
DIAGNOSTIC ASSESSMENT
History:
-cigarette smoking, ethanol intake
-occupational exposure to fumes
Physical examination:
-most early glottic tumours arise on membranous portion of true vocal cord
-20% extend to supraglottis
-20% extending 5 mm or more below glottic margin
-25% extending to anterior commissure
HISTOLOGICAL CLASSIFICATION
Mild Dysplasia:
-abnormal dyskaryotic squamous cells with mild atypical cytological alteration involving cell size,
shape, colour and organization
-not a significant risk factor for malignant degeneration
Moderate Dysplasia:
-atypical cytological alteration involving cell size, shape, colour and organization
-risk factor for malignant degeneration
884
-microscopic suspension laryngoscope with stripping of epithelium and a closely monitored
program of follow-up are indicated
-careful assessment q2-3 months for at least 5 years
-repeat biopsy if any changes
-some reports recommend radiation therapy initially and others advise radiation therapy if there is
recurrence after initial stripping
Microinvasive Carcinoma
-malignant cells extend through basement membrane of vocal cord epithelium but do not invade
vocalis muscle
-can be managed by endoscopic excisional biopsy, laser excision, or by radiation therapy
Invasive Carcinoma
-malignant cells that frankly invade through the basement membrane
-can be treated by endoscopic excision, laser excision, thyrotomy with cordectomy,
hemilaryngectomy, VPL with laryngoplasty, or radiation therapy
-traditionally radiation therapy has been offered as the preferred treatment
Ackerman’s Tumour
-aka: verrucous carcinoma
-rough, shaggy surface, a rounded pushing margin and no metastasis
-histopathology:
-benign-appearing (nonmitotic, no infiltration)
-well-differentiated squamous epithelium with papillary projections, extensive hyperkeratosis,
basement membrane intact
-“pushing margins”
-tumour less radiosensitive
-small lesions excised endoscopically; larger tumours managed by partial laryngectomy
-excellent prognosis
General
-options include for early invasive SCCa of glottis:
-single modality therapy:
-limited-field primary external beam radiation
-surgical management:
-endoscopic surgical excision
-thyrotomy with cordectomy
-hemilaryngectomy
-VPL with laryngoplasty
-elective neck dissections are NOT indicated for early glottic cancer
-microlaryngoscopic surgery is safe and effective management for T1 lesions
-LME is an acceptable alternative:
-relative contraindications:
-anterior commissure involvement
-subglottic extension
-T3 glottic cancer
-posterior commissure involvement
885
Open Partial Laryngectomy
-cordectomy:
-limited excision of true vocal cord
-for early lesions not extending to anterior commissure
or involve region of arytenoid cartilage
-true hemilaryngectomy:
-excision of ~50% of endolarynx with overlying thyroid
cartilage
-for larger lesions T1 and T2
-VPL:
-indications:
-transglottic or very extensive bilateral
glottic carcinoma
-select T1 and T2 glottic carcinoma
-tumour does not extend beyond 1/3 of
opposite cord
-less than 1 cm of anterior subglottic
extension or 5 mm of posterior
subglottic extension
-no posterior commissure involvement
-good pulmonary function
-patient must also give consent for possible
total laryngectomy
-technique:
-removes one vocal fold from anterior
commissure to vocal process
-up to ½ of opposite vocal fold may be
removed (frontolateral VPL)
-removes ipsilateral false vocal fold,
ventricle, paraglottic space, and
overlying thyroid cartilage (3 mm posterior strip of cartilage preserved
-advantages:
-allows decannulation, functional glottic voice
-disadvantages:
-risk of aspiration, requires initial tracheotmy
-extended hemilaryngectomy
-indications:
-select T3 lesions or arytenoid involvement
-removes one vocal fold, arytenoid and overlying thyroid cartilage
-outer thyroid perichondrium lines the laryngeal surface
-strap muscle used for laryngoplasty
886
-significant oropharyngeal extension
-tumour spread into neck
-most recurrent carcinomas do not meet these criteria, therefore total laryngectomy is usually necessary
-persistent edema following radiation therapy strongly suggests possibility of residual cancer
-if greater than 6 months must confirm with biopsy
COMPLICATIONS
Early
-subcutaneous emphysema, haemorrhage, tracheotomy tube obstruction
Late
-persistent aspiration, lingering infection, laryngeal stenosis, severe hoarseness, granulation tissue
formation, tumour recurrence
-two common causes for failure with hemilaryngectomy are inability to recognize inferior margin of
tumour and spread of cancer outward through cricothyroid membrane
EMERGENCIES
-airway obstruction
-aspiration
887
EARLY SUPRAGLOTTIC CARCINOMA
Supraglottic Laryngectomy
-cancers of epiglottis:
-tend to have pushing borders rather than infiltrating ones, which allows for resection with
millimetre tumour-free margins
-tend to remain supraglottic until late in their progression
Combined therapy
-if primary tumour is completely resected, there is no need for radiation (no neck node metastasis)
-a recent study finds no measurable benefit to combined therapy with either preoperative or postoperative
radiation and surgery
Nonsurgical options
-unsuccessful in a high percentage of pts with T2 and T3 lesions
-today, virtually all pts who have early supraglottic cancer can expect to have a lung-powered glottis voice
after treatment is completed
-supraglottic resection
-cricohyoidopexy
-near-total laryngectomy
TREATMENT PLANNING
888
Horizontal (Supraglottic) Hemilaryngectomy
-rationale:
-embryological boundary between false and true vocal folds results in independent lymphatic
drainage
-supraglottic cancer tends to have pushing borders rather than infiltrating borders
-patient selection criteria for supraglottic laryngectomy
-T1 or T2 lesion
-cordal mobility
-anterior commissure uninvolved by cancer
-tumour does not involve vocal fold, ventricle, arytenoid, interarytenoid, piriform, base of tongue
-thyroid cartilage uninvolved by cancer
-surmountable nodal metastasis
-general good health
-good pulmonary function (FEV1 > 50-60%)
-technique
-removes epiglottis, AE folds, false vocal cords, pre-epiglottic space, portion of hyoid bone and
thyroid cartilage
Tumour Variables:
-T1, T2 and some T3 are suitable for supraglottic partial operation
-paramount clinical feature is cordal mobility
Patient Variables:
-aspiration a big risk post-surgery
-obvious severe and uncorrectable chronic pulmonary disease will disqualify a patient
-uncorrectable swallowing disorders (ie. Scleroderma or serious stricture) usually disqualify a pt from sx
Clinical Assessment
-voice quality:
-pts with T1 and T2 supraglottic cancers do not have glottic hoarseness
-fiberoptic examination
Radiographic Examination
-supraglottic operation is safe with millimetre margins, but those margins must be identified accurately, and
if the surgeon lacks confidence in the pathology report, a safe operation is less likely
-most important clinical preoperative assessment relates to presence or absence of regional metastasis
-CT can be used to determine presence of metastasis
-failure to manage metastasis in the neck is the major cause of failure in the surgically treated early
supraglottic cancer
889
Extensions of the Supraglottic Operation
COMPLICATIONS
-major:
-airway obstruction
-pneumonia
-aspiration
-speech alteration
-minor:
-delayed feeding tube removal
-wound infection
-fistula
-supraglottic stenosis and redundant arytenoid mucosa (which sucks into the glottis and becomes an
obstruction)
-preserving the false vocal cords contributes to both problems
890
EARLY GLOTTIC AND SUPRAGLOTTIC CARCINOMA
Supracricoid Partial Laryngectomy
DIAGNOSTIC ASSESSMENT
Preoperative Evaluation
-history
-physical examination: careful examination of larynx for mobility of vocal cord or arytenoid
-CT scan
-panendoscopy
-CXR
-assessment of pulmonary reserve
-preoperative evaluation by radiation oncologists is recommended to explain the alternatives for treatment
Contraindications
-hyoid invasion
-massive preepiglottic space or vallecular invasion
-tongue base invasion
-arytenoid fixation
-subglottic extension to cricoid
-pharyngeal or interarytenoid involvement
-extensive thyroid cartilage invasion
-inadequate pulmonary reserve
-resectable by supraglottic laryngectomy
Technique
-remove:
-entire thyroid cartilage
-bilateral true and false vocal folds
-one arytenoid (may spare both arytenoids if not involved)
-paraglottic space
-spares:
-cricoid cartilage
-hyoid bone
891
-cricohyoidopexy:
-used for reconstruction for supraglottic cancer
-cricohyoidoepiglottopexy:
-used for transglottic cancer
-preservation of function requires at least a cricoarytenoid unit and cricoid ring
SUMMARY
-acceptable functional results can be maintained after SCPL-CHP provided one functional cricoarytenoid
unit and an intact or reconstituted cricoid ring are preserved
-combination chemotherapy with radiotherapy with laryngectomy as salvage treatment have not shown a
significant change in survival rates compared with conventional therapy
-conservation laryngeal surgery does not preserve the entire organ anatomically, but usually maintains a
functional organ
-the most practical use for the SCPL-CHP is for T2 or T3 supraglottic carcinoma extending to the glottic
level
-SCPL can be viewed as the most extensive partial laryngectomy that is compatible with speech and
swallowing without a permanent tracheotomy
892
ADVANCED CANCER OF THE LARYNX
EPIDEMIOLOGY
ANATOMY
-supraglottic region: tip of epiglottis apices of both ventricles including false cords
-glottic region: both true cords, floor of ventricle, anterior commissure, interarytenoid area
-subglottic region: extends from 5 mm inferior to free edge of true vocal cords to lower border of cricoid
cartilage
PATTERNS OF SPREAD
-pre-epiglottic space:
-superior: hyoepiglottic ligament
-anterior: thyroid cartilage and thyrohyoid membrane
-posterior: epiglottis and thyroepiglottic ligament
-spread to preepiglottic space soft tissues of neck via dehiscence in thyrohyoid membrane created by
superior laryngeal vessels and nerves
-paraglottic space:
-lateral to ventricles
-boundaries:
-anterior: continuous with pre-epiglottic space
-superior: aryepiglottic folds
-inferior: gap between thyroid and cricoid cartilage
-lateral: thyroid cartilage
-medial: conus elasticus and quadrangular membrane
-transglottic if inferior and superior to ventricle
-invasion of this space associated with high rate of subglottic or extralaryngeal spread of tumour
-most tumours involving the subglottic region are extensions of large laryngeal cancers rather than primary
tumours of the subglottis
893
-most common sites of cartilage invasion:
-anterior commissure tendon (Broyles’ ligament)
-attachments of cricothyroid membrane to adjacent cartilage
-anterior portion of thyroid lamina near origin of thyroarytenoid muscle
-posterior border of thyroid lamina adjacent to piriform sinus
-capsule of cricoarytenoid joint
-nodal metastasis:
-more common in supraglottic cancers than subglottic or glottic
-supraglottic tumours:
-upper and middle jugular lower jugular
-glottic tumours:
-delphian middle and lower jugular regions
-subglottic tumour:
-pretracheal, paratracheal, middle, and lower jugular lymph nodes
-in absence of tongue invasion, rare metastasis to submandibular/submental regions or to posterior
triangle
-preservation of zone I and V for laryngeal primary tumours with less than N2 disease
STAGING
-fixed vocal cord indicates deep invasion into the laryngeal musculature
-pathologic examinations have shown that the clinical staging of a laryngeal cancer is underestimated at
25% to 40%
-presence of mutant p53 clearly associated with diminished survival, but not included in staging system
Supraglottis
-approximately 30-40% of laryngeal cancer
-subsites:
-suprahyoid epiglottis
-infrahyoid epiglottis
-aryepiglottic folds
-false vocal cords
-arytenoids
-tumour invasion typically occurs superiorly toward base of tongue or pre-epiglottic space
-overall 25-75% risk of regional metastasis, primarily to nodal levels II, III, and IV
-staging:
-T1: primary tumour limited to one subsite
-T2: primary tumour involves mucosa of adjacent subsite or outside region of supraglottis
(glottis, base of tongue, medial wall of piriform sinus)
-T3: vocal cord fixation or primary tumour involves pre-epiglottic space, postcricoid, or deep
base of tongue
-T4: invades thyroid cartilage, soft tissues of neck, thyroid, or esophagus
Glottis
-approximately 50-75% of laryngeal cancer
-staging:
-T1: primary limited to vocal folds (1a = one cord; 1b = both cords) <5% regional metastasis
-T2: primary involves subglottis or supraglottis, impaired vocal fold mobility; 5-10% region
metastasis
894
-T3: vocal fold fixation; 10-20% regional metastasis
-T4: invades thyroid cartilage or beyond larynx; 25-40% regional metastasis
Subglottis
-rare primary site
-poor prognosis
-<20% regional metastasis
-staging:
-T1: primary tumour limited to subglottis
-T2: primary tumour involves vocal folds with normal mobility
-T3: primary tumour limited to larynx with fixed cords
-T4: primary tumour invades thyroid cartilage or beyond larynx
MANAGEMENT
Treatment
-primary goal is to cure pt with preservation of speech and swallowing
-extent of regional involvement determines survival
-involvement of preepiglottic space, cartilages or soft tissues associated with even higher rate of lymphatic
spread to prelaryngeal and deep cervical nodes
895
ADVANCED SUPRAGLOTTIC LESIONS
Supraglottic Laryngectomy:
-indications:
-supraglottic cancers classified as T3 d/t preepiglottic space invasion or minimal medial piriform
sinus involvement above level of true cords
-no extension to vocal cord
-good health and pulmonary reserve
-possibility of converting to total laryngectomy
Near-total layrngectomy:
-single arytenoid cartilage preserved to produce a lung-powered voice through a trachea esophageal conduit
-contraindications: subglottic extension below cricoid ring or failure of radiation therapy
-indications:
-large T3 or T4 lesions not amenable to supraglottic or supracricoid resection with one uninvolved
arytenoid and ventricle
-pts with lesions amenable to standard supraglottic procedure but with poor cardiopulmonary
function
-unilateral transglottic tumours with cord fixation
-poor pulmonary function and cardiac reserve negate conservation surgery, as does failure of prior full-
course radiation therapy
Total Laryngectomy:
-indications:
-all T3 cancers not amenable to supraglottic or supracricoid laryngectomy
-all T4 cancers not amenable to supracricoid or near-total laryngectomy
-tumours with extensive involvement of thyroid or cricoid cartilage
-invasion of surrounding soft tissue of the neck
-extension beyond posterior third of base of tongue
The Neck
-bilateral selective neck dissection would be treatment of choice of N0 pt
-most common site of recurrence is contralateral undissected neck
-for N0 or N1 regional disease, radiation has been shown to be equivalent to surgery
Adjuvant Radiation
-for patients at higher risk of recurrence:
-positive margins, T4 lesions, N2 neck or evidence of extracapsular lymph node spread, perineural
or vascular invasion, metastasis to inferior tracheoesophageal, lower jugular or mediastinal nodes,
multiple levels of nodal involvement, and subglottic extension
Survival
-rate for stage IV supraglottic cancer no better than 50% even with combined treatment
896
ADVANCED GLOTTIC LESIONS
Radiation or Surgery?
-primary radiation limited to pt with favourable T3 lesion
-total laryngectomy is procedure of choice for tumour recurrence if radiation therapy was delivered in
curative doses
The Neck
-most likely regions involved: jugular chain, paratracheal, pretracheal groups
COMPLICATIONS
Complications of Surgery
-haematoma, hypothyroidism aspiration pneumonia, wound infection, hypocalcemia, fistula
-late complications: structure, stomal stenosis, hypothyroidism
Complications of Radiation
-hoarseness, edema, dysphagia, odynophagia, mucositis, thick secretions, skin breakdown
-late effects chondronecrosis, fibrosis of skin/soft tissue/mucous membranes, severe dryness, stricture,
hypothyroidism, trismus, secondary neoplasm eg. Sarcoma (rare)
897
LARYNGEAL CARCINOMA TREATMENT OVERVIEW
Induction chemotherapy plus radiation compared with surgery plus radiation in patients with advanced
laryngeal cancer. The Department of Veterans Affairs Laryngeal Cancer Study Group.
898
chemotherapy group than in the surgery group. A total of 59 patients in the chemotherapy group (36
percent) required total laryngectomy. The larynx was preserved in 64 percent of the patients overall and 64
percent of the patients who were alive and free of disease. CONCLUSIONS. These preliminary results
suggest a new role for chemotherapy in patients with advanced laryngeal cancer and indicate that a
treatment strategy involving induction chemotherapy and definitive radiation therapy can be effective in
preserving the larynx in a high percentage of patients, without compromising overall survival.
899
TRACHEAL TUMOURS
RADIOLOGIC EVALUATION
-to determine location and linear extent of lesion, extra-tracheal involvement, and amount of airway not
involved
-standard views
-fluoroscopy functional asymmetry of vocal cords and provides information about extent of lesion
-polytomography gives additional detail, particularly of mediastinal involvement
-barium esophagography define esophageal involvement by extrinsic compression or invasion
-CT/MRI
AIRWAY MANAGEMENT
900
SIGNS AND SYMPTOMS
-SOBOE (54%)
-hemoptysis (41%) - usually for SCCa earlier diagnosis
-cough (37%)
-wheezing and stridor (35%)
-dysphagia or hoarseness (7%)
-recurrent pneumonitis
-CXR usually normal
DIAGNOSIS
ANESTHESIA
SURGICAL TECHNIQUE
901
Reconstruction
-neck flexion to provide anastomosis without tension
-options:
-primary anastomosis:
-pedicled strap muscle over anastomosis
-suprahyoid laryngeal release (Montgomery release):
-provides extra 1-2.5 cm of length (up to 5 cm of length)
-infrahyoid release described
-hilar release:
-mobilization of the right pulmonary hilum
-involves making a U-shaped incision in pericardium beneath inferior pulmonary vein
-incising septum, which extends inferiorly from the right inferior pulmonary vein and
joins lateral aspect of atrium and inferior vena cava to pericardium
-left mainstem bronchus divided and reanastomosed end-to-side with bronchus intermedius
-provides extra 2.7 cm length
-Marlex and Silicone grafts
-carinal involvement:
-approach via right posterolateral thoracotomy
-right or left main bronchus sutured to trachea in an end-to-end manner; anastomosis of other
bronchus to lower portion of trachea wall laterally above initial anastomosis is performed
Complications:
-anastomotic stenosis
-air leaks subcutaneous emphysema
-anastomotic separation
-suture line granuloma
-esophageal fistula
-vocal cord paralysis
-aspiration (after laryngeal release) pneumonia/empyema
-post-obstructive pulmonary edema
-haemorrhage from innominate artery
-operative death
Role of Radiation
-SCCa and ACC are radiosensitive
-resection combined with irradiation tripled survival time for both SCCa and ACCa
Recommendations
-benign primary tumours and tumours of intermediate aggressiveness are best managed by means of
surgical resection with reconstruction of airway
-for SCCa and ACC, resection followed by full-dose mediastinal irradiation advocated
902
VASCULAR TUMOURS OF THE HEAD AND NECK
BENIGN TUMOURS
VASCULAR TUMOURS OF THE
Localized Tumours HEAD AND NECK (Batstakis)
Lymphangioma
-most tend to progress
-commonly occur in neck and mucosal surfaces of oral cavity (tongue)
Angiofibroma
-predominantly among male adolescents
-consists of multiple vascular channels surrounded by tough fibrous connective tissue
-originates in lateral wall of nasopharynx and tends to invade posterior aspect of choana,
pterygopalatine fossa, orbit, and occasionally intracranial cavity
-most common feeding vessels from external carotid system
-IMAX and ascending pharyngeal arteries
-angiography and embolization
-surgical approaches:
-medial maxillectomy
-transpalatal approach
-facial degloving
-combination
-endoscopic approach for small tumours
-radiation reserved for large unresectable tumours
903
Generalized Tumours
-cystic hygroma:
-occurrence in posterior triangle associated with hydrops fetalis, Turner syndrome, chromosomal
aneuploidy, fetal death
-cytogenic analysis of fetuses born with cystic hydroma indicated
-extensive infiltration; CT/MRI to assess
-tx: surgical excision
Inflammatory Tumours
Telangiectasis
-Osler-Weber-Rendu
-familial occurrence
-autosomal dominant
-clinical triad:
-characteristic telangiectatic lesion
-hereditary incidence
-presence of haemorrhagic diathesis
-epistaxis is hallmark; bleeding from oral mucosa
-telangiectasia on facial skin, particularly cheeks
-for septal telangiectasia, treatment is septal dermoplasty
-estrogen and other hormones effective, as is laser treatment
MALIGNANT TUMOURS
Angiosarcoma
-malignant tumour of vascular endothelial cells
-extremely rare
-scalp > neck > mouth > antrum
-rapidly growing neoplasms with insidious onset and minimal symptoms
-50% cured by primary excision or die of disease within 3 years
-XRT for palliation
Hemangiopericytoma
-arise wherever there are capillaries
-tx is wide surgical excision
-XRT for palliation
904
Kaposi Sarcoma
-HIV
-non-pruritic, painless, flat or nodular, pigmented lesion on any skin or mucosa surface of H+N
-treatment geared toward local control, reduction of symptoms, and improvement of appearance
-XRT and chemotherapy effective but have serious side effects
-interferon can be effective, but recurrence common
-intralesional injection of vinblastine, cryotherapy, and laser excision
PARAGANGLIOMA
905
Carotid Body Tumours
-asymptomatic, slowly enlarging, nontender neck masses immediately anterior to SCM at level of hyoid
bone
-bruit on auscultation
-widening of carotid bifurcation by well-defined tumour blush splaying of vessel (Goblet/Lyre sign)
-MRI: “salt and pepper” appearance d/t flow voids
-Shamblin classification:
-Group I: -small and easily dissected away from vessels
-Group II: -medium-sized; intimately associated with vessels but separable with dissection
-Group III: -large tumours encasing the carotid necessitating partial or complete vessel
resection and replacement
-treatment:
-approach is similar to that of acoustic neuromas:
-young patient early resection advocated
-older patient, small lesion observation
-surgical treatment is mainstay of therapy - potential vascular replacement surgery considered
-palliative radiation if pt’s high surgical risk
-mortality rate 8%
-early operation desirable: less extensive procedure that is better tolerated
-surgical details:
-potential for vascular replacement
-adventitial plane can be developed tumour removed from bifurcation
-Fisch classification:
-Type A -Tumour limited to the middle ear cleft (glomus tympanicum)
-Type B -Tumour limited to the tympanomastoid area with no infralabyrinthine
compartment involvement
-Type C -Tumour involving the infralabyrinthine compartment of the temporal bone and
extending into the petrous apex
-Type C1 -Tumour with limited involvement of the vertical portion of the carotid canal
-Type C2 -Tumour invading the vertical portion of the carotid canal
-Type C3 -Tumour invasion of the horizontal portion of the carotid canal
-Type D1 -Tumour with an intracranial extension less than 2 cm in diameter
-Type D2 -Tumour with an intracranial extension greater than 2 cm in diameter
906
F.Ling - Vascular Tumours (5)
907
F.Ling - Vascular Tumours (6)
908
F.Ling - Vascular Tumours (7)
909
-surgical approach depends on the localization and extension of the tumour
-Fisch type A tumours:
-excised by a transmeatal or perimeatal approach
-Fisch type B tumours:
-require an extended posterior tympanotomy
-Fisch type C tumours:
-require radical resection via a standard combined transmastoid-infratemporal or
transtemporal-infratemporal approach with or without ICA trapping, preceded by
external carotid artery embolization or superselective embolization
-surgery leads to therapeutic success in about 90% of patients.
-Fisch type D tumours:
-treated with a combined otologic and neurosurgical approach
-infratemporal approach with a skull base resection and a posterior fossa exploration are
the most advisable in the attempt to remove the entire tumour
-partial resection is followed by radiation and follow-up MRI/CT scanning.
-classic fractionated radiation therapy (40-50 gray [Gy]) and stereotactic radiosurgery are successful in
long-term control of tumour growth and in decrease of catecholamine excretion in functional tumours
-radiation treatment is advised as the sole treatment modality for elderly or infirm patients who are
symptomatic, especially those with extensive or growing tumours
Intravagal Paraganglioma
-arises from nests of paraganglionic tissue within perineurium of vagus nerve immediately below or at level
of ganglion nodosum
-lie near skull base
-diagnostic clue:
-anteromedial displacement of internal carotid artery
-cf carotid body tumour splaying of internal and external carotid arteries
-may be “dumbbell” shaped into jugular foramen
-resection may cause laryngeal paralysis requires rehabilitation
SYNDROMES
Sturge-Weber Syndrome
-capillary malformation over trigeminal distribution
-ipsilateral meningeal vascular malformations
-possible association with seizure disorder and mental retardation
Maffucci Syndrome
-multiple cavernous hemangiomas
-dyschondroplaisa with shortening and deformity of involved bones
-occasional visceral vascular lesions
-25% incidence of chondrosarcoma
910
CRANIAL-BASE SURGERY
NEUROANATOMIC CONSIDERATIONS
Arterial Supply
1. vertebral artery
2. posterior inferior cerebellar artery (PICA)
3. basilary artery
4. anterior inferior cerebellar artery (AICA)
5. posterior cerebral artery (PCA)
6. posterior communicating artery
7. middle cerebral artery (MCA)
8. internal carotid artery
9. ophthalmic artery
10. anterior cerebral artery
11. anterior communicating artery
12. medial striate artery
13. anterior choroidal artery
NEUROPHYSIOLOGY
Intracranial Pressure
-edema usually is caused by prolonged or excessive retraction of brain during tumour resection
-correlates highly with postoperative course complicated by short-term decrease in mental function and
long-term neurologic deficit
-prevention of edema by means of removal of large segments of calvarium and base of skull to obviate
brain retraction
911
CSF Production
-produced at rate of 20 ml/h (500 ml/d)
-amount of CSF reabsorbed cannot be controlled pharmacologically
-amount produced can be altered with carbonic anhydrase inhibitors (ie. acetazolamide)
EVALUATION
Imaging Studies
MRI -can differentiate tumours on basis of signal response -longer image acquisition times
-can generate sagittal images -poorer bone evaluation
-can perform angiography (MRA)
-provide detailed images of soft tissue invasion
T1- weighted very dark very bright dark intermediate bright dark
912
SURGICAL ANATOMY
913
Anterior Cranial Base
-roof of ethmoidal and sphenoidal sinuses form floor of anterior cranial base between orbits
-portion of ethmoidal sinuses that contributes to anterior floor of base of skull is fovea ethmoidalis
-most common location of iatrogenic defects and CSF leaks through floor of anterior cranial base
after ethmoidal sinus surgery
-extracranial landmarks that identify floor of anterior cranial base:
-anterior and posterior ethmoidal arteries
-optic nerve located 5 mm posterior to posterior ethmoidal artery
-Cavernous sinus:
-contains:
-internal carotid artery
-CN III, IV, V1, V2, and
VI
-drained by paired superior and
inferior petrosal sinuses
-internal carotid artery located by
identifying GSPN
-course of GSPN directly above
and in same direction as
horizontal portion of petrous
portion of ICA
-most reliable intracranial
landmark for petrous portion of
ICA
-superior orbital fissure transmits several
vital structures
-inferior orbital fissure opens into
pterygopalatine fossa
-deep temporal artery provides primary
blood supply for temporalis muscle;
reconstructive flap most commonly used in
cranial-base surgery
Lacrimal (V1)
Frontal (V1)
Trochlear (IV)
Supraorbital vein
Oculomotor (III)
Abducens (VI)
Nasociliary (V1)
Zygomaticofacial (V2)
Zygomaticotemporal (V2)
Inferior ophthalmic vein
Orbital Fissure with annulus of
Zinn
914
Pterygopalatine fossa:
-space between posterior wall of maxillary sinus and pterygoid
plates
-boundaries:
-superior: -posterior part of the inferior orbital
fissure (a)
-orbital process of the palatine bone, body
of the sphenoid bone
-anterior: -posterior maxillary sinus wall (b)
-posterior: -lateral pterygoid plate
-inferior surface of greater wing of
sphenoid
-lateral: -pterygomaxillary fissure (c)
-medial: -vertical lamina of the palatine bone
-inferior: -hard palate
-communicates with:
-anterosuperior: inferior orbital fissure orbit
-posteriorsuperior: foramen rotundum, vidian canal middle cranial fossa
-medial: sphenopalatine foramen nasal cavity
-lateral: pterygomaxillary fissure infratemporal fossa
-inferior: greater and lesser palatine canals oral cavity
-contents:
-internal maxillary artery
-foramen rotundum maxillary division of trigeminal
-sphenopalatine ganglion and nerve
-vidian nerve
-formed by contributions of lesser petrosal and deep petrosal nerves
-passes through pterygoid canal to synapse in pterygopalatine ganglion
-provides autonomic innervation to nasal cavity, nasopharynx and lacrimal glands
915
Infratemporal fossa:
-contains:
-pterygoid muscles
-maxillary artery and its branches
-pterygoid venous plexus
-branches of the mandibular division of the trigeminal
nerve (foramen ovale)
-otic ganglion
-chorda tympani
-middle meningeal artery (foramen spinosum)
-boundaries:
-superior: -base of skull
-anterior: -posterior buttress of malar eminence and maxillary sinus
-posterior: -glenoid fossa, mandibular neck and condyle
-medial: -plane extending from lateral pterygoid plate to spine of sphenoid bone
-lateral: -medial surface of the ramus of mandible
-inferior: -medial pterygoid muscle
-important foramina:
-foramen ovale and spinosum
916
MANAGEMENT OF CRANIAL BASE TUMOURS
Surgical Approaches
917
-bifrontal craniotomy:
-to expose dura over frontal poles
-subfrontal craniotomy:
-Raveh approach
-segment of bone containing glabella and supraorbital rims removed between supraorbital foramen
-provide direct anterior exposure of ethmoidal sinuses and to maximize exposure of subfrontal
base
-may obviate the use of facial incision for selected tumours of paranasal sinus
-frontal poles and overlying dura separated from bony cranial base to allow transection of olfactory nerve
connection through cribriform plate
-exposes planum sphenoidale and optic chiasm
-facial incisions:
-lateral rhinotomy:
-exposes superior limit of nasal cavity and paranasal sinuses for complete tumour
removal
-can be combined with periorbital incisions: subciliary or transconjunctival
-facial degloving and transpalatal approach:
-exposes nasal cavity and nasopharynx without facial incisions
-provide more limited exposure of upper vault and ethmoidal sinuses
-extent of central cranial-base exposure can be increased by combining with LeFort I osteotomy of the
maxilla
-separates superior dental arch from midface at level just superior to roots of teeth
-causes down-fracturing of palate and provides wide exposure of clivus, craniocervical junction
and nasopharynx
918
Infratemporal Fossa Approach
-temporal and infratemporal regions are reached through:
-preauricular or postauricular incision that extends onto the cervical region
-hemicoronal or bicoronal incision
-removal of orbitozygomatic segment of bone allows elevation of temporalis muscle from temporal fossa to
gain access to infratemporal fossa
-+/- removal of mandibular neck and condylar head
-frontotemporal craniotomy can be performed to elevate brain
-internal carotid artery medial to osseous eustachian tube
-uncovered mobilized to allow access to medial petroclival structures
-sphenoid sinus entered between 2nd and 3rd division of CN V
-reconstruction:
-ipsilateral temporalis muscle or temporoparietal fascial flap OR
-temporalis flap obtains blood supply from deep temporal arteries
-free flap reconstruction
-reconstruction:
-temporalis muscle flap
-positioned within infratemporal fossa and below central cranial base
-free flap if no adequate coverage
-zygomaticomaxillary bone segment replaced
-lacrimal system reconstructed with silicone stents
919
F.Ling - Cranial-Base Surgery (10)
920
F.Ling - Cranial-Base Surgery (11)
921
Posterior Cranial Base
-approaches:
-transmastoid-translabyrinthine
-retromastoid-retrosigmoid
-sub-occipital craniotomy
-provide access to jugular bulb and CPA
ADJUVANT THERAPIES
COMPLICATIONS
CSF Fistula
-most common complication after cranial-base surgery (20%)
-determine type of leak:
-high flow: active flow seen from wound, ear canal, or nasal cavity
-usually managed by direct closure in OR
-CT cisternography used if source of leak not evident
-low flow: CSF on dressings
-lumbar drain placed
-draining too much CSF can cause air entrainment into cranial vault through cranial-base
defects pneumocephalus
-if a low-flow leak has not stopped within 5 days, reoperation usually is necessary
-CSF leak specifically confirmed by means of testing for protein B2-Transferrin
-contained in only three body fluids: CSF, perilymph, vitreous fluid of the eye
Meningitis
-N+V, headache, decreasing mental status
-positive Brudzinski sign (stiff neck) and Kernig sign (pain in hamstring muscles on knee
extension)
-diagnosis by LP and CSF analysis
-postsurgical aseptic meningitis caused by meningeal irritation from surgical manipulations,
blood, and blood breakdown products
-bacterial meningitis:
-posttraumatic: S.aureus, Pneumococcus
-postoperative: S.aureus, Enterococcus
-treatment: IV antibiotics
922
-any leak, regardless of causation, persists longer than 5 days, operative closure is
pursued
-long-term antibiotics does not prevent meningitis and specifically increases risk of meningitis or
wound infection with resistant microorganisms
-techniques:
-CSF leak in sphenoidal sinus after transsphenoidal hypophysectomy
-endoscopic closure with fibrin glue or hydroxyappatite cement or autografts +/- pre-
operative lumbar drainage
-dural patching: reestablishment of the continuity of dura
-Diabetes Insipidus:
-usually occurs after severe head trauma or removal of pituitary or hypothalamic tumours
-decreased secretion of ADH
-polyuria, dehydration, hypovolemia and polydipsia
-tx: fluid and electrolyte replacement; vasopressin can be given to control urine output
(temporary)
-SIADH:
-caused by head trauma or intraoperative manipulation
-can be cause by stroke, systemic metabolic disturbances, or intracranial bleeding
-inability to eliminate free water hyponatremia and hypoosmolality
-tx: fluid restriction to maximum of 1L day
-severe cases may require 3% hypertonic saline solution
Volume of urine output >250 mL/h for more than 2 h <30 mL/h
923
POTENTIAL COMPLICATIONS (Summary)
Category Complication Treatment Options
Mass lesions -brain edema -mannitol, diuretics, barbiturate coma, occasionally lobectomy
-haematoma -evacuation
CSF -leak -reexploration and repair; spinal fluid drainage; vascularized flap
EMERGENCIES
Air Embolus
-from open venous sinuses within diploe of skull, sigmoid sinus, jugular bulb or jugular vein
-fairly large amount of air needed but circulatory compromise can occur with volumes as low as 30 ml
-tx: -wound filled with wet packing
-patient turned to head-down, left lateral decubitus position traps air to right side of heart to
minimize embolization to lungs
-position maintained until circulatory stability returns or aspiration of air can be achieved with
transvenous catheter
-source of air-leak sealed
924
Postoperative Seizures
-manipulation or resection of temporal lobe particularly epileptogenic
-prophylactic antiseizure prophylaxis routine
-tx: IV phenytoin, phenobarbital, or diazepam
-search for metabolic or structural cause
925
SURGICAL TECHNIQUES TO ENHANCE PROSTHETIC REHABILITATION
-early dental intervention can decrease inpatient days by reducing sites of oral infection and decreasing risk factors
for oral complications, such as osteoradionecrosis
-note advanced periodontal disease, gross dental caries, tissue irritation, poor oral hygiene
-dentist’s evaluation:
-confirms existence of acute and chronic oral pathologic conditions such as dental abscess, teeth
with advanced periodontal disease, or dental calculus causing gingivitis
-Panorex obtained to demonstrate overall topographic features of dentition, maxilla, mandible, sinuses,
nasal cavity and TMJ
-teeth with poor or questionable prognosis are identified and extracted before or during primary ablative
surgical procedure
926
SURGICAL TECHNIQUES TO ENHANCE PROSTHETIC REHABILITATION
Maxilla
-alveolar cuts made through socket of an extracted tooth to prevent iatrogenic bone loss and to ensure
longevity of tooth next to this cut
-spare as much premaxilla as possible for support and retention of prosthesis
-STSG placed in maxillary defect to provide scar tissue band for retention of prosthesis, decrease mucous
secretion and crust formation
-palatal mucosa can be wrapped around midline portion of palatal cut
-removal of inferior and middle turbinates allows extension of prosthesis into defect area
-surgical obturator prosthesis placed to restore oral contour for immediate function and good postoperative
appearance
Soft Palate
-it is easier to rehabilitate a pt’s speech and swallowing if soft palate is removed totally
-if remaining soft palate is nonfunction, rehabilitation can be difficult or even impossible
Mandible
-three types of osseous free tissue transfer have been used:
-scapula
-iliac crest
-fibula
-fibular graft supplies length and quality of bone to reconstruct defects of mandible and is an excellent
recipient for dental implants and prostheses
-procedures to aid support of a prosthesis:
-vestibuloplasty with placement of STSG
-placement of dental implants
Tongue
-palatal augmentation prostheses approximated to maxilla to increase linguopalatal contact help normalize
speech and swallowing
-tongue prostheses are available but provide poor function
Extraoral Lesions
-prostheses are retained with adhesives and tissue undercuts or extraoral osseointegrated implants
Orbit
-surgical considerations to improve prosthetic rehabilitation
-eyelid resection while maintenance of brow position
-rough bony margins smoothed
-STSG placed in depth of defect to cover expose bone
Ear
-easier to replace complete ear than partial ear
-recipient area must be flat or concave
-skin devoid of hair provides good adhesive base
-if tissue can be spared, tragus is the first choice allows anterior margin of prosthesis to be hidden
927
GENERAL INFORMATION ABOUT OSSEOINTEGRATED DENTAL IMPLANTS
-implants are made of titanium and are cylindrically designed with threads that anchor them in bone
-stages:
-placement of implant into bony recipient site under local or general anesthesia
-covered by tissue flap and allowed to integrate with bone for 12 or more weeks
osseointegration
-superior portion of implant is uncovered and connector is placed on implant
928
CUTANEOUS MALIGNANCY
Merkel Cell Carcinoma
Epidemiology
-rare neoplasm - just over 600 cases reported
-6th and 7th decades of life (mean age, 67.8 y); M=F
Histology
-small, round, basophilic cells arranged in sheets, rests, or trabeculae
-originates in the dermis
-rounded nuclei, finely divided chromatin, scant cytoplasm, and high rate of mitosis
-three histologic subtypes of MCC:
-solid type (most common)
-trabecular type
-diffuse type (worst prognosis).
-immunohistochemical staining:
-cytokeratin (in the form of a perinuclear dotlike pattern typical of neuroendocrine tumors) and
neuron-specific enolase makes the definitive diagnosis
-absence of S-100 protein and homatropine methylbromide marker (HMB-45) essentially excludes
the diagnosis of malignant melanoma
Prognosis
-aggressive malignancy similar to malignant melanoma
-10-25% of pt with regional nodal involvement at presentation
-local recurrence after primary treatment in 25-45% of pts
-regional nodal involvement develops in 50-70%
-distant metastases occur in more than 30% of patients
-overall 5-year survival rate is 50-70%
Treatment
-surgical excision:
-wide local excision, to include 2-3 cm of normal-appearing skin
-Mohs micrographic surgery effective
-radiation therapy:
-radiosensitive tumor
-adjuvant XRT after excision recommended to reduce local recurrence
-45-60 Gy in standard fractions to surgical site and regional lymphatic bed are used
-N0 neck (Stage I disease):
-controversial: both elective lymph node dissection and radiotherapy are advocated
-N+ neck (Stage II disease):
-complete lymph node dissection
-postoperative XRT to regional site and neck is unknown at this time
-treatment of recurrence:
-reexcision with a 2-cm margin or with Mohs micrographic surgery
-distant metastasis (Stage III):
-lungs, liver, bone, or brain
-mean survival time of 8 months
929
-histochemically similar to small cell carcinoma of the lung: similar chemotherapeutic regimens
-carboplatin and etoposide
930
NECK CANCER, UNKNOWN PRIMARY
-when clinicians are unable to determine origin of metastatic cervical lymphadenopathy, cancer is said to
originate from an unknown primary site
-when primary site of carcinoma is known, one is able to administer focused therapy to primary site and
cervical lymphadenopathy
-if site is unknown must treat entire pharyngeal axis and larynx to cover possible origins of metastatic
carcinoma
-treatment results in a significant increase in morbidity
-occult primary carcinoma either metastasizes early to cervical lymphatics or develops in an anatomical site
that is not detectable by endoscopy or imaging techniques
-typical presentation is complaint of a painless neck mass
-thorough head and neck exam is performed
-if no primary site is found, one is obligated to perform a panendoscopy of upper aerodigestive tract with
biopsy samples obtained from designated high-yield anatomical sites and any other suspicious areas
-surgical treatment of cervical lymphadenopathy in certain clinical situations may be performed at same
time as panendoscopy.
Relevant Anatomy
Occipital nodes:
-drainage of posterior scalp
Postauricular nodes:
-lymphatic drainage of posterior scalp, mastoid, and posterior auricle
Parotid nodes:
-extraglandular nodes: drainage of anterior scalp (anterior to imaginary anatomical line)
-intraglandular nodes: same anatomical regions as extraglandular nodes as well as parotid gland
itself
Retropharyngeal nodes:
-drainage of posterior region of nasal cavity, sphenoid and ethmoid sinuses, hard and soft palate,
nasopharynx, and posterior pharyngeal wall
931
-when lymphadenopathy is located in supraclavicular space, lower deep lateral cervical chain, or lower
posterior triangle, primary lesion is often not from upper aerodigestive tract
Treatment:
Radiation therapy:
-Jesse et al demonstrated added advantage of radiation therapy to locoregional control following surgical
removal of cervical metastases
-locoregional failure rate of 13-32% when treated with surgery alone cf 0-18% when patients are treated
with primary surgery (neck dissection) followed by adjuvant external beam radiotherapy.
-field to be covered by radiation therapy is controversial
-pts treated with ipsilateral irradiation had a relative risk of recurrence in head and neck of 1.9
compared to patients treated with bilateral irradiation
-bilateral cervical irradiation with surgical therapy improves locoregional control of cancer and is
accepted as standard of care for patients with advanced cervical disease (>N2)
-mucosal sites that are to be included in radiation field of patients with occult primary lesions are generally
accepted as entire pharyngeal axis
-in theory, this should prevent occurrence of primary lesion
-some argue that, to decrease morbidity of radiation-induced xerostomia, nasopharynx should not
be included in radiation ports when results of endoscopy and findings on imaging studies are
negative
Chemotherapy:
-generally reserved for patients with clinical or pathologic indicators of aggressive disease or primary
nasopharyngeal carcinoma:
-extensive lymphadenopathy (>N2C)
-extracapsular spread of carcinoma
-unresectable local disease
-distant metastatic spread of carcinoma often undergo chemotherapy for possible cure or palliative
treatment
Surgical therapy:
-Panendoscopy:
-generous biopsy samples of nasopharynx are obtained for both frozen sectioning and permanent
sectioning
-inspection and palpation of oral cavity, oropharynx, hypopharynx, and larynx
-rigid cervical esophagoscope is used to examine esophagus
-biopsy samples are obtained by examiner of base of tongue
-unilateral tonsillectomy vs bilateral tonsillectomy
-depending on results of panendoscopy, either newly found primary lesion (other than nasopharynx) is
addressed surgically along with cervical lymphadenopathy or lymphadenopathy is addressed separately
with appropriate neck dissection.
932
OSTEORADIONECROSIS AND HYPERBARIC OXYGEN THERAPY
Osteoradionecrosis (ORN)
-condition of nonvital bone in a site of radiation injury
-can be spontaneous, but it most commonly results from tissue injury
-apparently innocuous forms of trauma as denture-related injury, ulcers, or tooth extraction can overwhelm
the reparative capacity of radiation-injured bone
-grades of disease:
-Grade I:
-most common presentation
-exposed alveolar bone is observed
-Grade II:
-ORN that does not respond to hyperbaric oxygen therapy and sequestrectomy/saucerization
-Grade III:
-full thickness involvement and/or pathologic fracture
Frequency:
-rare in patients who receive less than 60 gray (Gy) radiation therapy
-incidence is increased in patients receiving combined chemotherapy-radiation
Etiology:
-ORN can be either spontaneous (39% of cases) or the result of an insult (61%)
-cumulative progressive endarteritis caused by radiotherapy results in insufficient blood supply (tissue
oxygen delivery) to effect wound healing
Pathophysiology:
-irradiated mandible, periosteum, and overlying soft tissue undergo hyperemia, inflammation, and
endarteritis thrombosis, cellular death, progressive hypovascularity, and fibrosis
-radiated bed is hypocellular and devoid of fibroblasts, osteoblasts, and undifferentiated osteocompetent
cells
Work-up:
-rule out recurrence
-determine method of radiation treatment, total dose, and radiation portal
-CT/MRI of mandible
-future: SPECT scan
Treatment:
Medical therapy:
-pretreatment phase:
-dental evaluation for patients with oral cancer who may need radiotherapy
-dentist should perform prophylaxis, periodontal scaling, caries control, and fabrication of
fluoride trays
-teeth that cannot be salvaged with conservative endodontic therapy should be extracted
-fluoride treatment to prevent radiation caries
-posttreatment phase:
-primarily supportive: nutritional support along with superficial debridement and oral saline
irrigation for local wounds
-antibiotics are indicated only for definite secondary infection
933
Hyperbaric Oxygen:
-HBO transiently elevates tissue oxygen tension and stimulates fibroblastic proliferation and oxygen-
dependent collagen synthesis
-allows for angiogenesis in radiated bed
Microvascular reconstruction
-after resection of nonviable bone, vascular free tissue transfer offers immediate reconstruction and
restoration of mandibular continuity
-free tissue transfers offer patients a shorter treatment course without the need for HBO
Postoperative details:
-risk of developing ORN is cumulative in relation to radiation dose, and risk continues throughout pts life
-risk of ORN in patients who must undergo procedures involving the mandible following radiation
treatment increases with time from radiation therapy
-prophylactic use of HBO can decrease morbidity and increase success of dental therapy
-prior to dental extraction/implant placement, consider HBO if surgery will occur in a field of radiation that
is known to have received 60 Gy
-follow the standard HBO regimen of 20 preoperative treatments and 10 postoperative treatments
-perform surgery in as atraumatic a fashion as possible
934
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ORAL CAVITY
Lip
External upper lip (vermilion border)
External lower lip (vermilion border)
Commissures
Oral Cavity
Buccal mucosa
mucosa of upper and lower lip
cheek mucosa
retromolar areas
bucco- alveolar sulci, upper and lower (vestibule of mouth)
Upper alveolus and gingiva (upper gum)
Lower alveolus and gingiva (lower gum)
Hard palate
Tongue
anterior 2/3
inferior (ventral) surface
Floor of mouth
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Stage 0:ÇTis N0 M0
Stage I:ÇT1 N0 M0
Stage II:ÇT2 N0 M0
Stage III:ÇT3 N0 M0; T1- 3 N1 M0
Stage IVA:ÇÇÇT4 N1- 2 M0; Any T N2 M0
Stage IVB:ÇAny T N3 M0
Stage IVC:ÇAny T Any N M1
PHARYNX
Nasopharynx
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Stage 0:Ç
Tis N0 M0
Stage I:Ç
T1 N0 M0
Stage IIA:Ç
T2a N0 M0
Stage IIB:Ç
T1 N1 M0
T2 N1 M0
T2a N1 M0
T2b N0 M0
T2b N1 M0
Stage III:Ç
TI N2 M0
T2a N2 M0
T2b N2 M0
T3 N0 M0
T3 N1 M0
T3 N2 M0
Stage IVA:Ç
T4 N0 M0
T4 N1 M0
T4 N2 M0
Stage IVB:Ç
Any T N3 M0
Stage IVC:Ç
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Any T Any N M1
Oropharynx
Stage 0:ÇTis N0 M0
Stage I:ÇT1 N0 M0
Stage II:ÇT2 N0 M0
Stage III:ÇT3 N0 M0; T1- 3 N1 M0
Stage IVA:ÇÇÇT4 N1- 2 M0; Any T N2 M0
Stage IVB:ÇAny T N3 M0
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Hypopharynx
Stage 0:ÇTis N0 M0
Stage I:ÇT1 N0 M0
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Stage II:ÇT2 N0 M0
Stage III:ÇT3 N0 M0; T1- 3 N1 M0
Stage IVA:ÇÇÇT4 N1- 2 M0; Any T N2 M0
Stage IVB:ÇAny T N3 M0
Stage IVC:ÇAny T Any N M1
LARYNX
Supraglottis
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Glottis
vocal cords
anterior commissure
posterior commissure
Subglottis
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Stage 0:Ç
Tis N0 M0
Stage I:Ç
T1 N0 M0
Stage II:Ç
T2 N0 M0
Stage III:Ç
T3 N0 M0
TI N1 M0
T2 N1 M0
T3 N1 M0
Stage IVA:Ç
T4 N0 M0
T4 N1 M0
Any T N2 M0
Stage IVB:Ç
Any T N3 M0
Stage IVC:Ç
Any T Any N Ml
MAXILLARY SINUS
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T3: Tumor invades any of the following: bone of the posterior wall of the
maxillary sinus, subcutaneous tissues, skin of cheek, floor or medial wall of
orbit, infratemporal fossa, pterygoid plates, ethmoid sinuses
T4: Tumor invades orbital contents beyond the floor or medial wall including
any of the following: orbital apex, cribriform plate, base of skull,
nasopharynx, sphenoid, frontal sinuses
Stage 0:Ç
Tis N0 M0
Stage I:Ç
T1 N0 M0
Stage II:Ç
T2 N0 M0
Stage III:Ç
T3 N0 M0
T1 N1 M0
T2 N1 M0
T3 N1 M0
Stage IVA:Ç
T4 N0 M0
T4 N1 M0
Stage IVB:Ç
Any T N2 M0
Any T N3 M0
Stage IVC:Ç
Any T Any N M1
PAROTID GLAND
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Stage I:Ç
T1 N0 M0
T2 N0 M0
Stage II:Ç
T3 N0 M0
Stage III:Ç
T1 N1 M0
T2 N1 M0
Stage IV:Ç
T4 N0 M0
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T3 N1 M0
T4 N1 M0
Any T N2 M0
Any T N3 M0
Any T Any N M1
THYROID GLAND
Papillary or Follicular
Under 45 Years
Stage I:Ç
T1 N0 M0
Stage II:Ç
T2 N0 M0
T3 N0 M0
Stage III:Ç
T4 N0 M0
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Any T N 1 M0
Stage IV:Ç
Any T Any N M1
Medullary
Stage I:Ç
T1 N0 M0
Stage II:Ç
T2 N0 M0
T3 N0 M0
T4 N0 M0
Stage III:Ç
Any T N 1 M0
Stage IV:Ç
Any T Any N M1
Undifferentiated
The following regional node classification is applicable to all malignant head and
neck tumors. In clinical evaluation the actual size of the nodal mass should be
measured and allowance made for intervening soft tissues. It is recognized that
most masses over 3 cm in diameter are not single nodes but confluent nodes of
tumor in soft tissues of the neck. There are three stages of clinically positive
nodes: N1, N2, and N3. The use of subgroups a, b, and c is not required but is
recommended. Midline nodes are considered as ipsilateral nodes.
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TRACHEAL RESECTION WITH PRIMARY ANASTOMOSIS
-release manoeuvres:
-hilar release manoeuvres (uncommonly used today)
-division of right pulmonary ligament
-division of left main stem bronchus just distal to carina with end-to-side anastomosis to bronchus
intermedius
-pericardial dissection
-cervical flexion
-suprahyoid release (SHR)
948
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ORAL CAVITY
Lip Carcinoma
Regional metastasis:
relatively uncommon; ~10%
Locoregional control:Ç>90%
5- yr survival:
Overall:Ç91%
I- II:Ç>90%
III- IV:Ç30- 70%
Tongue Carcinoma
Regional metastasis:Çcommon
clinically apparent:Ç25- 33%
occult: 25- 33%
5- yr locoregional control:Ç91%
5- yr survival:
I- II:Ç60- 75%
III- IV:Ç25- 40%
Effect of extracapsular spread (ECS) - 5- yr survival and overall
N0:Ç88% and 75%
N+/ECS- :Ç65% and 50%
N+/ECS+:Ç48% and 30%
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neck:Ç18.5%
5- yr survival:
I- II:Ç60- 80%
III:Ç28- 68%
IV:Ç6- 36%
Regional metastasis:Çcommon
10- 20%
5- yr survival:
T1:Ç80%
T2:Ç57.8%
T3:Ç46.5%
T4:Ç65.2%
Overall survival:Ç26- 55%
Regional metastasis:
clinically apparent:Ç25- 30%
occult:Ç15%
Locoregional control:Ç70- 80%
Mandibular cortical invasion:Ç5- yr survivalÇ85% - - > 68%
Cervical metastasis:Ç5- yr survivalÇ86% - - > 59%
Palate Carcinoma
Local recurrence:Ç53%
Regional recurrence:Ç30%
5- yr survival:Ç44- 75%
Buccal Carcinoma
950
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I- II:Ç65- 78%
III- IV:Ç50- 60%
PHARYNX
Nasopharynx
Nodal metastasis:
clinically apparent:Ç87%; 20% bilateral
Locoregional control
radiation:Ç60%
chemoradiation:Ç70- 80%
5yr- survival
radiation:Ç36- 58%
chemoradiation:Ç70- 80%
10- yr survival:
10- 40%
Oropharynx - Tonsil
Locoregional control
I- II:Ç75- 90%
III:Ç50%
IV:Ç20- 50%
5yr- survival
I- II:Ç80%
III:Ç50%
IV:Ç20- 50%
Locoregional control
I- II:Ç75- 90%
III:Ç50%
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IV:Ç20%
5yr- survival
I- II:Ç85%
III- IV:Ç20- 50%
Locoregional control
I- II:Ç75- 90%
III:Ç75%
IV:Ç35%
5yr- survival
I- II:Ç70- 80%
III:Ç64%
IV:Ç20- 40%
Hypopharynx
LARYNX
Supraglottis
Glottis
Subglottis
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MAXILLARY SINUS
PAROTID GLAND
THYROID GLAND
Mortality:
low- risk group:Ç1- 2%
high- risk group:Ç40- 50%
Medullary Carcinoma
5- yr survival:Ç78- 91%
10- yr survival:Ç61- 75%
Anaplastic Carcinoma
953
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VELOPHARYNGEAL INSUFFICIENCY
Introduction:
-inadequate velopharyngeal closure (VPC) allows air to escape through nose during generation of
consonants requiring high oral pressure, leading to inappropriate nasal resonance during speech production
Problem:
-VPC is an important part of speech
-all phonemes in English language with the exception of 3 (/m/, /n/, /ng/) are produced with oral airflow
velopharynx closed
-nasal phonemes (/m/, /n/, /ng/) are produced with nasal resonance velopharynx open
-VPI is inadequate closure of velopharyngeal port resulting from a structural problem with the velum
-eg, submucous cleft palate, shorted velum relative to the depth of the posterior pharyngeal wall,
overt cleft palate
Etiology:
-overt cleft palate (most common)
-submucous cleft palate
-bifid or double uvula, muscular diastasis of the soft palate (zona pellucida), and notching of
posterior border of hard palate
-occult submucosal cleft palate
-absence or deficiency of musculus uvulae with a diastasis of levator veli palatini but without
presence of a bifid uvula or grooving of oral surface of soft palate
-best visualized endoscopically as absence of bulge on nasal surface of soft palate during speech.
-transient VPD with hypernasal resonance following adenoidectomy, with or without tonsillectomy
-Down syndrom:
-predisposition to VPD is present
-often have a narrow velopharynx and a shallower skull base, resulting in less distance for palate
to traverse to effect closure
-VCF syndrome
-autosomal dominant entity linked to microdeletions in long arm of chromosome 22
-major findings include cleft palate (overt, submucous, or occult submucous), conotruncal heart
anomalies, mental disabilities, and a characteristic facies
-common in patients with VCF syndrome due to presence of a cleft palate and pharyngeal
hypotonic
-low muscle tone:
-may be a feature of other syndromes (eg, neurofibromatosis, myotonic dystrophy, any syndrome
in which low muscle tone is a feature)
-tonsil hypertrophy that prevents palate from adequately moving superiorly during attempted VPC
-acquired causes include:
-stroke or head injury
-other neurologic diseases (eg, muscular dystrophy, multiple sclerosis, amyotrophic lateral
sclerosis [ALS], Parkinson disease)
Clinical:
-nasal resonance, and nasal emissions (ie, air escape through nasal passage with speech)
-nasal regurgitation
-recurrent and chronic sinus infections
954
Relevant Anatomy:
When viewed endoscopically, several topical anatomic features of velopharynx (nasopharynx) are important to note.
-Pharyngeal ostium of eustachian (auditory) tube: This opening and its associated structures comprise
lateral wall of nasopharynx
-Pharyngeal tonsil (ie, adenoid): adenoid, which is a closely aggregated collection of lymphoid nodules, is
directly posterior in nasopharynx and overlies basilar portions of sphenoid and occipital bones
-Posterior pharyngeal wall: comprises mainly superior pharyngeal constrictor muscle. Contraction of this
muscle in axial plane at level of VPC constitutes a structure known as Passavant ridge.
-Pharyngeal surface of soft palate
Diagnostic Procedures:
-Voice and resonance evaluation
-articulation assessment
-oral motor assessment
-measurement of nasal airflow:
-MacKay-Kummer sensory nerve action potential (SNAP) test
-assesses ratio of oral airflow to nasal airflow
-nasometer results are compared to normative data
-score 3 standard deviations above mean indicates hypernasal resonance
-Fiberoptic nasoendoscopy
-Videofluoroscopy
-allows more precise localization of level of VPC by measuring level against spine
TREATMENT
Speech therapy
-Speech therapy improves velopharyngeal function when VPD is minimal or due to articulation errors and
in postoperative patients
Prosthetics
-obturators can substitute for tissue deficiency and are attached to teeth by metal wire or bands
-palatal lifts are used when adequate palatal length exists but dynamic motion of palate is poor due to
neuromuscular etiologies
955
Surgical therapy:
Preoperative details:
1. Coronal:
-most common closure pattern (present in 55% of patients with normal velar function)
-major contribution to closure is from soft palate as it contacts a broad area of posterior
pharyngeal wall
-little medial motion of lateral pharyngeal walls occurs
2. Circular:
-present in approximately 20% of individuals with normal closure
-involves contribution from both soft palate and lateral pharyngeal walls
-closure that resembles a circle getting smaller
4. Sagittal:
-least common pattern (10%)
-palatal motion is minimal
-main contribution from medial motion of lateral pharyngeal walls
-pattern seen most commonly in patients with persistent VPD following repair of cleft
palate.
Other considerations
-placement of a pharyngeal flap increases degree of nasal airway obstruction and may worsen any
preexisting obstructive sleep apnea consider pharyngoplasty instead
-location of internal carotid arteries as they traverse lateral pharynx is an important consideration,
especially in VCF syndrome preoperative evaluation with contrast-enhanced CT scan or magnetic
resonance angiography
956
Intraoperative details:
Pharyngoplasty
-advantageous when coronal or circular closure is present and lateral pharyngeal wall motion is deficient
-goal is to develop a more functional sphincter by improving dynamics and bulk of velopharyngeal tissues
and by tightening and reducing size of velopharyngeal sphincter
-two superiorly based flaps comprising posterior tonsillar pillars with underlying palatopharyngeus muscles
-small inferiorly based posterior pharyngeal wall flap then was elevated, and 2 lateral flaps were rotated
90 ° and inserted onto posterior flap
-success rate: 78-100%
-incidence of postoperative hyponasality: 12-17%.
Pharyngeal flap
-preferred method in patients with good lateral pharyngeal wall motion who have a persistent central gap
due to poor palatal motion
-superiorly based posterior wall flap sutured to nasal surface of soft palate
-flap raised down to prevertebral fascia, creating a tissue flap of superior constrictor muscle with
its overlying mucosa
-flap then is sutured to nasal surface of palate by incorporating it into split repair
-normalization or resolution of hypernasality in 90% of patients
Postoperative details:
-immediate postoperative concerns deal mainly with upper airway obstruction
957
AUDIOLOGICAL TESTS
Audiogram
-frequencies tested: 250 to 8000 Hz
-interoctave frequencies and ultra-high frequencies on a case-by-case basis (ie. suspected
ototoxicity, hearing aid user, precipitous loss)
-inserts vs phones: 40 vs 60 dB interaural difference
-combined ART and ARD has sensitivity of 73% and specificity of 90% for prediction of acoustic
neuroma; sensitivity of 80% and specificity of 60% for CPA tumours
-reflex decay phenomenon is specifically associated with eighth-nerve lesions
958
PI-PB Function
-performance intensity (PI) function for phonetically balanced (PB) words
-aka rollover function
-list of one-syllable words presented at a comfortable intensity vs a loud intensity
-word lists are balanced to equally represent all of the speech sounds, therefore different
frequencies
-for a patient with hearing within normal limits, first list would be presented at 50 dB and the
second at 80 dB
-score at comfort level minus score at elevated level
-difference of more than 25% = positive result
-can be suggestive of retrocochlear pathology
Electrocochleography (EcoG)
3 main applications
-neurodiagnostic evaluation of Menière’s disease
-enhancement of ABR wave I
-intraoperative monitoring
-extratympanic, tympanic and transtympanic electrode options
-abnormally large summation potential (SP) is seen in most patients with Menière’s disease
-an elevated SP/AP amplitude ratio is seen in approximately 60% of Menière’s patients
-SP/AP > 0.4 considered abnormal
-sensitivity of 62% and specificity of 95%
Otoacoustic Emissions
-2 types: transient evoked (TEOAEs)and distortion product (DPOAEs)
-main applications:
-suspicion of auditory neuropathy
-malingering patients
-patients with tinnitus
-to monitor cochlear status over time
-TEOAE restricted to <5 kHz and cannot test ears with >30 dB loss
-DPOAE can test 1-8KHz range and can test to 55 dB loss
-able to test selected frequencies in detail as opposed to one response curve representing the
frequency range
959
-to verify presence of auditory neuropathy
-uses a 10 millisecond window to record five peaks which represent different areas along the auditory
pathway
-degree of loss
-more hearing = better results
-clear results are usually obtained when threshold at 4000 Hz is 70 dB or better
-examples of tests:
960
Stenger Test
-two tones presented in both ears at the same time but at different intensities
-10 dB above threshold in the better ear
-10 dB below threshold in the poorer ear
-when the patient fails to respond, it is a positive Stenger Test which suggests malingering
961
TYMPANOSTOMY TUBES
INDICATIONS
Persistent otitis media with effusion Factors making tympanostomy tube placement less desirable:
-various meta-analyses have reported -Mild symptoms with acute stages of infection
-Good response to medical therapy
short-term resolution rates between 16% and -Little or no hearing loss with OM with effusion
32%
-long-term resolution rates of 65% at 3 * A child with a history of four or more bouts of acute OM in the
months and 85% at 6 months last 6 months, six or more bouts in the last 12 months, three or more
months of bilateral OM with effusion, or 6 or more months of
-losses of 20 dB or more will certainly hinder unilateral OM with effusion.
the child’s understanding and appreciation of
his or her surroundings; whether it will also
lead to delays in short- or long-term speech
and language acquisition or have lasting consequences for cognitive development is debatable
-few small studies that have compared scholastic aptitude in children with unoperated OM with effusion
with those who had TT placement do not show significant differences
-TT placement should be seriously considered in cases of bilateral OM with effusion that has been present
for 3 or more months if the hearing loss in the better ear is 20 dB or greater
962
Frequent otitis media in patients with an underlying sensorineural hearing loss
-the additional 10- to 30-dB hearing loss produced by a middle-ear effusion can significantly complicate
efforts to take advantage of residual hearing in patients with an underlying hearing loss
Severe tympanic membrane retraction with hearing loss, impending cholesteatoma formation, or ossicular
chain erosion
-untreated TM atelectasis is frequently complicated by the difficult problems of cholesteatoma and erosion
of the long process of the incus and eventual ossicular chain discontinuity
-TT retraction/atelectasis can frequently be completely reversed by timely TT placement
PERIOPERATIVE CONSIDERATIONS
Tube selection
-most TTs are variations of the grommet or the T-tube
-generally speaking, the larger and stiffer the flange, the longer the tube remains in situ
-T-tubes will remain in situ for extended periods when designed with long, stiff flanges and is one of the
few tubes that is easily removed in the office without an anesthetic
-could potentially serve as either long- or short-term tubes
-disadvantage is the high reported rate of perforation
-perforation rate can be reduced to less than 10% if a short-flanged T-tube of soft
silicone is used
Insertion technique
-myringotomy is performed in the anterior portion of the TM to avoid the acoustically sensitive portion of
the drum
-classic dogma states that a radial incision is less damaging to the TM and that TTs will be retained longer
if placed in the anterosuperior quadrant
-a recent study showed no difference in TM sequelae with radial or circumferential incisions and no
difference in retention time based on location of incision
Antibiotic drops
-ototopic antibiotic drops can be considered in the immediate postoperative period in an effort to reduce
postoperative otorrhea, particularly when a mucoid effusion was evident during TT placement.
963
Swimming
-no consensus as to whether patients with TTs should be permitted to swim, and, if so, whether earplugs
are necessary
Follow-up
-assuming there are no other problems, the ears should be examined at least twice yearly to assess TT and
TM status
COMPLICATIONS
Anesthetic complications
Otorrhea
-most common complication following TT placement and will occur at some point during the life of the TT
for as many as 50% of patients
-likely to follow an upper-respiratory infection
Myringosclerosis
-tympanosclerotic plaques within the TM in 40% to over 50% of TMs after TT placement—which is much
higher than would be expected from a history of recurrent OM alone without TT placement
-a large series showed that this finding did not significantly affect hearing
Cholesteatoma
-may arise independently of the TTs in patients with longstanding eustachian tube dysfunction and
recurrent OM
-may also arise as a direct complication of TT placement, either in a retraction pocket that progresses to the
point of debris accumulation or as the result of ingrowth or transplantation of keratinized epithelium into
the middle-ear cleft
-longer retention associated with higher rates of cholesteatoma formation
964
DEVELOPMENT OF THE EAR
AURICULAR DEVELOPMENT
-5th week GA
-three hillocks arise from first branchial
(mandibular) arch: hillocks 1, 2, 3
-three hillocks arise from second branchial (hyoid)
arch: hillocks 4, 5, 6
-on either side of first branchial cleft
-8th week GA
-identifiable auricle
-hillock 1: tragus
-hillock 2: crus helices
-hillock 3: ascending helix
-hillock 4: horizontal helix, upper portion of scapha
and antihelix
-hillock 5: descending helix, middle portion of
scapha, antihelix
-hillock 6: antitragus and inferior aspect of helix
-18th week GA: auricle reaches adult form
-Fissures of Santorini:
-lymphatic channels that connect the lateral
cartilaginous EAC to the parotid and glenoid fossa
region, allows for extension of infection and
malignant tumours
-Foramen of Huschke:
-embryological remnant that forms a defect that connects the medial EAC to the parotid and
glenoid fossa region, allows for extension of infection and malignant tumours outside the
temporal bone
965
Tympanic Membrane
-trilaminar origin:
-ectoderm from floor of 1st branchial cleft epidermal layer
-endoderm of 1st pharyngeal pouch mucosa layer
-neural crest mesenchyme with cephalic mesoderm fibrous layer
-notch of Rivinus:
-notch of the squamose portion of the temporal bone located superiorly, within lies the pars
flaccida
Ossicles
-main source of development of ossicles is neural crest
mesenchyme of first and second branchial arches
-Meckel’s cartilage (first arch)
-head of malleus
-body and short process of incus
-mandibular branch of CN V and tensor
tympani muscle
-Reichert cartilage (second arch)
-long process of incus
-handle of malleus
-stapes superstructure and tympanic surface
of stapes footplate
-facial nerve and stapedius muscle
-mesoderm of otic capsule
-vestibular surface of footplate
-annular ligament
-ossification of malleus and incus by 16th week GA and almost complete by 30th week GA
-ossicles reach their adult size at birth
Maldevelopment
-ossicular abnormalities:
-middle ear deformities without coexisting outer ear defects are unusual
-incudomalleolar fusion or fixation a common defect
-stapedial abnormalities are less common
-footplate may have normal mobility because of its separate development from otic
capsule
-persistent stapedial artery
-usually regresses at 10 weeks
-when the artery persists, a vessel arises from internal cartotid artery in hypotympanum, which
courses through the crura of the stapes to the fallopian canal enters fallopian canal and courses
forward to geniculate ganglion and to dura
-risk of bleeding during middle ear surgery (ie. stapedectomy or cochlear implantation)
-congenital cholesteatoma
-failure of atrophy of epidermoid formation in the anterior mesotympanum
966
DEVELOPMENT OF THE FACIAL NERVE
Membranous Labyrinth
-develops from otic placode (3rd week GA)
-invaginate to become otocysts
subdivides into vestibular and cochlear
compartments and grows and
dramatically changes shape to achieve
adult form at 10 weeks and adult size
at 20 weeks GA
-sensory epithelium of cochlea develops at 7th
week GA as the duct grows and begins to coil
-hair cells begin to develop from base to
apex
-inner cells develop before outer cells
-afferent nerves develop before efferent
nerves
-endolymphatic duct and sac continue to grow
into the third trimester
-while otocysts is dividing into vestibular and
cochlear portions, the vestibulocochlear ganglion
divided into a superior and inferior division:
-superior:
-superior and lateral ampullae
of SCC
-utricle
-inferior:
-posterior ampulla
-saccule
-periotic duct:
-within cochlear aqueduct
-connects scala tympani to posterior cranial fossa
-ductus reunions:
-narrowest segment between cochlea and saccule
Osseous Labyrinth
-perilymph-filled osseous labyrinth
-derived from the labyrinthin capsule from periosteal and enchondral ossification (susceptible to bony
967
diseases such as Paget’s, osteodystrophies, or otosclerosis)
-most important aspect is resorptive process in mesoderm that separates membranous from developing
bony otic capsule
-cochlear aqueduct:
-begins in inner ear at base of scala tympani subarachnoid space in posterior cranial fossa
-vestibular aqueduct:
-contains endolymphatic duct and veins of vestibular aqueduct
-runs from vestibule to posterior surface of petrous pyramid in posterior cranial fossa (opening is
the operculum)
Otic Capsule
-develops from 14 centers of ossification
-achieves adult size by week 22 GA
-precartilaginous precursor appears in 7th week from cephalic
mesoderm
-oval window formed in the ninth week vestibular surface of
footplate
-rim of footplate and facing rim of window remain
cartilaginous
-round window forms adjacent to basal turn of cochlea
Maldevelopment
-categorization:
-membranous labyrinth anomalies alone (80%)
-osseous and membranous labyrinth anomalies (20%)
-inner ear abnormalities caused by arrested or aberrant
development
-genetically predetermined
-insult can occur before 5th week GA
968
-separate portions of developing system can be variably susceptible to teratogenic insult
-Scheibe:
-described the most common histopathologic finding in congenital deafness
-cochleosaccular dysplasia due to incomplete development of caudal portion of the otocysts (pars
inferior)
-organ of Corti typically partially or completely missing
-cochlear duct and saccule are collapsed
-stria vascularis is degenerated
-utricle and SCC are normal
-Bing-Siebemann dysplasia:
-complete membranous labyrinthine dysplasia
-rare
-most severe membranous abnormality
-Michel malformation:
-disruption of development before 4th week
-most severe abnormality of labyrinthine development
-complete aplasia
-failure of otic vesicle to develop
-disruptions at week:
-4 common cavity (can still be implanted)
-5 cochlear aplasia
-early 6 cochlear hypoplasia (severe)
-late 6 cochlear hypoplasia (mild)
-early 7 incomplete partition of cochlea: Mondini
malformation (severe)
-late 7 incomplete partition: Mondini malformation
(mild)
969
-narrow internal auditory canal
-can indicate failure of development of CN VIII
-if < 3 mm and normal facial function, it is likely that only the facial nerve is present
-this condition is a contraindication to cochlear implantation
970
ANATOMY AND PHYSIOLOGY OF HEARING
EXTERNAL EAR
971
MIDDLE EAR
-impedance matching device: couples low impedance of air to high impedance of fluid filled cochlea
-impedance matching achieved by
1. effective vibratory area of tympanic membrane ~17-20x greater than that of stapes footplate
2. lever action of ossicular chain
-arm of long process of incus shorter by factor of 1.3 than length of manubrium and neck of
malleus
3. shape of tympanic membrane
-transforming ratio:
-22:1 = (17x1.3):1
-results in pressure gain of ~ 25-30 dB
-TM protects round window by allowing a phase difference between sound conducting to the oval
window and sound directly reaching the round window; if sound waves would strike the oval and round
windows simultaneously, the resultant forces would suppress the cochlear fluid wave
972
-resonance frequencies:
-natural frequencies that vibrate a mass with the least amount of force
-concha: 4-6 kHz
-EAC: 2-3 kHz
-TM: 0.8-1.6 kHz
-ossicles: 0.5-2 kHz
-middle ear: 0.8 kHz
COCHLEA
973
-production of endolymph:
-marginal cells of stria vascularis
-dark cells of cristae and maculae of vestibule
-sound transmission and transduction:
-stapes footplate oval window perilymph of scala vestibuli helicotrema (opening at apex
of cochlea) perilymph of scala tympani
-basilar membrane
-0.12 mm wide at base and increases to 0.5 mm at apex
-base more stiff than flexible apex
-organ of Corti
-rests on basilar membrane and osseous spiral lamina
-components:
-outer and inner hair cells
-supporting cells: Deiters, Hensen, Claudius
-tectorial membrane
-reticular lamina-cuticular plate complex
-supporting cells provide structural and metabolic support for organ of Corti
-inner and outer hair cells
-differing morphology and innervation
-spiral ganglion: cell body of auditory nerve, axons to cochlear nucleus in brainstem and
dendrites project through osseous spiral lamina
-50,000 neurons innervate cochlea:
-90-95% synapse directly on inner hair cells (Type I neurons)
-predominantly afferent
-15-20 of these neurons innervate each inner hair cells
-5-10% synapse directly on outer hair cells (Type II neurons)
-predominantly efferent
-each type type II neuron branches to innervate ~ 10 outer hair cells
974
-transduction: displacement of basilar membrane
-basilar membrane stiffer at base than apex - travelling wave progresses from base to apex
-peak or maximum amplitude of basilar membrane displacement varies as function of stimulus
frequency:
-high frequency: max displacement at base
-low frequency: max displacement at apex
-cochlear amplifier:
-activity of outer hair cells that enhances motion of basilar membrane at frequencies near
the best frequency of the particular cochlear location
-out hair cells shorten and lengthen when stimulated by sound
-contributes to fine frequency-selective abilities of ear and sensitivity and ability to detect
extremely faint sounds
-produces the “tuning curve” seen when sound intensity is plotted against
frequency
-notion of cochlear amplification supported by phenomenon of otoacoustic emissions
-stereocilia-hair cell complex
-stereocilia of outer hair cells are in direct contact with tectorial membrane
-deflection of sterocilia by travelling wave opens and closes non-specific ion channels
influx of K depolarization of cell intracellular enzyme cascade (Ca++ mediated)
release of chemical transmitters (glutamate) activate afferent neural fibers
-recruitment:
-loudness in abnormal ear that grows abnormally quickly with intensity once threshold is
reached due to loss of outer hair cells (tips of tuning curve missing)
-four potentials:
-endolymphatic (endocochlear) potential
-cochlear microphonic
-summating potential
-whole-nerve action potential
-endolymphatic potential:
-not generated in response to acoustic stimuli
-DC potential of 80-100 mV recorded in scala media
-arises from stria vascularis
-related to heavy vasculature of stria vascularis and to Na-K-ATPase
-cochlear microphonic:
-alternating AC current
-represents potassium ion current flow though outer hair cells
-waveform mirrors motion of basilar membrane
-summating potential:
-DC potential recorded in response to sound
-largely reflects DC shifts caused by stimulus-driven intracellular potentials of outer hair cells
-represents asymmetry in basilar membrane movement resulting from pressure difference between
scala tympani and scala vestibuli during sound stimulation
-whole-nerve (compound) action potential:
-arises from all-or-none discharge of auditory nerve fibers
975
NONLINEAR PROPERTIES OF THE EAR
-cochlea cochlear nucleus superior olivary complex lateral lemniscus inferior colliculus medial
geniculate body of thalamus auditory cortex (at Sylvian Fissure of Temporal Lobe - Brodmann’s area 41)
-extensive contralateral innervation
976
VESTIBULAR FUNCTION AND ANATOMY
Hair Cells
-stereocilia and kinocilia extend from cell body and in contact with
gelatinous membrane
-bending of hair cells opens K-channels changes resting potential
-two cell body types:
-type I (chalice cells)
-totally engulfed by one afferent terminal
-efferent innervation is indirect with efferent
nerve synapsing on afferent nerve
-type II (cylindrical)
-may have one or more afferent nerve endings on
body of cell
-direct and indirect efferent innervation of hair
cell body
-kinocilium:
-longest and largest hair cell occurring near periphery of
cell body
-polarization vector of hair cells toward kinocilium
-deflection of hair cells toward excitation
-deflection of hair cells away inhibition
977
Semicircular Canals
Pairing of Canals
-functional canal pairs:
-R+L lateral SCCs
-R anterior SCC and L posterior SCC
-L anterior SCC and R posterior SCC
-angular rotation perpendicular to any of these planes produces maximum response from the two canals in
that plane
-operate in push-pull manner:
-movement directed along maximum excitation of one member of the pair produces maximum
inhibition in the other member
Blood supply
-labyrinthine artery (arises from anterior cerebellar artery, superior cerebellar artery or basilar artery)
anterior vestibular artery utricle, posterior and horizontal ampullae
common cochlear artery
proper cochlear artery
vestibulocochlear artery
cochlear ramus
vestibular ramus posterior ampulla, sacculus, utricle, horizontal and
superior ampullae
Otolith Organs
-inertial mass component: calcium carbonate crystals = otoconia
-hair cells project into gelatinous supporting substrate
-each has sensory hair cells arranged in wide variety of orientations of its polarization vectors
-striola: line of orientation of hair cells in the utricle and saccule around which the polarity of the sensory
cells changes 180o
-orientation of polarization vector:
-away from striola in saccular macula; toward striola in utricular macula
978
Afferent Connections
-afferent nerve fibers are bipolar: one synapse at hair cell, other in
vestibular nucleus
-cross-connections are present between right and left vestibular
nuclei
-superior vestibular nerve innervates:
-anterior SCCs
-horizontal SCCs
-utricle
-inferior vestibular nerve innervates:
-posterior SCCs
-saccule
PHYSIOLOGY OF BALANCE
Vestibulospinal Reflex
-otolithic organs modulate the antigravitational muscles in a similar way as the vestibulo-ocular reflex
modulates the eye to allow for postural control
-eg. simultaneous contraction of the extensor muscles with contralateral flexor muscles to maintain posture
-position and motion of muscles and joints may also modify vestibulospinal reflex via receptors found in
intervertebral joint receptors
-anterior SCC:
-excitatory: ipsilateral SR, contralateral IO
-inhibitory: ipsilateral IR, contralateral SO
-horizontal SCC:
-excitatory: ipsilateral MR, contralateral LR
-inhibitory: ipsilateral LR, contralateral MR
-posterior SCC:
-excitatory: ipsilateral SO, contralateral IR
-inhibitory: ipsilateral IO, contralateral SR
979
Caloric Testing
980
BALANCE FUNCTION TESTS
Type of Nystagmus
-gaze
-induced (eg. calorics)
-positional
-spontaneous
981
Positional and Positioning Tests
-patient moved slowly into series of stationary positions with eyes closed and presence or absence of
nystagmus is assessed
-Dix-Hallpike manoeuver used
-torsional nystagmus cannot be measured by ENG
-head hanging:
-right: counterclockwise torsional nystagmus
-left: clockwise torsional nystagmus
-peripheral lesion:
-direction of nystagmus does not change independently of head movement
-central lesion:
-direction-changing nystagmus without an accompanying change in head position
Saccadic System
-latency, maximum velocity, duration, gain (overshoot or undershoot), refixation saccades, glissade
(postsaccadic drift, or slip of the eye) measured
-abnormal saccadic response caused by lesions in cerebellum (dorsal cerebellar vermis), brainstem
(paramedian tontine reticular formation and MLF) or ocular muscles and nerves
-cerebellar lesions saccadic overshoot or undershoot dysmetria
-age, fatigue, lack of attention, sedatives, drug intoxication and other factors can cause slow saccades or
increase latency
Pursuit System
-healthy pts can pursue object moving at velocity of 30 degrees per second
-gain, phase lead or lag, symmetry are measured
-anatomic localization usually not possible
-saccadic pursuit suggests cerebellar disease
-reduced bilateral gain can be caused by brainstem lesion
Optokinetic System
-keeping pt stationary and moving environment
-separating smooth pursuit system and optokinetic system can be difficult
-if lights are extinguished, SP system response drops to zero pts continue to have nystagmus for ~25s
(optokinetic afternystagmus OKAN)
-abnormalities are not site specific
-not routinely used
982
ROTARY CHAIR, SINUSOIDAL HARMONIC ACCELERATION
-evaluates VOR
-pts wired with conventional EOG and fitted with head band with EOG amplifier and rotational velocity
sensor
-pt fixes on stationary target and rotate head in synchrony with auditory cue (max 6 Hz)
-vestibular system evaluated at frequencies more physiologic than ultralow frequencies used in ENG and
rotational chair testing
-clinical value questionable with sensitivity of only 27% and specificity of 85%
DYNAMIC POSTUROGRAPHY
-eliminates visual and somatosensory input and therefore better isolates the vestibular apparatus
-two tests:
-sensory organization test
-movement coordination test
983
-sensory organization test:
-evaluation under six conditions in which sensory and proprioceptive inputs are varied
-anterior and posterior body sway is recorded
984
F.Ling - Balance Function Tests (5)
985
ASSESSMENT OF PERIPHERAL
AND CENTRAL AUDITORY FUNCTION
PHYSICS OF SOUND
Measurements of Intensity
-decibel (dB):
-unit of measurement of sound pressure or intensity based on a logarithmic ratio
-dB = 10 log (Ioutput/Ireference) = 10 log (Poutput2/Preference2) = 20 log (Poutput/Preference)
-I = P2; P = unit of sound pressure level
-Preference = 2x10-4 dyne/cm2
Sound Intensity
-whispered speech ~ 25 dBHL
-conversational speech ~ 40-50 dBHL
-shouting ~80dBHL
Pure-Tone Audiometry
-degree of hearing loss:
-mild: 20-40 dBHL
-moderate: 40-60 dBHL
-moderate-severe: 60-80 dBHL
-severe: 80-100 dBHL
-profound: > 90-100 dBHL
-speech frequencies: 500-4000 Hz
-audiometry uses pure tones at 250, 500, 1000, 4000 and 8000 Hz (octave frequencies); interoctave
frequencies: 3000 and 6000 Hz
-Pure-Tone Average (PTA):
-average hearing thresholds for 500, 1000, and 2000
-typically should be within 10 dB of speech reception threshold
986
-crossover:
-occurs with sounds greater than 40 dBHL
-interaural attenuation for air conduction ~ 50dB for lower frequencies and 60 dB for higher
frequencies
-interaural attenuation for bone conduction assumed to be 0 dB
-masking required to prevent crossover phenomenon
-masking:
-uses “white noise” = narrow band noise for pure-tone signals and speech noise for speech signals
-bilateral ABG of 50 dB cannot be masked (masking dilemma)
-configuration:
-hearing loss as a function of test frequency
-low frequency SNHL: characteristic of endolymphatic hydrops
-high frequency SNHL: characteristic of presbycusis
-bilateral down-sloping high frequency SNHL: characteristic of presbycusis
-Carhart’s Notch: falsely depressed bone conduction peaking at 2000 Hz suggestive of
otosclerosis, secondary to a reduction of the inertial component of bone conduction
-4 kHz Notch (Boilermaker Notch): high frequcny SNHL at 4000-5000 Hz that occurs with NIHL
-Cookie Bite (U-shape): associated with hereditary hearing impairment
-Recruitment:
-increasing signal intensity produces an out-of-proportion perception of loudness
-suggests cochlear hearing loss
-recruitment causes discomfort within a shorter range of the SRT (normally 95 dB above SRT
causes discomfort)
Speech Audiometry
-speech reception threshold (SRT):
-softest intensity level at which pt can correctly repeat words ~50% of the time
-uses spondee words: two syllable words with equal stress on each syllable
-if difference between PTA and SRT exceeds +/- 7 dB - suspect malingering
-speech recognition
-uses phenomes: phonetically balanced words; 25-50 single-syllable words
-phenomes are presented at 30-40 dB above SRT/PTA
-percentage of correct words repeated is recorded
-rollover:
-a paradoxical decrease in discrimination ability with increasing signal intensity
-suggestive of a retrocochlear disorder
987
Tympanometry:
-dynamic recording of middle ear impedance as air pressure in EAC systematically increased or decreased
-classification of middle ear disorders:
-Type A:
-peak in compliance within +50 to -100 mmH2O
-normal
-Type As:
-s = “shallow”: peak compliance less than lower normal limit of compliance
-middle ear impedance abnormally high (stiff):
-otosclerosis, tympanosclerosis
-Type Ad:
-d= “deep”: peak compliance exceeds upper compliance limits
-ossicular disruption, flaccid TM, monomeric TM
-Type B:
-flat
-associated with presence of middle ear fluid
-sometimes seen for perforated TMs
-Type C:
-peak within negative pressure region beyond -100 mmH2O
-eustachian tube dysfunction and inadequate ventilation of middle ear space
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-absence of reflexes:
-minimal CHL (5-10 dB)
-SNHL (>60 dB)
-mild CN VIII impairment (0-40 dB)
-brainstem lesion
-CN VII dysfunction proximal to stapedial branch
-indications:
-asymmetric hearing loss
-unilateral vestibular weakness
-unilateral tinnitus suggestive of
retrocochlear pathology
-high risk children or with failed
auditory screening
-suspected malingerers
-intraoperative monitoring
-diagnosis of peripheral
neuropathies and brainstem lesions
-unaffected by sedation; affected by
phenytoin, lidocaine, diazepam, and
halothane
ABR waves:
-I: compound action potentials from distal
(cochlear end) of eighth CN
-II: proximal end of eighth CN
-III: caudal pons (cochlear nuclei, trapezoid
body, superior olivary complex)
-V: lateral lemniscus as it approaches inferior colliculus
-reproducible absolute latencies for each wave component and relative (interwave) latencies b/n
components are calculated in milliseconds
-latency data assessed for symmetry and compared to appropriate normative data
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-conductive or mixed hearing loss:
-well-formed and clear wave 1 at a
delayed latency value for
maximum stimulus intensity level
-cochlear hearing loss:
-small and poorly formed wave I
-normal interwave latency values
-wave I-V latency value < 4.60 ms
-retrocochlear auditory dysfunction
1. Abnormal interaural wave V
latency difference (IT5)
- > 0.2 msec
-may be relative to size of
tumour
2. Abnormal interaural wave I-
V latency difference (IT1-5)
3. Abnormal III-V latency
difference (IT3-5)
4. Prolonged interwave latency
between I-V(T1-5) or I-III
(T3-5)
5. Increased absolute latency
measurements:
-5.7 msec for wave V
-compared with normal standard
-may not be as accurate since latency may be affected by CHL
Electrocochleography (EcoG)
-indications:
-direct measurement of cochlear and auditory
nerve function
-for intraoperative monitoring of cochlear and
8th nerve status
-diagnosis of Menieres
-three major components:
-cochlear microphonic (CM)
-summating potential (SP)
-compound action potential (AP)
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-> 30% for transtympanic electrode (on promontory)
-Menieres:
-abnormal enlargement of relation b/n component amplitudes of SP and AP; large SP/AP ratio
highly suggestive of endolymphatic hydrops
-tympanic electrode: sensitivity 57%, specificity 94%
P300 response
-oddball paradigm: two stimuli, one frequent predictable stimulus, one rare or deviant stimulus
-pt try to attend to rare stimuli produces large positive peak in 300 ms region
-presumed generators are regions of medial temporal lobe (hippocampus) that are important in auditory
attention
-requires attention to the stimuli
OTOACOUSTIC EMMISIONS
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-occur among 60% of persons with normal hearing
-stimulus-frequency OAE:
-least studied of the evoked OAE
-distortion-product OAE:
-two pure-tone stimuli are presented to the ear simultaneously
-determined by the equation: 2f1-f2
-actual cochlear frequency region assessed is closer to f2 stimulus
-ideally ratio of f1/f2 ~ 0.22
-transiently evoked OAE:
-elicited with brief acoustic stimuli such as clicks or tonebursts
-when outer hair cells are structurally damaged or non functional, OAEs cannot be evoked
-OAE provide information about auditory function at far more frequencies than does an audiogram
-advantage: used in pts with tinnitus and normal audiogram (30% of outer hair cells can be
damaged without affected audiogram)
Test Battery
-auditory evoked responses
-behavioural tests
-dichotic word test, dichotic sentence test, speech-in-competition test, binaural stimulation on one
or more nonspeech measure (pitch pattern sequence and duration pattern tests)
-peripheral auditory function is normal
PSEUDOHYPACUSIS
Shadow curve:
-patient with severe to profound unilateral hearing loss will hear a tone in the opposite or
contralateral ear. The thresholds will mimic those in the better ear but will be reduced by about 50
to 60 dB.
-result is a shadow curve due to cross-over resulting from sound being perceived by the better ear
even through presented to the poorer ear
-failure to show a shadow effect is considered a positive indication of pseudohypoacusis
Stenger test
-based on principle that asymmetry in loudness of only a few decibels will cause any person to
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hear sound only in the louder side
-two acoustic stimuli identical in every way except intensity
-sound presented at 10 dB above threshold in good ear; 10 dB below threshold in poor ear
-if a sound is heard in good ear and patient acknowledges this negative Stenger; pt has genuine
hearing loss
-if pt does not acknowledge that they heard a sound in good ear positive Stenger; suspect
malingering
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ANATOMY OF THE SKULL BASE,
TEMPORAL BONE, EXTERNAL EAR, AND MIDDLE EAR
(Cummings Ch 132)
SKULL BASE
-temporal bone articulates with five other cranial bones: frontal, parietal, sphenoid, occipital, and zygomatic.
Fig. 132-1. Skull base and cervical neurovascular anatomy observed from the right side. The right half of the body
of the mandible has been cut through in the parasagittal plane.
Fig. 132-2. Skull base and cervical neurovascular anatomy seen from the medial side after removal of the
pharyngeal wall.
-Jugular foramen:
-internal jugular vein
-spinal accessory (CN XI), glossopharyngeal (CN IX), and vagus (CN X)
-CN XI is the most posterior of the three nerves, and CN X lies between it and CN IX
-nerves are medial to the internal jugular vein and internal carotid artery at the base of the skull,
but CN X shifts to a position between and posterior to the vessels lower in the neck.
-Stylomastoid foramen:
-facial nerve (CNVII): exits the skull anterior to the digastric notch and slightly posterolateral to the styloid
process
-Carotid canal:
-internal carotid artery enters anterior to the jugular fossa and medial to the styloid process
-Hypoglossal canal:
-between the carotid canal and the styloid process
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-hypoglossal nerve (CN XII) exits
-Foramen spinosum:
-middle meningeal artery enters the middle cranial fossa
-Foramen ovale:
-transmits the mandibular division of CN Vas it passes from the cranial fossa to the infratemporal fossa
TEMPORAL BONE
1. Squamous portion
-articulates with: parietal bone, frontal bone, and greater
wing of the sphenoid bone
-lateral surface defines boundary middle cranial fossa
-sulcus of middle meningeal artery scores medial surface
-caudal portion of bone extends medially to join
superior surface of petrous bone in the region of the
tegmen forms petrosquamous fissure
-forms posterosuperior portion of external auditory
meatus
-the hiatus between tympanic bone and squama
corresponds to notch of Rivinus (incisura typanica)
2. Mastoid portion
-squama forms anterosuperior portion of the mastoid
process
-petrous bone forms posteroinferior parts
-posterosuperior portion of external auditory meatus, is
the (suprameatal) spine of Henle
-pneumatization within the mastoid process varies
-squama of temporal bone forms a lateral wall of the
central air-containing space, the antrum, which
communicates with the middle ear by the aditus
-suprameatal spine and cribriform area provide
important landmarks for surgical access to the antrum -
from the region of the antrum, pneumatization may
extend inferiorly into the tip of the mastoid process,
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where the remnant of the petrosquamous suture may persist as a thin plate of bone, Körner’s septum
3. Petrous portion
-petrous portion of the temporal bone approximately assumes
the configuration of a four-sided pyramid
-within the body of petrous bone is the labyrinth; the internal carotid artery, CN VII, and CN VIII (acoustic and
vestibular portions)
-lateral dimension defines the medial limit of the middle ear cavity
-contains the first turn of the cochlea, or promontory; the dome of the lateral semicircular canal; and the
medial wall of the antrum.
Superoanterior surface
-forms part of the middle cranial fossa
-laterally the bone is fused with the squama and anteriorly it articulates with the sphenoid bone
-foramen lacerum is found between the apex of the petrous bone and the sphenoid bone and contains but
does not transmit the internal carotid artery
-at the bone’s anterior margin, the large wing of the sphenoid bone forms musculotubal canal
-contains the semicanal for tensor tympani and the semicanal of the eustachian tube
4. Tympanic portion
-forms anterior and inferior walls and part of the posterior wall of the external auditory meatus
MIDDLE EAR
The middle ear consists of the tympanic cavity and the osseous
eustachian tube.
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separating the space from the middle cranial fossa. The floor of the
tympanic cavity is a thin layer of bone over the bulb of the internal
jugular vein and an irregular collection of air cells. The posterior
boundary is more complex and contains many important anatomic
landmarks. The posterior wall is close to the mastoid air cell system;
the pyramidal eminence, a bony elevation that transmits the tendon
of the stapedius muscle, is attached to the superior aspect of this
wall. Part of the muscle is contained within the pyramidal process
itself. The chorda tympani nerve enters the tympanic cavity lateral to
the pyramidal process through its foramen, the tympanic opening of
the canal for the chorda tympani. The posterior sinus, or facial
recess, is between the pyramidal process and the chorda tympani
nerve (see Figure 132-6). The incudal fossa, where the posterior
ligament of the incus is attached, is cephalad to the facial recess. The
anterior boundary of the tympanic cavity partly consists of the wall
of the carotid canal, which may be very thin. The tensor tympani
muscle and its semicanal are found superiorly, and the eustachian
tube orifice is found more inferiorly along the anterior wall. The
medial wall consists of the promontory, or basal turn of the cochlea;
the oval and round windows; and the fallopian canal. A ridge of
bone found superiorly—the ponticulus—and a ridge of bone found
inferiorly—the subiculum—divide the medial wall into three main
depressions. The round window niche is inferior to the subiculum,
the oval window niche is superior to the ponticulus, and the
tympanic sinus is medial to the facial nerve between the subiculum
and ponticulus (see Figure 132-7). Inferior to the subiculum in the
round window niche, or fossula of the cochlear window, is the
cochlear window or round window orifice, which is closed by a
fibrous mucosa-covered membrane. Superior to the ponticulus is the
oval window niche, or fossula of the vestibular window, which leads
to the vestibular or oval window. The footplate of the stapes closes
the window. The prominent ridge of bone posterosuperior to the
fossulae contains the facial nerve, and posterosuperior to this
structure is the prominence of the lateral semicircular canal. The
lateral boundary of the tympanic cavity is the membranous wall
formed by the tympanic membrane and its annulus, the bony
tympanic sulcus, and the lateral wall of the epitympanic recess, the
tympanic scutum. The epitympanic recess is a space defined
superiorly by the tegmen tympani, medially by the prominence of the
facial cranial and semicircular canal, laterally by the scutum, and
posteriorly by the incudal fossa.
Click to enlarge
Fig. 132-6. Scanning electron
micrograph of posterior and superior
middle ear taken from a primate shows
the relationship of the facial canal to
the intact ossicular chain, stapedius
tendon, tensor tympani tendon, and
cochleariform process. The facial
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recess is caudal to the incudal fossa,
and the tympanic sinus extends a
variable distance medial to the facial
nerve (cranial nerve VII) in its vertical
segment. The chorda tympani nerve is
shown as it passes between the neck
of the malleus and the long process of
incus to the petrotympanic fissure. The
relationship between the facial recess,
the short process of the incus (outlined
in white), and the facial canal is clearly
shown. (´40.)
Click to enlarge
Fig. 132-7. A, Tympanic cavity,
showing the relationship of the
tympanic sinus to the ponticulus and
subiculum. B, Observation of a
pathologically altered left human
middle ear with a 25° 1.9-mm rigid
endoscope showing the relationship
between the facial nerve (FN) and
recess, round window (RW),
ponticulus (P), sinus tympani
(asterisk), subiculum (S), round
window (RW), and promontory (PR).
The incus and stapedial crura are
absent.
Click to enlarge
Fig. 132-8. Scanning electron
micrograph of mucosa overlying the
center of the promontory in a human.
Many nonciliated cells with surface
microvilli and few ciliated cells are
shown. (´1950.)
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the tympanic membrane, or the pouches of von Troltsch, are formed
from reflections of the anterior and posterior mallear folds among
the ossicles, their ligaments, and the tympanic membrane.
The middle ear cleft communicates with the tympanic antrum via the
aditus ad antrum in the posterosuperior wall of the epitympanic
recess. It is by this route that cholesteatoma extends from the middle
ear cleft into the mastoid cavity. The membranous folds and
pouches may influence the direction and location of spread.
The blood supply of the middle ear and mastoid cavity originates
from the internal and external carotid arteries. The anterior tympanic
artery is a terminal branch of the internal maxillary artery. Two of its
branches supply the bone and mucosa of the superior and lateral
walls of the epitympanic cavity, and a third branch provides the main
blood supply for the malleus and incus (Figure 132-9). Another
branch of the internal maxillary artery, the deep auricular artery,
provides two branches to the vascular ring of the tympanic
membrane. A posterior branch supplies most of the tympanic
membrane, whereas the anterior branch supplies a lesser portion of
the anterior and inferior region.
Click to enlarge
Fig. 132-9. Lateral views of the incus
and malleus show their blood supply
based on the anterior tympanic artery.
Portion of the posterior branch
(between cut ends) has been omitted.
Two arteries originate from the middle meningeal artery: the superior
petrosal and the superior tympanic. The superficial petrosal artery
enters the facial hiatus and divides into two main branches. Both
branches pass within the fallopian canal to provide a major blood
supply to the geniculate ganglion and the facial nerve. The blood
supply to the incudostapedial joint area derives from the superior
and inferior arteries of the stapedius tendon and posterior crural
artery (Figure 132-10). These arteries originate from the arterial
plexus, supplied by the superficial petrosal artery within the fallopian
canal and its anastomosis with a stylomastoid artery. The superior
tympanic artery enters the middle ear adjacent to the lesser petrosal
nerve. The artery supplies the tensor tympani and a portion of the
epitympanic space. It also forms an anastomotic plexus with the
inferior tympanic artery, giving rise to the anterior stapedial artery
and the anterior crural (femoral) artery (see Figure 132-10).
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Click to enlarge
Fig. 132-10. Normal blood supply to
the lenticular process of incus,
incudostapedial joint, and stapes.
The venous drainage from the middle ear cleft is principally via the
lateral sinus, jugular bulb, the petrosal sinuses, the pterygoid plexus
of veins, and the middle meningeal veins.
The sensory root of the facial nerve is the intermediate nerve. Fibers
from this nerve pass anteriorly from the geniculate ganglion as the
greater petrosal nerve or posteriorly within the facial nerve to exit as
the chorda tympani nerve. After exiting the facial hiatus, the greater
petrosal nerve enters the foramen lacerum, where it joins the deep
petrosal nerve to form the nerve of pterygoid canal (vidian nerve).
This nerve traverses the pterygoid (vidian) canal and then the
sphenopalatine ganglion, where the sensory fibers have their cell
bodies. These fibers are distributed to the soft palate and tongue.
Preganglionic secretory fibers from the cell bodies in the superior
salivatory nucleus also end in the sphenopalatine ganglion. Their
corresponding postganglionic fibers innervate the lacrimal gland and
provide secretory innervation to the nasal cavity. Sensory fibers of
the chorda tympani nerve have their cell bodies in the geniculate
ganglion and provide taste sensation to the anterior two thirds of the
tongue. The chorda tympani nerve also carries preganglionic
secretory fibers from cell bodies within the superior salivatory
nucleus, which synapse within the submaxillary ganglion, and then it
provides secretory motor impulses to the submaxillary and
sublingual glands.
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parotid gland via the otic ganglion. Small branches from the
tympanic nerve and lesser petrosal nerve appear to anastomose with
the facial nerve and greater petrosal nerve, respectively, as they
course close to each other within the middle ear cleft and substance
of the petrous bone.
A branch of the vagus nerve and a smaller branch from the inferior
ganglion of the glossopharyngeal nerve join to form Arnold’s nerve
(auricular ramus of the vagus). This nerve and branches of the facial
nerve provide cutaneous innervation to the posterior surface of the
external auditory canal.
Tympanic membrane
Click to enlarge
Fig. 132-11. A, Scanning electron
micrograph of radial fiber distribution
over the umbo viewed from the canal
side after removing the epidermal
layer. (´30.) B, Higher-magnification
electron micrograph of radial fibers.
(´4500.)
Both the pars tensa and pars flaccida consist of three layers: a lateral
epidermis continuous with the skin of the external auditory meatus, a
middle layer or lamina propria, and a medial mucosal layer
continuous with the mucosa of the tympanic cavity. Originally, it was
believed that Shrapnell’s membrane possessed no lamina propria
layer because it appears thinner and more distensible than the pars
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tensa. This is, however, not the case, and the appearance of this
membrane more likely is caused by the organization and content of
the connective tissue within the lamina propria. The lamina propria
of the pars tensa consists of connective tissue fibers arranged in two
basic layers. Outer radial fibers originate from the inferior four fifths
of the handle of the malleus and the umbo and insert into the
tympanic sulcus (see Figure 132-11, A). An inner layer of circular
fibers originates primarily from the short process of the malleus.
Transversely and parabolically oriented fibers intertwine these two
layers. The exact nature of the fibers is unknown; they are probably
neither pure collagen nor elastin (see Figure 132-11, B).
The tympanic nerve and the auricular branch of the vagus nerve
provide part of the nerve supply to the tympanic membrane. The
auriculotemporal branch of the mandibular nerve provides additional
sensory innervation.
Auditory ossicles
The three major auditory ossicles (Figure 132-12) are the malleus,
incus, and stapes. Together with the tympanic membrane and the
ligamentous attachments, the ossicular chain forms the
sound-pressure transformer mechanism of the middle ear. The
malleus is the most lateral of the three ossicles and is attached to the
tympanic membrane, whereas the stapes is attached to the vestibular
window.
Click to enlarge
Fig. 132-12. Articulated ossicles and
dimensions and form of the stapes.
The malleus bones consist of two main parts: the head and the
handle, or manubrium. The head of the malleus occupies a portion
of the upper tympanic space and has a tooth-like process that
articulates with the body of the incus. Between the head and the
elongated handle is the neck of the malleus. The anterior process
projects from the anterior surface of the neck. Opposite and just
inferior to the short process is a roughened area on the handle of the
malleus for the attachment of the tendon of the tensor tympani
muscle. The handle of the malleus is firmly attached to the tympanic
membrane on its lateral surface, giving rise to the mallear stripe (stria
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mallearis). Medially the handle is covered with middle ear mucosa.
The incus resembles a molar tooth. The crown of the tooth, or the
body, articulates with the head of the malleus. The short and long
processes of the incus correspond to the roots of the tooth. The
short process rests in the incudal fossa and is attached by a
ligament. The long process is thinner and more tapered than the
short process and articulates with the head of the stapes. A flattened
bony platform, the lenticular process, sits at the end of the long
process at the point of articulation.
The stapes bone is shaped like a stirrup and consists of two legs, the
anterior and posterior crura, and a footplate, which is attached by
an annular ligament to the margins of the vestibular window. The
two crura are joined superiorly at the head, which articulates with
the lenticular process of the incus. Each leg resembles a trough, with
the concave surfaces facing each other. Of the two legs, the anterior
crus is more delicate and less curved. On the posterior crus is a
roughened area in the region of the head for the attachment of the
tendon of the stapedius muscle. Cartilage covers the articulating
surface of the head.
Six ligaments support the ossicles within the tympanic cavity. The
anterior ligament of the malleus extends from the angular spine of the
sphenoid bone through the petrotympanic fissure to insert on the
neck of the malleus. The superior mallear ligament extends from the
upper tegmen tympani to insert on the head of the malleus. The
lateral mallear ligament extends from the neck of the malleus to the
upper edge of the notch of Rivinus. The superior incudal ligament
passes from the tegmen tympani to the body of the incus, whereas
the ligament of the short process passes from the incudal fossa to
the floor of the antrum. The annular ligament of the stapes attaches
the footplate to the margins of the vestibular window.
1003
malleus and incus. Many vessels pass through the ossicular complex
along the tendon of the stapedius muscle, first to the stapes and then
laterally to the incus and malleus. Other vessels pass directly from
the facial canal to the stapes.
Eustachian tube
Facial nerve
Click to enlarge
Fig. 132-13. A, Scanning electron
micrograph of the facial nerve in the
region of the fissula of the vestibular
window taken from a primate. The
facial nerve sheath is composed of
fibrous epineurium, vascular connective
tissue, and periosteum, which has been
removed with bony facial canal.
NF-nerve fibers. (´255.) B,
Higher-magnification electron
micrograph shows individual nerve
fibers invested by connected tissue
fibers making up the endoneurium.
Fibers appear to be hollow tubes
formed by the Schwann cell myelin
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sheath. Axoplasmic remnants (A) are
seen within some tubules. An
occasional Schwann cell nucleus
(asterisk) is seen bulging from within
the myelin sheath. (´3375.)
As it curves around the oval window niche, the nerve begins its
vertical segment anterior and inferior to the lateral semicircular canal.
In the region of the oval window niche, the facial nerve lies within
the medial wall of the tympanic cavity, where the bone of the facial
canal is very thin. The nerve may be in direct contact with the
mucosa of the tympanic cavity by dehiscences in the facial canal in
50% to 60% of healthy petrous bones. As the nerve begins its
vertical segment, it passes lateral to the tympanic sinus, which
extends a variable distance medial to the nerve.
As the facial nerve enters its vertical portion, it is medial to the short
process of the incus and lateral to the stapedius muscle. Inferior to
the short process of the incus, the facial sinus cells are delineated
superiorly by the incudal fossa, medially by the facial canal, and
laterally by the chorda tympani nerve. The facial recess within the
posterior wall of the tympanic cavity also may be called the
suprapyramidal process because of its relationship to the
pyramidal eminence.
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NEUROPHYSIOLOGIC INTRAOPERATIVE MONITORING
Electrocochleography
-near field technique
-wide-band click composed of many frequencies that stimulate the entire cochlea
-monitors cochlear microphonic and summating potential and eighth-nerve action potentials arising from a
stimulus
-cochlear microphonic:
-alternating current response generated by hair cells of organ of Corti
-summating potential:
-can represent asymmetry in basilar membrane caused by pressure differences between
the scala media and scala vestibuli that indicate changes in the endolymphatic fluid
-compound action potential:
-representative of responses from basal turn of the cochlea
-N1 latency is inversely related to stimulus rate; amplitude is directly related to stimulus rate
-EcoG can best sense changes in cochlear blood supply
-reduced amplitude or loss of ECochG action potential indicates injury to labyrinthine (internal
1006
auditory) artery
-decreased amplitude, or prolonged latency, of N1 or the cochlear microphonic has been associated with
postoperative hearing loss
-disadvantages:
-transtympanic needle placement
-may not be sensitive to medial intraoperative changes within the CPA
-may not be useful in detection of intraoperative damage or manipulation of the cochlear nerve
1007
INTRAOPERATIVE FACIAL NERVE MONITORING
1008
IMAGING STUDIES OF THE TEMPORAL BONE
1009
EXTERNAL AUDITORY CANAL
Benign Neoplasms
-EAC cholesteatomas usually present with focal bony erosion of bony ear canal
-CT will show soft tissue filling EAC with adjacent smooth bony erosion
-Keratosis obturans:
-abnormal epithelial migration of TM though to be responsible
-most pts present with otalgia, CHL and otorrhea
-CT demonstrates significantly diffuse widening of EAC
Malignant Neoplasms
-SCC:
-associated with irregular bony erosion or destruction of bony canal wall
-tumours involving cartilaginous lateral third of EAC can easily extend anteriorly through fissure
of Santorini to the parotid gland
1010
Infectious and Inflammatory Diseases
Inflammatory Disease
-because all pneumatized spaces of temporal bone are contiguous, OM involves inflammation in other
three regions of pneumatization (mastoid, perilabyrinthine and petrous apex)
-pneumatized areas in temporal bone pacified but integrity of mastoid bony septae, ossicular chain
and mastoid cortex would be intact
-coalescent mastoiditis:
-mastoid cavity filled with granulation tissue
and bony septae undergo enzymatic bony
resorption
-subperiosteal abscess can develop as a
result of direct inflammatory extension
through thin trabecular bone in lateral
mastoid cortex
-Bezold abscess:
-inflammatory debris erodes
mastoid tip medial to insertion of
SCM abscess in upper neck
-can spread via direct extension,
hematogenous spread or by retrograde
thrombophlebitis
sigmoid dural venous sinus
thrombosis, abscesses and
meningitis (most common
intracranial complication of AOM)
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-petrositis:
-Gradenigo triad: retroorbital pain, sixth nerve
palsy, chronic otorrhea
-CT: opacified petrous apex cells with lysis of bony
septae
-MRI: peripheral meningeal enhancement at petrous
apex as adjacent dura becomes thickened and covered
with granulation tissue
-cholesterol granulomas:
-caused by trapped chronic inflammatory mucosal
secretions within pneumatized petrous apex
-encapsulated cystic lesion filled with brownish liquid
containing cholesterol clefts
-clinical presentation: hearing loss, tinnitus,
hemifacial spasm and cranial nerve deficits
-MRI: high signal intensity in both T1 and T2
-cholesteatoma:
-MRI: -T1: isointense with brain
-T2: hyperintense
Cholesteatoma
-sac lined by keratinizing stratified squamous epithelium that gradually enlarges in air spaces inside middle
and mastoid cavity
-pars flaccida cholesteatomas:
-begin in Prussak space, between lateral attic wall and head of malleus
-usually erode lateral attic wall (scutum)
-extend posteriorly to involve posterolateral attic and antrum
-pars tensa cholestatomas:
-originate form postero-superior retraction and progress posteriorly to involve facial recess and
sinus tympani
-bony erosion:
1012
-ossicular chain destruction:
-long process of incus > body of incus > head of malleus
-labyrinthine fistula
-most common site is lateral semicircular canal
-cochlear fistula at promontory area
-facial paresis
-imaging:
-MRI: -T1: nonspecific signal intensity with some rim enhancement after contrast
-granulation tissue will enhance whereas cholesteatoma will not
-T2: moderately hyperinse
-glomus tympanicum:
-most common primary tumour of middle ear
-originates from glomus bodies along Jacobson’s
nerve (a branch of glossopharyngeal nerve) and
rarely from Arnold’s branch (vagus nerve)
-will enhance intensively after administration of
contrast in both CT and MRI
-congenital cholesteatoma:
-rare tumour
-arises from aberrant epithelial embryonic rests
left behind in middle ear
-propensity of its occurrence in anterosuperior
middle ear near eustachian tube opening
INNER EAR
Congenital Anomalies
-membranous labyrinth originates from neuroectodermal-derived otic placode starting in 4th GA
-formation of entire membranous labyrinth with 2.5-2.75 cochlear tumours is complete by 8th week
-otic capsule grows and ossifies to its full adult size by 24th week
-majority of congenital SNHL are limited to membranous labyrinth (80%) majority of pts have normal
CTs
-bony labyrinthine deformities (20%) believed to be d/t developmental defect between 4th and 8th weeks of
gestation
-Michel aplasia:
-absence of entire inner
ear including
vestibulocochlear nerve
-d/t arrested development
of otic placode during 3rd
GA
-common cavity deformity:
-d/t arrested development
in 4th and 5th GA
1013
-cochlear aplasia arrest in 5th week
-cochlear hyperplasia arrest in 6th week
-Mondini deformity:
-developmental arrest during 7th GA
-only 1.5 turns of cochlea with absence of interscalal septum between apical and middle
turns
1014
Inflammation of Inner Ear
-labyrinthitis:
-postcontrast T1 MRI demonstrates diffuse abnormal enhancement of the normally nonenhancing
labyrinth
-in haemorrhagic labyrinthitis, T1 images show increased signal intensity within labyrinth
-chronic labyrinthitis fibrous tissue fills membranous labyrinth (seen on T2)
-abnormal bone formation within membranous labyrinthine space labyrinthitis ossificans
Neoplasms
-intralabyrinthine schwannoma
-rare
-Meniere-like symptoms of recurrent vertigo and hearing loss
OTODYSTROPHIES
-otosclerosis:
-otospongiosis
-enchondral bone around otic capsule is replaced by multiple foci of spongy vascular irregular
bone spongy bone later becomes calcified and sclerotic
-commonly involved site is anterior oval window region (fistula ante fenestrum)
-“double ring sign”: CT appearance of otic capsule along basilar turn of cochlea
1015
-obliterative otosclerosis new bone formation
limited to round window and basilar turn of cochlea
-osteogenesis imperfecta:
-all or part of otic capsule can be demineralized,
similar to cochlear otosclerosis, but is more severe
Neoplasms
Inflammation
-Bell’s palsy caused by HSV I infection
-MRI demonstrates a linear uniformly enhancing facial nerve from distal IAC to mastoid segment
on contrast
-MR evaluation indicated in pts with facial paralysis persisting beyond 2 months, recurrent palsy
or slowly progressive palsy
1016
VASCULAR ANOMALIES AND DISEASES
Vascular Neoplasms
-paraganglioma:
-most common cause for objective pulsatile
tinnitus and a vascular hypotympanic mass
-MRI: enhances on T1 “salt and pepper”
appearance d/t flow voids
-glomus jugulare:
-supplied mostly by ascending pharyngeal
artery
-some contributions from posterior
auricular and occipital arteries
1017
-benign intracranial hypertension (pseudotumour cerebri)
-can also cause subjective pulsatile tinnitus
-MRI to r/o significant intracranial mass (none)
-LP to confirm and relieve elevated CSF pressure
-other causes of pulsatile tinnitus:
-arteriosclerosis, fibromuscular dysplasia, arterial dissection, arteritis
-IAC contents: vestibulocochlear nerve, facial nerve, nervus intermedius, labyrinthine artery, sometimes a
loop of AICA
Neoplasms
-meningioma
-second most common CPA tumour
-10% of all CPA tumours
-trigeminal neuropathy more common
-MRI: T1: isointense to brain; enhance intensely and homogeneously post-contrast
T2: isointense or hyperintense
1018
Congenital Lesions
-epidermoid cyst:
-third most common lesion of CPA
-MRI: T1: hypointense; no enhancement
T2: hyperintense
-arachnoid cysts:
-MRI: T1: low intensity
T2: high intensity
-lipoma:
-presumed to arise as a result of maldifferentiation of meningeal precursor tissues
-CT and MRI show fat-containing lesion in CPA
-CT: -dark
-MRI: T1: bright
T2: dark
Inflammatory
-granulomatous processes such as sarcoidosis can involve IAC and CPA
-postcontrast T1 images abnormal leptomeningeal thickening and enhancement
Vascular Lesions
1019
IMAGING STUDIES OF THE TEMPORAL BONE
1020
EXTERNAL AUDITORY CANAL
Benign Neoplasms
-EAC cholesteatomas usually present with focal bony erosion of bony ear canal
-CT will show soft tissue filling EAC with adjacent smooth bony erosion
-Keratosis obturans:
-abnormal epithelial migration of TM though to be responsible
-most pts present with otalgia, CHL and otorrhea
-CT demonstrates significantly diffuse widening of EAC
Malignant Neoplasms
-SCC:
-associated with irregular bony erosion or destruction of bony canal wall
-tumours involving cartilaginous lateral third of EAC can easily extend anteriorly through fissure
of Santorini to the parotid gland
1021
Infectious and Inflammatory Diseases
Inflammatory Disease
-because all pneumatized spaces of temporal bone are contiguous, OM involves inflammation in other
three regions of pneumatization (mastoid, perilabyrinthine and petrous apex)
-pneumatized areas in temporal bone opacified but integrity of mastoid bony septae, ossicular
chain and mastoid cortex would be intact
-coalescent mastoiditis:
-mastoid cavity filled with granulation tissue
and bony septae undergo enzymatic bony
resorption
-subperiosteal abscess can develop as a
result of direct inflammatory extension
through thin trabecular bone in lateral
mastoid cortex
-Bezold abscess:
-inflammatory debris erodes
mastoid tip medial to insertion of
SCM abscess in upper neck
-can spread via direct extension,
hematogenous spread or by retrograde
thrombophlebitis
sigmoid dural venous sinus
thrombosis, abscesses and
meningitis (most common
intracranial complication of AOM)
1022
-petrositis:
-Gradenigo triad: retroorbital pain, sixth nerve
palsy, chronic otorrhea
-CT: opacified petrous apex cells with lysis of bony
septae
-MRI: peripheral meningeal enhancement at petrous
apex as adjacent dura becomes thickened and covered
with granulation tissue
-cholesterol granulomas:
-caused by trapped chronic inflammatory mucosal
secretions within pneumatized petrous apex
-encapsulated cystic lesion filled with brownish liquid
containing cholesterol clefts
-clinical presentation: hearing loss, tinnitus,
hemifacial spasm and cranial nerve deficits
-MRI: high signal intensity in both T1 and T2
-cholesteatoma:
-MRI: -T1: isointense with brain - non-enhancing
-T2: hyperintense
Cholesteatoma
-sac lined by keratinizing stratified squamous epithelium that gradually enlarges in air spaces inside middle
and mastoid cavity
-pars flaccida cholesteatomas:
-begin in Prussak space, between lateral attic wall and head of malleus
-usually erode lateral attic wall (scutum)
-extend posteriorly to involve posterolateral attic and antrum
-pars tensa cholestatomas:
-originate from postero-superior retraction and progress posteriorly to involve facial recess and
sinus tympani
1023
-bony erosion:
-ossicular chain destruction:
-long process of incus > body of incus > head of malleus
-labyrinthine fistula
-most common site is lateral semicircular canal
-cochlear fistula at promontory area
-facial paresis
-imaging:
-MRI: -T1: nonspecific signal intensity with some rim enhancement after contrast
-granulation tissue will enhance whereas cholesteatoma will not
-T2: moderately hyperintense
-glomus tympanicum:
-most common primary tumour of middle ear
-originates from glomus bodies along Jacobson’s
nerve (a branch of glossopharyngeal nerve) and
rarely from Arnold’s branch (vagus nerve)
-will enhance intensively after administration of
contrast in both CT and MRI
-congenital cholesteatoma:
-rare tumour
-arises from aberrant epithelial embryonic rests
left behind in middle ear
-propensity of its occurrence in anterosuperior
middle ear near eustachian tube opening
INNER EAR
Congenital Anomalies
-membranous labyrinth originates from neuroectodermal-derived otic placode starting in 4th GA
-formation of entire membranous labyrinth with 2.5-2.75 cochlear turns is complete by 8th week
-otic capsule grows and ossifies to its full adult size by 24th week
-majority of congenital SNHL are limited to membranous labyrinth (80%) majority of pts have normal
CTs
-bony labyrinthine deformities (20%)
believed to be d/t developmental defect
between 4th and 8th weeks of gestation
-Michel aplasia:
-absence of entire
inner ear including
vestibulocochlear
nerve
-d/t arrested
development of otic
placode during 3rd
GA
1024
-common cavity deformity:
-d/t arrested development in 4th and 5th GA
-cochlear aplasia arrest in 5th week
-cochlear hypoplasia arrest in 6th week
-Mondini deformity:
-developmental arrest during 7th GA
-only 1.5 turns of cochlea with absence of interscalal septum between apical and middle
turns
1025
Inflammation of Inner Ear
-labyrinthitis:
-postcontrast T1 MRI demonstrates diffuse abnormal enhancement of the normally nonenhancing
labyrinth
-in haemorrhagic labyrinthitis, T1 images show increased signal intensity within labyrinth
-chronic labyrinthitis fibrous tissue fills membranous labyrinth (seen on T2)
-abnormal bone formation within membranous labyrinthine space labyrinthitis ossificans
Neoplasms
-intralabyrinthine schwannoma
-rare
-Meniere-like symptoms of recurrent vertigo and hearing loss
OTODYSTROPHIES
-otosclerosis:
-otospongiosis
-enchondral bone around otic capsule is replaced by multiple foci of spongy vascular irregular
bone spongy bone later becomes calcified and sclerotic
-commonly involved site is anterior oval window region (fistula ante fenestrum)
-“double ring sign”: CT appearance of demineralization of otic capsule along basilar turn of
cochlea
1026
-obliterative otosclerosis new bone formation
limited to round window and basilar turn of cochlea
-osteogenesis imperfecta:
-all or part of otic capsule can be demineralized,
similar to cochlear otosclerosis, but is more severe
Neoplasms
Inflammation
-Bell’s palsy caused by HSV I infection
-MRI demonstrates a linear uniformly enhancing facial nerve from distal IAC to mastoid segment
on contrast
-MR evaluation indicated in pts with facial paralysis persisting beyond 2 months, recurrent palsy
or slowly progressive palsy
1027
VASCULAR ANOMALIES AND DISEASES
Vascular Neoplasms
-paraganglioma:
-most common cause for objective pulsatile
tinnitus and a vascular hypotympanic mass
-MRI: enhances on T1 “salt and pepper”
appearance d/t flow voids
-glomus jugulare:
-supplied mostly by ascending pharyngeal
artery
-some contributions from posterior
auricular and occipital arteries
1028
-benign intracranial hypertension (pseudotumour cerebri)
-can also cause subjective pulsatile tinnitus
-MRI to r/o significant intracranial mass (none)
-LP to confirm and relieve elevated CSF pressure
-other causes of pulsatile tinnitus:
-arteriosclerosis, fibromuscular dysplasia, arterial dissection, arteritis
-IAC contents: vestibulocochlear nerve, facial nerve, nervus intermedius, labyrinthine artery, sometimes a
loop of AICA
Neoplasms
-meningioma
-second most common CPA tumour
-10% of all CPA tumours
-trigeminal neuropathy more common
-MRI: T1: isointense to brain; enhance intensely and homogeneously post-contrast
T2: isointense or hyperintense
1029
Congenital Lesions
-epidermoid cyst:
-third most common lesion of CPA
-MRI: T1: hypointense; no enhancement
T2: hyperintense
-arachnoid cysts:
-MRI: T1: low intensity
T2: high intensity
-lipoma:
-presumed to arise as a result of maldifferentiation of meningeal precursor tissues
-CT and MRI show fat-containing lesion in CPA
-CT: -dark
-MRI: T1: bright
T2: dark
Inflammatory
-granulomatous processes such as sarcoidosis can involve IAC and CPA
-postcontrast T1 images abnormal leptomeningeal thickening and enhancement
Vascular Lesions
1030
INFECTIONS OF THE EXTERNAL EAR
OTITIS EXTERNA
-acute OE:
-usually begins with itching instrumentation with Q-tip or fingernail
-removal of protective lipid film allows proliferation of bacteria “itch-scratch cycle”
-rapid bacterial growth purulent discharge
-may progress to subacute to chronic forms
History
-pain, fullness, itching, hearing loss
Bacteriology
-Pseudomonas aeruginaosa, Proteus mirabilis, staphylococci, streptococci, and various gram-negative
bacilli
-swabs usually taken for recalcitrant infections
Staging
-Senturia et al:
-preinflammatory
-acute inflammatory: mild, moderate or severe
-chronic inflammatory
-preinflammatory:
-stratum corneum becomes edematous d/t removal of protective lipid layer
-plugging of apopilosebaceous unit
-pt feels sense of fullness or itching
-acute inflammatory:
-pain and tenderness of auricle
-mild: mild erythema and minimal edema with small amount of cloudy secretion
-moderate: thicker more profuse exudate
-severe: increased pain and obliteration of lumen with profuse greenish-grey purulent exudate
1031
-chronic inflammatory:
-less pain but more profound itching for a longer period
-mild edema of canal skin may extend to skin of concha secondary changes:
-eczematization, lichenification and superficial ulceration
Differential Diagnosis
-necrotizing otitis externa
-bullous external otitis
-granular external otitis
-perichondritis
-chondritis
-relapsing polychondritis
-furunculosis
-carbunculosis
-other dermatomes: eg. psoriasis and seborrheic dermatitis
Natural History
-acute: spread of infection to adjacent preauricular tissues, face and neck
-may progress to perichondritis, chondritis, cellulitis, erysipelas
-chronic: excoriation canal skin becomes lichenified complete obliteration of canal
Medical Treatment
-fundamentals:
-frequent and thorough cleaning
-judicious use of appropriate antibiotics
-treatment of associated inflammation and pain
-recommendations regarding prevention of future infections
-in absence of purulence - brief course of acidifying drop efficacious in discouraging bacterial or fungal
growth
-antibiotic drops:
-Cortisporin: neomycin-hydrocortisone
-Cipro HC
-Moderate Stage:
-insert wick and instill drops on it expands and presses soft tissues and periosteum toward
nondistracted position may also relieve pain
-antibiotic drops continues for 2-3 days after cessation of pain
-oral antibiotics in mild and moderate stages is of no proven value
-Severe Stage:
-add oral antibiotics with broad-spectrum coverage for 10-14 days
-antistaphylococcal penicillins, 1o cephalosporins, antipseudamonal fluoroquinolones
(ciprofloxacin, levofloxacin, gatifloxacin)
-fluoroquinolones contraindicated in pts under age 18
-warm compresses and local wound care
-Chronic Stage:
-repeated cleaning and instillation of antibiotics and steroids
-triamcinolone acetonide 0.25% cream or ointment (Kenalog)
-dexamethasone sodium phosphate 0.1% (Decadron, Pred Forte 1%) ophthalmic drops
-avoid placing FB in ear canal
-may try acidifying drops: 1:1 vinegar:water or ethyl alcohol:water
1032
Surgical Management of Hypertrophic Chronic Otitis Externa
-when local measures are insufficient to eradicate infection must remove involved canal skin and any
adjacent involved cutaneous or cartilaginous tissue
-rarely required but performed through postauricular incision
-wide meatoplasty
-canal resurfaced with STSG
Diagnosis
-four salient features:
-persistent severe otalgia for longer than 1 month
-persistent purulent otorrhea with granulation tissue for several weeks
-diabetes mellitus, another immunocompromised state or advanced age
-cranial nerve involvement
1033
Medical Treatment
-control underlying medical condition if possible (eg. diabetic control)
-obtain cultures
-otic drops
-anti-Pseudomonas antibiotics for 6 weeks or more
-eg. 3rd generation cephalosporin (ceftazidime) + quinolone (ciprofloxacin)
-eg. pip/tazo +gentamycin or tobramycin or amikacin
-eg. imipenem or meropenem
-eg. gentamicin or tobramycin +/- ticarcillin or piperacillin
-eg. mezlocillin or azlocillin
-eg. ceftazidime, imipenem, aztreonam, amikacin, norfloxacin, ciprofloxacin
-must continue on antibiotics despite improvement of symptoms
-regular debridement
-other:
-HBO: thought to facilitate osteoneogenesis and promote repair of diseased bone; value
questionable
-indications of improvement:
-resolved otalgia
-resolution of granulation tissue
-improved gallium scan
Surgical Treatment
-controversial
-reserved for pts who do not respond to conventional therapy
-excision of underlying necrosis and replace it with vascularized tissue
-wide local excision of infected cartilage and soft tissues
-middle ear exploration
-mastoidectomy
-facial nerve decompression
-temporal bone resection if no response
Complications
-cranial neuropathy
-meningitis, brain abscess and death
-overall mortality:
-37% before introduction of Abx; 23% afterward
-60% if multiple cranial nerve involvement
1034
Granular External Otitis
-resembles earliest stage of NEO
-loss of TM for more than 1 month without middle ear disease
-pathogens: S. aureus, S. epidermidis, P. aeruginosa
-usually resolve with conventional treatment
-oral antibiotics if infection extends beyond canal
Relapsing Polychondritis
-intermittently progressive disease marked by inflammatory destruction of cartilage
-cartilage of external ear, larynx, trachea, bronchi, nose may be involved
-fever, anemia, erythema, swelling, pain and elevated ESR
-diagnosis based on hx and p/e supported by elevated ESR
-tx: oral corticosteroids
Otomycosis
-fungal infection of skin of EAC
-Aspergillus sp. most common (A. niger, A. flavum, A. fumigatus, A. albicans; C. albicans)
-pruritus
-white, black or dotted gray membrane
-treatment:
-acidifying solutions:
-aluminum sulfate-calcium acetate (Domeboro)
-boric acid
-Castellani’s paint (acetone, alcohol, phenol, fuschin, resorcinol)
-clotrimazole cream or solution (Lotrimin)
-powders (in TM perforations):
-Metacresyl acetate (Cresylate) painted on margin of perforation
-nystatin powder
-gentian violet
-fungizone powder (amphotericin B)
-chloromycetin-sulfanilamide-tinactin (tolnaftate)
1035
-?surgical decompression if facial nerve affected
-acyclovir, famcyclovir, valacyclovir ameliorate herpetic infections
-famcyclovir reduces duration of postherpetic neuralgia
Dermatoses
-allergic and irritant contact dermatomes
-erythema, weeping and vesiculation accompanied by itching
-tx: removal of causative agent and use of topical steroids and astringents
Psychocutaneous Diseases
-primary essential pruritus, neurodermatitis, delusions of parasitosis, factitial dermatitis
Keratitis Obturans
-cholesteatoma of EAC
-bony erosion of external auditory canal
-frequently associated with COPD, bronchiectasis, sinusitis
-tx: debridement
1036
NEOPLASMS OF THE EAR AND LATERAL SKULL BASE
Paraganglioma
Origins
-arise from glomus bodies that occur in:
-adventitia of jugular bulb
-along tympanic branch of CN IX (Jacobson nerve)
-along auricular branch of vagus nerve (Arnold nerve)
Histology
-clusters (zellballen) of chief cells containing norepinephrine and dopamine
-arise from neural crest cells
-lack affinity for chromium salts “nonchromaffin paraganglia”
-only 1-3% actually secrete norepeinephrine
Epidemiology
-whites
-L>R
-F:M = 6:1
-peak incidence: 5th decade
-multicentric in 5%; if secondary to AD disorder 50% multicentricity
-metastases uncommon (3-4%): lymph nodes, lungs, liver, spleen and bone
Clinical Manifestations
-glomus tympanicum
-originate on promontory of cochlea
-conductive hearing loss and pulsatile tinnitus most common
-otalgia or bloody otorrhea
-multiple cranial neuropathies
-reddish pulsatile mass medial to inferior TM:
-Brown Sign: positive pressure during pneumatic otoscopy causes blanching of mass
-Aquino Sign: diminished pulsations with ipsilateral carotid artery compression
-objective tinnitus with auscultation
-glomus jugulare
-arise in jugular fossae
-jugular foramen syndrome (Vernet syndrome); + Horner’s = Villaret syndrome
-erosion of jugular fossa anteriorly and superiorly exposes petrous carotid artery and allows
tumour to invade middle ear CHL and pulsatile tinnitus
-intracranial extension can occur
Investigations
-24h urine vanillylmandellic acid and metanephrine if symptomatic (flushing, diarrhea, palpitations,
headaches, orthostasis, perspiration)
-CT temporal bones (high resolution)
-erosion of caroticojugular spine usually indicates glomus jugulare tumour
-MRI to evaluate intracranial extension
1037
-vascular flow voids: salt and pepper appearance
-four vessel angiography
-for pre-operative planning
-pre-operative embolization to decrease intraoperative blood loss
Treatment
-complete surgical excision
-secreting tumours treated with adjunctive alpha- and beta-blockade
-glomus tympanicum:
-transcanal or hypotympanotomy approach
-extended facial recess approach
-glomus jugulare:
-transmastoid-transcervical exposure +/- facial nerve rerouting (Fisch A) or formal infratemporal
fossa dissection
-(see Vascular Tumours in Head and Neck Oncology section)
-XRT available but has little effect on primary tumour cells
-causes obliterative endarteritis in the vessels and controls rate of tumour growth
Epidermoid (Cholesteatoma)
-see Cholesteatoma notes
-most lesion of petrous apex and CPA are thought to be of congenital origin
-squamous metaplasia within temporal bone or intradural space proposed histogenesis
-developmental entrapment of ectodermal rests is more likely the cause
-slow infiltrative growth
-manifestations usually facial weakness, diminished facial sensation or facial pain
-histology:
-cyst lined with benign keratinizing squamous epithelium
-three components: sac or epithelial matrix, perimatrix, contents of cyst
-diagnosis:
-CT: well-defined homogeneous mass that contains areas of calcification
-MRI: low-signal intensity on T1; high signal intensity on T2; non-enhancing
-treatment:
-complete surgical excision by posterior fossa craniotomy
-complete excision difficult; 30% recurrence
-hemangiopericytoma:
-rare vascular tumour derived from pericytes
-metastatic spread in 50% lungs and bone
-treatment: wide excision; XRT and chemotx for extensive, recurrent or inoperable tumours
1038
Lymphoma, Plasmacytoma and Leukemia
-lymphoma:
-primary or metastatic
-conductive hearing loss, otalgia, otorrhea, fevers, facial nerve weakness, sensorineural hearing
loss
-treatment: chemotherapy and/or XRT
-extramedullary plasmacytoma:
-rare in temporal bone
-histology: sheets of monotonous round cells typical of plasma cells
-serum and urine analysis with monoclonal antibodies r/o multiple myeloma
-chemotherapy or XRT
-leukemia:
-marrow spaces in temporal bone infiltrated by leukemic cells
Cutaneous Carcinoma
1039
Glandular Tumours
-rare tumours of EAC
-ceruminous adenoma:
-arise from ceruminous glands
-well-differentiated proliferating ceruminous glands that form solid, cystic, and papillary patterns
-ceruminous adenocarcinoma:
-invasive; metastasis to regional lymph nodes
-pleomorphic adenoma
-invasive malignant tumours can extend radially through auricular cartilage and the fissures of Santorini
into the parotid gland or into surrounding periauricular tissue
-treatment:
-benign tumours: wide local excision
-malignant tumours:
-lateral temporal bone resection with parotidectomy and postoperative radiation +/-
cervical lymph node dissection for larger lesions
-osteoma:
-solitary pedunculate osseous lesions that originate on tympanosquamous and tympanomastoid
suture lines inside bony EAC
-if large CHL +/- OE
-removed with drill +/- STSG
-exostoses:
-broad-based osseous lesions that occur around circumference of medial aspect of bony EAC
-occurrence strongly associated with exposure to cold water
-postauricular approach; facial nerve at risk during drilling of posteroinferior aspect of bony canal
1040
-auricular endochondrial pseudocysts
-cyst-like degenerations of auricular cartilage
-from recurrent minor trauma
Adenomatous Tumours
-eosinophilic granuloma
-unifocal bony lesion - frontal and temporal bones, mandible
-histology: localized collection of histiocytes and polygonal and sheet formation
-dx: bone scan and open biopsy
-tx: surgical excision with XRT for recurrence
1041
-Hand-Schueller-Christian disease
-chronic disseminated form of LCH
-classic symptoms:
-chronic otorrhea
-diabetes insipidus
-exophthalmos
-polyostotic lesions: “punched-out” or “moth-eaten” appearance
-involvement of abdominal viscera and cutaneous lesions
-tx: vinblastine and corticosteroids or XRT
-Letterer-Siwe disease
-HSM, lymphadenopathy, bleeding diathesis, anemia, cutaneous lesions, generalized hyperplasia
of macrophages
-acute disseminated form of LCH
-highly fatal
-tx: chemotherapy
Sarcomas:
-exceptionally rare; in children however: most common primary malignancy of temporal bone
-rhabdomyosarcoma:
-30% of sarcomatous lesions (most common)
-80% pts <12 ya
-originate from pleuripotential mesenchymal cells in middle ear and eustachian tube
-histological subtypes:
-embryonal
-most common
-small round and spindle-shaped primitive mesenchymal cells in loose myxoid
or compact pattern
-botryoid
-alveolar
-sheets of round, oval, or straplike cells arranged in trabecular pattern
surrounding empty alveolar compartments
-pleomorphic
-anaplastic multinucleated spindle cells that form whorls and fascicles with
longitudinal striations
-dx: biopsy
-tx: limited surgical intervention, XRT and chemotherapy
-survival rarely exceeds 50%
-chondrosarcoma:
-petroclival region near foramen lacerum and petrous apex most common location of origin
-present with multiple CN neuropathies
-surgical excision primary therapy; recurrences common - resistant to XRT and chemotx
1042
Chordomas
-low- to intermediate-grade malignancies that result from defective embryonic remnants of notochord
-occurs in clivus but also as primary intracranial or nasopharyngeal soft tissue tumour
-histology:
-stellate, intermediate and vacuolated physaliphorus or soap-bubble cells in mucoid matrix
growing in nests, cords, or trabeculae
-stains positive for cytokeratin
-slow growing; metastasis unusual
-headache, diplopia and visual deficits common
-imaging:
-enhances with contrast
-CT scan:
-bony erosion of clivus or basiocciput in midline
-MRI:
-high signal on T1; low signal on T2
-tx: -surgical excision via transoral-transpalatal or infratemporal fossa approach
-recurrence common
-dermoids:
-rare cystic lesions in temporal bones
-thought to originate at point where 1st branchial cleft (anlage of EAC) lies adjacent to 1st
branchial pouch (anlage of middle ear and ET)
-suggests histogenesis related to incomplete closure at lines of fusion b/n branchial
elements
-have both mesodermal and ectodermal components
-lined by keratinizing stratified squamous epithelium that contains hair follicles, sebaceous glands,
smooth muscle and adipose tissue
-teratomas:
-rare in temporal bone
-arise from pluripotential stem cells near notochord
-contain all three embryonic germinal layers
-symptoms include facial paralysis, hearing loss and airway obstruction
-tx: surgical resection
-choristoma
-normal tissue that occurs in nonnative location
-eg. salivary tissue (most common), sebaceous glands and neural tissue in middle ear
-only require incisional or excisional biopsy
Cholesterol Granuloma
-mass lesion that results from reactive process within temporal bone
-hypothesis of pathogenesis:
-interference with drainage of middle ear
-haemorrhage
-obstruction of ventilation
-foreign body reaction to cholesterol crystals derived from haemoglobin catabolism
-thought to be start secondary to temporal bone trauma, ETD or mucosal edema
1043
-histology:
-cholesterol crystals surrounded by multinucleated giant cells, round cell infiltration, hemosiderin-
laden macrophages
-imaging: MRI: nonenhancing lesion bright on BOTH T1 and T2 weighted images
-treatment: drainage
Schwannoma
Meningioma
Lipoma
-rare
-imaging:
-T1 MRI: bright
-T2 MRI: dark
-nonenhancing
-confirmed with MRI fat suppression
-usually expectant management
-surgery for progressive or disabling symptoms
METASTATIC DISEASE
1044
CONGENITAL AURAL ATRESIA
EMBRYOLOGY
Facial Nerve
-abnormalities of facial nerve common in cases of aural atresia
-bony dehiscence frequently occurs and nerve may take an anomalous course
-typically, facial nerve makes an acute angle at second genu crossing middle ear in a more anterior
and lateral direction
-a correlation b/n degree of microtia and extent of facial nerve abnormality has been observed
PATIENT EVALUATION
-two principal objectives:
-assess overall hearing status and need for immediate amplification
-formulate a treatment plan that provides for consultation with members of other specialties
PHYSICAL EXAMINATION
-focus on overall craniofacial development
-look for abnormalities or syndromes involving first or second branchial arch
-evaluate facial nerve function:
-most common anomaly of facial function is congenital absence of depressor anguli oris muscle
Audiometric Evaluation
-essential to determine level of cochlear function in each ear to prevent operating on an only-hearing ear or
on an ear with little or no potential for hearing improvement
-bone conduction ABR can provide valuable information
Computed Tomography
-necessary in all pts being considered for surgery
-used to examine for possible cholesteatoma formation
-decision to operate depends primarily on degree of middle ear development, as reflected by size of
tympanum and status of ossicles
1045
MEDICAL MANAGEMENT
Unilateral Atresia
-no immediate intervention needed if contralateral hearing is normal
-bone conduction hearing aids for adults who want them
Bilateral Atresia
-early amplification essential in infants with bilateral atresia
SURGICAL MANAGEMENT
Selection Criteria
-risk of surgical complications will be minimized and chances for successful hearing result are increased if
middle ear and mastoid size are at least 2/3 of normal size and if all three ossicles, although deformed, can
be identified
-relationship of the facial nerve to the oval window is noted
-anterior displacement reduces the chance for successful hearing and increases the chance of
facial nerve injury
-unilateral cases: only ideal candidates are selected
-minimal criteria in bilateral cases:
-middle ear of at least ½ normal size and presence of an ossicular mass
Timing of Surgery
-can be performed as early as 5-6 years
-pneumatization of temporal bone is well advanced
-children old enough to cooperate with postop care
-permits microtia repair
Cholesteatoma
-pts with cholesteatoma should undergo surgery to eradicate disease process and if possible improve
hearing
-an average canal diameter of 4 mm or less 50% will develop cholesteatoma
-preponderance of cholesteatomas developed in canals 2 mm or less in diameter
-usually no cholesteatoma seen for child < 3 years of age
-therefore can wait far CT at age 6-8 years of age
1046
SURGICAL TECHNIQUE
Anterior Approach
Incision
-postauricular incision used to expose mastoid bone
-elevated anteriorly until a depression that represents the TMJ is encountered
Drilling a Canal
-middle cranial fossa dura is superior landmark
-TMJ is anterior landmark
-epitympanum will be entered and fused heads of malleus and incus identified
-facial nerve always lies medial to ossicular mass in epitympanum
-vulnerable to injury as external canal is enlarged in the posteroinferior direction
-in this area, may lie lateral to middle ear cavity in addition to being anteriorly displaced
Meatoplasty
-auricle undermined and soft tissue debulked from approximate area of meatus
-circular meatal opening about twice normal size is made
Skin Grafting
-STSG positioned in bony canal to overlap fascia graft
-packing used to maintain graft position
1047
SURGICAL FINDINGS
Ossicles
-expected finding is a fused and deformed malleus-incus complex
-malleus is typically more deformed than incus and has a short manubrium
-stapes is usually small and delicate with misshapen crura
Facial Nerve
-abnormalities common in major atresia pts
-anterior and lateral displacement of mastoid segment (most common)
-complete dehiscence of tympanic segment
-inferior displacement of tympanic segment
-higher incidence of facial nerve anomalies occur in pts with more severe microtia
HEARING RESULTS
-various results
-with carefully selected patients, hearing level of 20-30 dB in only 40-60% of patients
-near-normal hearing is not universally achieved even in carefully selected atresia pts
COMPLICATIONS
Labyrinthine Injury
-high frequency SNHL has been noted in some pts postop (2-4%)
-drilling on bone may be transmitted to inner ear
Canal Stenosis
-may develop in as many as 25% of pts
-secondary meatoplasty may be needed if significant stenosis causes trapping of debris leading to infection
-coverage of all bone by STSG needed to reduce granulation tissue formation
-stenosis may be due to displacement of pinna permanent suspension sutures to mastoid periosteum can
be used for proper realignment
Chronic Infection
-lack of normal migration of keratin debris and sebaceous and apocrine glands
-incidence of canal infections is higher
-may require regular cleaning
1048
Conductive Hearing Loss
-persistent CHL d/t:
-inadequate mobilization of ossicular mass from atretic bone
-unrecognized incudostapedial joint discontinuity
-fixed stapes footplate
-recurrence of CHL d/t:
-refixation of ossicular chain
-TM lateralization
1049
INTRATEMPORAL AND INTRACRANIAL
COMPLICATIONS OF OTITIS MEDIA
SYSTEMATIC APPROACH
Mastoiditis
-acute coalescent mastoiditis with subperiosteal abscess lateral to mastoid cortex and medial to concha
characteristically occurring 2 weeks after onset of acute suppurative otitis media
-pathogens:
- S. pneumoniae (most common)
-group A streptococcus (S. pyogenes)
-Staphylococcus epidermidis, Haemophilus influenzae, anaerobes
1050
-acute suppurative otitis media should respond within 3-5 days to appropriate antibiotic therapy
-if no response to Abx within first week, mastoiditis considered possible
-postauricular edema, subperiosteal abscess, or recurrence of pain within 2-3 weeks after onset of
acute suppurative otitis media, mastoiditis should be considered imminent
Subperiosteal Abscess
-mastoiditis that results in spread of infection to involve outer mastoid cortex elevating the periosteum
-SSx: edema, erythema, and tenderness over site of abscess; associated suppurative otitis media; fever
-postauricular abscess:
-most common site, spread through emissary veins or through bone
-may present with a pinna protruding outward from mass effect
-Bezold’s abscess:
-spread through a perforation in the mastoid cortex, tracts into SCM
-presents as a mass in the posterior triangle of the neck
-tx: parenteral antibiotics, mastoidectomy with drainage of the abscess
Petrositis
-Gradenigo syndrome:
-retroorbital pain, abducens palsy, ipsilateral acute or chronic otitis media
-tx: -parenteral antibiotics
-consider modified radical mastoidectomy extending toward petrous apex (if coalescent)
-approaches to the petrous apex:
-through the superior semicircular canal
-behind superior canal and above the horizontal canal
-infralabyrinthine
-through a triangle defined by the anterior border of the cochlea, the internal carotid
artery, and the middle fossa dura
-infracochlear
-through the root of the zygomatic arch
-anterior to the labyrinth
-treatment similar to treatment of acute mastoiditis
Labyrinthitis
-can be fatal if suppurative labyrinthitis (extremely rare) and meningitis occur
-serous labyrinthitis:
-toxic or metabolic products of bacteria or host inflammatory response enter inner ear through
round window membrane or cholesteatoma-induced fistula SNHL and vertigo with nystagmus
-hearing is recoverable
1051
-suppurative labyrinthitis:
-entrance of bacteria into labyrinth extensive inner ear and spiral ganglia cell loss
-profound HL that never resolves
-tx: clear up middle ear infection with Abx and myringotomy
-chronic infection surgical intervention
-removal of cholesteatoma
Labyrinthine Fistula
-chronic suppurative otitis media from a cholesteatoma erodes the bone of the labyrinth (most commonly at
the arch of the horizontal canal)
-dx: CT scan, fistula test (high false negative rate)
-tx: surgical exploration via a mastoidectomy with exteriorization of cholesteatoma
-matrix should be left intact over lateral SCC
-graft site if fistula is exposed; parenteral antibiotics if infected
Facial Paralysis
-facial paralysis in presence of subacute infection, acute coalescent mastoiditis, mask mastoiditis, petrositis,
or chronic suppurative otitis media may be destructive particularly in the tympanic segment
-cholesteatoma the most common cause of facial paralysis
-tx:
-clearing middle ear infection as rapidly as possible with Abx and myringotomy
-surgical intervention for subacute or chronic infection with evidence of neural degeneration
-do not open nerve sheath - perineurium is a barrier to infection; neural tissue lacks resistance to
infection
1052
septic emboli
-aspirate clot if suspect abscess
-anticoagulant therapy
-ligation of IJV if continued septic emboli despite initial surgery and postoperative antibiotics
Brain Abscess
-most common sites: temporal lobe or cerebellum
-four clinical stages:
-invasion (initial encephalitis)
-low-grade fever, drowsiness, headache, malaise
-localization (latent or quiescent abscess)
-silent, no symptoms usually
-enlargement (manifest abscess)
-abscess produces focal symptoms
-termination (abscess rupture) rapid death
-tx:
-surgical aspiration of abscess (intracranial and/or via ear)
-IV antibiotics
-surgical excision if gas within the abscess cavity
Meningitis
-most common intracranial complication of otitis media
-three pathways of spread:
-direct extension
-thrombophlebitis
-hematogenous dissemination
-severe Mondini malformation suspected if:
-rapid onset of meningitis within hours of acute suppurative OM in which organism is S.
pneumoniae or nontypable H. influenzae and unilateral or bilateral congenital profound SNHL
and vestibular deficit
-allow unusual connections b/n CSF through IAC, vestibule and stapes footplate
-communicating meningoencephalocele if above symptoms in adults
-pathogens:
-H. influenzae type B, Pneumococcus, hemolytic streptococcus
-dx:
-lumbar puncture for cells and culture
-elevated CSF pressure, decreased CSF glucose, presence of inflammatory cells and bacteria,
increase in protein content
1053
-tx:
-IV antibiotics and myringotomy
-33% of meningitis survivors suffer neurologic sequelae:
-behavioural disorders, mental retardation, deafness
-dexamethasone shown to reduce inflammatory sequelae and not interfere with antibiotic
treatment
-for subacute or chronic mastoiditis:
-ceftazidime for meningitis caused by P. aeruginosa
-metronidazole for anaerobic infection
-surgical debridement
Subdural Abscess
-pus collection between dura and arachnoid membrane
-three mechanisms:
-direct spread through dura
-retrograde venous thrombosis
-brain abscess rupture into subdural space
-dx: CT/MRI reveals crescent shaped enhancement (less resistance to spread) that does not cross midline
-tx: -clearing ear infection with IV antibiotics and myringotomy
-treating subdural abscess: mastoidectomy, careful exploration of dura with removal of excess
granulation tissue; neurosurgery consult
Epidural Abscess
-epidural abscess second most common of all intracranial complications arising from middle ear infections
-pus collection between skull and dura
-most commonly from direct extension via bone erosion
-tx: high-dose parenteral antibiotics and surgical drainage
COMPLICATIONS OF TREATMENT
Complications of Surgery
-excessive blood loss
-blood can be lost rapidly during course of mastoidectomy
-brain herniation
-pulmonary emboli
-air embolism
-tx: HBO and helium treatment
EMERGENCIES
1054
-headache lethargy/coma
-brain abscess
-otitis hydrocephalus
-meningitis
-subdural abscess
-seizure
-brain abscess
-focal neurologic deficits
-brain abscess
-subdural abscess
-meningismus
-meningitis
-ventriculitis
-subdural abscess
-carotid rupture
-reduction of visual fields or acuity
1055
MIDDLE EAR AND TEMPORAL BONE TRAUMA
History
Facial hypesthesia Intratemporal cranial nerve V deficit or Usually late onset if intracranial Spontaneous recovery is the
facial injuries general rule
Diplopia Cranial nerve VI deficit or eye injury Usually late Spontaneous recovery is the
general rule
Hearing Loss
-up to 40% HI pts suffer hearing loss
-transverse fractures have greatest propensity for severe SNHL
-longitudinal fractures more frequently with conductive and mixed hearing loss
-labyrinthine or cochlear concussions high frequency SNHL with associated vertigo
-mechanisms of SNHL:
-disruption of otic capsule
-concussion injury
-NIHL
-perilymphatic fistula
-injury to auditory CNS
Dizziness
-often late complaints
-notice once becoming ambulatory
-causes of vertigo with trauma:
-post concussion syndrome (most common)
-concessive injury to membranous labyrinth
-cupulolithiasis
-disruptive injury to labyrinth
-traumatic perilymphatic fistula
-trauma-induced endolymphatic hydrops
Facial Weakness
-easily overlooked
-determination of time of onset important
-late-onset paresis or paralysis common after temporal bone trauma and may be delayed for days or weeks
-areas of facial nerve injury:
-longitudinal fractures: perigeniculate area
-transverse fractures: labyrinthine segment
-penetrating injuries: extra-temporal, stylomastoid portion, vertical segment of nerve
1056
-mechanisms of injury:
-bony spicules
-perineural hematoma
-transection
-edema/swelling
Physical Examination
-three commonly seen findings for temporal bone trauma
-hemotympanum
-postauricular ecchymosis (Battle sign)
-periorbital ecchymosis (Raccoon eyes)
-facial nerve weakness requires careful evaluation
-CSF leakage: -diagnostic tests: chemical analysis, electrolyte determination, intrathecal dye injection,
and -2 transferrin protein identification
Radiologic Evaluation
-high-resolution CT scanning with bone algorithms
Location -through petrosquamous suture line and continues -involve otic capsule or internal auditory canal
anterior to otic capsule
-through superior EAC, middle ear, long axis of
petrous pyramid
1057
-gunshot wounds or other penetrating trauma requires evaluation with angiography or MRA greater
possibility of internal carotid artery injury
-options for carotid injury:
-embolization
-surgical revascularization
-ligation
Other Tests
Hearing Tests
-if early surgery is not a consideration, preliminary test is not critical; conductive losses may be repaired at
any time and sensorineural losses have poor prognosis that are not influenced by treatment
MANAGEMENT
Hearing loss May resolve if secondary to Amplification, conventional or Tympanoplasty with or without
hemotympanum CROS aid middle ear reconstruction
Facial Paralysis Complete recovery expected in Supportive eye care Decompression or repair of facial
cases of delayed onset -physical therapy if long-term nerve
paralysis expected Measures necessary for eye care
-structured rehabilitation with (gold weight, or tarsorrhaphy)
biofeedback techniques helpful to
improve function and avoid
synkinesis
CSF otorrhea or Spontaneous resolution in > 90% of Elevation of HOB; lumbar drainage Resorted to only after 2 weeks and
rhinorrhea cases failure of conservative measures
-indications for surgery:
-persistent leak
-recurrent meningitis
-persistent pneumocephalus
1058
FACIAL NERVE EXPLORATION AND REPAIR
Transmastoid Approach
-suitable only for lesions peripheral to geniculate ganglion
-not appropriate for transverse fractures
-lateral fracture defect involving mastoid cortex fracture line followed medially to facial nerve injury
-bone chips removed from nerve: examined for stretching, compression, laceration, or transection
-if intact decompression of epineural sheath in proximal and distal fashion until normal nerve
encountered
-partial transection repaired with onlay nerve graft
-if > 50% axon separation interpositioning graft
Transmastoid-Translabyrinthine Approach
-used if hearing is not useful and site of facial nerve injury proximal to geniculate ganglion
-usually for transverse fractures with involvement of otic capsule severe SNHL that will never recover
-makes visible the entire intratemporal course of the nerve and brainstem origin
-primary repair, grafting, or short-circuiting techniques are used from the posterior fossa to the parotid
portion of the nerve
POSTOPERATIVE CARE
1059
COMPLICATIONS
EMERGENCIES
-obvious brain herniation into middle ear, mastoid or external auditory canal
-massive bleeding from intratemporal carotid artery laceration
1060
CHOLESTEATOMA
CONGENITAL CHOLESTEATOMA
-embryonic rest of epithelial tissue in the ear without tympanic membrane perforation and without hx of ear
infection
-2/3 seen in anterior-superior quadrant
-mean age of presentation 4.5 years
-M:F = 3: 1
-usually dumbbell shaped
-pathogenesis unclear:
-failure of involution of ectodermal epithelial thickening in proximity to geniculate ganglion
-failure of “epidermoid formation” to involute development of cholesteatoma in anterior
mesotympanum
-other theory: metaplasia of middle ear mucosa
ACQUIRED CHOLESTEATOMA
Theories of Pathogenesis:
Primary acquired:
1. Invagination theory:
-blocked attic and localized negative pressure with retraction of pars flaccida
-pouch invagination occurs and eventually develops into an attic cholesteatoma as it accumulates
keratin
Secondary acquired:
1. Implantation theory:
-formation by iatrogenic implantation of skin into middle ear as result of surgery, FB or blast injury
2. Metaplasia theory:
-transformation of desquamated epithelium to keratinized stratified squamous epithelium secondary to
chronic or recurrent otitis media
1061
Factors involved in bone resorption
-mechanical
-pressure generated by expansion of cholesteatoma as it accumulates keratin debris
-biochemical
-bacterial elements (endotoxins)
-products of host granulation (collagenases, acid hydrolases)
-growth factors, cytokines
-cellular
-osteoclastic activity within subepithelial matrix of cholesteatoma
-release acid phosphatase, collagenase, and other proteolytic enzymes
SURGICAL ANATOMY
-Prussak’s Space:
-origin of epitympanic cholesteatomas
-floor: lateral process of malleus and its
associated mucosal folds lying in the horizontal
plane
-boundaries:
-anterior/superior/posterior: lateral
malleolar fold
-inferior: lateral process of malleus
-medial: neck of malleus
-lateral: pars flaccida
1062
-upper boundary defined by 3 well defined routes:
1. Posterior route:
-most common
-penetrates superior incudal space
lateral to body of incus then traverses
aditus ad antrum to enter mastoid
-AND/OR descends through floor of
Prussak space into posterior space of
von Troeltsch (pouch lying between
tympanic membrane and posterior
mallear fold) may involve stapes,
round window, sinus tympani, and
facial recess
1063
PREVENTION
PREOPERATIVE EVALUATION
-surgical goals*:
-1. treating complications (extradural abscess, brain abscess, facial nerve palsy, labyrinthitis)
-2. removing diseased bone
-3. obtain a dry ear
-4. preserve normal anatomy
-5. preserving or improving hearing
SURGICAL MANAGEMENT
1064
-provides good exposure and easier recognition of recurrent disease
-disadvantages:
-required cleaning of mastoid cavity, difficulty with hearing aid fitting, increased risk of infection
with water exposure
Bondy Procedure:
-removal of scutum and posterior canal wall with preservation of ossicles and middle ear space
Hearing Loss
-ossicular chain erosion in 30% of cases
Labyrinthine Fistula
-found in up to 10% of patients
-chronic ear disease, SNHL and /or vertigo induced by noise or pressure changes in middle ear
-fistulae of horizontal SCC most common
-tx: modified radical mastoidectomy
-leave matrix over fistula (1.5-2 mm) to prevent SNHL
Facial Paralysis
-due to infection or chronic expansion
-common site of nerve involvement is geniculate ganglion
Infections
-periosteal abscess: from blockage of aditus ad antrum or extensive erosion through mastoid cortex
-lateral sinus thrombosis
-intracranial abscess
Brain Hernia
-usually seen during revision surgery
-temporalis fascia graft to fix herniation
-large defect: repair from above via middle fossa approach
-small defect: repair from below with fascia patch
-defects larger than a few millimeters require conchal cartilage for support to prevent herniation
-area of brain in mastoid is necrotic and functionless remove it at the level of dural defect
1065
SURGERY OF THE MASTOID AND PETROSA
Incisions
Postauricular Incisions
-Wilde
-afford best exposure
-generally made 8-10 mm behind postauricular crease
-in infants and children under 2 ya, inferior portion placed more posteriorly to prevent injury to facial nerve
-exposure of temporalis fascia; horizontal incision created along temporal line which is inferior margin of
temporalis muscle
-mastoid emissary vein may be encountered in making incision to mastoid cortex should be occluded d/t
possibility of introducing air embolism
-periosteum elevated off mastoid cortex, exposing posterior wall of external auditory canal
Endaural Incisions
-Lempert I: -canal incision medial to bony cartilaginous junction extending along entire posterior half
of canal
-Lempert II: -superior incision extending from Lempert I incision laterally between tragus and root of
helix at meatus of ear canal
-small relaxing incision made at inferior margin of Lempert I incision to allow mobilization of posterior
skin
-endaural incision for access to mastoid have become less commonly used d/t limitations of exposure
Surface Landmarks
-temporal line:
-indicates level of floor of middle cranial
fossa
-root of zygoma:
-extends anteriorly along temporal line
-spine of Henle:
-suprameatal spine
-eminence located near the posterosuperior
wall of the EAC
-Macewen Triangle (cribriform fossa):
-depression in area just posterosuperior to
suprameatal spine with an irregular bony
surface
-the apex, the most lateral extent of
petrosquamous suture line, signifies
location of underlying mastoid antrum
-tympanomastoid suture line:
-located posteriorly in EAC, reliable
landmark for the exit of the facial nerve
-tympanosquamous suture line:
embryonic fusion plane located posteriorly and inferiorly in the EAC, divides tympanic and mastoid
portions of the temporal bone
-vascular strip:
-thickened vascular skin of superior canal between tympanosquamous and tympanomastoid suture line
1066
Simple Mastoidectomy
-used for: CLINICAL INDICATORS FOR MASTOIDECTOMY
-drainage of coalescent mastoiditis
-exposure of antrum, attic, labyrinth Indicators (one of the following)
-persistent or recurrent otorrhea
and endolymphatic sac -persistent or recurrent ear pain
-mastoid antrum generally located beneath -conductive hearing loss
point at intersection between a horizontal and -tympanic membrane perforation and/or cholesteatoma
vertical line drawn tangential to superior and -acute mastoiditis with osteitis
-neoplasm of temporal bone
posterior margins of external auditory canal -fracture of temporal bone with CSF leak
-cortex removed -facial nerve paralysis requiring decompression of facial nerve
-superior limit of dissection: temporal
line/tegmen
-Korner septum:
-bony plate lateral to actual antrum and is remnant of petrosquamous suture line
-divides mastoid air cells into medial and lateral regions
-posterior limit: sigmoid sinus
-in anterior protympanum, a projection of bone extending inferiorly from tegmen tympani, the “cog” can
obscure occult disease in anterior epitympanum and supratubal recess
-inferiorly, facial nerve may be encountered lateral to tympanic annulus in 65% of cases
-dehiscence of facial nerve in 55-57%
-most common area of dehiscence:
-tympanic portion, superior to oval window
-accounting over 50% of dehiscent nerves
-other areas:
-geniculate ganglion
-facial recess
1067
-tympanic sinus
-mastoid retrofacial air cell region
-most common site of injury to facial nerve: inferior to lateral semicircular canal after second genu
-other anomalies of the facial nerve:
-bifid nerve
-course inferior to oval window
-transmission of high-frequency sound from vibration of drill bit through incus and stapes could result in
SNHL d/t transmitted acoustic energy
-regions at risk for residual disease:
-most lateral part of facial recess approach at medial part of posterior ear canal wall
-sinus tympani:
-medial and anterior to mastoid portion of fallopian canal
Advantages Disadvantages
Canal-wall-down -residual cholesteatoma visible on follow-up -mastoid bowl maintenance can be a lifelong problem
-recurrent cholesteatoma is rare -middle ear is shallow and difficult to reconstruct
-total exteriorization of facial recess -position of pinna may be altered
-second stage sometimes required
Canal-Wall-Up (CWU):
-allows excellent view of facial recess and incus region while maintaining intact posterior ear canal
-may allow more physiologic ossicular reconstruction techniques with a deeper an better aerated middle ear
-increased risk of residual (20-35%) and recurrent disease (5-20%)
-most common site: mesotympanum
-increased likelihood of leaving cholesteatoma in lateral portion of facial recess
-“second-look” operation recommended at 6-12 months to reassess ear for residual disease and perform
planned reconstruction of sound-conducting system
Canal-Wall-Down (CWD):
-decreased risk of residual (2-17%) and recurrent disease (0-10%) cf CWU procedures
-equal or better hearing results reported
-lack of need for two surgeries
-indicated for advanced disease, noncompliant patients, only hearing ear
Radical mastoidectomy
-classic radical mastoidectomy:
-CWD mastoidectomy
-complete removal of TM, annulus, malleus, incus and middle ear mucosa
-eustachian tube plugged with fascia plug
1068
-goal: establish dry open cavity devoid of secretory epithelium
-precludes reconstruction of middle ear
-rarely performed today
-indications:
-unresectable cholesteatoma secondary to extension down ET, into cochlea, or into
perilabyrinthine region
-multiple failed prior modified radical mastoidectomies
Mastoid Obliteration
-mastoid bowl generally needs to be cleansed q6-12 months
-*techniques to minimize potential complications after CWD:
-wide saucerization
-avoidance of dependent pocket in mastoid tip lower floor of ear canal to same level as digastric
ridge
-lowering facial ridge
-generous meatoplasty
-exteriorize sinodural angle
-further modifications:
-Palva flap:
-postauricular musculoperiosteal flap
-temporalis muscle pedicled anteriorly or temporalis fascia pedicled on superficial
temporal artery
-using bone paté and bone chips placed deep to postauricular musculoperiosteal flap
Meatoplasty
-large meatus necessary for effective postoperative care and subsequent cleansing of mastoid bowl
-facilitate epithelialization and reduction of size of mastoid bowl
-crescent of conchal cartilage removed
-most important aspects of meatoplasty are adequate resection of cartilage and positioning of posterior
canal after cartilage removal
1069
Bondy Procedure
-variation of modified radical mastoidectomy performed through either endaural or postauricular incisions
-used in cases of large attic cholesteatomas in which middle ear is functioning well
-ossicular chain and middle ear are free of disease
-posterior ear canal wall removed down to annulus superiorly and facial ridge inferiorly
-scutum removed exposing epitympanum
-cholesteatoma marsupialized and keratin content debrided
-medial wall of cholesteatoma matrix left in place over body of incus and malleus and seals middle ear
space
-if cholesteatoma seen extending around ossicles standard MRM performed
-same principles as outlined apply to mastoid saucerization and reconstruction except middle ear is not
entered
Endoscopy
-to provide visualization of facial recess and sinus tympani
ENDOLYMPHATIC SHUNT
-procedures designed to “shunt” endolymph from lumen of endolymphatic sac into extracellular space in
treatment of intractable Meniere disease
-shunts established with Silastic strips or specially manufactured valves
-exposure of endolymphatic sac attained through complete mastoidectomy
-Donaldson’s Line:
-imaginary line drawn from lateral SCC that bisects perpendicularly the posterior SCC
-region where line crosses the sigmoid sinus marks the superior edge of the
endolymphatic sac
-bone over sigmoid sinus thinned
-bone overlying dura between inferior portion of posterior SCC and sigmoid sinus removed
-endolymphatic sac located between inferior portion of posterior semicircular canal and sigmoid
sinus
-bone over this region of dura is thinned and removed, exposing endolymphatic sac
-appears as a thickened whiter area of dura
-incision made with microscalpel, exposing luminal endothelium
-shunt inserted
1070
PETROUS APICECTOMY
-suppurative processes of petrous apex cause chronic infection and sometimes deep pain, abducens
paralysis, and facial paralysis
-divided into anterior and posterior portion by a coronal plane through internal auditory canal
-anterior portion: pneumatized in 9% pts
-posterior portion: pneumatized in 30% pts
-infection or cholesteatoma spread only to pneumatized apices
-surgical approaches:
-via middle cranial fossa
-via mastoid and middle ear
-surgeon can usually follow infected tracts:
-tracts into posterior apex:
-retrofacial tract
-subarcuate tract
-tracts along sinodural angle (retrolabyrinthine approach)
-tracts into anterior apex:
-infralabyrinthine tract:
-below posterior SCC and posterior to fallopian canal
-high jugular bulb may block entry through this route
-infracochlear tract:
-below cochlea
-carotid artery identified in anterior protympanum
-tensor tympani muscle in superior protympanum removed
-triangle made up of: carotid artery, cochlea and tegmen tympani
-triangle forms a direct opening into anterior petrous apex
-glenoid fossa approach:
-glenoid fossa exposed and contents displaced anterior
-medial wall of glenoid fossa then dissected
-location of carotid artery monitored
-all bone removed between carotid artery and dura of middle cranial fossa
-complete exenteration of anterior petrous apex is impossible without labyrinthectomy, but in most cases,
drainage of infected cells is sufficient to reverse suppurative process
1071
F.Ling - Surgery of the Mastoid and Petrosa (7)
1072
COMPLICATIONS AND EMERGENCIES
COMPLICATIONS
Vestibular Injury
-from trauma or subsequent infection
-results in acute vertigo with slow resolution over weeks to months
-chronic disequilibrium or vertigo may occur
Postoperative Infection
-perioperative oral antibiotics administered if infection occurs
Dysgeusia
-injury to chorda tympani
Brain Herniation
-if larger areas of dura are exposed, brain herniation into mastoid cavity and epitympanum can occur
-may result in cerebritis, meningitis and CSF leak
CSF Leak
-lacerated dura sutured and covered by fat, fascia or muscle graft to prevent CSF fistula
Bleeding
-laceration of sigmoid sinus or jugular bulb
-can be controlled by placing Gelfoam
-large lacerations secondary complications such as air embolism, sigmoid thrombosis
-early signs of air embolism:
-increases end-expiratory CO2, hypotension and abnormal cardiac sounds
-injury to carotid artery requires proximal and distal occlusion
1073
RECONSTRUCTION OF THE TYMPANIC
MEMBRANE AND OSSICULAR CHAIN
PREOPERATIVE ASSESSMENT
TECHNICAL CONSIDERATIONS
-pathologic TM abnormalities
-attic retraction cholesteatoma under
an eroded lateral attic wall
-sinus tympani retraction
cholesteatoma
-central perforation
Central Perforation
1074
-disadvantage:
-increased incidence of failure
1075
Lateral Attic Wall Erosion Cholesteatoma
-most common type of cholesteatoma problem requiring TM reconstruction
-key is to reconstruct lateral attic wall with cartilage
-postauricular approach
-superior elevation of fibrous annulus anteriorly and inferiorly
-pulls TM off short process of malleus onto the long process TM flap developed down to but not off the
umbo
-cholesteatoma removed from epitympanum
-lateral attic wall reconstructed with tragal cartilage; cartilage fixed against malleus neck
-saddle blanket graft placed over superior bony external canal and lateral attic walls
-prostheses:
-PORP = partial ossicular replacement prosthesis
-TORP = total ossicular replacement prosthesis
-plastic prostheses high extrusion rate; reduced with cartilage interposed over prosthesis platform
-hydroxyapatite prostheses tissue integration properties
1076
-synthetic incus strut
-constructed from a variety of materials
-eg. hydroxyapatite, titanium, porous polyethylene
-recreates connection from malleus to stapes suprastructure or footplate
-PORP/TORP
1077
OTOSCLEROSIS
EMBRYOLOGY
HISTOLOGY
-early lesions
-active otosclerosis (otospongiotic phase)
-numerous fibrovascular spaces and increased osteoblasts and osteoclasts
-bone resorption begins around existing vessels by osteocytes enlargement of vascular channels
-dilation of these vessels seen clinically as a reddish hue on the promontory as
Schwartze’s sign
-ground substance is deposited in areas of resorption formation of new spongy bone "blue
mantles of Manasse" on H+E staining
-late lesions
-inactive phase (otosclerotic phase)
-osteoclasts are slowly replaced by osteoblasts
-fibrovascular spaces look less active, less vascular, and may resemble the normal adjacent bone
of the cochlear capsule.
-formation of dense sclerotic bone in areas of previous bony resorption
-begins in endochondral bone, eventually endosteal and periosteal layers become involved as well
PHYSIOLOGY
1078
-audiogram with flat or “cookie-bite” curve with excellent discrimination
-progressive pure cochlear loss beginning at usual age at onset for otosclerosis
-CT revealing demineralization of cochlea typical of otosclerosis (“double ring” sign)
-stapedial reflex demonstrating “on-off effect” seen before stapedial fixation
EPIDEMIOLOGY
LABORATORY FINDINGS
-audiogram
-air-bone gap
-Carhart notch:
-loss of 20-30 dB in bone conduction at 2 kHz
-thought to be secondary to the mass effect and loss of resonance of ossicles/stapes
-typically improves after stapedectomy causing overclosure of the air-bone gap
suggesting that the cause of this audiological phenomenon is artefactual
-speech discrimination excellent
-tympanometry may show AS pattern
-on-off effect:
-early stapes fixation characteristic abnormal decrease in impedance noted at onset and
offset of eliciting signal
-absent stapedial reflexes towards late stages of disease
DIFFERENTIAL DIAGNOSIS
-ossicular discontinuity
-incus necrosis from recurrent chronic OM
-fibrous union of incudostapedial joint
-congenital stapedial footplate fixation
-malleus head fixation
1079
-Paget disease
-begins in periosteal layer and involved endochondral bone last
-excessive absorption of bone with fibrovascular replacement forming weak haphazard trabecular
bone
-usually diffuse involvement of the skull
-stapes involvement or fixation seldom occurs
-tx: hearing amplification, medical management to inhibit bone resorption (eg. mithramycin,
calcitonin)
-Osteogenesis imperfecta
-AD defect of osteoblast activity resulting in multiple fractures
-increased bone resorption and abnormal remodelling
-stapes fixation and blue sclera in 40-60% of affected pts
-Osteopetrosis (Albers-Schonberg Disease)
-rare dominant or recessive forms
-results in ossicular anomalies (otic capsule is resistant to the disease)
-thickened bones of the skull base, blindness (optic nerve atrophy), absent paranasal sinuses,
choanal atresia, facial paralysis, hepatosplenomegaly, brittle bones
MANAGEMENT
Natural History
-90% with only histologic evidence are asymptomatic - active lesions mature w/o stapedial fixation
-in symptomatic pt; slowly progressive conductive and sensorineural hearing loss begins by age 20
-maximum conductive loss of 50-60 dB
Amplification
-effective and safe alternative to surgery
-patient satisfaction an issue however
Medical Management
-sodium fluoride
-replaces hydroxyl ions fluorapatite complex more stable and theoretically resists osteoclastic
action
-20-120 mg/day
-vitamin D and calcium
-in conjunction with NaF
-may accelerate maturation of bony lesions
-with above treatment regimen, 50% pts show no worsening of symptoms, 30% improve, 20% continue to
worsen
Surgical Management
Patient Selection
-contraindications:
-only hearing ear
-active infection
-suspected active endolymphatic hydrops
-other considerations:
-age: -very young pts has higher incidence of oval window reclosure after a successful initial
procedure
-second operation greater risk of cochlear deafness
1080
-occupation:
-divers, pilots, flight attendants, frequent travellers are at greater risk for postoperative
fistula and prosthesis dislocation
-pts whose work or hobbies dictate excellent balance questionable candidates
-tympanic membrane perforations should be repaired before attempted stapedectomy
-history of cholesteatoma or severe ET dysfunction not good candidates
-middle ear effusion a strong relative contraindication
-worst hearing ear approached first
-minimum of 3-12 months before surgery attempted on second ear
Procedure
-stapes mobilization
-anterior crurotomy
-stapedectomy: entire stapes and footplate is removed
-stapedotomy:
-creation of fenestra in midportion of stapes - piston prosthesis is then positioned and connective
tissue placed at base of prosthesis to prevent fistula
-some reports suggest a decrease in postoperative cochlear deafness and improvement in air-bone
gap closure above 2kHz
Prosthesis
-connective tissue oval window graft
-wire or piston prosthesis
Intraoperative Complications
-high and dehiscent jugular bulb
-persistent stapedial artery
-courses b/n stapes crura
-some authors will attempt to cauterize; many will abort procedure
-note: artery may be only source to middle meningeal artery
-dehiscent and abnormally low facial nerve
-can obscure oval window
-may consider gently retracting nerve superiorly (controversial)
-abort procedure if surgeon believes nerve is in jeopardy
-profuse perilymph gusher
-patent cochlear aqueduct
-removal of footplate in presence of gusher increases risk of postoperative cochlear deafness
-risk of permanent SNHL
-tx: seal vestibular opening with a graft, place prosthesis, pack and close, manage for perilymph
fistula, may require lumbar drain
-fracture of long process of incus
-place prosthesis to remaining incus or use malleus to oval window prosthesis
-“floating footplate”
-might be pushed into vestibule and attempts to remove it can result in significant neurosensory
hearing loss
1081
Postoperative period
-no lifting or straining for 6 weeks
-postoperative audiogram at 4-6 weeks
-closure of air-bone gap to within 10 dB in ~ 90% of patients
-10% experience no improvement
-1-2% suffer persistent profound sensorineural loss
Postoperative Complications
-immediate:
-vertigo:
-usually self limited
-if persists > 1 week, corticosteroids may be of some benefit
-acute otitis media
-rare
-may lead to meningitis
-weeks postop:
-reparative granuloma
-1-2%
-progressive SNHL after earlier postoperative hearing improvement
-discrimination scores lower than expected
-requires immediate surgery
-findings: significant granulation tissue around oval window graft
-historically seen with Gelfoam graft
-weeks to years postop:
-oval window fistulae
-fluctuating or progressive hearing loss
-high clinical suspicion
-requires exploratory surgery
-postop expectations usually stabilization of SNHL and resolution of vertigo
-failure of stapedectomy:
-prosthesis displacement (most common)
-footplate refixation
-perilymph fistula
-otosclerotic regrowth
-lateralization of oval window membrane
-revision surgery
-provides improvement in symptoms in less than 65% of cases
-seven times higher risk of postoperative cochlear deafness
1082
ACUTE PARALYSIS OF THE FACIAL NERVE
Intracranial Segment
-23-24 mm
-segment from brainstem to internal auditory canal
-Nervus Intermedius: parasympathetic and sensory
root of facial nerve
-motor root joins with nervus intermedius in
CPA/IAC to form common facial nerve
Intratemporal Segments
-meatal
-labyrinthine
-tympanic (horizontal segment)
-mastoid (vertical segment)
1. Meatal
-8-10 mm
-from porus acousticus (fundus) to meatal foramen
-traverses in anterior superior quadrant of IAC
separated by falciform crest inferiorly and Bill’s
bar posteriorly
2. Labyrinthine
-3-5 mm
-from meatal foramen to geniculate ganglion
-narrowest segment of fallopian canal (0.68 mm
diameter)
-geniculate ganglion:
-located at first genu Middle fossa approach - GSPN (5); geniculate ganglion (7); facial nerve
-cells bodies of sensory cells and taste meatal segment (10), labyrinthine segment (9), tympanic segment (12)
cells from anterior 2/3 of tongue and
palate
-greater superficial petrosal nerve:
-first branch of facial nerve
-carries preganglionic parasympathetic
fibers to lacrimal gland
3. Tympanic
-8-11 mm
-from geniculate ganglion to pyramidal eminence
(at second genu)
-courses above cochleariform process, oval
window and stapes; below lateral semicircular
canal
-most common site of dehiscence (40-50%)
Lateral approach - facial nerve mastoid segment (1), tympanic segment (2),
labyrinthine segment (3), meatal segment (4); GSPN (5); cochleariform
process (6)
F.Ling - Facial Nerve (1)
1083
4. Mastoid
-10-14 mm
-from pyramidal process to stylomastoid foramen
-nerve to stapedius
-chorda tympani:
-preganglionic fibers to submandibular and sublingual glands
-special sensory taste fibers
Extratemporal Segments
-postauricular nerve
-branch to external auricular and occipitofrontalis muscles
-nerve to stylohyoid
-nerve to posterior digastric muscle
-nerves to muscles of facial expression
-pes anserinus
-branching point of extratemporal segments in parotid gland
-two divisions:
-superior - temporozygomatic
-inferior - cervicofacial
-temporal branch:
-frontalis
-corrugator supercillii
-procerus
-upper orbicularis oculi
-zygomatic branch:
-lower orbicularis oculi
-abundant anastomotic supply with
buccal branch
-buccal branch:
-zygomaticus major and minor
-levator anguli oris
-buccinator
-upper orbicularis oris
-marginal mandibular branch:
-lower orbicularis oris
-depressor anguli oris
-depressor labia inferioris
-mentalis
-cervical branch:
-platysma
1084
FUNCTIONAL ANATOMY
1085
SURGICAL ANATOMY
2. Translabyrinthine Approach:
-used when hearing preservation not an issue
-nerve usually found along a line drawn between the horizontal SCC and digastric ridge
EVALUATION
1086
Adjunctive Testing:
-CT and MRI
-electrophysiologic testing
-topognostic tests:
-generally not useful and have been replaced with electrophysiological testing
-Schirmer test:
-quantitate amount of tearing in involved eye
-significant if > 30% reduction in tears or < 25 mm tear in 5 mins
-audiometry: should be done in all cases of facial palsy
-treponemal studies: Lyme titers and VDRL/FTA-ABS
-CBC: may suggest inflammatory process
-ACE level: may suggest active sarcoidosis
Definitions:
Neurapraxia:
-lesion compresses flow of axoplasm
-nerve is viable and recovers normal function when blockade is removed
-NET, MST and ENOG normal; EMG abnormal
Axonotmesis:
-state of Wallerian degeneration distal to lesion characterized by preservation of endoneural
sheaths of motor axons
-NET, MST and ENOG will indicate rapid and complete degeneration
Neurotmesis:
-Wallerian degeneration and loss of endoneural tubules
-eletrophysiologic tests similar to axonotmesis
1087
-Class III:
-neurotmesis
-neural tube (axons, myelin sheath, and endoneurium) disruption
-Wallerian degeneration occurs distal to site of injury
-unpredictable outcome (loss of endoneural tubules results in high risk for synkinesis)
-Class IV:
-neurotmesis
-violates perineurium greater chance of incomplete and aberrant regeneration
-Class V:
-neurotmesis
-complete transection no regeneration without surgical reapproximation
-risk of a neuroma from nerve sprouts outside nerve sheath
Electrophysiologic Tests:
Nerve excitability test (NET) Complete paralysis < 3 wks < 3.5 mamp threshold Not useful in first 3 days after
duration difference: prognosis good onset or during recovery
Maximal stimulation test (MST) same as NET Marked weakness or no muscle Not objective
contraction: advanced
degeneration with guarded
prognosis
Electroneurography (ENOG) Same as NET and MST < 90% degeneration: prognosis False positive results in
good; > 90%: prognosis in deblocking phase
question
Electromyography Acute paralysis less than 1 wk Active mu: intact motor axons Cannot assess degree of
duration degeneration or prognosis for
recovery
-within first 3 days after onset of complete paralysis, results of NET, MST, and ENOG yield little useful
information, as Wallerian degeneration distal to the stimulation areas has not occurred; the results always
indicate incomplete degeneration and good prognosis
-prognosis cannot be established until the sixth or seventh day after onset of paralysis
-NET:
-current thresholds required to elicit just-visible muscle contraction on the normal side of the face are
compared with those values required over corresponding sites on the side of paralysis
-side-to-side threshold difference is calculated
-3.0 to 3.5 mA difference compatible with advanced degeneration
-MST:
-modification of NET that uses a level of current sufficient to depolarize all motor axons underlying the
stimulating probe
-muscular responses graded subjectively; markedly decreased or absent facial movement signifies advanced
degeneration
1088
-ENOG:
-supramaximal level of current applied with bipolar electrodes percutaneously over main trunk of facial
nerve
-compound myogenic action potential
-peak-to-peak amplitude directly proportional to number of intact motor axons
-ratio of abnormal side to normal side measured
-> 90% degeneration indicates a poor prognosis for immediate or complete restoration of facial function
-in Bell’s palsy, patients exceeding 95% degeneration within the first 2 weeks of onset fall into the guarded
prognostic category
-limitations: testing error: standard lead placement versus optimal lead placement
-EMG:
-electrodes inserted into muscle, measures muscle response to voluntary contraction
-useful to demonstrate the existence of functional motor units
-fibrillations from deinnervated nerve appear after 1-2 weeks
-polysynaptic signals indicate reinnervation
-presence of voluntary action potentials indicates at least partial continuity of nerve
II Mild Slight weakness noticed Very slight Normal Moderate-to- Complete Slight
on close inspection good function closure with asymmetry
minimal
effort
III Moderate Obvious, but not Noticeable Normal Slight-to- Complete Slightly weak
disfiguring difference but not moderate closure with with
between the two sides severe movement effort maximum
effort
Birth Trauma
-most common cause of unilateral facial paralysis in the neonate
-facial nerve is at risk for injury during delivery as ti courses the underdeveloped mastoid process
-nerve compression due to molding of head in birth canal
-risks: forceps delivery, prolonged delivery, large infant
-SSx: asymmetric crying facies, hemotympanum, periauricular ecchymosis
1089
-diagnosis:
-if complete paralysis within first 3 days of life EMG to provide conclusive evidence of
neuromuscular integrity
-later presentations, NET, MST and ENOG used initially followed by EMG if myogenic
responses are absent
-treatment: observation
-prognosis for spontaneous regeneration is excellent and surgical exploration not recommended unless
nerve has had an opportunity for recovery
-Mobius Syndrome:
-CN VI, VII palsy
-deformity of extremities: club foot (talipes equiovarus)
-tongue weakness
-mixed hearing loss
-mental retardation
-external ear deformities
-tx: treated later in life with muscle transfers and fascial slings
-thalidomide embryopathy:
-limb and ear anomalies and abducens nerve palsy
-Albers-Scheoenberg Disease:
-autosomal recessive inheritance
-disorder of bone metabolism resulting in osteopetrosis of bony IAC causing compression of
nerves (CN III, VII and VIII)
Bell’s Palsy
-most common cause of facial paralysis
-risks: diabetes mellitus, pregnancy, past history (7-12% recur)
-facial paralysis of acute onset (<48 hours) and limited duration, etiology idiopathic
-prognosis:
-1/3 paresis; > 95% recover without sequelae
-2/3 paralysis; > 85% some return of facial tone within 3 weeks; may not have return for 3 to 6
months
-70-85% will have full recovery by 6 months; 15-30% will have incomplete recovery
-longer the delay, the greater likelihood of adverse sequelae
-inflammatory infiltrates throughout course of facial nerve
-infecting agent: HSV in geniculate ganglion
-interventions:
-steroid treatment:
-thought to prevent denervation, speed recovery, lessen synkinesis and prevent
progression of paralysis
-some studies do not show any statistical difference between steroids and placebo
-prednisone 1 mg/kg/day in divided doses and tapered over 7 to 10 days
-acyclovir:
-added to steroid regimen at 2000 mg/day in five doses for 7 days
-delay > 3 days before beginning antiviral therapy likely precludes any additional
efficacy
1090
-surgical:
-still controversial
-considered only for > 90% degeneration on ENOG in first 2 weeks of paralysis
-postulated the maximal nerve injury occurs at the meatal foramen
-unroofing labyrinthine segment via middle fossa approach
-decompression performed within 14 days of onset significantly improves
outcome in patients with poor prognosis; after 14 days no additional benefit
-decompression of mastoid and tympanic segments has no effect on recovery
Otitis Media
-complication of acute suppurative otitis media, otitis media with effusion, chronic otitis media, and
mastoiditis
-incidence ~ 1:20,000
-prognosis excellent; rapid resolution after resolution of infection
-tx: M+T
Melkersson-Rosenthal Syndrome
-unknown familial condition
-symptoms usually begin in childhood and early adolescence
-SSx:
-chronic or recurrent facial edema of upper lip
-recurrent unilateral or bilateral facial motor dysfunction
-fissured tongue
-migraine headaches
-dx:
-clinical history and exam, lip biopsy reveals dilated lymphatics and granulomatous changes with
giant cells, may have elevated ACE levels during attacks
-tx:
-empiric management with corticosteroids
1091
Lyme Disease
-Borrelia burgdorferi transmitted by a deer tick
-SSx:
-10% of patients have ipsilateral or bilateral facial nerve involvement after 1-4 weeks incubation
period
-initial erythema migrans (bull’s eye rash), flu-like symptoms, meningitis, multiple neuropathies,
cardiac conduction disorders, meningoencephalitis, swollen joints
-facial paralysis resolves in 6-12 months (full recovery anticipated)
-tx:
-parenteral penicillin, ceftriaxone, or cefotaxime for severe cases
-for rash only consider oral therapy
TRAUMA
1092
-middle fossa approach in patients with good hearing
-transection rare requires end-to-end anastomosis or interpositional grafting
-edema and contusion more common requires incision of epineural sheath to evacuate hematomas
Gunshot injuries
-paralysis > 50% cases
-d/t direct transection, bony fragments, or secondary kinetic energy
-most common sites of injury are mastoid and tympanic segments and stylomastoid foramen area
-outcome of facial function is poorer
Iatrogenic causes
-less than 1%
-delayed onset paresis more common but usually due to viral reactivation
-common sites of injury:
-tympanic segment adjacent to oval window (d/t dehiscence)(1st)
-mastoid segment (2nd)
-management:
-partial injuries (< 50%) are best treated by decompression proximal and distal to injury
-injuries > 50% require primary anastomosis or cable grafting
-postoperative weakness:
-wait for local anesthetics to wear off
-may consider corticosteroids and follow progression
-consider re-exploration for complete paralysis in select cases
-Interpositional grafts:
-donor sites: greater auricular, median antebrachial cutaneous, sural nerves
1093
-skull base tumours:
Anterior transposition:
-spares greater superficial petrosal nerve and preserves normal tearing
-preferred for benign tumours of infralabyrinthine compartment
Posterior transposition:
-provides access to petrous apex
Division and reanastomosis:
-may aid exposure to parapharyngeal space
-avoid this approach because of complications
-when tumour is benign, continuity of nerve is preserved using mobilization techniques EXCEPT
for:
-facial nerve schwannomas
-benign tumour invading the nerve
-recurrent tumour adherent to the nerve
-malignant tumours:
-require tumour-free excision
-exceptions:
-lymphomatous and leukemic invasion of nerve
-low-grade malignancies of parotid
-Parotid Tumours:
-mucoepidermoid carcinoma most common parotid tumour to cause paralysis
-adenoid cystic carcinoma has higher rate of neural involvement
-other neoplasms:
-cholesteatomas
-hemangiomas
-glomus jugulare or tympanicum
-meningioma
-metastatic carcinoma
Stroke
-presents with an acute, forehead sparing facial paralysis associated with other lateralizing neurological
signs
Guillain-Barre Syndrome
-common cause of acute bilateral facial nerve palsy
-associated with generalized weakness, central nervous and autonomic dysfunction
Myasthenia Gravis
-autoimmune disease with antibodies against the acetylcholine receptor at the neuromuscular junction
which causes progressive motor weakness with repetitive function
-associated with ptosis, difficulty chewing, talking, weakness, and thymic tumours
EYE CARE
-most common complication is corneal desiccation
-precautions: ophthalmic lubricants, closure of eye with tape at night, moisture chambers or shielded
glasses, avoidance of wind/fans/vents
-surgical options: gold weight implants, canthoplasty, tarsorrhaphy, and upper eyelid springs
1094
OTOLOGIC MANIFESTATIONS OF SYSTEMIC DISEASE
INFECTIOUS DISEASES
SYSTEMIC DISEASES
Mumps
-RNA paramyxovirus transmitted by salivary secretions
-salivary adenitis, epididymo-orchitis, pancreatitis, thyroiditis, polyarthritis, myocarditis
-hearing loss in 5/10000
-80% unilateral, high-frequency hearing loss
-usually permanent
-no specific treatment
-corticosteroids reported to help diminish fever and pain resulting from parotid and testicular
swelling
Measles
-caused by highly contagious RNA virus
-pre-vaccination era, was common cause of acquired SNHL
-HL occurs in fewer than 0.1% of all measles infections
-bilateral SNHL and occurs at same time as macular rash
-45% with profound hearing loss
-permanent hearing loss
-asymmetric hearing loss maximal at higher frequencies
1095
Syphilis
-middle ear and mastoid affected by both congenital and acquired syphilis
-Treponema pallidum
-tertiary syphilis:
-gumma: granulomatous lesion with central necrosis and obliterative arteritis
-may affect middle ear with TM perforation
-labyrinthine involvement in secondary or tertiary stages
-secondary stage:
-abrupt, bilateral and rapidly progressive hearing loss
-vestibular symptoms unusual
-rash
-CSF: lymphocytosis with elevated total protein and normal glucose levels
-tertiary stage:
-asymmetric and fluctuating hearing loss
-progressive tinnitus and vertigo may occur
-positive fistula test (Hennebert’s sign) may be seen
-loss of speech discrimination out of proportion to pure-tone thresholds
-diagnosis:
-positive serum fluorescent treponemal antibody absorption test (FTA-ABS)
-microhemagglutination assay-Treponema pallidum (MHA-TP)
-treatment:
-penicillin 2.4 MU IM weekly for 6-12 weeks
-penicillin 0.6 MU IM daily for 6-12 weeks
-prednisone 30-60 mg per day on alternate days for 3-6 months with slow taper
Lyme Disease
-Borrelia burgdorferi
-transmitted by ticks
-early symptoms: rash, severe headache, neck stiffness, fever, chills, myalgia, profound fatigue
-late symptoms: multiple neuropathies, arthritis, meningitis, myocarditis
-ENT symptoms: facial paralysis, TMJ pain, tinnitus, SNHL, sudden hearing loss, otalgia, facial pain,
cervical adenopathy, vertigo
-common cause of facial paralysis (bilateral)
-usually resolves slowly over 6-12 months
-antibiotics often used to hasten resolution and prevent disease progression
-responds well to doxycycline, amoxicillin, penicillin, tetracycline, or cefuroxime axetil
Leprosy
-Hansen’s disease
-endemic in tropical countries
-Mycobacterium leprae
-nasal mucosa thought to be primary site of transmission from infected persons
-nervous, cutaneous and ocular involvement can lead to extremity mutilation, leonine features, and
keratoconjunctivitis
-bacillus infects nerves and immune response to infection causes nerves to thicken considerably
-greater auricular nerve, ulnar nerve, peroneal nerve and radial nerve commonly affected
-lesions of external ear in 70%: infiltrating nodules, loss of cartilage, ulceration
-dx: biopsy
-tx: dapsone and rifampin; clofazimine
1096
Tuberculosis
-Mycobacterium tuberculosis
-most infected people are asymptomatic carriers with 5-10% lifetime risk of developing clinical disease
-aural tuberculosis may present as facial paralysis, persistent aural discharge, refractory chronic otitis
media, profuse granulation tissue, bone sequestra or necrosis, perichondritis, or failed otologic surgery
-otitis media:
-may result from hematogenous and lymphatic spread
-generally painless, with multiple small perforations that may quickly coalesce to total tympanic
membrane perforation
-CHL from ossicular destruction
-dx:
-AFB in exudate or tissue preparations
-definite diagnosis made by isolation and identification of M. tuberculosis in culture from
diagnostic specimen
-culture of exudate negative in 60% of cases
-tx:
-antituberculous chemotherapy
-may require surgery to remove intractably pathologic tissue and sequestrated bone
IMMUNOLOGIC DISEASES
Wegener’s Granulomatosis
-otologic involvement seen in ~35% of cases
-most common otologic manifestation are facial or postauricular pain, otitis media with effusion, acute
otitis media, hearing loss, and vertigo
-OM may result from obstruction of ET
-CSOM may resolve with treatment of WG and may be used as an indicator of remission or
recurrence
-SNHL may be d/t immune complex deposits in cochlea, vasculitis of vasa vasorum of cochlea, or
pressure on acoustic nerve by a granulomatous lesion
-dx:
-c-ANCA found in 90% of pts with active WG and in 60% with limited disease
-tx:
-corticosteroids and cyclophosphamide
Relapsing Polychondritis
-episodic inflammation of cartilaginous structures
-over time, recurrent inflammation leads to atrophy, scarring and distortion of involved cartilage
-otologic manifestations:
-red, tender, edematous pinna with sparing of external ear canal
1097
-diagnosis is clinical; biopsy of acutely inflamed pinna avoided because of risk of infection
-lab findings: elevated ESR, anemia and positive RF
-tx: corticosteroids; dapsone, indomethacin and salicylates; MTX has been described
Polyarteritis Nodosa
-necrotizing vasculitis of small- and medium-diameter arteries
-diagnosis based on biopsy:
-PMN infiltrating all layers of vessel wall and perivascular areas intimal proliferation and
degradation of vessel wall
-lesions are segmental and tend to affect areas of arterial bifurcation
-hepatitis B surface antigen can be demonstrated in serum of 30-40% of patients
-predominant otologic symptom is usually hearing loss (conductive or sensorineural)
-tx: systemic corticosteroids combined with cyclophosphamide
Rheumatoid Arthritis
-persistent inflammatory synovitis causing progressive cartilage and bone destruction within joints
-affects 1% of population; F>M
-association with expression of HLA-DR4
-rheumatoid nodules are both cutaneous and subcutaneous and may involve external ear
-conductive and sensorineural hearing loss can occur
-significantly higher incidence of SNHL than normal persons, possibly d/t autoimmune inner-ear
disease
-CHL thought to be d/t abnormal middle-ear stiffness
METABOLIC DISORDERS
Gout
-disorder of purine metabolisms that causes abnormally high levels of uric acid
-overproducers treated with allopurinol, underexcreters are treated with uricosuric drugs such as
probenecid
-tophus found on auricle no treatment necessary
Ochronosis
-form of alkaptonuria
-AR disorder of homogentisic acid metabolism
-affected persons accumulate homogentisic acid oxidized to black compound that adheres to cartilage
and discolours ear, fingers, buccal mucosa and nose
-tx: low-protein diet
1098
Mucopolysaccharidoses
-inherited deficiencies of enzymes needed of degradation of mucopolysaccharides
-Hunter syndrome:
-deficiency of alpha-iduronidase
-X-linked inheritance
-Hurler syndrome:
-deficiency of alpha-iduronidase but inherited as AR
-Morquio syndrome:
-deficiency of N-acetylgalactosamine-6-sulfatase or of beta-galactosidae
-hearing loss is usually mixed with conductive component d/t ETD and SOM
-SNHL may be d/t abnormal lipid metabolism within nerve cells
DISEASES OF BONE
Osteogenesis Imperfecta
-AD disorder of connective tissue
-mutations in either of two chains that form type I procollagen
-both conductive and sensorineural hearing loss found in 90% pts over age of 30
-CHL associated with blue sclera
-caused by involvement of ossicles with pathologic fractures of long process of incus or stapes
crura
-SNHL associated with gray or white sclera
Osteopetrosis
-inherited disorder causing faulty remodelling of bone
-AD or AR
-dominant form
-progressive enlargement of head and mandible and long-bone clubbing
-progressive cranial neuropathies caused by nerve compression at foramina optic atrophy,
trigeminal hypoesthesia, recurrent facial paralysis, SNHL
-CHL d/t involvement of ossicles and bone of epitympanum
Paget’s Disease
-chronic, often progressive disorder of bone metabolism
-characterized by bony hypertrophy and remodelling d/t increased activity of both osteoclasts and
osteoblasts
-affects 3% of population over 40 years of age and up to 11% of those over 80
-temporal bone involvement can cause SNHL and CHL
-otologic symptoms:
-hearing loss, tinnitus, mild vestibular complaints
-facial nerve not affected
-other signs:
-calvarial enlargement, enlargement of superficial temporal artery, elevated ALP and typical
findings of radiographic studies
-radiographic findings:
-thickening of calvarium
-mixture of dense and radiolucent areas of fibrosis
-areas of cortical erosion
-characteristic coarse bony trabeculae
-treatment:
-calcitonins and etidronate disodium to decrease osteoclast activity
1099
Fibrous Dysplasia
-replacement of normal cancellous bone by spicules of woven bone in a fibrous stroma
-most common presenting symptoms of temporal bone fibrous dysplasia are CHL (80%), progressive
occlusion of EAC (85%), and canal cholesteatoma (40%)
-facial nerve paralysis or paresis and SNHL are other possible complications
-indications for surgical treatment:
-CHL and cholesteatoma secondary to EAC stenosis
IDIOPATHIC DISEASES
Histiocytosis X
-characterized by an accumulation of histiocytes, lymphocytes, and eosinophil in skin, bone marrow, lymph
nodes, lung, liver, thymus, spleen, and CNS
-most pts have deficiency of suppressor lymphocytes and an elevated amount of helper lymphocytes
-definitive diagnosis made by showing presence of Birbeck granules on EM or immunohistochemical
testing showing presence of CD1 antigen
-head and neck involvement seen in 73%
-cranial vault, EAC, temporal bone, lymph nodes, maxilla, mandible
-otologic symptoms:
-otorrhea, aural granulation tissue, mastoid swelling, deafness, collapse of external
auditory canal and swelling of mandible or maxilla
-tx:
-systemic disease: steroids etoposide, vincristine, vinblastine if no response
-topical or intralesional steroids for localized lesions
-eosinophilic granuloma:
-unifocal process affected children and young adults
-osteolytic lesion in temporal bone pain, swelling, purulent otorrhea, CHL
-destructive lesion within temporal bone seen on CT
-tx: XRT is curative and prognosis is excellent
-Hand-Schuller-Christian disease
-multifocal process
-occurs in children under 5 years
-prognosis less favourable than EG
-low-dose chemotherapy may be needed
-Letterer-Siwe disease
-rapidly progressive fulminant form of histiocytosis X
-occurs in children under 3 ya
-rapid fatal course
-death occurs from bleeding or infection caused by bone marrow failure from replacement by
immature histiocytes
1100
INFECTIONS OF THE LABYRINTH
Anatomy
-permeability of round window is implicated in spread of middle-ear infections to labyrinth
-patency of cochlear aqueduct diminishes with age:
-age < 16y 82% have patent aqueducts
-age > 60y 30% have patent aqueducts
-passage of particulate matter from CSF to inner ear possible
-8th nerve termini penetrate to their end organs through cribrose areas and provide potential route
for passage of infectious organisms from CSF
-stria vascularis has rich vascular supply: vestibulocochlear and spiral modiolar arteries
-organisms infect spiral ganglion cells after gaining access by cochlear vasculature
Physiology
-hyperactivity or hypoactivity in one labyrinth produces an imbalance that is perceived as vertigo
-compensation occurs - intervestibular commissural fibers undergo reorganization that is thought to be
important in functional recovery
MENINGITIS
Bacterial Meningitis
Etiology:
-Haemophilus influenzae, Neisseria meningitidis, Streptococcus pneumoniae account for 71% of cases
-incidence of partial or complete SNHL after meningitis ranges from 10-20%
-same three organisms were related to 83% of cases of hearing loss
-S. pneumoniae most detriment to hearing: associated with hearing loss in nearly 25% of cases
-initial bacteremia precipitates eventual hearing loss before any symptoms or signs develop
Pathology:
-acute toxic labyrinthitis
-acute suppurative labyrinthitis
-chronic labyrinthitis
-labyrinthine sclerosis
Viral Meningitis
-it has been difficult to link viral meningitis to hearing loss and imbalance
1101
Fungal Meningitis
-Rare: Cryptococcus neoformans, Aspergillus, Candida albicans, Coccidiodes immitis causative agents in
only 1.3% of meningitis cases
-neural involvement: granulomas in IAC and Rosenthal’s canal
-associated with retrocochlear lesions rather than cochlear hearing losses seen with bacterial meningitis
VIRAL LABYRINTHITIS
-difficult to prove
-only two viruses: CMV and mumps virus have been isolated and cultured from inner ear of affected humans
Cytomegalovirus
-DNA-containing virus
-cochlear alterations, most severe in basal turn, include hydrops or collapse of Reissner membrane and
inclusion bodies in cells of stria vascularis and endolymphatic surface of Reissner membrane
-most common cause of viral congenital deafness
-symptomatic disease (cytomegalic inclusion disease)
-only 1-2% of all congenital CMV infections
-hemolytic anemia, hepatosplenomegaly, jaundice, purpura
-30-60% develop severe, symmetric SNHL
-asymptomatic disease:
-majority of congenital CMV infections
-8-15% have mild to moderate SNHL
-diagnosis:
-suggested by radiographic demonstration of intracerebral calcium deposits in a
microcephalic child
-isolation of CMV from fresh urine during first 3 weeks of life can clinch dx in
symptomatic and asymptomatic cases
-identification of anti-CMV IgM in infant’s serum
-may be a role for ganciclovir for improvement and stabilization of hearing
Rubella
-produces multiple malformations including those of the temporal bone:
-cochleosaccular degeneration and strial atrophy
-symptomatic disease:
-implies infection in first trimester
-produces hearing loss in ~50%
-congenital cardiac malformations, visual loss, motor deficits, thrombocytopenic purpura,
hepatosplenomegaly, icterus, anemia, low birth weight, mental retardation
-asymptomatic disease:
-implies infection during second or third trimesters
-associated with hearing loss in 10-20%
-although rubella vaccine, if given to a nonimmune pregnant woman, can cross the placental barrier to
infect the fetus, the risk of subsequent hearing loss is small
-laboratory testing: isolating rubella virus from urine
-SNHL:
-most commonly profound
-in some pts hearing loss may progress
1102
-generally, all frequencies are affected equally; speech discrimination may be poor
-hypoactive vestibular response or frank unilateral or bilateral canal paresis may occur
Neurolabyrinthitis
-acute viral labyrinthitis: involvement of auditory or vestibular end organs
-acute neuritis: disruption of cochlear or vestibular peripheral nerve function
-therapy is not altered by the distinction
Mumps
-paramyxovirus
-symptom complex of parotitis, orchitis, meningoencephalitis, and in 0.05% of cases, hearing loss
-hearing loss usually occurs at end of first week of parotitis
-unilateral in 80%
-ranges from mild, high frequence SNHL to profound SNHL
-evidence supports hypothesis that a subclinical mumps infection can cause ISSNHL in an
otherwise healthy person
-vestibular involvement uncommon
-histopathology:
-alterations of cochlear duct structures
1103
-atrophy of organ of Corti and stria vascularis with collapse of Reissner membrane
-deformation and detachment of tectorial membrane and moderate loss of spiral ganglion cells in
basal turn
-no data exist to support steroid therapy - studies are still needed to evaluate steroid and antiviral therapies
Measles
-rubeola virus: RNA myxovirus
-rash, conjunctivitis and buccal mucosal lesions known as Koplik spots
-permanent SNHL in < 0.1%
-usually bilateral, worst in high frequencies
-mild to moderate (55%) or profound (45%)
-loss of vestibular function, manifested by reduced or absent caloric responses in as many as 72%
-vaccine has markedly decreased incidence of measles-related hearing loss
-temporal bone findings:
-atrophy of organ of Corti, which is worst at basal aspect of cochlea
-degenerative changes in spiral ganglion, stria vascularis, and tectorial membrane
-collapse of Reissner membrane
-alterations consist of multinucleated giant cells known as Warthin-Finkelday cells
-acute phase:
-xanthematous rash
-Koplik spots (small white foci representing necrotic lesions of buccal mucosa)
-mild conjunctivitis
-acute otitis media (rarely)
-diagnosis:
-isolating rubeola virus from throat cultures, documenting a fourfold increase in titers of antibody
to rubeola virus between acute and convalescent sera, or immunofluorescent staining of exfoliated
epithelium from oropharynx or conjunctiva, which can demonstrate rubeola antigen
-no clear documentation that steroid or antiviral therapy can benefit acute disease by preventing or
ameliorating SNHL
Varicella-Zoster
-herpesvirus VZV
-primary infection manifested clinically as chickenpox
-pustular rash
-Ramsay-Hunt syndrome:
-develops when latent virus is reactivated and consists of variable severity of facial nerve
paralysis, SNHL, and vertigo in associated with a painful vesicular rash of external auditory canal
and concha
-inflammatory neuritis of facial, cochlear, and vestibular nerves
-histopathology:
-atrophy of cochlear neurons and sensorineural elements of vestibular labyrinth
-collapse of Reissner membrane and fibrous tissue and neoossification in perilymphatic
compartment of lateral semicircular canal
-pts may be immunocompromised
-SNHL worse in high frequencies
-ENG may reveal a reduced or absent vestibular response in involved ear
-treatment:
-corticosteroids and acyclovir
-severe SNHL rarely recovers completely
1104
DELAYED ENDOLYMPHATIC HYDROPS
Etiology
-light microscopy variably reveals:
-cryptococcosis of inner ear and IAC
-CMV-associated inclusion bodies in IAC and inner ear
-no alterations
LUETIC LABYRINTHITIS
Etiology
-T. pallidum
-SNHL develops in congenital and acquired forms with variable frequency
-congenital:
-early: generally fatal
-late: sudden SNHL in childhood generally symmetric and profound with vestibular symptoms
-in 51% SNHL appears suddenly and asymmetrically between ages of 25 and 35 years
-acquired:
-SNHL can occur in primary, secondary, and tertiary forms
-histopathology:
-mononuclear leukocytic infiltrates and obliterative endarteritis
-inflammatory fibrosis with round cell infiltration can obliterate endolymphatic sac and duct
hydrops
-gummas, central necrosis, and lymphocytic infiltrates are most frequent in vestibular otic capsule
and can result in degeneration of sensory and neural structures of labyrinth and eighth cranial
nerve
-gummatous involvement of ossicles CHL
1105
-serologic testing:
-VDRL
-FTA-ABS
-false positives in connective tissue diseases, leprosy, infectious mononucleosis,
pregnancy
-treatment:
-at least 3 months
-penicillin G 2.4 MU IM for early stage
-procaine penicillin 1.8 MU IM daily for 3 weeks with 500 mg of probenecid po q6h, then 2.4
MU of benzathine penicillin G IM weekly to total of 3 months for late-stage disease
1106
NOISE-INDUCED HEARING LOSS
PATHOGENESIS
Pathology
-primary site if injury = rootlets of sterocilia
-TTS: outer hair cells’ stereocilia become less stiff respond poorly to stimulation
-stereocilia are able to recover
-PTS: fusion of adjacent stereocilia and loss of stereocilia
Acoustic Trauma
-single exposure to intense short-duration sound can cause permanent HL not preceded by TTS
-sound mechanically damages organ of Corti, tearing membranes, rupturing cells, allowing perilymph and
endolymph to mix
-impulse noise:
-range in 0.2 ms duration with peak energy at 2-3 kHz
-most hazardous (eg. small arms gunfire): above critical level of 140 dB
-impact noise:
-caused by collision of metal objects
-can cause acoustic trauma, but less likely than impulse noise to reach critical levels
1107
Interactions
-Aging: additivity: net hearing loss is the decibel sum of threshold shifts from aging and from noise
-Vibration: interacts with noise to damage ear (seen in “vibration induced white finger”)
-Drugs and Chemicals: no definite interactions
-Susceptibility: not well studied
Epidemiology
Nonoccupational Exposures
-gunfire
-most important non-occupational cause of NIHL
-impulses can range up to 170 dB
-exposures to leaf blowers, chain saws, and rock concerts can reach the 110-120 dBA range but few
persons accrue significant time in these exposures except in an occupational setting
1108
MANAGEMENT
Hearing Conservation
-OSHA requires hearing protection for workers exposed to 85 dBA
-prevent exposures exceeding 90 dBA for an 8-hour day
-5 dB “trading rule”:
-exposure time cut in half for each 5 dB increment exposure level
-eg. 8-h exposure to 90 dBA = 4-h exposure to 95 dBA = 2-h exposure to 100 dBA
-maximum permissible exposure (without hearing protection) is 90 dB TWA (time weighted average =
constant exposure for 8 hours)
-impulse noise exposure is limited to 140 dB peak level
-In Canada:
-workplace regulations vary from province to province
-it has been proposed that 85 dB(A) be used as the level for mandatory hearing testing and the
implementation of a hearing conservation program
-Canadian standards restrict noise levels in the workplace to 87 decibels for an eight-hour daily
exposure
-for each increase of 3 decibels, the duration of the worker'
s exposure to noise must be
reduced by half
1109
OTOTOXICITY
Aminoglycosides
-mechanism of action:
-act on bacterial ribosomes to stop synthesis of bacterial cell protein
-bactericidal against gram-negative aerobic bacilli
-mechanism of ototoxicity (theory):
-aminoglycosides form complexes with iron free radicals damage to outer hair cells and
vestibular receptors
-histopathology (order of progression):
1. early damage to first row of outer hair cells beginning at basal turn of cochlea high
frequency SNHL
2. progression to apex
3. second and third rows of outer hair cells
4. inner hair cells
-may be genetic predisposition
-damage is permanent if symptoms persist beyond 2-3 months
-vestibulotoxic:
-streptomycin and gentamicin
-manifested by vertigo or disequilibrium
-overall incidence of 15% for gentamicin
-cochleotoxic:
-amikacin, neomycin, kanamycin, tobramycin
-onset heralded by tinnitus
-agents that potentiate or synergise with aminoglycosides to cause ototoxicity:
-ethacrynic acid (facilitates gentamicin diffusion into endolymph)
-furosemide
-cisplatin
-flagyl
Macrolides
-ototoxicity reported mainly in pts receiving long-term, high-dose therapy such as for HIV-related
infections
-MOA for ototoxicity unknown
-most common manifestation is hearing loss in conversational frequencies
-hearing loss is reversible
Vancomycin
-rare reports of cochleotoxicity
-tinnitus and high-frequency hearing loss
Antineoplastic Agents
Cisplatin
-usually permanent hearing loss, bilateral and symmetric
-high-frequency hearing loss:
-histopathology: outer hair cell damage and cell loss most extensive in basal turn
-MOA for ototoxicity thought to be d/t generation of oxygen free radicals within inner ear and
depletion of glutathione in auditory hair cells
->50% receiving > 400 mg/m2 permanent ototoxicity
1110
-risk factors:
-high cumulative dose of cisplatin
-hx of noise exposure
-high dose of vincristine
-high dose of individual cycle than total dose
-elderly or young children
Carboplatin
-79% of patients experience hearing loss
-inner rather than outer hair cells are damaged
Diuretics
-furosemide and ethacrynic acid
-SNHL, tinnitus and vertigo
-transient and permanent loss reported
-incidence of ototoxicity ~ 6%
-MOA: injury to stria vascularis
-disturbance of K-ion transport with subsequent reduction of endocochlear potential
-keeping the rate of continuous infusion at rates less than 15 mg/min
Salicylates
-typically from high-dose aspirin therapy for arthritis
-limited to cochlea flat, bilateral, SNHL and tinnitus
-serum salicylate levels > 30 mg/100L
-threshold shifts of 30-40 dB
-complete reversibility within 2-3 days after cessation
Ototopicals
-human studies estimate incidence ~1/10 000
-avoid prolonged use especially when a tympanic membrane perforation present
-avoid use in a healthy ear
-studies in guinea pigs failed to show evidence of ototoxity with topical quinolones
MONITORING
1111
CEREBELLOPONTINE ANGLE TUMOURS
ANATOMY
1112
VESTIBULAR SCHWANNOMAS
Epidemiology
-incidence: 1/100 000 per year
Tumour Biology
-arise from vestibular segment of eighth cranial nerve (superior = inferior nerves)
-most commonly occur at Scarpa ganglion
-sporadic (98%)
-bilateral in type 2 neurofibromatosis
-genetic defect on long arm of chromosome 22
-autosomal-dominant
-tumours tend to occur in younger patients
-more adherent to facial nerve greater chance of losing hearing with surgical treatment
Clinical Manifestations
-symptoms:
-unilateral auditory or vestibular symptoms (true vertigo in 19%)
-hearing loss (85%), tinnitus (56%) and vestibular dysfunction
-disequilibrium (50%)
-fifth cranial nerve compression mid-facial hypesthesia (maxillary division)
-brainstem compression hydrocephalus headache and visual loss
-loss of speech discrimination out of proportion to hearing loss
-SSNHL presenting symptom in 26%
-cause of sudden loss from vestibular schwannoma in 1-2.5% of pts with SSNHL
-d/t sudden vascular occlusion of labyrinthine artery
-others: ocular symptoms (CN VI), dysphagia, hoarseness, aspiration, cerebellar dysfunction
-signs:
-Hitselberger sign: decreased sensation in EAC - sensory branch of seventh nerve affected
-decreased cranial nerve function: eg. decreased corneal reflex
Histology
-Antoni Type A:
-histologically parallel nuclei (palisading Verocay bodies)
-uniform spindle cells
-compact cells
-Antoni Type B:
-histologically less uniform
-may have fatty or hyaline degeneration
-less cellular
-more cystic
Diagnostic Tests
-audiometric testing:
-pure-tone testing: SNHL - most commonly unilateral high frequency (65%)
-speech discrimination: scores out of proportion with pure-tone thresholds
-rollover phenomenon: performance decreases significantly when the intensity of
speech signal is raised
-reflex thresholds typically elevated or absent
-if present reflex then reflex decay measured:
-signal presented 10 dB above reflex threshold for 10s if contraction of
1113
stapedius cannot be maintained for at least half strength for the 10s positive
retrocochlear finding
-electrophysiologic testing:
-ABR most sensitive and specific audiologic test
-electrical potentials measured in response to broad-band clicks of short duration
-abnormalities seen:
-interaural difference in latency of wave V with delay of more than 0.2 msec (40-60%)
-no identifiable waveforms in pt without significant hearing loss in higher frequencies (20-
30%)
-presence of wave I but absence of other waves (10-20%)
-normal in 10-15% of patients: sensitivity is 85-90%
-summary of ABR findings suggestive of retrocochlear lesion:
-vestibular testing:
-ENG: unilateral weakness of involved side on caloric testing
-tumours originating form inferior vestibular nerve may be missed (ENG only tests
superior nerve)
-no abnormality for smaller tumours
-hypoactive response on ENG indicates tumour probably on SVN favourable
prognosis for hearing
-hearing preservation more difficult with tumour in IVN b/c of proximity to
cochlear nerve and possible shared blood supply
-imaging studies:
-CT scan:
-90% of AN are enhanced
-intracanalicular tumours often missed
-CT only 63% accurate in diagnosing AN (may miss tumours smaller than 1 cm)
-intrathecal contrast or air CT cisternography improves diagnostic yield (historical)
-gadolinium enhanced MRI
-sensitive
-differentiation between AN and meningioma:
-AN: centered on IAC and has globular appearance causing acute angle formed
between posterior face of temporal bone and tumour surface; generally extends
into IAC “ice cream cone” appearance
-usually more non-homogenous than meningiomas
1114
Management
-goals: preserve life > avoid serious neurologic sequelae > complete tumour removal > preserve facial
nerve function preserve hearing
-observation:
-growth potential (3 groups):
-no growth or very limited growth (0.2 mm/y) (40%)
-limited growth (2 mm/y)
-rapid growth (10 mm/y)
-observation reserved for elderly pt or those with serious medical disorders who have small slow-
growing tumours
-younger pt better served by having tumour removed
-surgery:
-Translabyrinthine Approach
-indications:
-approach of choice for non-serviceable hearing
-advantages:
-most direct route to CPA
-requires minimal cerebellar retraction
-widely exposes fundus of IAC for better tumour removal
-offers best opportunity for immediate repair of CN VII if it is injured
-disadvantages:
-hearing is sacrificed
-approach used for tumours of all sizes
-results:
-mortality rate low (0.4%) and directly proportional to tumour size
-recurrence rate low (0.3-0.5%)
-complications:
-facial nerve paralysis (usually temporary) - most common
-CSF leak (4-14%)
-meningitis
-Retrosigmoid-Suboccipital Approach
-indications:
-for good preoperative hearing and tumour medially located within IAC and
protrudes >2cm into CPA
-large tumours, tumours of the medial IAC
-advantage:
-potential for hearing preservation
-ability to remove tumours of all sizes
-good visualization of brainstem and lower cranial nerves
-lower risk of facial nerve injury than middle cranial fossa approach
-disadvantage:
-potential for air embolism
-higher incidence of postoperative headaches
-limited exposure to lateral IAC
-higher risk of facial nerve injury than translabyrinthine approach
-requires cerebellar retraction
1115
-results:
-complete resection in 95%
-hearing preservation: 17-63%
-complications:
-CSF leak: 11-15%
-meningitis: 1-7%
-recurrence: <1%-3%
-Stereotactic Radiosurgery
-controversial
-radiation doses six times more than clinical maximum failed to eradicate
schwannoma cells in vitro
-no long term results
-significant hearing loss, facial nerve dysfunction
-multisource cobalt 60 gamma unit or linear accelerator
-usually for small tumours (< 1 cm)
-usually used for elderly or otherwise poor surgical candidates
1116
OTHER TUMOURS OF THE CEREBELLOPONTINE ANGLE
Meningiomas
-second most common tumour originating within CPA (3% of tumours in this region)
-arise from cap cells (endothelial cells)- collect in clusters around tips of arachnoid villi
-two types:
-globular
-en plaque (flat and sessile)
-histologic subtypes:
-meningotheliomatous meningiomas (55%)
-fibrous meningiomas (15%)
-transitional meningiomas (30%)
-angioblastic meningiomas (5%)
-generally larger than AN before causing hearing loss or vestibular symptoms
-ABR may be normal in 25% of pts
-CT scans:
-meningiomas:
-more dense appearance and generally are homogenous in taking up contrast medium
-evidence of hyperostosis and calcification within tumour
-sessile and broad based (“dural tail”) - no widening of IAC
-AN usually non-homogeneous because of areas of central necrosis
-MRI scans:
-“washed out” appearance because of vascularity less bright image than that of AN
-surgical resection for treatment:
-translabyrinthine approach:
-poor hearing and tumour at CPA
-transcochlear approach:
-medial extension of tumour to IAC and onto clivus
-GSPN section, facial nerve removed and transposed posteriorly, cochlea drilled away
-other combined approaches: middle fossa, retrosigmoid
Epidermoids
-may arise either within temporal bone or CPA
-hemifacial spasm is common early distinguishing feature and progressive facial paralysis frequently noted
-thought to arise from epithelial rests within temporal bone
-identical to cholesteatomas of middle ear
-MRI: dark on T1, extremely bright T2 signal; non-enhancing
-complete surgical resection usually difficult because of propensity of tumour to infiltrate between cranial
nerves and blood vessels
1117
Vascular Tumours
-glomus jugulare tumours
-non-chromaffin paragangliomas that arise from chemoreceptor cells along ninth and tenth cranial
nerves in jugular bulb
-pulsatile tinnitus
-CT: irregular destruction of jugular foramen
-tx: surgical resection through infratemporal fossa approach
-haemangiomas, hemangioblastomas
-often arise from geniculate ganglion
-slowly progressive facial paralysis
-tx: surgical excision by middle fossa approach
1118
F.Ling - CPA Tumours (8)
1119
SUDDEN SENSORY HEARING LOSS
DEFINITION
-any noticeable and measurable loss of hearing function - pitch or speech perception - occurring over a
matter of minutes to days
-loss of significant hearing (>30 dB) in at least 3 adjacent frequencies that occurs over less then 3 days
EPIDEMIOLOGY
-5-20 per 100 000
-M=F
-bilateral in 1-2% of cases
-median age at presentation: 40-54 years
DIFFERENTIAL DIAGNOSIS
-defined vs. idiopathic (ISSHL) DDx IN SUDDEN HEARING LOSS
-most cases idiopathic (85-90%); four theories: (defined)
-viral infection Infection Bacterial
-vascular compromise Meningitis
-intracochlear membrane rupture Labyrinthitis
-immune inner ear disease Syphilis
Viral
Mumps
Viral Infection CMV
-high prevalence of recent viral type illness, recent viral
seroconversion, temporal bone histopathology Inflammation Autoimmune
Cogan syndrome
-rates of seroconversion for herpesvirus family significantly SLE
higher in SHL population MS
-viral cause implicated but cannot be proved
Trauma Temporal bone fracture
Acoustic Trauma
Vascular Compromise Perilymphatic fistula
-cochlea: labyrinthine artery - no collaterals
-cochlear function sensitive to changes in blood supply Tumour CPA tumour
Temporal bone metastasis
-reduced O2 tension to stria vascularis
Toxins Aminoglycosides
Intracochlear Membrane Rupture ASA
-a leak of perilymph fluid into middle ear via round window
Vascular Thromoembolism
or oval window postulated to produce hearing loss by creating
Macroglobulinemia
a state of relative endolymphatic hydrops by producing Sickle cell disease
intracochlear membrane breaks Coronary bypass graft surgery
-break in membrane mixing of endolymph and perilymph
alters endocochlear potential
1120
EVALUATION
-history, physical
LABORATORY TESTS
-pneumotoscopy search for fistula sign
-audiogram CBC polycythemia, leukemia,
-ABR, OAEs, +/- ENG thrombocytosis
-laboratory tests (see table)
ESR nonspecific screen for autoimmune or
-CT/MRI of CPA eventually inflammatory disease, follow with ANA
-1-2% of pts with ISSHL have IAC or
CPA tumours FTA-ABs/MHA-TP syphilis
-also looking for cochlear dysplasia,
Coagulation studies if indicated, by history
Mondini malformation, or enlarged Thyroid function if indicated by history
vestibular aqueduct
TREATMENT
Empiric Therapy
-corticosteroids
-presumed reduction of cochlea and auditory nerve inflammation
-Prednisone 1 mg/kg po qd x 7-14 days then recheck hearing
-antivirals
-acyclovir: no real benefit if started after 5-7 days
-others: amantadine, famciclovir, valaciclovir
-effects of treatment not yet reported
Other Therapies
Vasodilators
-improve cochlear blood supply
-histamine, nicotinic acid, papaverine, procaine, niacin, carbogen have been used
-few data support vasodilator therapy
Rheologic agents
-alters viscosity of blood to improve blood flow
-LMW dextrans, anticoagulants, pentoxifylline (Trental)
Diuretics
-presumed cochlear endolymphatic hydrops
-mechanism of action for diuretics in SHL not understood
Surgery
-repair of oval and round window perilymph fistulae
1121
PROGNOSIS
1122
TINNITUS
DEFINITION
Objective Tinnitus
-perception of sound caused by an internal body sound or vibration
Subjective Tinnitus
-perception of sound in the absence of any acoustic, electrical or external stimulation
-more common than objective tinnitus
-typically associated with high frequency hearing loss
-prevalent b/n ages 40-70
-M > F
WORK-UP
-similar work-up as hearing loss
-special attention to retrotympanic masses, audible bruits, history of trauma, medications, presence of TMJ
and psychological factors
-character of tinnitus:
-unilateral or bilateral
-high-pitched or low-pitched (roaring, buzzing)
-pulsatile
-clicking
-progression and frequency
-loudness, pure or multiple tones
-level of discomfort
1123
OBJECTIVE TINNITUS
Vascular Causes
-pulsatile; synchronous with heartbeat
AV shunts
-congenital
-interconnections between occipital artery and transverse sinus, internal carotid and vertebral
vessels, or middle meningeal artery and greater superficial petrosal artery have been reported
-acquired
-most common cause: glomus tympanicum or glomus jugulare
-dx: CT of middle ear showing erosion of caroticojugular spine or lesion lying within middle-ear
space
Arterial Bruits
-carotid stenosis (most common cause of objective tinnitus)
Venous Hums
-hypertension or abnormal high placement of jugular bulb
-partial occlusion or narrowing of transverse sinus
-near transverse sinus/sigmoid sinus junction; result of ingrowth of arachnoid granulation
turbulence
-no specific management
Mechanical Causes
Palatomyoclonus
-sxs: irregular clicking sound, ear fullness, distortion of hearing
-muscle spasm postoccipital headache and TMJ pain
-tx: muscle relaxants, Botox injections into active muscle
1124
SUBJECTIVE TINNITUS
-more common than objective tinnitus (35-45% population experience tinnitus)
-major sleep difficulty in 8%
Treatment
-treat any reversible otologic or medical disorder
-majority of tinnitus cases resolve spontaneously:
-75% improve; 25% remain unchanged
-avoid: chocolate, coffee, tea, cola (caffeine)
-stop smoking
-re-evaluate medications
-radio on at night
-treat depression/anxiety
Masking
-minimal masking level provides some indication as to whether masking can be used successfully
-if level required is greater than 10-15 dB sensation level success is doubtful
-usually ~60% of those with severe tinnitus benefit from masking
-approximately 80% of patients will have their tinnitus masked with 6 dB or less of sound pressure
Hearing Aid
-can be a first-trial device
-only 25% are relieved by this method alone
Tinnitus Instrument
-combination hearing aid and masking device
-produces sound from 1.5 to 8 kHz with volume potential from 45-90 dB
-ability to modify input of hearing aid and masking device independently
Masker
-limited to patients with normal or near normal hearing
-only 1/3 find this device useful
Habituation therapy
-patient stimulated with broad-band noise up to 16 hours a day
-over period of months (10-18) patient may become unaware of or untroubled by the tinnitus
Medications
-only medications that have proved useful have been drugs that affect emotional status of patients through
anxiety reduction, improved sleep pattern, and antidepressant effect
-consider benzodiazepines, tricyclics antidepressants, and carbamazepine
1125
Electrical Stimulation
-investigational
-initial results not encouraging
Surgery
-currently rarely has a role in treating tinnitus
1126
AUTOIMMUNE INNER-EAR DISEASE
1127
AUTOIMMUNE IMMUNOPATHOLOGY
TREATMENT
1128
AGING AND THE AUDITORY AND VESTIBULAR SYSTEM
1. Cochlear
-epithelial atrophy with loss of sensory cells and supporting cells of organ of Corti
-progressive hair cell reduction begins at age 40
-high-frequency hearing loss with speech discrimination preserved in initial phases
2. Neuronal
-reduction of number of functioning cochlear neurons
-when reduction has reached 50% or more, hearing loss develops
-nonprecipitous, generalized loss of pure tone thresholds with speech discrimination
impaired out of proportion to the threshold shift
3. Metabolic
-atrophy of stria vascularis
-loss of 30% or more of strial tissue can result in clinical hearing loss
-flat hearing loss with good preservation of speech discrimination
1129
CAUSES OF BILATERALLY SYMMETRIC SNHL
Disorder Characteristics Diagnosis Treatment
Meniere disease -episodic attacks of fluctuant SNHL, -hx of typical attacks with medical: diuretics and low-salt diet
vertigo, tinnitus, aural fullness or symptom-free intervals; hearing surgical: decompression or shunt
pressure; bilateral in 20-30% of cases loss involves low tones initially of endolymphatic sac; section of
and later all frequencies; rule out vestibular nerve
neurosyphilis
Luetic hearing -often bilateral SNHL with no -positive FTA-ABS test, with or -penicillin and oral steroids
loss (late acquired characteristic audiometric pattern without clinical history of syphilis
syphilis) -speech discrimination score often worse
than would be predicted on basis of pure
tone thresholds
-often associated with vestibular
symptom
-may mimic Meniere disease
Paget disease -slowly progressive SNHL and CHL -skeletal deformities of skull and -calcitonins
-SNHL worse in high frequencies long bones of extremities, elevated
-maximum CHL of 20-30 dB at 500 Hz serum alkaline phosphatase and
urinary hydroxyproline
Hypothyroidism -slowly progressive SNHL affecting all -usual clinical stigmata of -thyroid replacement
frequencies daily hypothyroidism
-decreased serum T4
PRESBYCUSIS
1130
-tests of central auditory function suggest that older pts have poorer speech discrimination than younger pts
because of changes in central auditory processing
VESTIBULAR DYSFUNCTIONS
TYPES OF DIZZINESS
Category Sensation Diagnosis
Vertigo -illusion of motion, either linear or rotating -vestibular disturbance d/t peripheral or central disease
Presyncope -impending faint -diffuse cerebral ischemic d/t vasovagal response, cardiac disease, or
metabolic disorders
Dysequilibrium -impaired balance and gaze -impaired motor control d/t neuromuscular disease, severe bilateral
vestibular disease, stroke, multisensory deficits, or medications
Nonspecific -light-headeness, “confusion”, “wooziness”, -often psychological disorders (anxiety, depression, panic),
“foggy-headed” hyperventilation
NONSPECIFIC THERAPY
-drugs:
-five main classes of drugs used to control acute vestibular and autonomic symptoms:
-antihistamines (eg. meclizine - 12.5-25 mg po tid)
-phenothiazine (eg. promethazine)
-anticholinergics (eg. scopolamine)
-5HT3 antagonists (eg. ondansetron)
-benzodiazepines (eg. diazepam - 2.5-7.5 mg po daily)
-should be used sparingly and for short durations because they can cause reduction in CNS compensation
-vestibular rehabilitation
-involves specific habituation exercises designed to enhance normal adaptive mechanisms in CNS
-components: gaze stabilization, balance retraining, desensitization
ABLATIVE THERAPY
-for pts who continue to suffer from incapacitating, lifestyle limiting vertigo despite maximum medical
therapy
1131
COCHLEAR IMPLANTS AND OTHER
IMPLANTABLE AUDITORY PROSTHESES
-typical response range of a deaf ear to electrical stimulation is on the order of only 10-20 dB
-cochlear implants convert sound into an electric signal and stimulate the cochlear nerve directly
-strategies of encoding sounds:
-tonotopic organization:
-providing improved sense of pitch by delivering signals to different locations in the
cochlea
-temporal/rate coding:
-recognition from rate of presenting stimulus
-slow rate low pitch sound perceived
-fast rate high pitched sound perceived
-intensity coding:
-varying the intensity of the stimulus
-takes advantage of tonotopic arrangement: incoming speech signal is filtered into a number of frequency
band, each corresponding to a given electrode in the array
PATIENT SELECTION
Considerations
-age
-duration of deafness
-language
-mode of communication (auditory, speech cues, sign language etc..)
-other handicaps
-motivation
1132
Adults
-implantation of ear with any residual, Adult criteria:
aidable hearing carries risk that the implanted -> 18 years of age
ear could be made worse than the ear with a -bilateral severe-to-profound hearing loss (> 70 dB)
hearing aid -minimal benefit from conventional hearing aids (SRS
-adults with prelingual hearing loss generally < 30-50% in best aided condition)
are not considered good candidates for -HINT < 50% in best aided condition
cochlear implantation -no medical contraindications
Children
-both pre- and postlingually deafened children are candidates for cochlear implantation
-trend towards earlier implantation; electrical stimulation appears to be capable of preventing some of the
degenerative changes in the central auditory pathways
-age limit currently 12 months
-early implantation important in meningitis because progressive intracochlear ossification can occur and
precludes standard electrode insertion
-high incidence of OM in children < 2 y might compromise biosafety of cochlear implants
-cochlea is adult size at birth
-by 1 year, facial recess and mastoid antrum are adequately developed
1133
AUDIOLOGIC ASSESSMENT
-all potential candidates must have completed a period of experience with a properly fitted hearing aid
-parent questionnaires are used to determine hearing aid benefit
-various tests:
-HINT: hearing in noise test
-ESP: early speech perception test
-MAIS: meaningful auditory integration scale
-LNT: lexical neighbourhood test
-MLNT: multisyllabic lexical neighbourhood test
-PBK: phonetically balanced kindergarten
MEDICAL ASSESSMENT
PSYCHOLOGICAL ASSESSMENT
-exclusion: organic brain dysfunction, mental retardation, undetected psychosis, or unrealistic expectations
SURGICAL IMPLANTATION
1134
Complications
-most commonly encountered:
-postauricular flap problems
-facial nerve injury
-others:
-CSF gushers
-infected implant
-meningitis
-device failure
-device migration or extrusion
-residual hearing will be lost
-temporary dizziness, tinnitus or taste disturbance
CLINICAL RESULTS
Adult Outcomes
-many adults now demonstrate substantial speech understanding as early as 3 months following cochlear
implantation
-great deal of variability in performance
-factors affecting success:
-age at implantation and duration of deafness:
-younger age - shorter period of auditory deprivation more likely to achieve good
outcomes
-others:
-IQ associated with good speech perception skills
-lip-reading ability
-degree of residual hearing
Pediatric Outcomes
-assessment of performance in prelingually acquired hearing loss can be challenging
-battery of tests are required for assessment:
1135
MIDDLE EAR IMPLANTS
Principles
-vibrate ossicular chain by electromagnetic or piezoelectric means
-direct transmission of mechanical energy of amplified sound vibrations to ossicular chain
-MEI is coupled to ossicular chain or OW, eliminating acoustic coupling via EAC
-conversion of electric mechanical energy by 2 mechanisms
-electromagnetic (em): max output 140 dBSPL
-piezoelectric (PZ): max output 110 dBSPL
-impedance of electromagnetic implant is 1/5 that of piezoelectric crystal
Components
-external audio processor (battery, digital signal processor, microphone):
-mic picks up acoustic input & transmits electromagnetic signal to implanted receiver
-surgically implanted internal receiver (magnet):
-also incl a floating mass transducer crimped onto long process of incus
-coupling to ossicular chain driven by conductor link / induction coil
-placed via mastoid-facial recess approach
Advantages
-eliminate acoustic feedback
-wider frequency response
-eliminate tight-fitting EAC mold
-improve perception of auditory signal
-usable in professions eg musicians, athletes, headsets
-usable in enviro of heat, moisture, dust
Disadvantages
-for limited range of mod SNHL only
-SD must be > 50%
-not for CHL or retrocochlear HL
-need stable middle ear system
-need intact TM
-need good earmold fit
-very costly!
-risks of surgery: facial nerve injury, dysgeusia, bleed / infection / anesthesia
1136
-normal tympanometry
-normal middle ear anatomy
-no previous history of chronic middle ear disease or middle ear surgery
-no inner ear disorder
-dissatisfied with or unable to wear HA
1137
HEARING AIDS AND ASSISTIVE LISTENING DEVICES
-amplification (gain):
-linear:
-direct relationship maintained b/n signal input and output
-input/output slope = 1.0
-nonlinear:
-vary gain via amplitude compression or expansion
-input/output slope < 1.0; slope reduced by a constant
-sound level at output remains audible and comfortable over broad range of input
intensity
-compression most useful for those with reduced dynamic range (threshold of hearing
and discomfort)
-as hearing input increases, the amount of gain is automatically reduced to avoid
reaching an uncomfortable level
-saturation sound pressure level:
-maximum amount of sound pressure output that a hearing aid can produce
-venting:
-reduced the “occlusion effect” (relative increase in low-frequency sounds muffled sounds)
1138
-Signal to Noise Ratio (SNR)
-quantifies degree to which signal of interest is audible above the interfering noise at any given
moment in time
-directional microphone HA allow for improved SNR based on spatial location of signal of
interest
-offers improved speech intelligibility in noisy environments
-effectiveness is reduced when:
-signal of interest is located at great distance
-increased level of reflected (as opposed to direct) sound energy
BTE -range of power sufficient to reach severe and profound -earmold must fit snugly in EAC to eliminate feedback
hearing loss -may be difficult to hold in place for those with small
-allows adequate space to accommodate gain, output, and pinna or children
frequency response controls on analogue instruments for -cosmesis
adjustment by dispenser
-allow for placement of directional microphone
ITE -cosmetically appealing -amount of real ear gain may be limited because of
-placement of microphone takes advantage of pinna and feedback problems secondary to close proximity of
concha effects enhancing amplification in high frequencies microphone and receiver especially in cases of severe-
-microphone placement improves sound source profound high-frequency hearing loss
localization as head is moved
-may be easier to insert because only one component is
involved
-allows for placement of directional microphone
ITC -more cosmetically appealing -amount of gain sufficient for no more than moderate
-microphone placement takes advantage of pinna and hearing loss
concha effects boosting gain in high frequencies -requires good dexterity to insert
-microphone placement improves localization to sound -small size limits number of output/response controls in
source as head is moved analogue instruments
-venting options limited
-deep placement precludes use of directional microphone
CIC -most cosmetically appealing -amount of gain is sufficient for no more than moderate
-not visible in ear hearing loss
-takes full advantage of pinna and concha effects and -requires good dexterity to insert/change batteries
reduces occlusion effect -limits number of output/response controls in analogue
instruments
-deep placement precludes use of directional microphone
-venting options very limited
-deep tight fit requires precision and not possible on all pts
d/t ear geometry
1139
4. In the Canal (ITC)
-allows for normal acoustics provided by pinna
-increases gain in high frequencies
-helps with localization of sound
-patients who demonstrate the greatest improvements in speech intelligibility from amplification are those
who demonstrate a moderate to moderately severe hearing loss
-because they use hearing aids all the time
-hearing aid satisfaction, perceived hearing aid benefit and performance are not significantly correlated
with hearing loss
-important factors are motivation and acceptance of hearing loss
-subjectively, individuals who wear two hearing aids often indicate that they find speech easier to
understand even in noisier listening conditions
1140
-advantages of binaural amplification:
-better speech discrimination
-binaural squelch:
-release from masking
-improved speech intelligibility in noise when listening binaurally d/t phase
differences of the signal and noise
-improved sound localization with binaural hearing
-eliminates head shadow effects which reduce high-frequency cues necessary for hearing many
consonants
-binaural summation
-minimizes “auditory deprivation effect” of the unaided ear.
-failure to fit hearing aids on both ears of patients with binaural hearing loss can result in
temporary and perhaps permanent decrease in the auditory function in the unaided ear
-more natural and less stressful listening
-improved speech clarity
FM Wireless System
-affords acceptable SNR for speech understanding
-improves SNR in noisy environments
-improve speech perception in noise, reading/spelling ability, behaviour, psychosocial function, on-task
behaviours, and psychoeducational achievement in children
-talker has microphone FM broadcast to receiver unit worn by listener
Soundfield System
-deliver speech signal through a loudspeaker placed strategically in classroom environments
-proved improved SNR in classroom, which is beneficial for children with minimal hearing loss as well as
for those whose hearing loss has not been identified
1141
Infrared Systems
-signals transmitted via infrared light
-for public facilities
-speaker uses FM microphone/transmitter FM receiver/IR transmitter several light-emitting radiators
placed throughout room for uniform distribution
Other ALDS
-telephone, TV, radio and signalling devices
1142
PERIPHERAL VESTIBULAR DISORDERS
1143
Bilateral Vestibular Lesions
-symptoms caused by reduction in vestibular sensitivity and inaccuracy of VOR
-rapid head movement requires intact VOR
-without an intact VOR, quick head movements cause a slip of the visual field on the retina, and visual
acuity degrades
-patients report visual disturbance and light-headedness
-cerebellar compensation occurs; but cannot accommodate total or near total loss of bilateral vestibular
function results in oscillopsia (severe visual disturbances with head movement)
DIAGNOSIS
-history:
-describe dizziness:
-vertigo: illusion of rotational, linear, or tilting movement
-disequilibrium: sensation of instability of body positions, walking, or standing
-oscillopsia: inability to focus on objects with motion
-lightheadedness: sense of impending faint, presyncope
-physiologic dizziness: motion sickness, height vertigo
-multisensory dizziness: diabetes, aging resulting in partial los of multisensory systems
-onset and duration
-seconds to minutes: BPPV, VBI, epilepsy, arrhythmia
-hours: Ménière’s migraine
-days: vestibular neuritis, labyrinthitis
-constant: central causes
-severity, frequency
-associated symptoms:
-auditory (hearing loss, aural fullness, tinnitus, phonophobia)
-visual (blurred vision, diplopia, scotoma, photophobia)
-vegetative (nausea, vomiting)
-neurologic (dysphagia, dysarthria, hemipareisis, paraesthesia, etc..)
-precipitating factors (head movement or motion, stress, diet)
-medications
-PMHx:
-hypertension, cardiac arrhythmia, diabetes, thyroid disorders, vascular disease, otologic
problems, depression, neurologic disease, migraine, PMS
-recent head trauma, loud noise exposure, flying, diving, or heavy lifting
1144
-physical examination:
-head and neck examination, cranial nerve examination, eye movement examination, gait and
posture
-otologic testing
-penumatoscopy (induce nystagmus or dizziness) - fistula test
-inspection of TM and middle ear
-tuning forks
-vestibular testing:
-eye motility (check pursuit with convergence and divergence) test using Frenzel lenses
-spontaneous and gaze-evoked nystagmus
-Dix-Hallpike manoeuver
-head-shake nystagmus
-head motion in horizontal plane for 20-30 seconds, then suddenly stop to
evaluate for nystagmus
-head thrust test:
-examiner briskly moves pt’s head to one side while pt is directed to maintain
visual fixation on examiner’s face
-if unilateral vestibular weakness and inadequate VOR in one direction, pt
performs a refixation saccade after the head thrust to maintain visual fixation on
the target
-dynamic visual acuity test:
-pt asked to read lowest line on Snellen chart with head stationary and then
again during 2-Hz head oscillation
-for bilateral vestibular loss visual blurring during head oscillation
-neurologic exam:
-cranial nerve testing, Romberg’s test, gait
-investigations:
-audiogram
-ENG
-CT scan or MRI
1145
TREATMENT
Vestibular Rehabilitation
-most effective for rehabilitation of pts with sudden loss of vestibular function or positional vertigo
-also used in the management of vertigo of unknown causation
-head movements that produce the greatest symptoms of disequilibrium often are most useful in
rehabilitation
Psychogenic Disorders
-pts with dizziness frequently have history of chronic pain syndromes or panic attacks
-difficulty coping with disagreeable life situations
-dizziness disproportionate to objective findings often is part of a mechanism to manipulate family
members or to seek compensation for injury
1146
CENTRAL VESTIBULOPATHY
-central vestibular disorder implies abnormal processing of normal peripheral vestibular sensory inputs by
the CNS
-estimates of incidence among dizzy pts: 10-20%
-central compensation:
-ability of vestibular system to recover much of its overall effectiveness despite permanent
damage to some parts of the central processor
-hastened by repeated stimulation
DIAGNOSIS
-most pts have disequilibrium not vertigo, longer duration of symptoms with gradual onset, minimal
vegetative symptoms
-characteristics of nystagmus usually associated with central causes:
-direction: vertical, horizontal or torsional
-direction changing
-minimal nausea and suppression with visual fixation
-no latency or fatigue
-ENG: -abnormal smooth pursuit, saccadic, optokinetic nystagmus
Degenerative:
-age-related degenerative disease
Infectious:
-otitis meningitis, encephalitis, epidural abscess
-epidemic vertigo (antecedent viral infection)
-congenital syphilis
Circulatory:
-vertebrobasilar insufficiency
-Wallenberg syndrome (lateral medullary infarction)
-cerebellar haemorrhage
Autoimmune:
-Cogan syndrome: interstitial keratitis, fluctuating unilateral or bilateral hearing loss, episodic
vertigo
-acute cerebellar syndrome
Structural:
-Arnold-Chiari malformation: oscillopsia, hydrocephalus or tonsillar herniation
-hydrocephalus
Systemic:
-multiple sclerosis
-Parkinson disease
Primary or secondary neoplasms
Inherited:
-Waardenburg syndrome
-Huntington disease
-Familial periodic vertigo
Other:
-toxin exposure
-motion sickness
-vestibular epilepsy
1147
Migraine
-vascular syndrome caused by serial constriction and dilatation of intracranial blood vessels
-vestibular symptoms:
-motion intolerance, episodic vertigo, disequilibrium
-usually precede headache, during aura phase
-migraine-related vestibulopathy suspected when pt has personal or family history of migraine headache,
even if pt does not currently have headaches
-migraine-related vestibulopathy not associated with specific findings at ENG:
-most have no ENG findings
-abnormal findings include: unilateral or bilateral caloric weakness, spontaneous nystagmus,
positional nystagmus
-most common auditory symptom is phonophobia
-variants:
-Basilar migraine:
-headache preceded by symptoms of scotoma, transient blindness, vertigo, paresthesia,
slurred speech, ataxia, tinnitus, diplopia, loss of consciousness, motor weakness, hearing
loss
-Benign Paroxysmal Vertigo of Childhood:
-may represent early manifestations of migraine
-an episodic disorder in children under the age of 4 years
-completely normal child suddenly becomes frightened, cries out, clings to the parent or
staggers as though drunk, and exhibits pallor, diaphoresis, and often vomiting
-symptoms are accentuated by head movements and sometimes nystagmus and torticollis
are observed
-spells typically last for several minutes
-afterward the child is immediately normal and can resume playing as though nothing had
happened
-spells typically begin before age of 4 and occur up to several times a month
-after a period of 2 to 3 years, they decrease in number and gradually disappear
-most have no further spells after age of 7 or 8
-cause might be due to a vascular disturbance affecting the posterior circulation
-most eventually develop migraine
-look for dietary triggers: tyramine, alcohol, caffeine
-treatment:
-symptomatic: promethazine, diazepam, meclizine
-prophylaxis: B-blockers, CCBs, antidepressants
-medications to control headaches are not useful in controlling vertigo (eg. sumatriptan, NSAIDs)
Vertebrobasilar Insufficiency
-compression of vertebral artery compromises flow to posterior and anterior inferior cerebellar arteries
-SSx:
-transient vertigo with neck hyperextension or excessive rotation
-“4 D’s”: dizziness, diplopia, dysphagia, drop attacks
-dysarthria, headaches, hallucinations, ataxia, hemiparesis
-Wallenberg Syndrome:
-aka: lateral medullary syndrome
-infarction of PICA results in infarction of lateral medullary region of brainstem, spares
cochlear nucleus
1148
-SSx:
-acute vertigo (spontaneous nystagmus, nausea and vomiting)
-ataxia from incoordination of the ipsilateral limbs
-ipsilateral Horner Syndrome (anhydrosis, ptosis, miosis) from damage to sympathetic
fibers
-ipsilateral palatal paresis (dysphagia) and vocal fold paralysis (dysphonia) from
destruction of nucleus ambiguus
-ipsilateral numbness of face from involvement of spinal tract of trigeminal nerve
-ipsilateral lateral pulsion, diplopia from damage to CN VI
-ipsilateral loss of P+T sensation on face, contralateral loss of P+T on body, ipsilateral
paralysis of palate, pharynx and larynx
-Infarction of AICA:
-similar findings as above without Horner syndrome and abducens palsy
-hearing loss and tinnitus present (involves cochlear nucleus)
-Chiari Malformation:
-Classification:
-Type I: Protrusion of cerebellar tonsils
-Type II:Protrusion of cerebellar vermis, lower pons, and medulla (Arnold-Chiari
malformation) most common
-Type III: Herniation of cerebellum, forming a high cervical meningocele
-Type IV: Cerebellar hypoplasia, (variant of Dandy-Walker syndrome)
-symptoms:
-dissociated sensory loss:
-loss of P+T with relative sparing of vibratory sense and proprioception
-lower cranial nerve dysfunction:
-bilateral vocal cord paralysis, weakness, ataxia
-treatment:
-extensive surgical procedure consisting of surgical decompression of foramen magnum
with or without cervical laminectomy
-Other Anomalies:
-Basilar impression:
-occipital bone around foramen magnum deforms to cause posterior and superior
displacement of odontoid process
-Assimilation of the atlas
-bony union between atlas and skull base
-associated with posterior displacement of odontoid process
-Atlantoaxial dislocation:
-Down syndrome, Hurler syndrome, Morquio syndrome, achondroplastic dwarfism
Multiple Sclerosis
-multifocal demyelinating disease affecting the nervous system
-clinical course consists of multiple exacerbations followed by remissions
-although dizziness is not a common initial symptom of multiple sclerosis, as many as 50% of pts
eventually have some type of vestibular symptoms
-management of vestibular symptoms is supportive
1149
Miscellaneous Central Vestibular Disorders
-vestibular schwannoma:
-vestibulopathy present before surgical treatment may still be present after surgery
-vascular loop compression of eighth cranial nerve:
-controversial
-limited amount of histopathologic evidence suggests that this syndrome exists
-treatment would require intracranial procedure
1150
MEDICAL MANAGEMENT OF VESTIBULAR DISORDERS
AND VESTIBULAR REHABILITATION
MÉNIÈRE DISEASE
OTOSYPHILIS
-presumptive diagnosis of otosyphilis made when pt has unexplained cochleovestibular dysfunction and
positive results of FTAB absorption test
-penicillin and steroid therapy has been reported to improve vertigo among 58-86% of patients with
symptoms of otosyphilis
MIGRAINE
-migraine abortive therapy
-ergotamine tartrate
-sumatriptan
-migraine prophylaxis
-propranolol, flunarizine, nortriptyline, methysergide, verapamil
-TCA used for prophylaxis of vestibular migraine
-amitriptyline and imipramine have been used but have anti-cholinergic effects
-secondary amines (desipramine or nortiptyline) have fewer side effects and are the TCAs of
choice
1151
FAMILIAL ATAXIA SYNDROME
-autosomal dominant inheritance
-recurrent episodes of vertigo and ataxia among several members of a family
-acetazolamide effectively prevents episodic vertigo and ataxia
SYMPTOMATIC PHARMACOTHERAPY
VESTIBULAR REHABILITATION
1152
SURGICAL MANAGEMENT OF VESTIBULAR DISORDERS
PREOPERATIVE ASSESSMENT
-non-surgical techniques:
-Epley: canalith repositioning procedure
-Semont: liberatory manoeuver
-improved symptoms in 90%
-failure of one or both maneuvers after multiple repeated trials with debilitating symptoms is a prerequisite
for surgery
-surgical techniques:
-singular neurectomy
-nerve exits lateral aspect of IAC in the singular canal and courses inferiorly and
posteriorly to ampulla of PSCC
-intermediate segment is inferior-posterior to round window niche (sever the nerve at this
location)
-most common location is lateral to round window membrane (50%); 14-27% medial to
membrane
-transcanal approach
-complications:
-vertigo
-SNHL (20%; severe in 5%)
-extraordinarily difficult procedure
-PSCC occlusion
-transmastoid approach
-PSCC identified and bluelined
-laser partitioning of membranous labyrinth or packing with fascia or bone pate or bone
wax
-postoperative: dysequilibrium, transient sensorineural hearing loss
1153
OPERATIONS ON THE ENDOLYMPHATIC SAC (EXTERNAL SHUNTING)
-unknown therapeutic mechanism of sac surgery fuels controversy about its role in the management of
vertigo
-no controlled studies have documented the efficacy of sac surgery
-it appears that the benefit of sac surgery is limited in duration and that less invasive procedures can
provide similar benefit, although studies are not conclusive
-complete elimination of vertigo can be achieved by as many as 50% of patients, improvement occurs
among an additional 25%
-complications:
-SNHL (total 1%; mild-moderate 20%)
-facial nerve injury
-CSF leak
-bleeding from injury to sigmoid sinus or jugular bulb
LABYRINTHECTOMY
1154
SUPERIOR CANAL DEHISCENCE SYNDROME
PERILYMPH FISTULA
-definition: abnormal patency between inner and middle ear that allows flow of perilymph
-causes:
-temporal bone trauma:
-subluxations or fracture of stapes footplate and rupture of round window membrane
-minor changes in middle ear or intracranial pressure (less accepted theory)
-diagnosis by surgical exploration of middle ear with visualization of fluid leak in oval or round window
but it is still very subjective
-no good objective tests
-commonly reported symptoms:
-aural pressure
-disequilibrium exacerbated by exertion
-conductive or sensorineural hearing loss
-tx:
-initial bed rest - some defects seal spontaneously
-surgery only if symptoms are progressive and dizziness is debilitating
-transtympanic endoscopic approach used
-oval and round windows scrutinized for presence of fluid
-if fluid identified blood patch is placed
1155
TEMPORAL BONE NEOPLASMS AND LATERAL CRANIAL BASE SURGERY
(From Cummings - Ch 167)
Incision
-large C-shaped postauricular incision or Y-shaped incision
can be designed with a central island removed
-preauricular incision may be used for EAC involvement
Temporal craniotomy
-temporal craniotomy expose superior surface of petrous
bone
Osteotomy
-a groove may be drilled along floor of middle fossa
connecting glenoid fossa area, lateral IAC, and
posterosuperior mastoid
-osteotome is inserted into carotid canal just distal to first
genu and pointed toward internal auditory canal
-temporal bone specimen is brought out Subtotal temporal bone resection
1156
Total temporal bone resection
(A) frontotemporal-
retroauricular-cervical skin flap is
rotated forward
-external ear canal has been
transected
-facial nerve has been transected
just beyond stylomastoid foramen
-TMJ opened, and
mandibular ramus resected
-cranial nerves IX through XII and
jugular and carotid vessels are
exposed to neck
(E) with cerebellum retracted medially, cranial nerves V and VII through XI can be seen. labyrinthine (internal
auditory) artery has been transected at its origin from anterior inferior cerebellar artery
(F) cranial nerves VII through XI have been transected, and underlying dura has been incised as posterior border of
en bloc resection of petrous bone. petrous bone specimen then is disconnected from any remaining attachments and
removed. PICA—Posterior inferior cerebellar artery
1157
Reconstruction
-facial nerve and other appropriate CN can be cable grafted
-dural defects are closed as needed with fascia or pericranium
-temporalis muscle can be rotated and sutured to surrounding soft tissue
Cervical dissection
-done as needed to expose inferior margins of tumor
-to gain cervical control of vascular structures if needed
Radical mastoidectomy
-radical mastoidectomy removes air cell tracts lateral and
adjacent to otic capsule
-stapes suprastructure is removed to prevent inner ear
trauma
-facial nerve is skeletonized in preparation for transposition
-eustachian tube is obliterated with bone wax impregnated
with bone dust and a muscle plug
-removal of EAC, tympanic membrane, ossicles, and air
cells of temporal bone lateral to otic capsule constitute
radical mastoidectomy.
1158
Type A approach
-facial nerve transposition
-facial nerve skeletonized and freed of its bony
canal 180° circumferentially from geniculate
ganglion distally to stylomastoid foramen
-air cells of mastoid tip are exenterated lateral to
digastric ridge
-occlusion of sigmoid sinus
-bone is removed over posterior fossa dura anterior
and posterior to sigmoid sinus to allow ligation
-exposure of jugular bulb and internal carotid artery
-exposure of posterior infratemporal fossa now
permits isolation of vertical intrapetrous ICA
-with removal of bone over carotid artery and
beneath otic capsule, jugular fossa is exposed for
tumor removal
-tumor removal
-after exposure and distal control of ICA is
accomplished, tumor may be carefully removed
-jugular vein is ligated to prevent tumor and air
embolism
-closure of wound
-fascia lata provides best material for reconstruction, although lyophilized dura can be used to seal
defect
Type B approach
-differs from type A approach as facial nerve transposition usually is not required
-reflection of temporalis muscle still attached to coronoid process and zygoma allows retractor to expose
superior infratemporal fossa
-limits of operative exposure in type B approach are defined by middle cranial fossa (MCF) floor,
mandibular condyle, and reflected temporalis muscle
-thinning bone under MCF dura improves exposure
-petrous apex lesions, such as cholesteatoma or low-grade chondrosarcomas, may be removed at this point
with careful anterolateral retraction of ICA
Type C approach
-type C approach is an anterior extension of type B
approach
-permits posterolateral access to rostral clivus,
cavernous sinus, sphenoid sinus, peritubal space,
pterygopalatine fossa, and nasopharynx and to areas
exposed by type B approach
-in essence, permits access anterior to foramen
lacerum up to posterior aspect of maxillary sinus and
nasopharynx
1159
AGING AND AUDITORY SYSTEMS - PRESBYCUSIS
(From Cummings)
-characteristically results in bilateral symmetric neurosensory hearing loss in the frequencies above 2000
Hz
-increasing difficulty discriminating consonants in words
-ability to ignore competing speech also becomes impaired
-maintaining communication requires increasingly greater effort and energy
-30% of population over age 65 have significant hearing impairment
TYPES OF PRESBYCUSIS
Sensory presbycusis
-characterized by hair cell loss
-high-frequency, bilaterally symmetric sensorineural loss most frequently diagnosed in the elderly in the
clinical setting
-eventually, speech frequencies are lost
-degeneration of the organ of Corti - initially in the most basilar region and progressing apically about 15
mm along cochlear duct
-flattening and distortion with eventual loss of hair cells
-accumulation of lipofuscin, the aging pigment
Neural presbycusis
-associated with loss of spiral ganglion cells and axons; relative sparing of the organ of Corti
-gradual hearing loss with moderate slope towards high frequencies
-disproportionately severe decrease in speech discrimination
-basilar turn hearing usually normal
-apical innervation affected encoding of speech frequency and auditory information severely hampered
-associated with other neural deficits
1160
PROPOSED ETIOLOGIES
Vascular
-proposed as the cause of hearing loss in aging persons but insufficient histopathologic evidence
-progressive involution of human cochlear vasculature from fetus through the aged
-devascularization of capillaries and arterioles found in spiral ligament associated with aging
Diabetic presbycusis
-diabetic angiopathy narrowing of vessel lumens
-clinical audiologic and pathologic studies of the correlation between diabetes and presbycusis are
conflicting and contradictory
-in well-controlled studies, no correlation between sensorineural hearing loss and diabetes was found
Noise
-noise-induced HL may arise from mechanical damage, metabolic exhaustion or vascular changes
GENETIC CONSIDERATIONS
-typical hearing loss is basin-shaped curve with good discrimination and no recruitment
-pathologically, the most prominent feature in this disorder is atrophy of the stria vascularis, which is
parallel to Schuknecht’s strial atrophy category
-studies of the cochlea in temporal bones from patients with confirmed Alzheimer’s disease showed lack of
degeneration in the cochlea, which is typical of Alzheimer’s patients
TREATMENT
1161
CONGENITAL AURAL ATRESIA
(From Schuknecht - Laryngoscope 99; Sept 1989)
INTRODUCTION
-hypoplasia of EAC
-bilateral in ~30% of cases
-associated ipsicranial cephalic anomalies when they occur in syndrome are generally negative
prognosticators for successful corrective surgery for conductive hearing loss
-surgery delayed until the process of pneumatization of temporal bone is advanced: about 5 yoa
-aids:
-amplification and assistive auditory devices
-lip-reading instruction
-special education
-parental guidance
-immediate surgery for:
-partial meatal atresia that is developing obvious canal cholesteatoma
-total atresia with otologic or radiologic evidence of cholesteatoma, otitis media, or mastoiditis
-pre-surgical work-up:
-audiometry to determine status of better hearing ear
-ECoG to determine bilaterality of hearing
-CT scan to assess:
-extent of pneumatization
-appearance of ossicles
-location of facial canal
-configuration of bony labyrinth
-presence of possible cholesteatoma formation
CLASSIFICATION
1162
TECHNIQUE OF ATRESIAPLASTY
1163
COMPLICATIONS OF SURGERY
DISCUSSION
-if average canal diameter < 4mm then risk of cholesteatoma formation is ~ 50%
-preponderance of cholesteatomas developed in canals < 2mm
Hearing results
-standard to obtain minimal CHL with < 25 dB hearing threshold in at least 75% of pts
-Chandrasekhar: ABG of 30 dB in 60%
-Schuchtnecht: 50% of pts with 30 dB or better hearing
Alternatives
-bone anchored hearing aids
-bone conduction hearing aids
1164
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TEMPORAL BONE
Five segments:
squamous
mastoid
tympanic
zygomatic
petrous
contains portions of carotid artery and jugular venous drainage system
intimately related to dura of middle and posterior fossa
articulates anteriorly with condyle of mandible
mastoid air cell system communicates with middle ear
facial nerve passes through en route to muscles of facial expression.
EAR
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A. External Ear
protects tympanic membrane
collects and directs sound waves and plays a role in sound
localization
skin of external ear normally migrates laterally from umbo of malleus
in tympanic membrane to external auditory meatus (at a rate of 2- 3
mm per day)
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B. Middle Ear
communicates with nasopharynx via eustachian tube
transmits and amplifies sound waves from tympanic membrane to
stapes footplate converting energy from air medium to a fluid medium
of membranous labyrinth
three ossicles
tympanic membrane
ovoid, three- layered structure consisting of squamous epithelium
laterally, respiratory mucosa medially, and an intervening fibrous
layer
apex maintained medially by support of malleus
fibrous layer thickens laterally to form annulus, an incomplete ring
which is attached to surrounding bone
superior to lateral process of malleus, ring is deficient, andÇarea is
known as pars flaccida
majority of drum is composed of pars tensa.
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Ossicles
from lateral to medial: malleus, incus, and stapes
handle and lateral process of malleus attached to tympanic
membrane
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Protympanum
in this anterior recess of middle ear, eustachian tube exits to
communicate with nasopharynx
ETT runs in close proximity to carotid artery.
Hypotympanum
jugular bulb curves through hypotympanum
usually covered by bone, but may be dehiscent and extend into
middle ear space.
C. Inner Ear
consists of a fluid- filled labyrinth which functions to convert
mechanical energy into neural impulses
bony labyrinth is subdivided into smaller compartments by
membranous labyrinth
fluid surrounding membranous labyrinth is called perilymph; fluid
within is called endolymph
There are three main divisions of bony labyrinth.
Vestibule
just medial to oval window, and contains utricle and saccule
vestibule is an antechamber, leading to both cochlear and
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semicircular canal.
Cochlea
anterior to vestibule
bulges into middle ear and its bony covering is promontory
communicates with middle ear via round window
Semicircular Canals
project posteriorly from vestibule
detect angular acceleration
superior, posterior and lateral, or horizontal canals.
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ELECTRONYSTAGMOGRAPHY
OVERVIEW
-calibration:
-upward swing of pen right
-downward swing of pen left
-limitations:
-deals primarily with only one major vestibular tracts (VOR)
-ignores vestibular-spinal tracts
-limited to horizontal SCC and superior branch of vestibular nerves
-anterior posterior, otolith organs and inferior branch of vestibular nerves not stimulated
-results can be affected by attention and medications
-therefore ENG provides limited information about total vestibular system function
-purpose of ENG:
-detect organic pathology within at least a portion of vestibular system
-monitor change in vestibular function
-identify central vs peripheral vestibular pathways
-vestibular lesions involving the vestibular end organs and vestibular nerve are classified as
peripheral
CENTRAL SUBTESTS
-Alexander’s Law:
-nystagmus beats most intensely when eyes are deviated toward side of the fast phase of
the nystagmus
-true rotatory gaze nystagmus will not register on strip chart recorder
-antiseizure medications, barbiturates, alcohol may cause direction-changing gaze nystagmus and
poor ocular fixation
-deviation of eyes beyond 30o causes physiologic "end point" nystagmus
1171
-Rotatory gaze nystagmus:
-brainstem lesion, often vestibular nuclei (eg. MS, 4th ventricle cysts, masses in 4th ventricle)
-cerebellar disease
1172
-in conjunction with direction-changing nystagmus: lesion in brainstem or cerebellum
-spontaneous nystagmus generated from acute unilateral, peripheral vestibular lesion can cause an
optokinetic asymmetry that is dominant in the direction of the peripheral spontaneous nystagmus
-degree of asymmetry increases with the OKN target speed
PERIPHERAL SUBTESTS
1. Positional Tests
-to determine if changes in head position cause or modify nystagmus
-eyes close to eliminate effects of visual suppression
-positional nystagmus is considered to be nonlocalizing: can be peripheral or central lesion
-direction-fixed, positional nystagmus seen more commonly in peripheral vestibular lesions
-direction-changing, ageotropic positional nystagmus
-nystagmus that changes direction when head position changes and beats away from the
down ear in the supine-head-left (or right) positions
-more commonly in central lesions and in bilateral, peripheral vestibular lesions
-geotropic: fast phase beats toward undermost ear
-nystagmus needs to be at least 6-8 degrees/s to be considered significant
-if both peripheral vestibular systems are in fact neurologically equal, a nystagmus should not be
present, regardless of velocity
3. Caloric tests
-non-physiologic procedure to induce endolymph flow in SCC (primarily horizontal)
-creates temperature gradient from lateral to medial part of canal
-neck ventroflexed 30o horizontal SCC are placed in vertical plane
-water temperatures of 30oC and 44oC
-cold water:
-cooling endolymph causing fluid to become dense
-falls in vertically positioned canal
-bends cupula away from utricle (ampullofugal) neural inhibition relative to opposite
ear
-slow phase toward and fast phase away ("cold opposite") side of irrigation
-warm water:
-heating endolymph fluid less dense
-bends cupula toward urtricle (ampullopetal) neural stimulation relative to opposite
ear
-slow phase away and fast phase toward ("warm same") side of irrigation
-note slow-phase velocities are measured
1173
-Unilateral weakness: [(RW+RC)-(LC+LW)]/[RC+RW+LC+LW] x 100; abnormal if > 25%
-Directional preponderance: [(RW+LC)-(RC+LW)]/ [RC+RW+LC+LW] x 100; abnormal if >
30%
1174
MENIERE’S DISEASE
-Endolymphatic hydrops: condition of increased hydraulic pressure within inner ear endolymphatic system
-excess pressure accumulation causes a tetrad of symptoms as follows:
-Fluctuating hearing loss
-Occasional episodic vertigo (usually a spinning sensation, sometimes violent)
-Tinnitus or ringing in the ears (usually low-tone roaring)
-Aural fullness (eg, pressure, discomfort, fullness sensation in the ears)
Pathophysiology:
-two fluids chambers inner ear: endolymph and perilymph
-attacks of hydrops caused by increase in endolymphatic pressure break in membrane separating
perilymph (a potassium-poor extracellular fluid) and the endolymph (a potassium-rich intracellular fluid)
-chemical mixture bathes the vestibular nerve receptors depolarization blockade and transient
function loss creates an acute vestibular imbalance vertigo.
-mechanical disturbance of the otolithic organs responsible for linear and translational motion detection
may produce nonrotational vestibular symptoms
-mechanical disturbance of the organ of Corti hearing loss and tinnitus
-apex of the cochlea is wound much tighter than the base
-more sensitive to pressure changes than base affects low frequencies (located at the
apex) more than high frequencies (located at the relatively wider base of the cochlea)
-symptoms improve after membrane is repaired and normal sodium and potassium concentrations are
restored.
Causes:
-Increased pressure of endolymph may be caused by a wide range of disorders (eg, metabolic imbalance,
hormonal problems, infections). Autoimmune diseases (eg, lupus, rheumatoid arthritis) may cause an
inflammatory response within the labyrinth. Allergy also has been implicated in many difficult-to-treat
Ménière cases.
Differential Diagnoses:
-Benign Paroxysmal Positional Vertigo
-CNS Causes of Vertigo
-Inner Ear, Autoimmune Disease
-Inner Ear, Evaluation of Dizziness
-Inner Ear, Labyrinthitis
-Inner Ear, Ménière Disease, Surgical Treatment Inner Ear, Perilymphatic Fistula
-Inner Ear, Tinnitus
-Thyroid, Thyrotoxic Storm Following Thyroidectomy
1175
-Lyme disease
-Microvascular compression syndromes
-Multiple sclerosis
-Neurosyphilis
-Otosclerosis
-Perilymphatic fistula
-Salt or water imbalance
-Thyroid disease
-Thyroid hormone disease
-Transient ischemic attacks and stroke
-Trauma
-Vestibular migraine
-Viral infections
Investigations:
-audiometry
-transtympanic electrocochleography (ECoG)
-to detect distortion of nerve-containing membranes of the inner ear (presumably due to pressure
fluctuations of the perilymph pressure) and may show evidence of cochlear involvement
-ECoG measures ratio of summating potential (probably arising from movement of the basilar
membrane) and action potential on the nerve in response to auditory stimuli
-Hydrops is suggested when the ratio is greater than 35%
-ECoG is most accurate when Ménière disease is active
-ENG
1176
ELECTRONYSTAGMOGRAPHY
The visual system provides information about whether the environment is stationary or mobile. This is
accomplished by means of foveation. The visual system is subserved by the motor system, the premotor
system, and the command (control) eye movement system, which controls saccadic eye movements,
pursuit, and vergence.
The oculomotor portion of ENG assesses eye movement function for the various command eye movement
systems in the absence of vestibular stimulation. For oculomotor evaluation, the patient is presented with
various visual stimuli and asked to follow them while his or her eye movements are recorded.
SACCADES (calibration)
-also called the calibration test, evaluates the saccadic eye movement system
-this system is responsible for rapid eye movements and refixation of the target on the fovea.
Administration
-For saccadic testing, one may place dots on the wall or ceiling at specified distances from each other
(usually center and 10°, 20°, and 30° off center) and then instruct the patient to look back and forth
between the dots, keeping the head fixed
Interpretation
-test results are influenced by patient cooperation and visual acuity
-various drugs can also affect performance. Accuracy, latency, and velocity should all be taken into
consideration when interpreting saccades
Normal Saccades
1177
Accuracy
Hypermetric
-aka calibration overshoot,
hypermetric saccades occur
when a patient has difficulty
measuring the distance
required for the muscular act
necessary for following the
target
-patients who consistently
exhibit hypermetric saccades
may have ocular dysmetria,
which is suggestive of a CNS
lesion at the level of the
cerebellum (fastigial nuclei)
Ocular flutter
-spiky overshoot; the patient
overshoots the target several
times with a short duration
between overshoots
-caused by brainstem and
CNS lesions:
-brainstem
encephalitis,
paraneoplastic
syndromes,
meningitis, and
intracranial tumours
Hypometric
-patient undershoots the
target
-patient fails to reach target
with first saccades and
makes successive saccades,
each one brining the eyes
closer and finally onto the
target
-suggestive of basal ganglia
pathology and lesions of the
dorsal vermis of the
cerebellum
Multistep saccades
-occur when a patient undershoots the target and then attempts to correct with multiple small
saccades; also suggestive of CNS pathology
Postsaccadic drift
-called glissade, it is seen as a drifting of eye movement after the saccade; consistent with
cerebellar pathology
1178
Pulsion
-seen in vertical saccades
in patients with posterior
inferior (Wallengberg’s
syndrome) or superior
cerebellar artery syndrome.
The pattern includes a
pulling to the left or right
of the eyes when
completing vertical
saccades.
Latency
Delayed Saccades
-disorders in latency are due
to prolongation of saccades
-examiner should rule out
inattention or uncooperative
behaviour, drowsiness, drug
intoxications
-prolongations of more than
400 ms in attentive and
cooperative patients may be
suggestive of CNS
pathology: lesions of frontal
or frontoparietal cortex or
basal ganglia
Asymmetrical latencies
-can occur in patients with
lesions in the occipital or
parietal cortex
-saccades in one direction
may be fine with a
prolongation of saccades in
the opposite direction
1179
Velocity
Saccadic slowing
-first rule out drowsiness
or drug effects
-saccadic slowing is
consistent with various
CNS or ocular disorders,
including oculomotor
weakness, degenerative
conditions (Huntington’s
disease, progressive
supranuclear palsy), basal
ganglia pathology
(Parkinson’s disease), and
cerebellar disorders.
Asymmetrical velocity
-can be observed as an asymmetry between the eyes or between directions
-may suspect ocular nerve or muscle pathology (ie, lesions or palsies)
-CNS pathology may also be indicated
-lesion in the medial longitudinal fasciculus causing internuclear ophthalmoplegia may
evidence as asymmetrical saccadic velocity
-two primary etiologies:
-multiple sclerosis: usually causes bilateral (but sometimes highly asymmetric) INO
-brainstem infarction: usually causes unilateral INO
1180
GAZE
-conducted to evaluate for the presence
of nystagmus in the absence of
vestibular stimulation
-essentially 3 types of information are
obtained:
-presence or absence of
spontaneous nystagmus (no
task or center gaze)
-presence, absence, or
exacerbation of nystagmus
with addition of off-center
gaze tasks to stress the system
-fixation suppression of
spontaneous nystagmus
Administration
-patient is instructed to look straight
ahead and then to fixate on a target 30°
to the right, left, up, and down -fixation
is maintained approximately 30
seconds in center gaze and 10 seconds
in eccentric gaze
-fixation suppression can be eliminated by having the patient'
s eyes open in a dark room with Frenzel
lenses or with dark goggles used for infrared assessment
Interpretation
Square-wave jerks
-caution must be exercised
in interpretation of
square-wave jerks
-many healthy
patients exhibit this
pattern with their
eyes closed, with
increasing
frequency with
increasing age
-in young patients,
considered abnormal if they
occur more frequently than 1 per second or with eyes open suggestive of a cerebellar disorder,
progressive supranuclear palsy, and cerebral hemispheric disease
Spontaneous nystagmus
-may indicate either central or peripheral pathology
-presence of nystagmus with eyes open is always diagnostically significant
-peripheral indicators
Horizontal or horizontal rotary
Suppressed by visual fixation
Nondirection changing
Exacerbated by gazing in the direction of the fast phase
1181
-central indicators
Vertical
Not suppressed by fixation
Direction changing
Alexander's law
-nystagmus evident with eyes open always beats in the same direction and increases when the
patient gazes in the direction of the fast phase
-nystagmus decreases or disappears when the patient gazes in the direction opposite to the fast
phase; often seen in peripheral vestibular disorders and occasionally in central disorders
Brun’s nystagmus
-combination of unilateral
gaze-paretic nystagmus and
vestibular nystagmus, which
is evidenced as nystagmus
in both directions of a gaze
that is asymmetrical
-associated with extra-axial
mass lesions on the side of
the gaze-paretic nystagmus
-ie. tumours of
CPA such as
acoustic neuroma
-damage floccules
of cerebellum,
causing ipsilateral
gaze-paretic
nystagmus, and
also damage
vestibular nerve,
causing contralateral vestibular nystagmus
1182
Congenital nystagmus
-present at birth or develops
during infancy
-nearly always conjugate,
horizontal and quite intense
-often has a spiky
appearance and increases
with lateral gaze
-may decrease in velocity or
completely disappear with
eyes closed
-often has a null point
Rebound nystagmus
-burst of nystagmus lasting
approximately 5 seconds
that begins when the eyes
are returned to center gaze
-when present, may suspect
brainstem or cerebellar
lesions
Fixation suppression
-for peripheral lesions,
nystagmus that is evident
with eyes closed or in the dark should be suppressed by visual fixation
-if visual fixation does not suppress nystagmus, CNS pathology is possible
Downbeat Nystagmus
-form of central vestibular
nystagmus
-caused by lesions of
vestibulocerebellum and
underlying medulla
-cerebellar degeneration,
craniocervical anomalies,
and brainstem infarction
1183
Upbeat Nystagmus
-caused by lesions of the medulla or anterior vermis of the cerebellum
-infarctions, tumours, degenerations and atrophies of the cerebellum, medulla and midbrain, and
multiple sclerosis
Administration
-patient is instructed to
follow a sinusoidal
moving target with his or
her eyes only.
Interpretation
-tracking test results should
resemble a smooth sinusoid
-breakup of movement may
indicate CNS pathology in various
locations
-nystagmus may be seen in
tracking test results when also
observed in spontaneous (center
gaze) recordings
OPTOKINETIC
Administration
-patient tracks multiple stimuli
-may be in the form of stripes on a
rotating drum or a stream of
lighted dots across a light bar or
the field of an oculomotor
stimulator
-stimuli are moved at a rate of
300, 400, or 600 per second in
each direction
1184
Interpretation
-eye movements that are generated by moving fields resemble nystagmus
-if responses are not symmetrical, CNS pathology may be suspected
Positioning
Dix-Hallpike maneuver
-to assess the presence or absence of nystagmus associated with BPPV
-when test results are classically positive, canalith repositioning and vestibular rehabilitation therapy may
be indicated
Administration
-performed by turning a patient's head to the right or left and then briskly assisting him or her to a supine
position with the head hanging to the right or left
-if nystagmus is observed, the test is repeated to evaluate fatigability of the response
-maneuver should be completed prior to any other positional testing
-patients with BPPV present with a geotropic rotary nystagmus
Interpretation
-if rotary nystagmus is observed, the results must have the following 4 characteristics to be considered
classically positive:
-delayed onset - need to observe patient for at least 20 seconds
-transient burst of nystagmus - lasts about 10-15 seconds
-subjective report of vertigo
-fatigability
-when BPPV occurs, a peripheral lesion on the side that is down when the nystagmus occurs may be
indicated.
Positional tests
Administration
-examiner places the patient in each position and evaluates him or her for a minimum of 20-30 seconds
-mental tasking is used to keep the patient from suppressing nystagmus
-some standard positions used are as follows:
-head hanging
-supine
-supine, head right
-supine, head left
-lateral right
-lateral left
Interpretation
-if results are normal, no nystagmus is present
-for results to be considered abnormal:
-nystagmus observed in positional testing should exceed 60 per second
-change direction in any 1 position
-persist in at least 3 different positions
-be intermittent in all positions
1185
-peripheral indicators include the following:
-direction-fixed
-if direction changing in different positions, may be peripheral if geotropic; however, a horizontal
canal variant of BPPV should also be considered
-latency of onset
-fatigable
CALORIC STIMULATION
Caloric stimulation
-vestibular stimulators include
water, air, and closed-loop cuff;
water and air are commonly used
Administration
-cool irrigations - the fast phase of
nystagmus beats in the direction
opposite to the stimulated ear (ie,
cool irrigation in the right ear
causes left-beating nystagmus)
-warm irrigations - nystagmus beats
in the direction of the stimulated ear
(ie, warm stimulation of the right
ear produces right-beating
nystagmus)
-when adequate data have been
recorded, fixation suppression
testing is conducted
Monothermal
-some clinics use monothermal calorics as a screening test for patients who have normal oculomotor,
positional, and positioning test
-only warm calorics are conducted
-if the responses from each ear are equivalent, testing is terminated
-if a difference in responses exists between the 2 ears, bithermal caloric testing is conducted.
Interpretation
-in the normal vestibular system, adequate, equivalent responses should be obtained from each ear
-slow phase velocity is determined for each recording for use in the following calculations:
1186
-Unilateral weakness (UW) is used
to evaluate symmetry
-in many clinics, a UW
greater than 25% is
significant
-%UW = [(RC + RW - LC
+ LW)/(RC + RW + LC +
LW)] X 100
-a negative number
indicates a right unilateral
weakness, and a positive
number indicates a left
unilateral weakness
-unilateral weakness is
indicative of a peripheral
vestibular lesion involving
the nerve or end-organ on
the side of the weakness
-Bilateral weakness
-average caloric responses
of 60 per second or less are
consistent with a bilateral
weakness
-borderline bilateral
weakness is noted when the
average responses are
between 70-90 per second
-abnormally weak bilateral
responses may be due to
bilateral peripheral
vestibular pathology or
central interruption of VOR
1187
Fixation suppression
-after each caloric stimulus, the patient is instructed to fixate on a light or other object
-fixation should normally eliminate or greatly reduce the induced nystagmus
-if visual fixation does not inhibit nystagmus, central pathology at the level of the brain stem is indicated
Interpretation
-compute the fixation index (FI):
-an FI of 0.60 or greater is considered significant (FI = EO/EC, where EO = nystagmus with eyes
open and EC = nystagmus with eyes closed)
SPECIAL APPLICATIONS
Administration
The patient is placed in an upright position. While the patient is involved in mental tasks, recordings are
conducted with his or her eyes open in the dark (infrared goggles) or eyes closed with electrodes. The
presence or absence of spontaneous nystagmus is noted. Next, a probe from an immittance bridge is placed
in the ear canal, and a seal is obtained. Pressure is then varied from 0-200 mm H2O and held for
approximately 15 seconds. Pressure is then decreased to - 400 mm H2O and held for 15 seconds. The
patient is questioned for subjective symptoms.
Interpretation
The presence of a fistula is confirmed if pressure causes nystagmus.
Tullio phenomenon
This is not as routinely used as pressure fistula testing, but the Tullio phenomenon is an option for patients
on whom a hermetic seal cannot be obtained.
Administration
Follow the procedure for a pressure fistula test, but instead of varying the air pressure, present a 500-Hz
tone at 95 dB for no longer than 3 seconds. Monitor eye movements and ask the patient about his or her
subjective experience.
Interpretation
The Tullio phenomenon is positive if nystagmus is observed.
1188
CRANIAL NERVE VII
FACIAL NERVE ANATOMY
STRUCTURAL ANATOMY
Intracranial Segment
-23-24 mm
-segment from brainstem to internal auditory canal
-Nervus Intermedius: parasympathetic and sensory
root of facial nerve
-motor root joins with nervus intermedius in
CPA/IAC to form common facial nerve
Intratemporal Segments
-meatal
-labyrinthine
-tympanic (horizontal segment)
-mastoid (vertical segment)
1. Meatal
-8-10 mm
-from porus acousticus (fundus) to meatal foramen
-traverses in anterior superior quadrant of IAC
separated by falciform crest inferiorly and Bill’s
bar posteriorly
2. Labyrinthine
-3-5 mm
-from meatal foramen to geniculate ganglion
-narrowest segment of fallopian canal (0.68 mm
diameter)
-geniculate ganglion:
-located at first genu Middle fossa approach - GSPN (5); geniculate ganglion (7); facial nerve
meatal segment (10), labyrinthine segment (9), tympanic segment (12)
-cells bodies of sensory cells and taste
cells from anterior 2/3 of tongue and
palate
-greater superficial petrosal nerve:
-first branch of facial nerve
-carries preganglionic parasympathetic
fibers to lacrimal gland
3. Tympanic
-8-11 mm
-from geniculate ganglion to pyramidal eminence
(at second genu)
-courses above cochleariform process, oval
window and stapes; below lateral semicircular
canal
-most common site of dehiscence (40-50%) Lateral approach - facial nerve mastoid segment (1), tympanic segment (2),
labyrinthine segment (3), meatal segment (4); GSPN (5); cochleariform
process (6)
F.Ling - Facial Nerve (1)
1189
4. Mastoid
-10-14 mm
-from pyramidal process to stylomastoid foramen
-nerve to stapedius
-chorda tympani:
-preganglionic fibers to submandibular and sublingual glands
-special sensory taste fibers
Extratemporal Segments
-postauricular nerve
-branch to external auricular and occipitofrontalis muscles
-nerve to stylohyoid
-nerve to posterior digastric muscle
-nerves to muscles of facial expression
-pes anserinus
-branching point of extratemporal segments in parotid gland
-two divisions:
-superior - temporozygomatic
-inferior - cervicofacial
-temporal branch:
-frontalis
-corrugator supercillii
-procerus
-upper orbicularis oculi
-zygomatic branch:
-lower orbicularis oculi
-abundant anastomotic supply with
buccal branch
-buccal branch:
-zygomaticus major and minor
-levator anguli oris
-buccinator
-upper orbicularis oris
-marginal mandibular branch:
-lower orbicularis oris
-depressor anguli oris
-depressor labia inferioris
-mentalis
-cervical branch:
-platysma
1190
FUNCTIONAL ANATOMY
1191
The Halmagyi (Head Impulse)Test
What is it?
A clinical test of severe unilateral loss of horizontal SCC function: one large or several
small oppositely directed, compensatory, re-fixation saccades elicited by rapid horizontal
head rotation toward the damaged side.
How is it done?
• Patients sit upright and fix their gaze on a target about 3 m away. The examiner
stands in front, but to the side of the patient. The patient is instructed to look at
the target while your head is turned from one side to the other (ie. passively). The
patient’s head is then rapidly turned.
• The examiner looks for saccades. A patient will not make any saccades if the
horizontal canal on the side to which the head was turned is intact. If not intact, a
patient will make saccades in the direction opposite to which the head was turned.
These saccades can be recorded with standard ENG equipment.
• Initially tested on 12 patients with a surgically created complete unilateral canal
paresis. All 12 demonstrated predictable, clinically evident saccades with this
manoeuvre. None of the control patients demonstrated saccadic movement. The
response was equally strong in patients who had had a paresis for 1 week or 1
year.1
Conclusions
The head impulse test is a useful clinical test for the detection of severe unilateral
horizontal SCC paresis. Head impulse testing will not replace caloric testing but is a very
useful adjunct to it. This test is poor at detecting mild to moderate canal paresis.
References
1. Halmagyi GM, Curthoys IS. A clinical sign of canal paresis. Arch Neurol 1988;45:737-9.
2. Perez N, Rama-Lopez J. Head-impulse and caloric tests in patients with dizziness. Otol Neurotol
2003;24:913-7.
3. Beynon GJ, Jani P, Baguley DM. A clinical evaluation of head impulse testing. Clin Otolaryngol
1998;23:117-22.
How is it done?
• Originally described by Kamei et al1, it required the patient to shake their head 30 times in a)the
horizontal plane, bent forward 30o b)in the horizontal plane, positioned normally, c)in the coronal
plane, and d)in the sagittal plane.
• An alternative method has been described that requires the patient to shake their head rapidly in a
sinusoidal manner at a frequency of 2 cycles/s for at least 20 cycles.2
• After the head shaking, the patient’s eye movements are observed for 30-60 s.
• It has been described using Frenzel glasses, but it is thought to be more accurately performed
when done with standard ENG monitoring equipment.
• Three types of nystagmus have been described:
1) Deficiency-type: nystagmus with a predominate horizontal component and a fast phase
directed toward the intact end organ. Occurs in nearly 75% of cases.
2) Recovery-type: nystagmus directed toward the the affected side, occurs following a 20
second latent period. Occurs in nearly 23% of cases.
3) Biphasic-type: a combination of the latter two types. Occurs in 1-2% of cases.
Conclusions
HSN is neither sensitive nor specific and is not to be used as a screening test. It is complementary to the
standard ENG examination, but generally does not provide any new information to the examination.
References
1. Kamei T, Kimura K, Kaneko H, Noro H. Reevaluation of the head shaking test as a method of nystagmus
provocation. J Otolaryngol (Japan) 1964;67:1530-4.
2. Hain TC, Fetter M, Zee DS. Head-shaking nystagmus in patients with unilateral peripheral vestibular lesions.
Am J Otolaryngol 1987;8:36-47.
3. Fujimoto M, Rutka J, Mai M. A study into the phenomenon of head-shaking nystagmus : Its presence in a
dizzy population. J Otolaryngol 1993;22:376-9.
4. Asawavichianginda S, Fujimoto M, Mai M, Rutka J. Prevalence of head-shaking nystagmus in patients
according to their diagnostic classification in a dizziness unit. J Otolaryngol 1997;26:20-25.
5. Asawavichianginda S, Fujimoto M, Mai M, Desroches H, Rutka J. Significance of head-shaking nystagmus
in the evaluation of the dizzy patient. Acta Otolaryngol (Stockh) 1999;Suppl 540:27-33.
Imaging Studies:
CT scan and MRI both are useful for evaluating anatomic extent of soft tissue inflammation, abscess formation, and
intracranial complications.
-CT scan fails to diagnose early osteomyelitis because 30-50% of bone destruction is required to detect
osteomyelitis by CT scan.
-MRI provides poor bone resolution
-soft tissue manifestations regress on CT scan and MRI with response to therapy.
-one changes remain persistently abnormal on CT scan for at least one year and are not well demonstrated
by MRI. Thus, neither of tests can be used to determine osteomyelitis resolution.
-Most authors advocate obtaining a CT scan with initial evaluation for all patients, whereas Benecke
advocates obtaining this test selectively for patients with cranial neuropathy, extensive bone changes on
technetium scan, or poor clinical response to treatment.
-MRI and CT scan are equally sensitive in detecting soft tissue extent of disease, but MRI is more sensitive
for detecting intracranial complications
1194
NEOPLASMS OF THE EAR AND LATERAL SKULL BASE
PATHOLOGY
1195
Embryonal rhabdomyosarcoma: small round and Alveolar rhabdomyosarcoma: sheets of round, oval, or
spindle-shaped primitive mesenchymal cells in loose straplike cells arranged in trabecular pattern surrounding
myxoid or compact pattern empty alveolar compartments
1196
OTOPLASTY
PATIENT EVALUATION
SURGICAL TECHNIQUE
-postauricular incision created - ellipse of skin removed for conchal set back
-resulting auriculomastoid angle should be no less than 30o
-creation of antihelix
-incorporation of adequate amounts of both perichondral layers when placing the Mustarde and conchal sutures
-achievement of symmetry
COMPLICATIONS
1197
PERIPHERAL VESTIBULAR DISORDERS
Definition: Vertigo is the hallucination of movement, either of self (subjective) or the environment (objective).
History
A minimum vertigo history should address the following:
1. duration of individual attack (hours vs days)
2. frequency (daily vs monthly)
3. effect of head movements (worse, better, or no effect)
4. inducing position or posture (eg. rolling onto right side in bed)
5. associated aural symptoms such as hearing loss and tinnitus
6. concomitant or prior ear disease and/or ear surgery
Vertigo duration
MÉNIÈRE'S DISEASE
-endolymphatic hydrops and Ménière's disease in particular are final manifestation of a variety of
pathological insults which may be congenital, inflammatory, traumatic or idiopathic
-cause of Ménière's still remains unknown
-syphilis cause in ~7% of patients with Ménière-like syndromes and otosclerosis is associated with ~4% of
Ménière's
-viral infections postulated as one possible cause of endolymphatic hydrops but no specific viruses have
been associated with disease, and pathologic studies have not found histologic changes suggestive of viral
infection
1198
-Definite Ménière disease:
-two or more episodes of spontaneous rotational vertigo that lasts 20 minutes or longer
-audiometrically documented hearing loss on at least one occasion
-tinnitus or aural fullness in affected ear
-other causes excluded
-Certain Ménière disease:
-histopathologic confirmation to definition criteria
-Probable Ménière disease:
-one definitive episode of vertigo despite fulfilment of all other criteria
-Possible Ménière disease:
-cochlear or vestibular variants of Ménière disease when other causes have been excluded
Pathophysiology
-overaccumulation of endolymphatic fluid
-endolymph is produced at stria vascularis and is absorbed primarily by endolymphatic sac
-mechanisms that may lead to a disturbance of this system:
-an imbalance with the normal side is created, this being perceived as vertigo and hearing loss
Diagnosis
Clinical presentation
-recurring attacks of vertigo (96.2%) with tinnitus (91.1%) and ipsilateral hearing loss (87.7%)
-attacks often preceded by aura consisting of a sense of fullness in ear, increasing tinnitus, and a decrease
in hearing
-acute period of vertiginous symptoms lasts 2 to 6 hours
Disease course
-highly variable
-cluster of attacks separated by long remissions, there may be single, sporadic attacks or periods of
unrelenting, recurring attacks
-vertigo will cease spontaneously in 57% of patients in 2 years and in 71% after 8.3 years
-pts may be minimally inconvenienced or completely incapacitated
1199
-long term studies indicate that patients experience:
1. Average pure-tone hearing loss of 50 dB
2. Mean speech discrimination score of 53%
3. Average caloric response reduction of 50%.
4. Mean frequency of attacks: 6-11/year for first 20 years
5. Mean frequency of attacks diminishing to 3-4 /year after 20 years.
6. Bilateral disease occurred in 47% of patients observed for 20 years or more
Vertigo
-severe vertigo in horizontal plane which is maximal at onset of attack characterizes
-head movement exacerbates this symptom
-Otolithic crisis of Tumarkin:
-sudden unexplained falls without loss of consciousness or associated vertigo are occasionally
described
-a consequence of an abrupt change in otolithic input, an erroneous vertical gravity reference
occurs generates an inappropriate postural adjustment via vestibulospinal pathway sudden fall
-occur in less than 2% of Ménière's patients
-Lermoyez variant:
-resolution of hearing loss and tinnitus with onset of vertigo
-Cochlear hydrops:
-fluctuating hearing loss, aural fullness, tinnitus without vertigo
Nystagmus
-direction varies over time course of attack
-phases of nystagmus:
-"irritative nystagmus": early in attack, nystagmus is often noted beating toward affected ear
-"paralytic nystagmus": later, nystagmus beats toward healthy ear
-"recovery nystagmus": as attack subsides and vestibular function improves, nystagmus often
reverses toward affected ear
-nystagmus is not reliable in establishing validity of this diagnosis
1200
Investigations
-audiogram low frequency hearing loss
-ENG unilateral weakness
-ECoG increased SP/AP ratio
-glycerol dehydration test (historical):
-oral glycerol ingestion causes osmotic diuresis will improve symptoms temporarily within 30-
60 seconds
-help diagnosis only if patient seen during acute phase
Medical therapy
Prophylaxis
-medical treatment aimed at prevention of vertigo employ strategy of reduction in endolymph accumulation
-such protocols include
1. dietary modification
2. intermittent dehydration
3. diuretics
4. enhanced microcirculation of ear such as:
-adenosine triphosphate, isosorbide, histamine, and betahistine
5. reduction in immune reactivity with corticosteroid, immunoglobulin, and allergy therapy
6. stress reduction
Vasodilators
-in belief that Ménière's disease is result of strial ischemia, vasodilating agents such as betahistine have
been used without any effect
-other agents utilized with same rationale include: papaverine analog eupavarine, nicotinic acid, adenosine
triphosphate, and dipyridamole
Symptomatic relief
Antivertiginous medications:
1. Antihistamines
2. Mild sedatives
3. Benzodiazepines
4. Antidepressants
5. Antinausea medications
-these are aimed at dampening severity of attack and primarily diminishing autonomic symptoms associated
with vertigo such as nausea and vomiting.
Surgical treatment
-reserved for those patients who have failed medical management and is estimated to be necessary in 10%
of individuals
-some patients will continue to experience motion intolerance and mild positional instability despite
effective surgical management, this is attributed to incomplete adaptation
1201
Hearing sparing procedures without damage to vestibular labyrinth
1. Vestibular neurectomy
a. Middle fossa approach
b. Suboccipital approach
-Both procedures require sectioning of vestibular nerve and sparing of facial and cochlear nerves
-do not interfere with progression of hearing loss which continues unabated
-both have similar results in controlling vertigo:
-approximately 95% will have complete symptomatic relief
2. Chemical vestibular ablation
-streptomycin and gentamicin, by virtue of their more selective vestibular toxicity, have been
instilled locally into middle ear as a treatment for unilateral Ménière's disease
-current protocols utilize injection of concentrated gentamicin into middle ear through a pressure
equalizing tube several times a day for two to four days
-effective in controlling vertigo in 90% of patients and produces inadvertent hearing loss in10 to
30%
-contraindications:
-infection
-only hearing ear
-contralateral dysfunction
-Labyrinthectomy
-an effective treatment for vertigo in Ménière's patient when serviceable hearing is absent (pure-
tone average > 60 dB and discrimination < 50%)
-excellent results are reported using all aforementioned techniques, with resolution of symptoms
in greater than 90% of cases
Parenteral Streptomycin
-utilized only for bilateral Ménière's
-resultant ablation of peripheral vestibular function while leaving hearing largely unchanged
-low dose parenteral streptomycin is used to preserve some degree of vestibular function to
prevent oscillopsia and ataxia
1202
SECONDARY ENDOLYMPHATIC HYDROPS
Otologic syphilis
-early syphilis
-vestibular symptoms are less frequent
-vary from mild imbalance to symptoms of protracted vertigo with vegetative features lasting days
-late syphilis
-can present up to 50 years or more after exposure
-cochleovestibular symptoms indistinguishable from Ménière's disease
-early syphilis, disorder is due to treponemal meningoencephalitis affecting arachnoid space
-late syphilis disorder is due to gummatous involvement of otic capsule
Cogan's syndrome
-characterized by interstitial keratitis and bilateral, rapidly progressive audiovestibular dysfunction
-autoimmune etiology
-progression to complete absence of vestibular function, manifested by ataxia and oscillopsia, is common
-hearing loss is bilateral and progressive, without spontaneous improvement and frequently becoming
profound
-treatment with high dose steroids
-if no improvement or progression, further immunosuppression with cyclophosphamide is
indicated
-Vogt-Koyanagi-Harada Syndrome
-similar to Cogan syndrome
-associated with granulomatous uveitis, depigmentation of hair and skin, aseptic meningitis, and
loss of eyelashes
Recurrent vestibulopathy
-individuals describe attacks of vertigo similar to those of Ménière's disease without audiologic symptoms
such as tinnitus, hearing loss, or a sensation of fullness in ear
-only 15% of recurrent vestibulopathy diagnoses will change over time to Ménière's disease because there
is addition of cochlear symptoms
-patients with this condition have better vestibular function on caloric testing than Ménière's and majority
(>80%) go on to resolution over several years
-cause is unknown and it occurs in younger people than Ménière's on average
-given good outcome of this disease recommendation for treatment is symptomatic control.
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VERTIGO LASTING SECONDS
-utricular degeneration liberate otoconia, which then float downward into inferior-most region of vestibule,
ampulla of posterior semicircular canal, once they deposit there, they alter specific gravity of cupola,
changing its response characteristics from a purely angular acceleration detector to one that is stimulated by
linear movements and gravity
-Hallpike position:
-nystagmus is torsional; top of eye beats toward undermost ear (geotropic) nystagmus
-nystagmus is counterclockwise, as viewed by observer, when head is hanging to right, and
clockwise in head-hanging-left position
-result of isolated stimulation of Posterior Semicircular Canal which results in activation of
ipsilateral superior oblique and inferior rectus muscles
-one of most common forms of vertigo, estimated at least as twice incidence of Ménière's
Diagnosis
History
-severe vertigo associated with change in head position
-symptoms on rising from a bending position, looking up to take an object off a shelf, tilting their heads
back to shave, or turning rapidly
-symptoms occur suddenly and last in order of seconds, but never in excess of a minute
-most common identifiable cause of BPPV is felt to be closed head injury
-other cited predisposing events include vestibular neuronitis, infections, and following stapedectomy
Physical findings
-clear-cut diagnosis of this disease entity is made by
(1) observing classic eye movements in association with Hallpike maneuver and
(2) a suggestive history
-nystagmus pattern that is pathognomonic of BPPV consists of following:
1. nystagmus is rotational and geotropic
2. there is a latency of onset (seconds)
3. duration of nystagmus is short (< 1 minute)
4. vertiginous symptoms are invariably associated
5. nystagmus disappears with repeated testing (fatigable)
6. nystagmus reverses its direction on return of head to upright position
Treatment
-majority of patients experience spontaneous resolution of BPPV within several months of onset
Medical treatment
1. Vestibular suppressants are ineffective.
2. Liberatory maneuvers
-Semont manoeuver
-Epley manoeuver
Surgical treatment
1. singular neurectomy
2. vestibular neurectomy
3. posterior semicircular canal occlusion
1204
VERTIGO LASTING DAYS TO WEEKS
Vestibular neuronitis
-typically presents with dramatic, sudden onset of vertigo and attendant vegetative symptoms, dizziness
lasts days, with gradual, definite improvement throughout course
-complete absence of auditory dysfunction or symptoms
-invariably follows a viral upper respiratory tract infection
-postural instability and motion instability with certain head movements is present for months subsequently
and in addition BPPV occurs subsequently in up to 15% of patients
-slow phase of nystagmus is toward affected side and hypofunction is observed on caloric responses
-treatment is supportive and symptomatic for vertigo and related vegetative symptoms
History
-considered as a possibility following trauma to inner ear
-mechanism of trauma can vary:
-barotrauma
-penetrating trauma
-surgical trauma such as stapedectomy, cholesteatoma surgery or trauma
-following physical exertion
-vestibular symptoms are variable and include episodic incapacitating vertigo, equivalent to a Ménière's
attack, positional vertigo, motion intolerance, or occasional disequilibrium
-disequilibrium following increases in CSF pressure such as nose blowing or lifting (so-called
Hennebert's phenomenon) has been noted, as has vertigo following exposure to loud noises (Tulio's
phenomenon)
Examination
-fistula test:
-positive pressure is introduced into suspect ear, either by rapid pressure on tragus, compressing
external canal, or via a pneumatic otoscope, while observing eyes
-positive fistula sign: conjugate contralateral slow deviation of eyes followed by three or four
ipsilaterally directed beats of nystagmus
-high false negative rate
-fiberoptic examination to middle ear through a myringotomy is currently investigational but holds promise
to select appropriate patients for surgical exploration
Treatment
-consist of following:
1. bed rest
2. head elevation
3. laxatives to reduce risk of increased intracranial pressure
4. monitoring of both hearing and vestibular function.
-if hearing loss worsens or vestibular symptoms persist, surgical exploration is warranted
-intraoperative identification of a fistula, reported in about 50% of individuals explored
1205
TRAUMA
Vertigo and ataxia are common sequelae of head trauma and may be caused by:
1. cervical trauma
2. central nervous system trauma
3. peripheral vestibular damage
Labyrinthine concussion
-often associated with hearing loss of variable degree, is result usually of blunt head trauma or barotrauma
-usually transient, with spontaneous resolution occurring over a matter of days to weeks
-hemorrhage in labyrinth may initiate a series of inflammatory steps that lead to fibrosis and ossification
with attendant audiovestibular dysfunction
Blast trauma
-includes such occurrences as open-handed slap to ear as well as actual explosions.
-tympanic membrane and ossicles can be injured but inner ear damage is most severe when conductive
mechanism is not damaged
-auditory loss most common in high frequencies and frequently recovers and vestibular damage is less
frequent
Penetrating trauma
-violation of labyrinth or 8th nerve by either fracture or stapes subluxation or direct injury results in
permanent and total audiovestibular dysfunction
-nystagmus beats in direction of healthy ear, and patient will fall and demonstrate past pointing in direction
of slow phase of nystagmus
-vertigo will gradually subside over ensuing days to weeks
Barotrauma
-relatively uncommon
-during flying and especially during diving in deep water, visual and proprioceptive cues are less effective
-acute vestibular dysfunction leading to disequilibrium, disorientation, nausea, and vomiting can be
devastating in such a setting
Alternobaric trauma
-transient vestibular or auditory dysfunction believed to occur as a result of elevated and probably
asymmetric middle ear pressure
-a function of eustachian tube opening pressures
Treatment:
1. Conservative:
-Bed rest, head elevation, and close monitoring of hearing- and balance-related symptoms are
suggested.
2. Surgical:
-Tympanotomy and middle ear exploration are reserved for those cases with progressive hearing
1206
loss or failure of resolution of vestibular symptoms in 3 to 5 days
3. Individuals suspected of having sustained IEBT and have complete recovery should be advised to
refrain from diving for at least 3 months
4. In all instances, patient should be counseled to perform gentle Valsalva maneuvers at frequent intervals
during descent and to abort dive if middle ear pressure equilibration cannot be achieved easily.
1207
Otolaryngology - Head and Neck Surgery Page 1 of 5
Dr. F. Ling's
1. Koerner's septum
1. Temporal line
2. M astoid air cells
2. M astoid cortex
3. External auditory canal skin
4. Emissary veins
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Otolaryngology - Head and Neck Surgery Page 3 of 5
1. Sigmoid sinus
1. Jugular bulb
2. Tegmen tympani
2. Facial nerve (mastoid segment)
3. Endolymphatic sac
3. Subarcuate artery
in dura of posterior fossa between posterior SCC and sigmoid
4. Posterior semicircular canal (ampullated end)
sinus
5. Superior semicircular canal (ampullated end)
enters temporal bone at operculum which lies posterioinferiorly
6. Horizontal semicircular canal (ampullated end)
from IAC
7. Facial nerve (tympanic segment)
lies at or below a line projected from axis of horizontal SCC
8. Incus
(Donaldson's line)
9. Malleus
4. Epitympanum
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Otolaryngology - Head and Neck Surgery Page 1 of 2
Dr. F. Ling's
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Temporal Bone Anatomy
1215
a. Anterior crus of
superior
semicircular
canal
b. Posterior crus of
superior
semicircular
canal
c. Mastoid air cells
d. Koerner’s
septum
e. Posterior margin
of temporal bone
or cerebellar
plate
1216
a. Anterior crus of
anterior
semicircular
canal
b. Crus communis
c. Posterior
semicircular
canal
d. Mastoid air cells
and cerebellar
plate
1217
a. Sigmoid sinus
b. Vestibular
aqueduct
c. Posterior
semicircular
canal
d. Anterior
semicircular
canal
e. Lateral
semicircular
canal
f. Internal auditory
meatus
1218
a. Internal auditory
meatus
b. Vesibule
c. Endolymphatic
sac
d. Vestibular
aqueduct
e. Posterior
semicircular
canal
f. Sigmoid sinus
g. Petrous apex
h. Lateral
semicircular
canal
i. Malleus head;
body an short
process of incus
1219
a. Internal auditory
canal
b. Facial nerve
(labyrinthine
segment)
c. Geniculate
ganglion
d. Facial nerve
(tympanic
segment)
e. Malleus
f. Incus
1220
a. Basal turn of the
cochlea
b. Geniculate
ganglion
c. Facial nerve
(tympanic
segment)
d. Malleus
e. Internal auditory
meatus
f. Vestibule
1221
a. Pyramidal
eminence
b. External auditory
canal
c. Round window
niche
d. Tensor tympani
e. Tympanic
membrane
1222
a. Jugular bulb
b. Internal carotid
artery
c. Eustachian tube
d. Tensor tympani
1223
a. Glenoid fossa,
temporo-
mandibular joint
b. Internal carotid
artery
c. Jugular bulb
d. Sphenoid sinus
1224
a. Supra-
labyrinthine cells
b. Cochlea
c. Malleus head
d. Tegmen tympani
e. Mastoid air cells
f. Carotid artery
1225
a. Internal carotid
artery
b. Cochlea
c. Facial nerve
(labyrinthine
segment)
d. Facial nerve
(tympanic
segment)
e. Middle ear
(hypotympanum)
1226
a. Internal auditory
canal
b. Tensor tympani
c. Facial nerve
(tympanic
segment)
1227
a. Facial nerve
(tympanic
segment)
b. Lateral
semicircular
canal
c. Scutum
d. Ossicles
e. Superior
semicircular
canal
1228
a. Posterior
semicircular
canal
b. Tegmen tympani
c. Vestibular
aqueduct
1229
Vestibulo-Ocular Reflex (VOR)
Caloric Testing
1230
LOCAL SKIN FLAPS:
ANATOMY, PHYSIOLOGY AND GENERAL TYPES
LOCAL FLAPS
-advantages:
-use of local tissue with better donor site match
-one stage in most instances
-low donor site morbidity
-disadvantages:
-random pattern blood supply with limited length
-distortion of surrounding structures
-not enough bulk for deep defects
VASCULAR ANATOMY
-hierarchy:
-subdermal plexus
-basis for random-
pattern flaps
-direct cutaneous arteries
-run on top of muscles
and send branches to
skin
-basis for axial-pattern
flaps
-segmental blood vessels
-large named branches
of aorta that run
below muscle masses
-form basis for
musculocutaneous
flaps
-perforating branches
-pass through
overlying muscles
-supplies muscles and overlying subcutaneous tissue and skin
-most common vessel supplying local facial skin flaps
-angiosome: overlying portion of skin supplied by a single perforating vessel
-adjacent angiosomes interconnected by small choke vessels in subdermis
1231
Random-Pattern Flaps
-rely on flow through dermal and subermal plexus
-limits length and width
-causes of skin flap failure:
-extrinsic: -wound infection
-systemic hypotension
-excessive tension
-haematoma
-intrinsic: -excessive flap length and random pattern blood supply
-pharmacologic vasoconstriction
-smoking
-peripheral vascular disease
Axial-Pattern Flaps
AXIAL-PATTERN FLAPS
-rely on blood from named direct cutaneous
arteries and veins that course along Nasolabial Flap -angular artery
longitudinal axis of flap Forehead flap -supratrochlear artery
Lateral forehead flap -superficial temporal artery
-blood supply considered secure for at least
Deltapectoral flap -perforating vessels of internal mammary
length of these vessels artery
Musculocutaneous Flaps
-designed around segmental artery and vein
-raised as a unit (skin, subcutaneous tissue, muscle and segmental vessels)
-eg. pectoralis major, trapezius, latisimus dorsi flaps
-random-pattern blood supply refers to interconnecting anastomoses within dermis and subdermal plexus
-arterial resistance is the primary determinant of the rate of
cutaneous blood flow
-changes in venous capacitance determine total amount of blood in
skin at any one moment
-arteriovenous shunts are ubiquitous precapillary communications
between arterial and venous circulations
-allow blood to bypass capillary bed and thus function as
regulators of blood flow
-shunts innervated by sympathetic nervous system
-increased sympathetic tone shunts narrow provide less
blood to the skin
-speculated that with complete opening (from sympathetic
denervation), blood shunted away from capillary bed and
compromises viability of distal end of flap
1232
Delay Phenomenon
-skin flaps that are partially incised and undermined but not transposed survive to a greater length when
raised at a later date
-most likely d/t closure of arteriovenous shunts, increase in vessel caliber, increased vessel numbers with
reorientation along flap axis and conditioning of distal flap to tolerate ischemia
-delays of 10-21 days most common
-beneficial effect is lost after 3 weeks to 3 months
-random-pattern flaps:
-parallel incision along sides of flap, leaving ends connected
-flap undermined to disrupt perforating vessels
-end of flap incised at time of transfer
-axial-pattern flap:
-incising proposed margins of flap sufficient; undermining not needed
SKIN BIOMECHANICS
-most common cause is vascular insufficiency d/t excessive flap length with a random blood supply or
excessive tension
-vasoconstriction: nicotine, epinephrine, dopamine
-haematoma under flap:
-increases wound tension and pressure on feeding vessels
-haematoma breakdown products contributes to flap necrosis
-diabetes, hypertension, infection and compression of flap pedicle also affect viability
1233
Transposition Flaps
-eg. rhomboid, bilobed, nasolabial flaps, Z-plasty, Dufourmental
Rhomboid Flaps
-for each rhomboid defect, four possible flap orientations can be used for closure
-advantage is that main area of tension is across closure of donor site and spares any compromise of the
flap tip
Dufourmental Flaps
-variant of rhomboid flap
-used for defects that do not correspond to classic 60- to 120-degree dimensions
-imaginary lines extended from diameter of defect and one of the sides of the defect
-angle made by these lines is bisected by a line the same length as a side of the defect
-back cut made that runs parallel to long axis of defect and same length as one side of defect
1234
Bilobed Flaps
-uses skin laxity to distribute tension
over two flaps
-first flap designed to be as long as
defect, somewhat narrower and angled
at ~45o
-second flap is smaller than first and
again angled at ~90o
-work best on nose where tissue can be
borrowed from perinasal area
-advantages:
-distributes tension evenly
-disadvantages:
-risk of pin cushioning
-lengthy incision that rarely
exploits ideal RSTLs
-common uses:
-nasal tip/dorsum, lateral cheek
Interpolated flap
-donor site is separated from recipient site and pedicle must pass over or under intervening tissue to reach
recipient site
Advancement Flaps
-monopedicled:
-usually rectangular and are moved forward into a defect from one side
-bipedicled:
-advanced from both sides of defect
-useful in lips and forehead
-V-Y advancement flaps
-preserve underlying subcutaneous circulation and preventing pincushioning edema by means of
providing adequate venous and lymphatic drainage
-common uses:
-forehead, lateral lip, eyelid
1235
-midline forehead
-temporal
-latissimus dorsi:
-advantage:
-large amount of available skin and soft tissue
-long vascular pedicle with extended arc of rotation (to vertex of scalp)
-less hair transfer
-potential for bilobed skin islands
-out of irradiated field
-disadvantage:
-requires repositioning
-propensity for seroma formation at donor site
-may be bulky in large patients
-requires extended tunnelling between pectoralis major/minor
-arterial supply: thoracodorsal artery
-common uses:
-similar to pectoralis major flaps
-trapezius:
-advantage:
-3 forms allows for versatility
-relatively flat and thin flap
-one-stage procedure
-disadvantage:
-relatively limited arc of rotation
-significant donor site morbidity (weakness of upper extremities, may require skin graft
for closure)
-weaker blood supply
-awkward positioning
-common uses:
-oropharyngeal and hypopharyngeal defects, lateral neck, posterior face
1236
-Flap Designs:
-superiorly based (upper) flap:
-vascular supply from occipital artery and paraspinal perforators
-reliable flap
-limited arc or rotation
-donor site may require a skin graft
-lateral island trapezius flap:
-vascular supply from superficial branches of transverse cervical artery
-may cover defects of the oropharynx, posterior oral cavity, and hypopharynx
-inferior (lower) flap:
-vascular supply from descending branches of transverse cervical artery and
dorsal scapular artery
-provides a long pedicle
-most commonly used trapezius flap
-sternocleidomastoid:
-advantage: donor site located close to defect
-disadvantage:
-tenuous blood supply to skin (not a true axial flap)
-rotation limited by accessory nerve
-arterial supply: occipital artery, superior thyroid artery, transverse cervical artery
-common uses:
-small defects in anterior lateral oral cavity and lateral oropharynx
1237
MICROVASCULAR FREE FLAPS
IN HEAD AND NECK RECONSTRUCTION
INTRODUCTION
Advantage:
-single-stage procedure, excellent perfusion, ability to preselect tissue characteristics of donor
tissue for given recipient site defect
-potential two-team approach
-possible functional restoration (sensation/motor)
-improved ability for spatial positioning of donor tissue
Disadvantage:
-requires microsurgical expertise and specialized instrumentation
-may require longer operating time
-possible colour and texture mismatch
-5-15% failure, most occur in first 24-72 hours; salvage rate on re-exploration ~50%
-neovascularization complete after 8 days
-vascularized muscle reduces to ~20% of tis mass, vascularized fat reduces to 40-60% of its mass
-may monitor flap clinically by examining colour, turgor, capillary refill, temperature, and quality of
dermal-mucosal bleeding
-revisions should be completed as possible to avoid no-reflow phenomenon, survival time may be extended
with free radical scavengers
-critical time of warm ischemia:
-jejunal flaps ~ 2 hours
-skeletal flaps ~ 6 hours
-cutaneous flaps ~ 8 hours
Radial Forearm thin, pliable versatility, ease limited bulk, skin graft donor site
Lateral arm moderately thin primary closure of donor site small-caliber pedicle
Lateral thigh moderately thick large surface area of tissue, long pedicle challenging harvest
Temporoparietal fascia ultrathin can be transferred as pedicle flap challenging harvest, limited pedicle length
Latissimus dorsi moderate bulk large surface area, ease of harvest lateral decubitus positioning
Gracilis thin muscle can be separated into functional units limited tissue available
Description
-skin of entire forearm, from antecubital fossa to flexor crease can be harvested
-most often used in reconstruction of oral cavity and base of tongue, partial and circumferential
reconstruction of pharynx, reconstruction of soft palate
-can be transferred as osteocutaneous flap with a segment of radius 10-12 cm long
1238
-disadvantage is limited amount of bone
available and risk of pathologic fracture of
radius
Neurovascular Pedicle
-based on radial artery and its venae comitantes or
cephalic vein
-lateral antebrachial cutaneous nerve is primary
sensory nerve
Anatomic Variations
-greatest concern is integrity of ulnar arterial supply
to hand through palmar arches
-incomplete palmar arch puts vascular supply of
thumb and index finger in jeopardy
-detect with Allen test
Potential Morbidity
-vascular compromise to hand
-radius fracture for osteocutaneous flaps
-cosmesis of site
Description
-moderately thin fasciocutaneous flap that
can be reinnervated for cutaneous
sensation with posterior cutaneous nerve
of arm
-donor side usually can be closed
primarily when width of harvested skin
limited to 6-8 cm
Neurovascular Pedicle
-based on terminal branch of profunda
brachii artery and posterior radial
collateral artery and its venae comitantes
-maximum pedicle length of 8-10 cm
-posterior cutaneous nerve of the
forearm used as vascularized nerve graft
Potential Morbidity
-radial nerve which lies in spiral groove of
humerus identified and protected
-injury leads to wrist drop
Technical Considerations
-lateral intermuscular septum 1 cm posterior to line drawn from insertion of deltoid and lateral epicondyle
-central axis of flap is based on intermuscular septum
1239
Lateral Thigh Flap
Description
-provides large surface area with expendable tissue
-flaps as large as 25x14 cm harvested
-most useful for intraoral and pharyngeal
reconstruction
Neurvascular bundle
-based on third perforator of profunda femoris
system
-pedicle length 8-12 cm
-lateral femoral cutaneous nerve of thigh for
reinnervation
Anatomic Variations
-terminal cutaneous branch of second or fourth
perforator of profunda femoris may provide
dominant arterial pedicle to skin
Potential Morbidity
-atherosclerosis of arteries
-proximity and vulnerability of sciatic nerve after adductor muscles are detached from linea aspera
Description
-most commonly transferred as pedicled flap, but
can be used as free flap when arc of rotation is
inadequate
-ultrathin, highly vascular, pliable, and durable
-can be harvested with dimensions of 17x14 cm
-used for reconstruction of oral cavity, middle and
upper regions face, hemilaryngectomy defects
Neurovascular Pedicle
-temporoparietal fascia deep to skin and
subcutaneous tissue and superficial to temporalis
muscle fascia
-superficial temporal artery and vein located 3
cm superior to root of helix where vessels branch
into frontal and parietal division
Potential Morbidity
-injury to frontal branch of facial nerve
-secondary alopecia from dissection too superficial
Preoperative Considerations
-relative contraindications:
-preoperative XRT, neck surgery, previous bicoronal incision, external carotid embolization
1240
MUSCLE AND MUSCULOCUTANEOUS FLAPS
Description
-easy to harvest, long vascular pedicle and extremely
reliable
-used to reconstruct high-volume defects such as total
glossectomy defects, skull base defects and large
cutaneous defects
-disadvantages: poor colour match to facial skin and
tendency to become ptotic
Neurovascular Pedicle
-based on deep inferior epigastric system
-larger caliber vessels cf superior system
-musculocutaneous perforators are direct
branches and can supply much larger territory
of skin
-neurosensory supply: lower six intercostal nerves
Potential Morbidity
-can weaken anterior abdominal wall and predispose pt
to ventral herniation
-below arcuate line, anterior sheath must be
reapproximated to prevent herniation
-ileus can occur
Description
-used either as free or pedicled flap
-when transferred as muscle alone, muscle atrophies to
thickness of ~4 mm
-ideal for scalp reconstruction but poor for large
neck defects
-large volume defects require transfer as
musculocutaneous flap
Neurovascular Pedicle
-thoracodorsal artery and vein from subscapular vessels
-average length of pedicle is 9.3 cm (range 6 to 16.5 cm)
-thoracodorsal nerve provides motor innervation
Potential Morbidity
-if flap is pedicled, then risk of kinking and occlusion of
vessels flap necrosis
Technical Considerations
-pt positioned on bean bag in semi-decubitus position
-previous axillary lymph node dissection a relative
contraindication to use of flap
1241
Gracilis Flap
Description
-thin muscle flap from medial thigh
-primary use in head and neck has been facial
reanimation
-advantages of flap for facial reanimation are its
neuromuscular structure, long vascular pedicle and ease
of dissection
Neurovascular Pedicle
-terminal branch of adductor artery arising from
profunda femoris artery
-point of entrance of vascular pedicle into muscle is
consistently between 8 and 10 cm inferior to pubic
tubercle
-motor supply is anterior branch of obturator nerve
Description
-used for long-bone replacement after trauma or
cancer
-provides longest possible segment of
revascularized bone (25 cm)
-used for reconstruction of almost any mandibular
defect
Neurovascular Pedicle
-peroneal artery and vein provide primary blood
supply
-preoperative angiography or MRA are
recommended to ensure adequate arterial supply to
foot when peroneal artery is sacrificed
-peroneal communicated branch can be
harvested as vascularized nerve graft
Potential Morbidity
-in 5-10% of cases, blood supply to skin paddle is
inadequate
-functional deficits include weakness in
dorsiflexion of great toe
1242
Iliac Crest (Osteocutaneous and Osteomusculocutaneous) Flaps
Description
-used for reconstruction of segmental
mandibular defects
-up to 16 cm of bone can be harvested
Neurovascular Pedicle
-deep circumflex iliac artery and
vein which aries from lateral aspect of
external iliac artery
Potential Morbidity
-herniation of abdominal wall
Description
-long length and caliber of vascular pedicle;
abundant surface area of relatively thin skin;
separation of soft tissue and bone flaps; ability
to combine scapular flap with latissimus dorsi
and serratus anterior muscles
-10 cm of bone can be reliably transferred;
adequate for placement of osseointegrated
implants
Neurovascular Pedicle
-based on circumflex scapular artery
-horizontally oriented scapular flap
based on transverse cutaneous
branch
-vertically oriented parascapular flap
based on descending cutaneous
branch
-pedicle length:
-7-10 cm when circumflex scapular
artery harvested at its takeoff from
subscapular vessels
-11-14 cm if subscapular vessels
transected at their junction with axillary artery and vein
Potential Morbidity
-injury to joint space (glenoid)
-harvest of scapular osteocutaneous flap requires detachment of teres major and minor muscles shoulder
weakness and limited ROM
-previous axillary node dissection is a contraindication to use of these flaps
1243
VISCERAL FLAPS
Jejunum
Description
-used in reconstructing circumferential pharyngoesophageal defects
Neurovascular Pedicle
-mesenteric vessels
Potential Morbidity
-most susceptible to primary ischemia
-stricture of upper or lower anastomosis in ~10% (lower than tubed cutaneous flaps)
Other Considerations
-extension of disease into proximal thoracic esophagus is an absolute indication for esophagectomy and
gastric pull-up
-external monitoring segment of jejunum is removed at beside on POD#7 by means of suture ligation of its
mesentery
Flap Description
-used to cover large scalp defects, repair extensive midfacial defects, management of osteoradionecrosis
and osteomyelitis, facial contouring
-gastroomental free flap used for oral or pharyngeal defects; omentum used to provide carotid coverage
Neurovascular Pedicle
-right gastroepiploic artery
Potential Morbidity
-intraabdominal complications:
-gastric leak with peritonitis and intraabdominal abscess formation
-gastric outlet obstruction
-history of gastric outlet obstruction or peptic ulcer disease is a contraindication to this procedure
Pharyngoesophageal Defects
-classified according to circumferential involvement (partial, near total and total)
-mechanism of postop voice production and use of postop radiation therapy also considered
-partial defects (50% of pharynx) and near-total (1 cm strip remains):
-primary closure cannot be performed without high risk of pharyngeal stenosis
-reconstructed with pedicled regional flaps or free tissue transfer
-if carotid protection believed beneficial, a pedicled regional flap can be used to protect vessel
-total defects:
-complete defect
-free tissue transfer has greatest effect
-three types of reconstructions commonly used:
-gastric transposition
-for tumour extension below cricopharyngeus into cervical esophagus
1244
transposition for technical and oncologic reasons (possibility of skip lesions in
proximal esophagus)
-not optimal for long oropharyngeal extensions because it can put tension on
mucosal closure
-free jejunal transfer
-large free fasciocutaneous transfers (RFFF, lateral thigh)
-provide better voice, less dysphagia and less donor-site morbidity than does
jejunum
Midfacial Defects
-free flaps used to in reconstructing maxilla to maintain midfacial projection in premaxillary, zygomatic
and infraorbital regions
-restore contour and projection of midface
-facilitate rehabilitation of an occlusal surface in upper jaw for mastication
-provide oronasal separation
-close orbit or provide platform for prosthetic rehabilitation of the eye
-to maintain functioning lacrimal system if globe is intact
-infrastructure defects (oral palate)
-combined infrastructure and suprastructure defects:
-maxillectomy with intact orbital rim
-effectively reconstructed with an obturator
-maxillectomy including infraorbital rim
-best reconstructed with free tissue transfer, either alone or in concert with prosthesis
-eg. osseocutaneous forearm flap for infraorbital rim reconstruction
-eg. iliac crest, fibular or scapular flap with osseointegrated implants
-maxillectomy including infraorbital rim and orbital contents
-additional tissue volume required for the orbit
-osseocutaneous scapular flap alone or osseocutaneous radial forearm flap in
combination with maxillary prosthesis used
-composite defects
-any of the other defects combined with facial skin
-osseocutaneous scapular flap has been most useful
-adequate bone stock to recontour most maxillary defects
1245
osseocutaneous scapular flap or a rectus flap
-lateral defects best reconstructed with scapular flap or lateral arm flap
SUMMARY
Radial -thin, pliable -yes 3+ -radial artery 10-12 -no -only 40% of radial bone may be
Forearm -lateral antecubital cm transferred
cutaneous nerve bone -donor site requires skin graft
Lateral Arm -moderately -yes 3+ -profunda brachii 8-10 -no -difficult to close primarily if > 6 cm
thin -posterior cutaneous cm -unattractive scar at donor site
nerve of arm -difficult to position for two-team
approach
Scapula -moderate bulk -no 2+ -circumflex scapular 10 cm -yes -requires detachment of shoulder girdle
-thin skin artery bone muscles
(transverse cutaneous -7-10 -requires lateral decubitus positioning
branch; descending cm or -smaller volume bone stock for
cutaneous branch) 11-14 endosseous implants
cm
pedicle
Fibula -moderate bulk -yes 1+ -peroneal artery 25 cm -yes -variable and tenuous blood supply to
-lateral cutaneous bone skin paddle
branch of peroneal -skin graft may be requires at donor
nerve site for osseocutaneous harvest
Iliac Crest -bulky -no 2+ -deep circumflex iliac 16 cm -yes -risk of inguinal hernia
artery bone -poor colour match to face
-temporary hip weakness with
paraesthesia
Latissimus -moderate bulk -no 3+ -thoracodorsal artery 6-16.5 -no -poor colour match
Dorsi -thoracodorsal nerve cm -potential shoulder disability
(maintains bulk) -awkward position for two-team
approach
Lateral -moderately -yes 3+ -third perforator of 8-12 -no -more difficult to harvest
Thigh thick profunda femoris cm -atherosclerosis of arteries
-large flaps -lateral femoral
(25x14 cm) cutaneous nerve
1246
MANDIBULAR RECONSTRUCTION
PREOPERATIVE EVALUATION
Bony Defect
-a lateral (mandibular body) defect often causes minimal cosmetic and functional deformities
-some pts compensate well for malocclusion, making reconstruction unnecessary
-when mandibular symphysis is missing, severe functional and cosmetic deficits necessitate mandibular
reconstruction
-ramus defects - three scenarios:
a) proximal segment of condyle, coronoid process, and ramus superior to lingula
-allows superomedial proximal segment displacement by means of unopposed temporalis
and pterygoid muscle pull
-coronoidectomy aids proximal segment relocation and helps to obtain a better
neomandibular range of motion
b) complete disarticulation
-alloplastic joint replacement system can be used
-use of autogenous bone or costochondral graft for condylar reconstruction
c) oblique subcondylar osteotomy
-preserves condyle and posterior border of ascending ramus
-“Andy Gump” deformity: resection of anterior mandibular arch; difficult to reconstruct
Soft-tissue Defects
-pts who need additional soft tissue benefit from pedicled or free skin and muscle transplantation
-conventional mandibular reconstruction of irradiated tissue beds has low success rate (20-60%) and a high
complication rate (20-65%)
-Hyperbaric Oxygen therapy can improve quality of recipient bed
-improves radiation-related hypocellularity, hypovascularity, and hypoxia
-after 20 HBO tx (100% oxygen at 2.5 atm for 90 min), there is a greater cellular matrix of viable
fibroblasts and neoangiogenesis
-transcutaneous oxygen tension measurements after HBO therapy increased 150%
-vascular density plateaued at 80-85% for normal non-irradiated tissues after 18-22 HBO
treatments
-response of irradiated tissue to HBO has three phases:
-phase I:
-lag phase
-during first 8 treatments
-little change in tissue oxygen tension (30-50%)
-increased collagen synthesis and capillary budding
-phase II:
-rapid response phase
-18th to 22nd treatments
-oxygen tension increases logarithmically to plateau at ~82%
-neoangiogenesis with multiple capillaries in previously hypovascular tissue
-heightened fibroplasias evident
-phase III:
-plateau phase
-oxygen tension plateaus at 85% of the value for nonirradiated tissue
-correction of tissue hypoxia reduces stimulus to angiogenesis and further
treatments do not affect tissue oxygenation
1247
-HBO enhances perfusion and allows healing and supports transplantation of nonvascularized bone
-success rate of HBO therapy for secondary mandibular reconstruction among pts who have
undergone radiation therapy is ~92%
-additional HBO is not needed even if there is a long delay between completion of HBO therapy
and surgery
MATERIALS
Alloplast
-implants include pins, trays and plates
-used as spacers or for internal fixation of bone grafts
-obviate prolonged maxillomandibular fixation
-metal mesh trays and retention screws can be used as spacers with autogenous corticocancellous bone
chips
-main disadvantage is difficulty of augmenting the neoalveolar ridge for dental implantation
without removing the tray
-bone plates and screws are alloplastic materials most widely used in mandibular reconstruction
Bone Grafts
-osteogenesis (Axhausen):
-initial bone formation in a transplant arises form cells that survive transplantation and proliferate
to form new osteoid
-phase I:
-starts after grafting and continues for 4 weeks
-determines the final size of bone graft, because phase II replaces phase I bone rather
than producing new bone
-phase II:
-pluripotential host cells are transformed into osteoblastic cells
-these cells remodel phase I bone and organize the graft
-host fibroblast are induced to grow into graft mediated by bone morphogenic protein
(BMP)
-influences genetic transformation of host pluripotential cells along osteoblastic
lines involved in synthesis of type I collagen and hydroxyapatite salts needed for
formation of bone matrix
-begins 2 weeks after start of osteogenesis, peaks at 6 weeks and wanes until 6 months
-four types of autogenous free bone graft material
-corticocancellous blocks
-cancellous bone
-cortical bone
-particular bone combined with cancellous marrow (PBCM)
-corticocancellous blocks:
-late resorption of central graft causes fractures
-d/t diminished phase I bone formation and poor early revascularization because thick cortical
bone makes a physical barrier that separates cancellous graft bone from host tissue
-cancellous bone:
-provide sufficient phase I bone formation
-gives excellent clinical results in management of selected small defects if mandibular structural
integrity has not been compromised
-in larger defect, pure cancellous bone provides insufficient rigidity
1248
-PBCM:
-offers best osteogenic potential
-provides sufficient viable endosteal osteoblasts and mesenchymal cells to support both phases of
osteogenesis
-allows rapid revascularization
-disadvantage is lack of structural integrity, which necessitates use of a crib as carrier
-allogeneic cribs of mandible, rib or iliac bone are used in mandibular reconstruction
-allogeneic mandible is most useful in reconstruction of ramus and TMJ or symphysis
-allogeneic mandible is hollowed out to form a crib
-crib is packed with PBCM
-allogeneic rib is split longitudinally and the two cortical strips are contoured to the surgical defect
-allogeneic iliac: ipsilateral ilium best mimics that of hemimandible
SURGICAL TECHNIQUE
-for nonvascularized bone grafting, an external approach eliminates contamination and infection of oral
cavity
-coronoidectomy releases fibrosed temporalis muscle
-if a plate is being used for graft fixation, it is contoured and fastened to proximal and distal segments with
three or four bicortical screws in each segment
Pedicled Flaps
Deltopectoral Flap
-based on perforating branches of internal mammary artery
-limited reach of flap, need for staging
-limited use in contemporary reconstruction of oral cavity
1249
Temporalis Muscle Flap
-based on deep temporal artery and vein
-used to resurface limited defects of palatal and buccal mucosa
Vascularized Bone
-vascularized bone resists infection and extrusion
-particularly useful in previously irradiated oral cavity, where nonvascularized methods are prone to failure
-bony healing of vascularized bone is similar to fracture-type healing, rather than creeping substitution of
nonvascularized bone grafts
Distraction Osteogenesis
-process by which bone is stretched to elongate it or fill a bony defect
Timing of Reconstruction
-mastication muscle fibrosis and soft-tissue contracture make delayed reconstruction difficult
-avoiding primary reconstruction hinders functional and cosmetic results
-microvascular free vascularized bone transfer has greatly enhanced success of primary reconstruction of
segmental mandibular defects
-goals of primary oromandibular reconstruction:
-restore mandibular continuity
-restore lower facial contour
-maintain mobility of residual tongue
-reconstruct anatomic configuration of sulcus
-provide rehabilitation with functional lower denture
-improve mastication, deglutition, and speech
-restore sensation to denervated lower lip
-restore sensation to resurfaced portions of oral cavity
1250
-STSG usually placed over muscle
-donor site morbidity includes early gait disturbance and ventral hernia
Scapular Flap
-provides a large amount of soft tissue and 10-12 cm of bone
-based on circumflex scapular branches of subscapular vessels
-bone quality often is inadequate for dental implants
-harvesting requires intraoperative repositioning
Graft Fixation
-advantages:
-prevents shearing of neocapillaries revascularizing graft
-provide stability
1251
-disadvantages:
-stress shielding will interfere with bone remodelling
-screws can loosen and from cutaneous sinus tracks
Dental Rehabilitation
-use of dental implantation after bony mandibular reconstruction allows stable and retentive prosthetic
restoration
-types:
-conventional tissue-borne denture - least stable
-implant-born denture
-fixed retrievable prosthesis, most stable
-load is completely supported by the implants
-implant-assisted denture:
-load is shared by mucosa and the implants
-less expensive than implant-borne prosthesis
FUNCTIONAL ASSESSMENT
-functions of oral cavity:
-deglutition
-mastication
-oral competence
-taste
-articulation
-oral hygiene
-respiration
-airway protection
1252
SURGICAL RECONSTRUCTION AFTER MOHS SURGERY
ONCOLOGIC CONSIDERATIONS
RECONSTRUCTION OPTIONS
1253
-supraclavicular area
-upper eyelid
Local Flaps
-provide excellent colour and texture match and minimal contraction
-most commonly used: advancement, rotation, transposition, and V-Y flaps
Regional Flaps
-forehead flaps and neck flaps often are considered regional flaps for facial reconstruction
Distant Flaps
-pectoralis major musculocutaneous flap
-deltopectoral flap
-trapezius flap
-latisimus dorsi
Free Flaps
-required for massive defects
-requires microvascular anastomosis
Tissue Expanders
-used when there is inadequate adjacent tissue for reconstruction
-expansion performed over 6-12 weeks
-useful for scalp and forehead defects
-rapid expansion used for immediate acquisition of additional tissue
-expansion over 15-30 minutes
-0.5 to 2.5 cm of additional skin can be gained
Nose
-for smaller skin defects, primary closure or local skin flaps usually are appropriate on dorsum, sidewall, or
tip
-larger defects may require paramedian forehead flap
Cheek
-small defects closed primarily
-small to moderate defects best closed with local flaps
-rhomboid flap
-rhomboid flap with M-plasty modification
-triangular advancement flap from melolabial region
1254
-moderate to large defects:
-rotation flap of cheek skin
-elevated superficial to parotid gland and facial musculature
-rotation flap of neck skin
-preauricular incision extended into neck and flap elevated superficially to platysma
-lower cheek defects can be closed with cervical transposition flaps
-can be elevated deep to platysma to enhance flap blood supply
Forehead
-skin less mobile
-small lesions excised along horizontal axis and closed primarily
-moderate defects closed with advancement, rotation, and transposition flaps
-skin graft or healing by secondary intention may be reasonable
Temple Region
-small defects closed primarily with M-plasty
-moderate defects: V-Y closure
-large defects: secondary intention, skin grafting or tissue expanders
Eyelid
-skin defects usually amenable to primary closure, FTSG, or use of rotation flaps
Auricle
-small helical skin defects closed primarily
-small skin defects in other auricular areas repaired with skin grafts or allowed to heal by secondary
intention
Lips
-defects less than one-half lip width:
-closed primarily
-shield incision or W-plasty
1255
SCAR CAMOUFLAGE
SCAR ANALYSIS
-upon maturation, an ideal scar is level with the surrounding skin, is of good colour match, is narrow, is
parallel to or lies within favourable skin tension lies, and lacks obvious straight lines
-early revision with realignment of scar can accelerate its maturation
-healing wounds incorporate high fibroblastic activity, thus dermabrasion can be beneficial as early as 6
weeks after wounding
Excisional Techniques
TECHNIQUES OF SCAR REVISION
AND CAMOUFLAGE
Fusiform Excision
-useful only when scar lies in favourable position Excisional Techniques
-incision placement
-scar excised elliptically with opposing angles of 30o or less
-fusiform excision
-shave excision
Shave Excision -scar repositioning
-for scars that are acceptable narrow but have contours elevated a -serial partial excision
few millimetres above surrounding skin can be improved by means
Irregularization Techniques
of shave excision -Z-plasty
-healing occurs by re-epithelialization -W-plasty
-Geometric broken-line resurfacing
Scar Repositioning
Adjunctive techniques
-small scars that lie close to relaxed skin tension line can be -steroids
repositioned by means of excision -dressings, medications
-often involves sacrifice of tissue between scar and desirable site -cosmetics
Scar Irregularization
Z-Plasty
-lengthens scar and changes its direction
-helpful for scars that cross relaxed skin
tension lines, distort anatomic landmarks,
or make bands or webs across concavities
-two angles and three limbs of equal length
-60o increases length of scar
75%
-45o increases length of scar
50%
-30o increases length of scar
25%
-correctly designed Z-plasty uses lateral
limbs that parallel relaxed skin tension line
of interest
1256
W-Plasty
-useful around areas of convex curvature,
such as along mandibular border, antihelical
fold or dorsum of the nose
-advantages: segments with shorter limbs are
used and technique does not cause overall
lengthening of the scar
-usefulness is limited on broad, flat surfaces
such as the cheek, because result is a
predictable, regularly irregular scar that is
somewhat conspicuous
ADJUNCTIVE TECHNIQUES
Steroids
-to manage or prevent hypertrophic scars and/or keloids
-intralesional injection of triamcinolone acetonide
-injection into fat can cause atrophy
-concentration used varies from 10-40 mg/mL
-other complications:
-dermal and subcutaneous atrophy
-hypopigmentation
-telangiectasias
Mechanical Forces
-pressure and massage aid in resolution of hypertrophic scars
1257
Dressings, Medications, and Cosmetics
-topical antibiotic or pure petrolatum ointment used on sutured wounds minimizes crusting and retards
bacterial contamination
1258
NASAL RESTORATION WITH FLAPS AND GRAFTS
Large Nasal Defects
-nasal subunits:
-dorsum
-nasal side wall (2)
-alar/nostril sill (2)
-soft triangle (2)
-columella
-tip
-type of skin:
-thin, smooth mobile:
-dorsum and sidewalls, columella
-thick, pitted, with sebaceous glands:
-alae and upper part of nasal tip
BLOOD SUPPLY
1259
Large Superficial Defects:
1260
Reconstruction of a Framework for
Nasal Tip:
1261
Lining, Support, and Coverage for Large Full-
thickness Defects
-lining for defects that involve lower two
thirds of nasal vestibule can be harvested
from remaining vestibule and from
ipsilateral septum as a bipartite flap
consisting of a bipedicled portion and a
septal portion that have a common base
-two-part flap mobilized by means of
transverse incision of vestibular skin and
cartilage 8 mm above defect
-vestibular lining skin and cartilage are
mobilized and delivered to alar margin and
fixed with sutures
-septal flap incised and delivered to
maintain a 1.2 cm base over upper lip and
nasal spine
-two flaps sutured together to form a soft
and vascular vestibular lining
-subsurface framework of cartilage
reconstructed
-complications:
-vascular compromise of flap
-infection
-epistaxis
-emergencies:
-local vascular compromise: managed by
means of releasing tight sutures within 24
hours
-infection: antibiotics and aspiration of
hematoma
1262
NASAL RESTORATION WITH FLAPS AND SMALL GRAFTS
Small Nasal Defects
-upper third:
-nasal bones
-thin skin
-little functional concern with defects in this zone
-middle third:
-skin thin medially but thick laterally
-lateral nasal artery immediately cephalic to supra-alar crease
-lower third:
-tip, alar lobule, columella, and soft-tissue triangle
-thick sebaceous skin
-poorly healing scars
-dynamic collapse of external nasal valve may occur - requires nonanatomic cartilage grafting to
prevent collapse
TECHNIQUES
1263
Primary Closure
-for midline defects of middle or lower third of nose
Rhomboid Flap
-versatile flap with predictable scars and vectors of tension
-laxity usually from lateral nasal wall and medial cheek
-inferiorly based flap tends to cause fewer problems with postoperative congestion and edema
Bilobed Flap
-allows distribution of tension farther from primary defect to control degree of tension along alar margin
-wide undermining in the supraperichondrial plane essential for all transposition flaps
Reiger Flap
-glabellar skin with unilateral base on medial brow and supratrochlear region
-for large defects of upper third of nose
1264
SURGERY FOR EXOPHTHALMOS
-exophthalmos:
-condition of altered thyroid metabolism that causes protein depositions within EOMs, increasing
bulk as much as 10-fold
-an abnormal autoimmune response caused by T lymphocyte
-consequences:
-thickening of muscles
-fat herniation
-proptosis
-upper and lower eyelid retraction
-divergence of gaze
PATIENT EVALUATION
-any pt with unilateral or bilateral exophthalmos should be presumed to have thyroid disease
-Graves disease:
-increased total and free T3, total and free T4, reverse T3 uptake, clearance and release of iodine
131 and serum assays of TRH
-US of orbit can confirm suspicion of orbital thyroid disease thickening of EOMs
-CT/MRI: pathognomonic enlargement of recti muscles readily identified
-a particularly revealing physical sign is a hyperaemia over lateral rectus muscles
DIFFERENTIAL DIAGNOSIS
-pseudotumour cerebri
-most common differential diagnosis to consider
-CT/MRI can show generalized edema of soft tissues
-use of high-dose steroids usually improves proptosis within 24-48 hours
-lymphoma of the orbit
-usually elderly pt
-more localized mass seen on scan usually near apex, proptosis may be acentric
-space-occupying masses:
-metastatic tumour, vascular anomaly, neurofibroma retinoblastoma unilateral proptosis
-congenital shallowness of orbits (eg. Apert syndrome and Crouzon disease)
MANAGEMENT
1265
SURGICAL TREATMENT
Orbital Decompression
1266
-lateral rim can be removed by drill, osteotome or saw still attached to periosteum and then later
replacement into its proper position to maintain cosmesis
-lateral orbital bone removed as much as possible until thick bone of skull base encountered
-periorbita incised and orbital fat gently teased out to protrude into newly created space
-lateral extension of orbital fat limited by position of temporalis muscle
COMPLICATIONS
-untreated disease:
-progressive optic neuropathy blindness
-corneal exposure keratitis
-endophthalmitis
-diplopia
-corneal abrasion after decompression
-scleral protector, Frost suture, lubrication for protection
-optic nerve compromise
-from lengthy retraction
-retrobulbar hematoma
-injury to infraorbital nerve
-ectropion
-retinal hemorrhage
-occurs almost exclusively in diabetic patients
-orbital cellulitis or abscess if significant sinusitis occurs
EMERGENCIES
-retrobulbar hematoma
-retinal vascular oclusion
-corneal ulcer
1267
FACIAL REANIMATION
INTRODUCTION
ANATOMY
GENERAL CONSIDERATIONS
1268
TECHNIQUES
Crossover Technique
-three basic techniques:
-hypoglossal facial
-spinal accessory facial
-facial facial
-require following conditions:
-irreversible facial nerve injury
-intact mimetic function
-intact motor endplate function
-intact proximal donor nerve
-intact distal facial nerve
-commonly used in pts post-excision of acoustic neuromas
-results unpredictable: many pts have synkinesis
-7-to-11 crossover:
-morbidity: loss of trapezius function
-try to use only branch to SCM
-7-to-7 crossover:
-inconsistent results
-more sophisticated free muscle flaps or second
donor nerve usually required
-7-to-12 crossover:
-identify and cut facial nerve at stylomastoid foramen via parotidectomy approach
-nerve then isolated to pes anserinus
-identification of hypoglossal nerve inferior to digastric muscle nerve transected as distal as
possible and sutured directly to main trunk
-pts may have subtle articulation problems
1269
-other cranial nerves sacrificed and cannot use crossover techniques
1270
Ancillary Procedures
-include:
-facial plastic procedures (rhytidectomy, blepharoplasty, browlift)
-prosthetic implants (gold implants, spring implants)
-canthopexy and lid tightening techniques
-lateral tarsal strip procedure:
-used for ectropion or lower lid laxity
-tarsorrhaphy:
-partial suturing of eyelids, permanent procedure, does not reanimate, results in visual
field deficits and cosmetic deformity
1271
F.Ling - Facial Reanimation (5)
1272
FACIAL ANALYSIS
DEFINITION OF TERMS
1273
-nasofrontal angle (NFA)
-nasofacial angle (NfcA)
-nasolabial angle (NLA)
-male: ~90o-105o
-female: ~95o-120o
-mentocervical angle (MCA)
1274
Forehead
-most important characteristic of forehead from surgical standpoint is the NFA
-advancing NFA superiorly will effectively lengthen nose
-deepening the angle at surgery will alter dorsal profile nasal projection effectively increased
Eyes
-inner intercanthal distance ~ width of one eye ~ 3.5cm
-interpupillary distance ~ 6.5 cm
-outer intercanthal distance ~ 9.5 cm
1275
Nose
-nasal length: nasion to tip defining point
-desirable nasal width ~ 70-75% of nasal length
-polly-beak deformity caused by fullness in the supratip region
-tip projection: extent of protusion of nasal tip from anterior facial plane
1276
Lips
-lateral aspect of oral commissures should lie along vertical line tangent to medial limbus of iris
-interlabial gap: no more than 3 mm
-incisor exposure:
-no more than 2 mm with lips in repose
-no more than 2/3 of maxillary incisor on full smile
Ears
-top of helix should be on horizontal line with lateral eyebrow
-inferior attachment at level of alar-facial junction
-longitudinal axis on lateral view posteriorly inclined ~20o off vertical
-angle of protrusion from posterior scalp ~
20o
Dental Occlusion
-mesial: toward midline of dental arch
-distal: away from midline of dental arch
-buccal: toward cheek
-lingual: toward tongue
Angle’s Classification:
1277
PREOPERATIVE EVALUATION
OF THE AESTHETIC SURGERY PATIENT
SELECTION OF PATIENTS
Concept of Deformity
-surgeon needs to understand pt’s self-image, what the pt describes as the deformity and how the pt wants
the defect corrected
-surgeon mus also counsel pt about the surgeon’s perception of the problem
-pt and surgeon must agree on existence of deformity and the style and degree of desired change before
surgery is undertaken
Preoperative Interviews
-pt’s ability to accept the surgical result is highly correlated with the degree to which pt has been prepared
-interviews should address:
-what are the pt’s expectations
-are the expectations realistic and reasonable
-can the expectations be fulfilled
-can the pt be satisfied
-computer imaging:
-greatest danger in its use is “implied promises”
1278
Traditional and Contemporary Views
-paranoid schizophrenic is a potentially dangerous patient - thorough psychiatric evaluation recommended
-borderline personality disorders:
-poorer candidates for aesthetic surgery
-predominant in malpractice cases
-existence of preoperative depression is not an absolute contraindications to surgery, but there is a risk of
the depression intensifying
1279
SURGICAL ANATOMY OF THE NOSE
1280
TOPOGRAPHIC ANATOMY AND LANDMARKS
-topographic subunits:
-in reconstruction of external nasal defects, it is often
preferable to resect and replace an entire topographic
subunit with skin of like colour, character, and texture
rather than simply filling the existing primary defect with a
skin graft or pedicle flap
-consist of:
-nasal dorsum
-nasal sidewalls (2)
-nasal tip (including infratip lobule and columella)
-alar lobules (2)
-depressions of supraalar facets (2)
-nasal skin thinner, more mobile, and more easily repositioned in cephalic 3/5 of nose
-relatively devoid of subcutaneous tissue and sebaceous glands
-skin more thicker, glandular quality caudally
-skin is thin at rhinion and thick at nasion and supratip area
-slight skeletal hump at rhinion exists even when external epithelial profile line is relatively
straight and devoid of an external humped appearance
DISSECTION PLANES
-ideal soft-tissue preservation for potential cushioning and camouflage achieved by dissection in immediate
supraperichondrial plane (sub-SMAS) over upper and lower lateral cartilages and subperiosteal elevation
over bony dorsum
-ideally, anaesthetic infiltration should be placed precisely in this supraperichondrial (sub-SMAS) plane in
the lower half of the nose to aid in vascular dissection
-elevator muscles
-procerus
-levator labia-superioris alaeque nasi
-anomalous nasi
-depressor muscles
-alar nasalis
-depressor septi nasi
-compressor muscles
-transverse nasalis
-compressor narium minor
-minor dilator muscles
-dilator naris anterior
-synergistic action of levator labia superioris and depressor septi nasi can profoundly depress nasal tip
caudally, “round up” supratip area, and temporarily lengthen nose considerably
1281
-mimetic muscles encased and interconnected within SMAS
-dissection deep to SMAS layer results in ease of dissection, minimal bleeding, minimal damage to
neurovascular structures supplying nasal tip skin, avoidance of damage to intact SMAS layer, and reduced
scarring during healing more predictable healing
BONY SKELETON
CARTILAGINOUS SKELETON
Cartilaginous Pyramid
-composed of quadrangular septal cartilage and upper lateral cartilages
-cephalic end rigid and fixed while caudal end very flexible
-upper lateral cartilages extend a variable distance beneath caudal portion of nasal bones and are securely
fixed to bony undersurface
-reconstruction of certain twisted noses may require division of upper lateral cartilages from septum to
realign the nasal framework
-profile alignment often requires greater quantitative reduction of cartilaginous hump
-mucoperichondrium continuous from septal cartilage to undersurface of upper lateral cartilages should be
preserved in most pts
-division of this anatomic area of the valve as a “routine’ step in rhinoplasty serves no useful
purpose
-upper lateral cartilage to alar cartilage attachment represents one of the major supports to projection of the
tip and is interrupted by almost all incisional approaches for access to nose in rhinoplasty
-“scroll”
-inferior edge of upper lateral cartilage may recurve outwardly and met with a corresponding
incurving of cephalic margin of alar cartilage
-may result in abnormal width of nose in middle third or supratip area
-nasal valve:
-angle between caudal quadrangular cartilage and distal upper lateral cartilages
Nasal Septum
-mucoperichondrium enveloping quadrangular cartilage inserts into bony-cartilaginous articulation with
maxillary crest at base of septum, where mucoperiosteum covering bony nasal floor also is inserted
-maxillary-premaxillary approach:
-gaining access to bony septal floor by elevating and bringing into continuity two subperichondrial
and mucoperiosteal flaps by sharp or semisharp dissection (“superior and inferior tunnels”)
-portion of septum anterior to piriform aperture provides vital support for nasal dorsum and tip
1282
-angles of the caudal septum:
-anterior septal angle
-midseptal angle
-posterior septal angle
-membranous septum:
-composed of bilateral external layers
of the vestibular skin with intervening
subcutaneous areolar tissue
-in pts with overactivity of tip while
speaking, it is desirable to divide fibers
of depressor septi nasi that traverse
membranous septum to insert over
caudal septum
-complete transfixion incisions sacrifice the
attachment of medial crura footplates to caudal
septum, thereby at least temporarily diminishing
one of the major tip support structures
Major
-size, shape, and resilience of medial and lateral crura of lower lateral cartilages
-medial crural footplate attachment to caudal border of quadrangular cartilage
-attachment of upper lateral cartilages (caudal border) to alar cartilages (cephalic border)
Minor
-ligamentous sling spanning paired domes of alar cartilages
-cartilaginous septal dorsum
-sesamoid complex extending the support of the lateral crura to piriform aperture
-attachment of alar cartilages to overlying skin and musculature
-nasal spine
-membranous septum
1283
INTRODUCTION TO RHINOPLASTY
INITIAL CONSULTATION
1284
ANAESTHESIA
-local anaesthesia:
-advantages:
-less bleeding
-recovery faster
-lower cost
-cocaine:
-4% solution (maximum dose ~5 mL for most adults)
-maximum dose = 3 mg/kg
-effective for 2 hours
-mechanism of action: blocks re-uptake of NE and dobutamine at adrenergic endings
-lidocaine:
-maximum dose: 3-5 mg/kg
-with epinephrine, max dose: 7 mg/kg
-0.5% lasts 1 hour (2 hours with epi)
-1% lasts 1.5 hours (3.5 with epi)
-bupivicaine:
-maximum dose = 3 mg/kg
-lasts 3-10 hours
OVERVIEW OF SURGERY
Incisions
-hemitransfixion:
-allows access to columella, medial crura, and premaxillary area
-open incision:
-best access for tip and dorsal nasal work
-intercartilaginous incision:
-for minimal tip work
-intracartilaginous incision:
-parallels LLC cephalic border, 2-6 mm closer to nostril opening
-incision through LLC
-trims cephalic border of LLC, removing a 3-5 mm strip of cartilage
-rim incision:
-made at caudal border of LLC
-often combined with intercartilaginous incision for delivery of LLC
Hump Reduction
-skin of upper nose separated from bone and cartilage
-periosteum is incised and subperiosteal plane undermined to nasofrontal angle
-dorsal line needs slight middorsal “hump” to compensate for thinner skin here
-reduction begun with scalpel removal of cartilage
-bony hump then reduced to join with cartilaginous dorsum
-small bony humps or irregularities can be adjusted by rasping
-larger humps usually removed with osteotomes
1285
Medial and Lateral Osteotomies
-“open roof” deformity after hump is
removed
-osteotomies disconnect bones both medially
and laterally mobilized nasal bones are
repositioned medially
-medial osteotomy performed first
-beginning at open roof superior
edge, cut starts with osteotomes
next to septum and curves gently
outward and upward to nasofrontal
suture line
-lateral osteotomy:
-begins above floor of piriform
aperture, lateral to anterior inferior
turbinate
-if begun lower, may narrow nasal
valve, causing obstruction
-osteotomes kept parallel to floor during
main length of osteotomy; if angled the underlying bone cannot support repositioned bones and a step-off
or asymmetric positioning can occur
-“high” osteotomies: result in obvious step-off in bone at middorsal level
-lateral osteotomy usually not carried superior to intercanthal line
-intermediate osteotomy:
-performed between medial and lateral ones
-permit satisfactory narrowing of flattened noses
1286
F.Ling - Rhinoplasty (4)
1287
EXTERNAL RHINOPLASTY APPROACH
-external rhinoplasty approach provides maximal exposure of upper and lower lateral cartilages
-advantages:
-helpful in diagnosis, cartilage manipulation, and precise application of cartilage grafts
-disadvantages:
-transcolumellar incision, increased surgical time, increased tip edema
-result in minimal loss of tip support by dividing only skin attachments to lower lateral cartilages (minor tip
support mechanism)
-prior surgical incision such as lateral rhinotomy, extended bilateral alotomies, or excessive thinning of
overlying skin can compromise blood supply to skin-soft tissue envelope
-major arteries, veins and lymphatics of nasal tip run above SMAS of nose
-arteries:
-lateral nasal a. - from facial artery
-follow cephalic margin of lateral crura to meet paired columellar vessels
-dorsal nasal a.
-columellar a.
-important to dissect below musculoaponeurotic layer of the nose minimizes tip edema
SURGICAL TECHNIQUE
-1% lidocaine with 1:100000 epinephrine injected into nasal tip, columella and along caudal margin of
lateral crura
-incisions: transcolumellar incision made at level of midcolumella and bilateral marginal incisions
-cone incisions are made, converse scissors are used to dissect caudal to medial crura without damaging
caudal margin of lower lateral cartilage
-submuscular plane just above lateral crura is identified and tissue is bluntly dissected toward cephalic
margin of lateral crura
-fibrous connections released in midline
-blunt dissection continued toward osseocartilaginous junction
-options:
-columellar strut:
-sutured into precise pocket between medial crura to provide support or correct buckled medial or
intermediate crura
-caudal extension graft:
-appropriately shaped flat piece of septal cartilage harvested from posteroinferior region of
septum
-will enhance nasal length, tip projection and alar-columellar relationship
-dome-binding suture:
-increases tip projection and narrows domes
-dome division with excision of superiorly based triangle of cartilage:
-to narrow the domes
-cartilage usually excised at the domes if decreased projection is desired
-if tip rotation is needed, cartilage can be excised lateral to domes
-shield-shaped tip grafts can be used to increase tip support and projection, provide shape to infratip lobule
and camouflage tip asymmetries
1288
-thin skin is a relative contraindication for tip grafts because graft may become visible when
edema resolves and skin thins over time
-cases that require extended surgical exposure for diagnostic or technical reasons
-asymmetry of nasal tip cartilages or middle nasal vault
-inadequate tip projection
-structural deficiency
-specific nasal deformities:
-crooked nose deformity
-secondary and revision rhinoplasty
-cleft-lip nasal deformity
-saddle-nose deformity
-benign nasal tumours
-closure of septal perforations
COMPLICATIONS
-dissection out of submuscular plane excessive bleeding, postop edema, scarring and irregularity of skin-
soft tissue envelope
-irregularity of transcolumellar incision
-lateral notching of transcolumellar incision
-results from stretching of upper columellar flap effectively increases horizontal width of
columellar flap
1289
REFINEMENT OF THE NASAL TIP
-quality of skin:
-essential indicator of surgical outcome and plays significant role in preoperative planning
-extremely thick skin, rich in sebaceous glands and subcutaneous tissue least likely to achieve
desirable refinement and definition
-thin skin: offers no cushion to camouflage or contour imperfections
-undesirable progressive skin retraction over years
-tip recoil:
-tests the inherent strength and support of the nasal tip
-weak tips may require additional struts or grafts
-note asymmetry of alar cartilage
-assess septum, columella
-evaluation of nasal spine and caudal septal angle
-position and inclination of nasofrontal and nasolabial angles,
shape and size of alae, overall width of middle and upper thirds of
nose, and relationship of nose to rest of the facial features and
landmarks are evaluated
SURGICAL TECHNIQUES
1290
-preservation, reduction or enhancement of tip projection are considered
-preferred nasal tip surgery terms:
-incisions: transcartilaginous, intercartilaginous, marginal
-approaches: delivery, nondelivery (cartilage splitting, retrograde), open (external)
-techniques:
-volume reduction with residual complete strip; weakened complete strip; suture
modification of complete strip; interrupted strip
Nondelivery Approaches
-cartilage splitting:
-for pts who need only conservative or minimal tip refinement and rotation
-few millimetres of medial-cephalic portion of lateral crus removed
-disturbs little of normal anatomy and consistently heals predictably and with symmetry with
minimal scarring
Delivery Approaches
-visual presentation of alar cartilages as bipedicle chondrocutaneous flaps
-must maintain a complete strip at least 5 mm wide
-can achieve greater volume reduction
-used when significant defatting or scar resection is required
-transdomal suturing:
-pts with extremely thin skin, delicate alar sidewalls and bulbous cartilage, predictable refinement
with horizontal mattress suture
-strengthen tip support and can be used to enhance tip projection
-interrupted strip techniques
-used when more significant cephalic tip rotation is indicated in more severe tip deformities
-residual complete strip is divided somewhere along its course, excessive portions of lateral and
occasionally medial crus removed, and cartilages are reconstructed
-dangers:
-asymmetric healing and scarring
-sacrifice of tip support
-over-rotation of tip
1291
Tip Projection
-preservation:
-ensure major and minor tip supports are left largely intact or reconstructed
-complete strip techniques recommended
-avoid complete transfixion incision which destroys vital support provided by medial crural
footplate overlap of caudal septum
-techniques to increase projection:
1. autogenous cartilage struts positioned below or between medial crura
2. plumping grafts of cartilage into base of columella through low lateral columellar incision
3. for widely splayed medial crural footplates resecting excessive intercrural soft tissue and
suturing medial crura (transdomal or interdomal suture)
4. autogenous cartilage tip grafts (supradomal graft or shield graft)
5. cephalic rotation of tip
-techniques to decrease tip projection:
1. full transfixion incision
2. lower septal angle
3. shorten medial and/or lateral crura
Tip Rotation
1292
-techniques to decrease tip rotation:
1. excise caudal septum near
spine
2. dorsum augmentation
Tip Volume
1293
SPECIAL CONSIDERATIONS IN RHINOPLASTY
CLEFT-LIP NOSE
3 mo -tip rhinoplasty
-cleft-lip repair
-closure nasal floor
-myringotomy and tube
placement
12-18 mo -palatoplasty
4-7 yr -columellar lengthening
8-16 yr -orthodontic treatment
9-11 yr -alveolar cancellous bone grafting
14-16 yr -definitive nasal reconstruction
14-17 yr -orthognathic surgery
-nonwhite pt generally has thicker skin with more subcutaneous adipose tissue in nasal tip
-nasal bones usually small in both length and height
-low dorsum gives appearance of wider nose
-nasal spine usually much less significant structure
-augmentation may be needed to increase nasal height
-Gore-Tex usually used to build up significant depression but cannot provide support
-irradiated cartilage may be used
-other materials: Silastic, Mersilene mesh
-tip definition may be required cartilage graft used
SADDLE-NOSE DEFORMITY
1294
-cartilage grafts:
-septal cartilage
-rib graft
-auricular graft
-bone grafts:
-mastoid cortex
-iliac crest
-calvarial bone
-alloplastic materials:
-risk of infections and extrusion
-Silastic, Gore-Tex, Mersiline, Proplast, Supramid,
-heterografts:
-bovine cartilage and bone (largely abandoned d/t resorption)
-homografts:
-demineralized bone
-high resorption rate
-irradiated cartilage
-high resorption rate
-unnatural feel
-acellular dermis (Alloderm)
1295
TWISTED NOSE
-evaluation:
-examine overall facial symmetry
-examine relationship of nose to face
-evaluate septum
-evaluate nasal spine: shape and position relative to
midline and medial crura
-evaluate bony pyramid: length height and any
convexity or concavity
-middle third of nose: depressions of one or both
upper lateral cartilages, deviation of dorsal septum,
profile abnormalities
-tip: position of domes, deficits of medial or lateral
crura, problems with support, contour
abnormalities
-alae, nostrils examined from frontal, basal and
lateral views
Surgical Technique
-an inadequately straightened septum is most
common reason for less-than-ideal postoperative
result
-high septal deviation in keystone area (region of
overlap of upper lateral cartilage by nasal bones)
associated with C-shaped external deviation at rhinion
-corrected via septoplasty
1296
-sequential osteotomies performed
-if above inadequate to straighten the angulation, light morselization, cross-hatching or
partial-thickness cuts can be performed on dorsal septum in keystone area
-sequential osteotomies:
-“opening a book”
-if pyramid deviated to left, lateral osteotomy cut made on opposite side medial
osteotomy made on right medial osteotomy made on left left lateral osteotomy made
-tip-work:
-free all soft-tissue attachments from lower lateral cartilages to allow them to return to
midline position
-existing cartilage is rearranged and grafting of deficits performed
-middle-third:
-contoured if needed
-simple depressions usually treated with onlay grafts
-C-shaped depressions can be camouflaged with onlay grafting
-collapse of one or both upper lateral cartilages can be addressed with spreader graft
placed between septum and upper lateral cartilage
-for children, cosmetic nasal surgery should be delayed until child has reached an age of essentially full
nasal growth (age arbitrary: 15-17)
-aging and the nose:
-changes in position of nasal tip
-major and minor tip support weakens with age descent of the nasal tip over the years
-changes in quality of nasal cartilage and bone
-changes in thickness and elasticity of skin
-nose divided into three parts:
-fixed upper part: nasal bones
-semimobile midportion: upper lateral cartilages and septum
-lower mobile part: lower lateral cartilages
-with age, the middle and lower parts become longer and more prominent; nasolabial angle becomes less
than the ideal 90o
-loss of bone and fat in premaxillary area may make nose appear more prominent
-goal is to reconstitute tip support mechanisms whenever possible
-dorsal-hump removal is performed conservatively in the older patient
1297
REVISION RHINOPLASTY
-as a general rule, revision rhinoplasty is not undertaken for at least 1 year after primary rhinoplasty
-most frequent complications requiring surgical intervention include knuckling (bosseleation), pinching,
columellar retraction, polly beak, alar retraction, midnasal asymmetry, saddling
BOSSELATION
PINCHING
ALAR RETRACTION
-etiology:
-excessive cartilage and vestibular skin excision that results in scarring and retraction of the ala
-prevented by leaving at least 2-3 mm rim strip and not sacrificing any vestibular skin in
the primary rhinoplasty
-poor alar-columellar relationship
-congenital causes
-lateral crural cartilage and membrane excised
1298
-treatment:
-shorten columella
-shorten contralateral ala
-cartilage graft (minimal retraction)
-auricular minicomposite (severe retraction)
-cymba concha graft
-ideally best to replace left ala with right cymba concha and vice versa
-skin is rolled out and graft placed in the vestibule
COLUMELLAR RETRACTION
-etiology:
-congenital
-alar-columellar disproportion
-traumatic
-iatrogenic resection of caudal septum
-treatment:
-raise ala
-cartilage graft
-composite graft
-used if membrane and cartilage are deficient
POLLY-BEAK FORMATION
-definition:
-postsurgical convexity of supratip relative to rest of nose, such that the lower two-thirds of nose
takes on the convex profile of a parrot’s beak
-etiology:
-inadequate dorsal cartilaginous septal resection
-excessive dorsal septal resection
-results in dead space in supratip area
-excessive tip cartilage resection
-leads to loss of tip support
-exuberant supratip scar tissue
-excessive bony pyramid reduction
-shortened columella
-excessive excision of domes of alar cartilage
-treatment:
-supratip massage
-high cartilaginous septum or exuberant scar tissue excise tissue excess through unilateral
intercartilaginous and complete septocolumellar incision
-augmentation of tip support and projections
-augmentation of dorsal profile
-steroid injections
1299
MIDNASAL ASYMMETRY
-etiology:
-nasal bone disparity
SADDLE-NOSE DEFORMITY
-etiology:
-congenital
-traumatic
-iatrogenic
-excessive resection of bone or cartilage from nasal dorsum
-treatment:
-retrodisplacement of tip
-for overprojecting tip causing relative concavities of pyramid
-lateral osteotomies
-raises dorsal profile line slightly and aids in closing open roof deformity
-autogenous graft
-septal cartilage best choice
-can be layered
1300
-other materials:
-conchal cartilage, temporalis fascia
-autogenous outer table cranial bone, iliac bone, rib cartilage implants
-disadvantages:
-irregularities, resorption, morbidity associated with harvesting body sites
-alloplastic graft
-supramid, gore-tex, mersiline, proplast
-silastic implants
-disadvantages:
-inflammation
-dislocation
-rejection
1301
BLEPHAROPLASTY
SURGICAL ANATOMY
EVALUATION
Indications
-blepharochalasis:
-rare condition of unknown cause
-may be familial, characterized by recurrent attacks of lid edema resulting in thin, redundant eyelid
skin and sunken appearance from fat herniation
-hereditary hypertrophy of skin and orbicularis muscle
1302
-dermatochalasis:
-laxity of eyelid d/t aging
-acquired draping of excess kin over lids, usually from actinic damage, thins eyelid skin, allows
for prolapse of orbital fat, progressive ptosis occurs with aging
-pseudoherniation:
-orbital fat protrudes through a lax orbital septum behind orbicularis muscle, baggy lids
Motivational History
-family history of baggy lids
-long-term desire for reversal of progressively deteriorating lid appearance
-no pt should expect external-world changes as a result of surgery
Medical History
-control fluid retention
-no ophthalmic conditions
-pt with full-blown dry-eye syndrome should not undergo blepharoplasty
-previous blepharoplasty
-secondary procedure must be conservative to avoid lagophthalmos or significant scleral show
Ophthalmic Evaluation
-check visual acuity, visual field tests, motility, ocular tension, measure scleral show, proptosis,
fundoscopic exam
-normal Bell’s phenomenon:
-assess adequate protection of the globe, evaluating by forcing the lids open and observing the
upward rotation of the globe to protect the cornea
1303
muscle flap
-palpate orbital rim to determine extent of bony margin contributing to lower lid appearance
THE OPERATION
Anesthesia
-local anaesthesia
-eyelids maintain anaesthesia for the shortest period
Upper Lid
-complete before beginning surgery on lower
lids
-mark upper lid crease: upper anatomic
boundary of tarsal plate
-should be at least 8 mm above upper
lid margin
-carry line medially into sulcus into
nasal junction
-carry line laterally to sulcus between
lateral orbital rim and lid
-grasp redundant skin with forceps:
-lower blade is at marked lid crease, upper blade is in region of maximum estimated excision
-with forceps blade closure, the upper lid margin should not elevate
-skin marked at several points and then connected into a line
-medial skin redundancy should always be underestimated slightly if pt has large medial fat compartment
-prevents tenting of skin and hypertrophic scarring
-depth of excision is to orbital septum
-orbital septum is opened sharply and fat is teased into wound and removed
-skin closed with subcuticular Prolene sutures
Lower Lid
Skin-Flap Approach:
-start at lateral canthal mark 2.5 mm below lid margin in subciliary crease
-small skin flap developed for 3 mm to expose and preserve pretarsal fibers orbicularis
oculi (preserves tension)
-separate pretarsal and preseptal muscle to puncta exposes lateral, central and medial
fat compartments
-fat removal done in lateral to medial direction
-before clamping medial fat pocket, observe and preserve inferior oblique muscle
-hemostasis must be absolute to avoid bleeding medial fat stump that could retract back
into the orbit
-skin-muscle flap draped superiorly and excision done with small scissors while patient is looking
upward with mouth open thus placing maximum tension on lower lid
-there should be no wound gap after excision
1304
Transconjunctival Approach:
-local anaesthetic injected into subconjunctival space from puncta medially to the lateral canthus
-incision made with fine electrodissection needle (Colorado needle) through conjunctiva along
inferior tarsal border
-dissection carried immediately over orbital septum and under orbicularis
-separate orbital septum from orbicularis down to orbital rim
-exposes the three fat compartments removed after clamping
-sutures not required to close transconjunctival incision
POSTOPERATIVE CARE
-avoid looking downward for next 24 hours: downward gaze could allow skin-muscle flap to slide
inferiorly over underlying orbicularis septum
-sedentary activities for the first 3 days
-mild activities may resume on POD 10
-contact lenses may be safely used at POD 9-10
COMPLICATIONS
COMPLICATIONS
-severe cutaneous ecchymosis
Hematoma -haematoma
-more common after lower lid blepharoplasty -subconjunctival ecchymosis
-chemosis
-has palpable firmness
-lagophthalmos
-wound reopened and bleeding vessel cauterized -scleral show
-ectropion
Subconjunctival Ecchymosis -pigmented, wide, too low scars
-loss of vision
-resolves completely in 3 weeks
-dry-eye syndrome
-reassurance
EMERGENCIES
Chemosis -progressive haematoma
-severe dry-eye syndrome
-related to lower lid blepharoplasty -vision loss
-can resolve quickly (days) or remain for up to 6 weeks
-reassurance
Lagophthalmos
-usually mild after upper eyelid surgery
-minor tearing treated with ointments
Ectropion
-postoperative squint exercises and upward massage can reverse minor scleral show
-if caused by horizontal lid laxity that was unrecognized, horizontal lid-shortening procedure required
-may be due to downward displacement of skin-muscle flap simple releasing incision which elevates the
flap and redrapes it may resolve the problem
Poor Scars
-requires secondary scar excision
-scars result when wound is repaired over a large dead space
-can be treated by injecting very small amounts of Kenalog
Loss of Vision
-usually follow haematoma formation
-rapid decompression of a progressing retrobulbar haematoma is essential to preserve vision
1305
THE AGING FACE (RHYTIDECTOMY)
ANATOMY
-Temporal Branch:
-courses along line from earlobe to
zygomatic arch at point midway
between tragus and lateral canthus
-over zygomatic arch then
penetrates deep temporal fascia into
undersurface of superficial temporal
fascia
-Zygomatic Branch:
-courses 1 cm below zygomatic arch in a superior and medial direction from tragus to lateral
canthus
-Marginal Branch:
-exits the parotid 1 cm below mandibular angle, deep to platysma within the submandibular gland
fascia (superficial to the facial vein)
1306
PATHOPHYSIOLOGY
-intrinsic factors:
-histological changes in aging skin:
-thinning of epidermis
-retraction of rete pegs
-decreasing numbers of protective melanocytes
-dermal elastic filaments become thin and fragmented
-dermal collagen thickens but is reduced in amount
-reduced vascular supply to skin
-subcutaneous fat atrophy with gravitational redistribution of soft tissues
-extrinsic factors:
-sun-damage:
-actinic damage from UVA
-reduction in structural elements wrinkles
-growth of thickened, poorly organized fibers: elastosis
-increased amount of immature type III collagen
-decreasing vascular supply
-increasing cellular dysplasias actinic keratoses
-cigarette smoking decreases vascular supply
-increases skin slough 12x
ASSESSING CANDIDACY
1307
PREOPERATIVE EVALUATION
General Considerations
-must assess the full face
-consideration for facial resurfacing, brow-lift, blepharoplasty, or rhinoplasty done
-adjunctive chin an cheek augmentation may be necessary
-assess position of hyoid bone:
-high and posterior hyoid bone is ideal, allowing maximum elevation of submental contour and
greatest definition between submentum and neck in profile
-evaluate for jowling
-evaluate for deepened melolabial crease, chin ptosis, increased distance from ciliary margin to malar
crescent
-generally, older pt with voluminous sagging skin or pt with fat face and neck would not be as good a
candidate as thinner 40- to 50-yo pt because postoperative skin draping with such excess is less satisfactory
-ideal candidate:
-40-50' s, good bony framework, strong cheekbones and chin, normally placed hyoid bone, thin
face, good elasticity, and stable weight
Avoiding Problems
-full evaluation of facial nerve function
-note any facial asymmetry
-note any scars or lesions
-deep nasolabial folds and downturned oral commissure will not be adequately addressed with
rhytidectomy
-smokers have 12x more risk of skin slough 2o vasoconstriction and higher incidence of haematoma
formation
-prior face-lift may complicate proposed procedure
PREOPERATIVE PREPARATION
SURGICAL PLANNING
1308
OPERATIVE STAGE
Flap Elevation
-+/- submental liposuction through submental incision: can help provide wider undermining
-+/- playsmaplasty: inspect submental fat, plication of platysma
-incisions made through pre-auricular incision
-earlobe dissected completely free
-superficial flap elevation in region of temporalis fascia prevents injury to frontal branch of facial nerve,
which crosses zygomatic arch
-flap may be liposuctioned under direct vision
SMAS Suspension
-imbrication techniques:
-involve direct incision, resection or undermining of SMAS fascia with reapproximation or
overlap of cut SMAS fascia edges
-increased sharp dissection increases risks of bleeding, nerve injury and skin slough
-plication techniques:
-avoids direct cutting and undermining of SMAS layer
-folding of SMAS fascia on itself and secures tissues with buried sutures
-suspension vectors:
-first vector:
-from angle to mandible to fascia near superior mastoid cortex
-affects cervicomental angle and angular bony contour of mandible
-second vector:
-originates in SMAS of cheek and mandibular ramus near anterior border of parotid and
extends posterosuperiorly toward preauricular sulcus and tragus
-third vector:
-extends from posterior border of cervical platysma in a predominantly superior direction
to SCM fascia in region of mastoid tip
-pull that is too posterior creates a distinctly unattractive and artificial appearance: widen and flatten the
oral commissure
Flap Closure
-skin is redraped over ear
-excess skin is removed
-“pixie or satyr” earlobe:
-complication in which an elongated earlobe is directly attached to facial cheek skin
-prevented by leaving generous amount of perilobular flap skin around ear lobe
-leave a generous portion of extra skin for post-tragal incisions in order to sufficiently cover tragal cartilage
without tension
1309
COMPLICATIONS
Nerve Injury
-incidence 0.4-2.6%
-most commonly injured nerve is sensory greater auricular nerve
-motor branch most vulnerable to direct, technical injury is frontal branch of zygomatic-temporal division
-superficial location
-traverses mid-portion of zygomatic arch
-avoid deep-plane dissection
-other nerve branches:
-marginal mandibular nerve
-platysma transsection and excessive SMAS traction in region near angle of mandible
and inferior mandibular border can result in nerve paralysis
-buccal nerve:
-aggressive dissection medial to anterior border of parotid
Hematoma
-most common and feared complication (15%)
-require immediate evacuation and control of bleeding source
-pain, swelling or firmness of buccal region
-reduction of haematoma incidence:
-intraop hemostasis
-closed suction drainage
-shorter flaps and two-layer face-lift
-liposuction preservation of vascular septae
-sequelae:
-skin necrosis
-infection
-prolonged ecchymosis
-alopecia
-subcutaneous nodules and skin puckering
-scar contracture
Incisional Problems
-active hypertrophic scars
-satyr earlobe
-elongated earlobe from excessive inferior tension at lobule
-tx: V-Y advancement flap
-blunted and anteriorly dislocated tragus
-elevated temporal hairline
-ingrown hairs
-persistent hemosiderin deposits
Alopecia
-from poorly planned incisions and excessive tension
-avoid poorly placed incisions or tension
1310
THE AGING NECK
ANATOMY
-ideal neck has an acute cervicomental angle of 90o or less with hyoid bone at the apex of this angle
-aging of the neck
-collagen fragments and elastin fibers degenerate overlying integument atrophies and stretches
-perforating septa from underlying platysma support skin against gravity and create horizontal
rhytids
-insulating layer of fat thickens
-platysma is intimately connected to lower facial musculature (SMAS)
-function of the platysma is to stabilize chest muscles against the jaw during heavy lifting
-mandibular projection is important in determining strength or weakness of cervical profile
-a congenitally weak chin or one acquired by bone absorption and ptosis of mental muscles and
soft tissues allows enhancement of postoperative profile by simple augmentation
MANAGEMENT
1311
THE AGING FOREHEAD
FOREHEAD ANATOMY
-blood supply:
-lateral: external carotid superficial temporal artery zygomaticotemporal artery
-medial: ophthalmic artery supraorbital artery and supratrochlear artery
-nerve supply:
-central forehead: supraorbital and supratrochlear nerves (branches of V1)
-lateral sensation: lacrimal (V1), zygomaticofacial (V2), zygomaticotemporal (V2),
auriculotemporal (V3)
-motor function: temporal branch of facial nerve
-layers of scalp:
-S: skin
-C: subcutaneous tissue
-A: aponeurosis and frontalis
-L: loose areolar tissue
-P: pericranium
-muscles:
-frontalis muscle:
-interdigitates with orbicularis oculi
muscle, skin of eyebrows and root of
nose
-raises eyebrows forms horizontal
forehead rhytids
-corrugator supercilii muscles:
-draws eyebrows medially
-associated with vertical glabellar
rhytids
-procerus muscle:
-draws medial edge of eyebrow downward
-causes horizontal glabellar rhytids
1312
PHYSIOLOGY OF AGING
Forehead Aesthetics
-eyebrow position:
-medial end in line with vertical drawn at ala of nose
-apex in between vertical drawn from lateral limbus and lateral canthus
-lateral end at an oblique line drawn through ala of nose and lateral canthus
-in men brow is more commonly at level of supraorbital rim; women brow arches higher
Ptosis
-must differentiate between lateral eyelid hooding that is a result of upper eyelid skin redundancy and that
due to ptosis of the eyebrow
-relaxation of frontalis muscle to assess
-aggressive upper eyelid blepharoplasty may result in further brow ptosis
-correction of temple ptosis improves lateral canthal crow’s feet
Rhytids
-note forehead, glabellar, and temple rhytids
Hairline Patterns
-women with medium to low hairlines are candidates for standard coronal or endoscopic forehead lift
-women with high hairline might benefit from trichophytic lift, which maintains their hairline position and
reduces vertical height of their high forehead
-male patients beware of male pattern baldness
-may require direct and mid-forehead lifts, which seek to camouflage incision in natural subunit
boundaries
Skin Type
-fair- and thin-skinned pts usually heal with more ideal scars that those with dark and thicker or sebaceous
skin
Asymmetries
-passive and dynamic asymmetries of eyebrows noted
-dynamic eyebrow asymmetries should not be altered surgically
1313
-passive asymmetries are not usually corrected unless it is the pt’s expressed wish may alter unique facial
characteristics
Bony Contour
-women with prominent supraorbital rim and excessive forehead bossing may appear masculinized may
benefit from bone reduction
MANAGEMENT
1314
Coronal Forehead Lift
-standard procedure of choice for rejuvenation of upper face
-ideally for pt with generalized ptosis and rhytids of upper face and normal or low hairline
-relative contraindications:
-high hair lines in women and male pattern baldness
-not useful to correct brow asymmetries
-advantages:
-well-concealed incision behind hairline
-good exposure of forehead muscles allowing accurate and extensive myoplasty
-disadvantages:
-elevation of frontal hairline
-hypesthesia posterior to incision line
Technique:
-incision made 4-6 cm posterior to frontal hairline; cant incision parallel to hair follicles to
minimize hair loss
-dissection in subgaleal (supraperiosteal) plane and superficial to superficial layer of deep
temporal fascia
-beware of frontal branch over zygomatic arch
-perform myotomy of corrugators, procerus, and central frontalis muscle
-make skin excision anterior to incision (usually 12-18 mm of scalp)
-expect up to 5 mm of stretch-back
-place suction drain for 24 hours if needed
Pretrichial Lift
-primary indication is for a high hairline and long vertical height to forehead in women
-does not raise anterior hairline to unaesthetically high level
-resection of redundant forehead skin reduces vertical height of forehead
-advantage:
-allows same wide access to forehead musculature as coronal lift
-disadvantages:
-broader area of anesthesia
Mid-forehead Lift
-for pts with significant forehead rhytids in which the scar can be camouflaged
-more closer and more direct approach to glabella and does not distort hairline
-major disadvantage is potentially unsatisfactory scar
1315
Direct Brow Lift
-indicated primarily for men with bushy eyebrows
-advantages:
-long-lasting lift as a result of excellent orbicularis
muscle suspension
-best technique to correct brow asymmetries or
unilateral brow ptosis
-more effective to correct marked ptosis of lateral
eyebrow
-disadvantage:
-eyebrow scar
-loss of hair follicles
-no effect on forehead, glabellar or temple ptosis and
cannot be used to improve forehead or glabellar
rhytids
Technique:
-skin incised directly above brows, inferior edge of incision just within brow hairs
-skin excised down to but not including frontalis
-supratrochlear and supraorbital nerves preserved
-includes suspension of orbicularis oculi to pericranium
Browpexy
-performed through infrabrow incision
-may be indicated in pt primarily concerned about fullness or puffiness in lateral portion of upper eyelids
-lateral prominence in infrabrow region d/t prominent supraorbital margin or brow fat pad may be
improved with this technique
-use restricted to pts who have only mild to moderate eyebrow ptosis
Technique:
-performed through upper blepharoplasty incision
-dissection plane suborbicularis oculi
-fusiform fat excision
-may or may not also elevate brow
-if used to elevate brow, permanent suture suspension needed
1316
and lack of skin excision
-relative contraindications:
-high hairlines in women
-male pattern baldness
-tight, thick skin
-extensive bony attachements in Asians and American Indians
Technique:
-three to six small vertical incision just behind frontal hairline
-subperiosteal dissection plane
-dissection anteriorly and posteriorly
-endoscopic visualization and instrumentation
-supraorbital and supratrochlear nerves preserved
-myoplasty may be performed
-no scalp excision, therefore most surgeons fixate scalp in elevated position (screws, sutures,
tissue glue etc.)
COMPLICATIONS
-bleeding
-may be encountered from superficial temporal artery in coronal, pretrichial or trichopytic lifts or
from supratrochlear or supraorbital arteries
-lagophthalmos
-usually a problem in cases of previous or concurrent upper blepharoplasty with excessive skin
removal
-scar widening
-most often occurs in temporal region
-infection
-rare
-increased following haematoma development in diabetic pts
EMERGENCIES
1317
CONGENITAL AURICULAR MALFORMATION
-important landmarks:
-helix
-superior crus
-inferior crus
-scapha
-antihelix
-cymba conchae and cavum conchae
-external ear located in lower neck
as mandible develops, ear ascends to side of head
-hillocks:
1 tragus
2 helix
3 cymbum
4 scapha
5 antihelix
6 antitragus
-muscles:
-intrinsic: major and minor helices, tragus, antitragus, transverse and oblique
-external: anterior auricularis, superior auricularis, posterior auricularis
-blood supply:
-superficial temporal a.
-posterior auricular a.
-occipital a.
-venous drainage:
-posterior auricular v.
-external jugular v.
-superficial temporal v.
-retromandibular v.
-lymphatics:
-parotid nodes
-cervical lymph nodes
-motor innervation:
-CN VII:
-temporal branch anterior and superior auricularis
-posterior auricular branch posterior auricularis
-sensory innervation:
-lesser occipital nerve
-mastoid branch of lesser occipital nerve
-greater auricular nerve (C2, C3)
-auriculotemporal nerve (CN V3)
-Arnold’s nerve (CN X) supplies concha
1318
COMMON AURICULAR DEFECTS
-protruding ear:
-auriculocephalic angle > 30o
-cryptotia:
-pocket ear deformity
-cup ear deformity:
-constriction of helix and scapha
-colobomata:
-clefts of the ear
-lobule deformities
-microtia and anotia
PROTRUDING EARS
Preoperative Evaluation
-auricular landmarks of deformity:
-very poor antihelical fold
-overdeveloped concha
-abnormally formed scapha
-obvious lack of superior and inferior crus surrounding fossa triangularis
-otoplasty best begun before child starts school, b/n ages 5 and 6
-ear is at 85% of adult size and before the age of social stigmatization
Surgical Techniques
Mustarde Technique
-to correct underdeveloped antihelical fold
-involves placing several horizontal mattress sutures along scapha in a curved line to create an antihelical
sulcus
-problems: -sutures may become noticeable or could erode trough postauricular skin
-may fail to maintain proper curve of antihelical fold
Converse Technique
-to correct underdeveloped antihelical fold
-an island of cartilage is created that sits anteriorly to the rest of the conchal cartilage
-cartilage produces a normal appearing fold
-allows more permanent retraction of auricle and is potentially more permanent correction of antihelix
1319
Farrior Technique
-to correct underdeveloped antihelical fold
-combination suture and cartilage sculpting technique
-incisions made through cartilage on conchal rim only; then longitudinal wedges are removed at level of
superior crus and future antihelical fold
-an incision then is made through cartilage at level of antihelical fold, creating an island
Pitanguy Technique
-to correct underdeveloped antihelical fold
-uses smaller island flap and conchal set back suture
-for pts with small amount of antihelical cartilage
Furnas Technique
-for overdeveloped concha
-if conchal bowl too large, an island of cartilage can be removed to narrow it and allow proximal portion to
lie firmly against mastoid
-placement of conchal mastoid sutures as far posteriorly to avoid narrowing of EAC
CONGENITAL MALFORMATIONS
Classification
-Marx:
-Grade 1: abnormal auricle with all identifiable landmarks
-Grade 2: abnormal auricle without some identifiable landmarks
-Grade 3: microtia is recognized by a very small auricular tag (“peanut ear”)
-Grade 4: anotia
-Weerda:
-Grade I: mild deformity with a slightly dysmorphic helix and antihelix
-major structures are present, and no additional cartilage is necessary during surgical
repair
-Grade II: all major structures present to some degree, but repair requires cartilage or skin
-Grade III: few, if any, landmarks; peanut and anotic ears
1320
Surgical Planning and Treatment
TREATMENT OF CONGENITAL MALFORMATION OF
-photodocumentation AURICLE
-high-resolution CT scan of temporal bones
obtained Stage I: -auricular reconstruction (creation of cartilaginous
-at least 2-3 months allowed between stages framework with autogenous rib cartilage)
Stage II: -Lobule transposition
of reconstruction Stage III: -atresia repair (by otologist)
Stage IV: -tragal reconstruction
-Auricular Reconstruction (I): Stage V: -auricular elevation
-no stripping of perichondrium
during rib harvesting
-most common complication: atelectasis
-others: PTX, pneumomediastium, pneumonia
-sculpt cartilage to form framework
-framework implanted on side of head
Complications
-skin necrosis overlying cartilage framework
-chondritis
-reabsorption of cartilage
-malposition of auricle implant
-tissue breakdown of skin graft or posterior aspect of ear
-keloid formation
1321
CHIN AND MALAR AUGMENTATION
CHIN AUGMENTATION
1322
Complications
-displaced implant:
-implant may slide too far superiorly and obliterate anterior gingival-lip sulcus abnormal smile
-lateral displacement implant should be appropriately sutured to periosteum
-infection of tissue reaction:
-extremely rare
-antibiotics given if reaction does not resolve within 10 days, implant is removed and 8 weeks
should elapse before attempting to reinsert it
-bony resorption:
-occurs in almost all alloplastic implants
-may cause a problem to underlying teeth
-results in loss of projection
-improper size selection
-should wait at least 3 months before replacing implant to see what swelling and tissue reaction
will actually do to the appearance
-mental nerve injury from lateral dissection
-hypertrophic scar
Sliding Genioplasty
-indications:
-more severe cases of retrognathia
-insufficient vertical height
-hemifacial atrophy
-failed implant
-advantages:
-using pt’s own tissue
-can be used to decrease vertical
height of chin if necessary
-disadvantages:
-increased surgical time
-longer healing time
-risk of injury of anterior teeth and membranes around chin and lip area
-loss of lip competence (poor reapproximation of mentalis muscle)
Operative technique:
-incision made anterior to gingivobuccal sulcus and extends just laterally to cuspid teeth
-carried through orbicularis and mentalis muscles which will be reconstructed later
-periosteum is elevated inferiorly and laterally
-an osteotomy is made below cuspid apices and mental foramina at an appropriate angle
-inferior segment is advanced and held in place with four-screw cross-plate
-incision closed in two layers
-procedure can be combined with chin implantation to enhance contour
MALAR AUGMENTATION
-indications:
-lack of malar prominence
-adjunct to face-lift surgery if pt has deepened melolabial folds
-accentuation of malar prominence, creating a more pleasing aesthetic appearance
-asymmetry of malar prominence from congenital deformity, surgical resection or incomplete
reduction of malar fracture
1323
Evaluation
-decision mainly based on aesthetic appreciation than actual measurements
-when malar prominence falls more than 5 mm posterior to nasolabial groove on a true lateral projection,
there is usually a deficiency of the malar area
Implant Selection
-silastic:
-advantages:
-can be inserted into smaller pocket
-infection can be treated with implant in place
-disadvantages:
-tends not to stay in original position and must be anchored with suture at initial insertion
-forms surrounding capsule that may be palpated as surgical site matures
-reinforced e-PTFE:
-advantages:
-forms no capsule and has good tissue fixation
-disadvantages:
-large pocket required for insertion
-must be removed if infection occurs in immediate area
-porous polyethylene:
-advantages:
-has average pore size that ranges from 100-250 um
-allows for tissue ingrowth with minimal soft-tissue reaction
-disadvantages:
-not as flexible as silastic or reinforced e-PTFE
-must be removed if infection occurs
Operative Procedure
-intraoral incision placed just inferior and slighly anterior to parotid duct, 3 cm long
-incision carried down to periosteum
-elevation superior and lateral over malar and zygoma
-porous implants pressure loaded with clindamycin and saline
-implant placed over cheek
-incision closed in two layers
Complications
-malpositioned implant
-must be surgically removed and replaced
-infection
-implant removed
-new implant should not be reinserted for 6-8 weeks
-intraoral implant exposure
-implant removed, size adjusted, and reinserted
1324
CHEMICAL PEELING
Skin Anatomy
Epidermis
-stratum corneum: no nucleus, keratin in cytoplasm,
loosens then desquamates
-stratum granulosum: 3-5 layers thick, flattened,
keratohyalin granules
-stratum spinosum: basophilic cells
-stratum basale: single layer of cuboidal cells at basal
lamina
Epidermal-Dermal Junction:
-rete pegs: epidermal projections into dermal layer
-papillae: dermal, vascularized projections into
epidermal layer
Dermis:
-papillary dermis: collagen and elastin fibers
-reticular dermis: denser layer
Subcutaneous layer:
-contains fat and fibrous tissue
-reparative processes:
-epidermis growth and thickening triggered by removal of stratum corneum as well as with deeper
damage of epidermis to basal layer
-deposition of some collagen and dermal glycosaminoglycans activated by epidermal wounds
-production of collagen and dermal ground substance generated with dermal wounds
-timeline:
-5 days: epidermis regenerates
-1 weeks: epidermis loosely attached to dermis
-2 weeks: new collagen deposits, youthful look
-1 month: pigment returns
-6 months: epidermis at normal thickness
-10 months: dermis normalizes
1325
-depth of penetration factors:
-agents used and their concentrations
-method of applications and layers of application
-use of pre-peel keratolytic agents
-use of degreasing agents
-use of occlusion or semi-occlusion of peeled skin
-skin thickness
-pilosebaceous gland activity and density
-anatomic location
-contraindications:
-active herpetic lesions
-pustular acne
-history of keloids
-collagen diseases
Jessner peel
-mixture of resorcinol, salicylic acid, and lactic acid in ethanol
-used to freshen skin, to treat acne and to lighten epidermal pigmentation
Phenol peels
-indications:
-aging skin with fine and deep wrinkles
-photodamaged skin
-multiple, diffuse actinic keratoses
-pigmentary abnormalities
-superficial acne scars
-stucco keratoses
-mechanism of action:
-deep dermal peel
-liquefaction necrosis resulting in deep dermal injury
-complications and caveats:
-pigmentary changes for darker skinned pts: hyperpigmentation or hypopigmentation
-relative contraindication: skin treated with x-rays destroyed adnexal structures needed for
1326
cutaneous regeneration
-previous used of systemic Accutane is a risk factor for scarring
-flap necrosis and scarring if used in conjunction with facelift
-toxicity:
-phenol is absorbed into circulation
-significant cardiac arrhythmias
-related to surface area of phenol applied: face is peeled in segment of no more than 25%
of facial area with 10-15 minute pause between segments
-renal and hepatic toxicity
-contraindications:
-areas treated with external beam radiation
-renal, cardiac, hepatic disease
-formulations:
-Baker’s solution:
-contains liquid phenol (88% phenol concentrate), distilled or tap water, liquid soap,
croton oil (enhances keratolytic and penetrating action)
COMPLICATIONS
-hyperpigmentation
-hypopigmentation
-scarring
risk factors:
-deep peels in keloid-forming patients
-peels that extend into reticular dermis
-post-radiation skin (lack of adnexal structures)
-Accutane therapy (wait 12 months to allow sebaceous glands to recover)
-excessive abrasion prior to application
-cardiac arrhythmia (with phenol)
-renal toxicity (with phenol)
-herpes simplex activation
-prophylactic valcyclovir started 48 hours before the peel and continued for 10-12 days
-cutaneous infection
-streptococcus or staphylococcus infection (uncommon)
-pseudomonas infections (uncommon)
1327
CERVICOFACIAL LIPOSURGERY
-adipose tissue
-mesodermal origin
-subdermal perivascular connective tissue containing adipoblasts preadipocytes adipocytes
-blood supply:
-< 1cm: from descending branches of subdermal plexus
-suctioning fat in direction upward toward subdermal plexus will cause greater
fat atrophy
-> 1cm: from ascending fascial arteries
-suctioning fat over fascia will cause greater fat atrophy
-volume and distribution of cervicofacial fat are strongly influenced by genetic factors
-surgical changes in fat volume should be considered permanent in cervicofacial region
-fat transplantation:
-reinjection of liposuctioned fat small cystic cavities lined with fibrous tissue in center or fat
which provide a useful matrix for providing volume
-6-9 months required for graft stabilization
-small, uniform quantities that maximize surface area-to-volume ratio
-indications:
-improve contour for correcting congenital or traumatic deformity
-correct lipoma and lipodystrophies
-defat flaps
-removal of localized fat deposits (wattles and jowls)
-correction of asymmetries
-adjunct to face/neck lift
-enhancement of malar eminences
-limited to subdermal volume changes
-difficult to obtain good results with pts with thin and lax skin
-fine rhytids cannot be corrected
-excessive or loose skin will remain redundant
-absolute contraindications:
-generalized obesity
-collagen vascular diseases
-endocrine disorders
-bleeding disorders
-relative contraindications:
-inelastic skin, cellulitis or pitting defects, stretch marks, minimal to minor wrinkling, age of 55
and older, history of hypertension or diabetes
1328
PREOPERATIVE ASSESSMENT AND WORKUP
Liposuction
-standard: blunt suction technique of Illouz
-less damage to vascular and lymphatic arcades
-septae are left to nourish skin with perforating vessels less possibility of skin loss
-small suction cannula creates more subcutaneous tunnels and decreases likelihood of surface
irregularities
-start with blunt tipped 4- or 6- mm cannula with suction apertures 8 to 10 mm from end
-cobra-tipped cannula for dense fibrotic tissue but more likely to cause neural, vascular and skin damage
-“wet technique”
-tumescence solution (hypotonic salt solution with lidocaine and epinephrine)
-advantages:
-decreases blood loss and aids in dislodgement and separation of tissue planes
-disadvantage:
-fluid distorts surgical area, more difficult to determine actual volume of fat removed
-higher incidence of post-surgical edema and ecchymosis
-“dry technique” more applicable in head and neck
-does not use tumescence solution
-ultrasound-assisted liposuction:
-20-40 kHz ultrasonic frequency at cannula tip forms microcavities or bubbles eventually
bubbles implode
Lipoinjection
-harvest with 18-gauge or larger cannula
-inject small quantities (usually in 0.1 ml increments) beginning distally
-overcorrect by about 30%
1329
-inframalar groove
-cheek hollows
-nasolabial fold
-oral commissure
-mentum
COMPLICATIONS
-Minor:
-ecchymosis
-dyesthesia
-irregularities, bulges, depressions
-pigmentation changes
-Major (rare)
-neural and vascular injury
-haematoma/seroma
-infection
-skin loss
1330
MANAGEMENT OF BENIGN FACIAL LESIONS
EPIDERMAL LESIONS
Actinic Keratosis:
-small multiple erythematous lesions on sun-exposed areas
-10-20% develop into SCCa
-actinic cheilitis: occurs on vermilion border of lips
-tx: -usually cryotherapy
-multiple lesions: dermabrasion, chemical peeling or topical 5-FU
Actinic keratosis
Cutaneous Horn:
-hyperkeratotic conical lesions whose height is at lease half their largest diameter
-various types of lesion may be present at their bases (actinic keratosis, verruca,
SCC, seborrheic keratosis)
Cutaneous horn
Seborrheic Keratoses:
-brownish black verrucous stuck-on appearance
-tx: -dermal curettage
Keratoacanthoma:
Seborrheic keratosis
-clinically and histologically can resemble SCC
-occur in elderly people on sun-exposed areas
-rapid growing reaching full size in 6-8 weeks then involuting spontaneously (less
than 6 months)
-can also occur with Muir-Torre Syndrome
-genetic syndrome characterized by a combination of sebaceous tumors of
the skin and one or more internal malignancies, most often colon cancer
-types of sebaceous skin neoplasia include sebaceous adenoma, sebaceous
Keratoacanthoma
epithelioma, sebaceous carcinoma, and keratoacanthoma
-tx: -observation or complete excision
-avoid shave biopsy because histologic changes at lesion base are
important in differentiating from SCCa
Cysts:
-often compressible and may have visible puncta
Epidermoid cyst
Millia:
-small, yellowish white, 1-2 mm papules
Comedones:
-open (blackheads) - occur with acne vulgaris
-closed (whiteheads)
-histologically: dilated cystic hair follicles filled with keratinous and lipoid material
1331
SKIN-APPENDAGE TUMOURS
Trichofolliculomas:
-solitary
-central pore with white wool-like tuft of hair
-tx: -shaving, punch excision or CO2 laser
Tricoepitheliomas: Tricofolliculoma
-small, flesh-coloured papules
-solitary or multiple (AD) cluster around central face
-can occur with cylindromas
-tx: -shaving, punch excision or CO2 laser
Trichilemmomas:
-small pink to brown facial papules
-multiple hamartoma syndrome (Cowden disease) Multiple tricoepitheliomas
-AD
-associated with high incidence of breast cancer, other visceral
malignancies
-fibrous hamartomas of breasts, thyroid and GI tract
Sebaceous Hyperplasia:
-2-3 mm yellow to orange lobulated papules with slight umbilications
-can occur with cyclosporine use Syringoma
-feature of acne rosacea
Syringomas:
-intraepidermal eccrine duct adenomas
-predominantly in women at puberty - multiple lower eyelid lesions
-tx: -excision
Hydrocystomas:
Hydrocystoma
-uncommon cystic periorbital lesions
-translucent bluish quality
-tx: -excision
Pilomatrixomas:
-tumours differentiating toward hair cells
-solitary, hard, deep-seated nodules
-common in children and young adults
-tx: -excision Pilomatrixoma
Nevus Sebaceus:
-tumour differentiating toward sebaceous glands
-congenital lesion presenting as a solitary, often linear, slightly raised, orange-
yellow hairless plaque on scalp or face
-basal cell carcinoma develops in 5-7%
-tx: -excision
Nevus sebaceus
1332
NON-SKIN-APPENDAGE TUMOURS
Vascular Tumours:
Hemangiomas:
-congenital:
-nevus flammeus
-vascular malformation (port wine stain)
-medial nevus flammeus:
-lightens with age and not associated with
underlying abnormalities
-lateral nevus flammeus:
-darkens with age
-associated with leptomeningeal angiomatosis
(Sturge-Weber syndrome) or osteohypertrophy
and arteriovenous fistulae (Klippel-Trenaunay Nevus flammeus
syndrome)
-tx: tunable dye lasers
-capillary haemangiomas
-appear b/n 3rd and 5th weeks of life
-grow for months and then regress
-70% regress by age 7
-tx: -usually resolve spontaneously
-treat those that ulcerate, encroach on vital structure
(nose, eyes, mouth) or are frequently traumatized
Capillary hemangioma
intralesional corticosteroids used
-cavernous haemangiomas
-appear at any age
-association with Maffucci syndrome (dyschondroplasia
and osteochondromas) or blue rubber-bleb nevus syndrome
Ectasias:
-telangiectasias
-occur in many conditions:
-scleroderma, dermatomyositis, radiation dermatitis, chronic Pyogenic granuloma
alcoholism, liver disease, pregnancy, childhood, Osler-
Rendu-Weber disease
-venous lakes
-deep blue cutaneous nodules typically on lips, ears, or face
-arteriovenous malformations
1333
Fibrous Tumours
-skin tags
-fibrous papules
-adenoma sebaceum
-uncommon but characteristic feature of tuberous sclerosis
-actually angiofibromas
-tx: dermabrasion, CO2 laser, or argon laser
-hypertrophic scars Adenoma sebaceum
-keloids
Fatty/Muscular Tumours
-lipoma
-leiomyomas: arise from erector pili hair follicle smooth muscle
Neural Tumours
-neurofibromas
-benign nerve sheath tumours
Melanocytic Tumours
-tumours of nevus cells (melanocytic nevi), epidermal melanocytes, or dermal
melanocytes
-melanocytic nevi:
congenital or acquired
-histological classification:
-Junctional: flat pigmented Junctional nevi
-Dermal: flesh coloured and dome shaped or pedunculate
-Compound: in between
-Spitz nevus:
-epithelioid and spindle cell nevus
-benign but can resemble malignant melanoma histologically
-epidermal melanocytes:
Dermal nevi
-freckles (ephelides)
-lentigines
-lentigo senilis (actinically induced)
-lentigo simplex
-may become malignant lentigo maligna or lentigo maligna
melanoma
-dermal melanocytes:
-nevi of Ota
-unilateral blue-brown-black discolourations of the periorbital Compound nevi
region, temple, forehead, malar area and nose
-rarely undergo malignant degeneration
-blue nevi
-no malignant potential
Spitz nevus
1334
Inflammatory Lesions
-warts (verruca vulgaris)
-HPV infection
-molluscum contagiosum
-poxvirus
-shiny, flesh-coloured to pink, dome-shaped, firm papules with central umbilications
THERAPEUTIC CONSIDERATIONS:
Dermal Curette
-semi-sharp round to oval blade of variable size
-blade will not normally cut through normal collagen
Electrosurgery
-electrodesiccation
-healing by secondary intent may take 2-3 weeks
Cryotherapy
-tissue destruction determined by volume of cryogen applied, duration of exposure and technique used
-NO, fluorocarbon sprays and liquid nitrogen
Chemical Peeling
-actinically damaged skin
Dermabrasion
-can be more predictable than chemical peeling because extent of wounding can be more precisely
controlled
Laser Surgery
-precise margination, good control of destruction depth, good hemostasis, decreased postoperative pain,
and target specificity
Hemostatic Agents
-Monsel solution (ferric subsulfate) - protein coagulant; permanent discolouration
-aluminium chloride
-silver nitrate
1335
MANAGEMENT OF ALOPECIA
METHODS OF TREATMENT
Donor Site
-found on sides and back of head and is limited anteriorly be a vertical line through the EAC
-superior border of safe donor area in mid-occipital region generally located beneath horizontal line that
intersects superior attachment of auricles to the scalp
-strip of follicles no larger than 1 cm is removed
-ensure no transection of follicles
-individual grafts are then made
Recipient Site
-grafting requires 2-4 sessions
-grafts inserted, evenly spaced apart and maintaining adequate circumferential bridge around each graft
-this maintains adequate circulation around each graft
-maintain consistent graft angling of follicles
-two methods to achieve density and refinement within transplanted hairline regions:
1336
b) Combination of minigrafts and micrografts
-minigrafts contain 3-8 hairs
-create higher-density hair more posteriorly
-micrografts have only 1-2 hairs
-refine outer perimeter of transplanted recipient site
-soften transition zone between bald forehead skin and transplanted frontal
hairline
-wait 4 months between each session
-newly transplanted grafts enter telogen effluvium phase and lose preexistent hair over 2-6 weeks
-new hair begins growth in about 10-16 weeks
Scalp Reduction
-excision of bald skin from crown and central scalp regions
-hair bearing scalp is undermined and advanced superiorly to cover excision site
-scalp reduction patterns:
-midline sagittal ellipse, Y pattern, lateral crescent
Tissue Expansion
-useful in pts with MPB who would benefit from hair-bearing flap or a scalp reduction but are limited by
poor scalp flexibility
-scalp expanders: temporoparietal and occipital donor regions
-does not provide coverage to frontal regions
-frequent expansion (2-3x/wk) until pain tolerance reached
-scalp reduction is then performed
-complications: infection, haematoma, exposure of implant, implant failure
Juri Flap
-pedicled transposition flap based on STA
-for frontal hairline restoration
1337
LASER SKIN RESURFACING
-laser produces thermally induced exfoliation with superior precision, depth control, and uniformity with
additional beneficial therapeutic effects on collagen
SKIN ANATOMY
-epidermis: 0.04-1.5 mm
-keratinocytes
-melanocytes in basal layer
-dermis:
-superficial papillary dermis
-deeper, thicker reticular dermis layer
-contains fibroblasts: collagen and elastin production
-appendiceal structures
-hair, sebaceous glands, sweat glands
-neck skin has relative lack of pilosebaceous glands increased risk of scarring and delayed
healing
-age related changes in skin:
-thinning of epidermis and dermis
-flattening of dermal-epidermal junction
-collagen and elastin fibers become fragmented and degenerate
-decrease in number of appendiceal structures
1338
INDICATIONS AND PATIENT SELECTION
-indications:
-rhytids
-dyschromias
-scarring conditions:
-superficial/shallow acne
-elevated scars more favourable than depressed scars
-immature more favourable than mature scars - ideally 6-8 weeks following scar
formation for optimal results
-skin lesions:
-lentigines and seborrheic keratoses
-actinic keratoses
-early superficial basal cell carcinoma
-adjunct to other facial rejuvenation procedures (eg. blepharoplasty, rhytidectomy)
-avoid using laser on area where there is subdermal undermining
-contraindications:
-active or recent use of isotretinoin (Accutane) impaired ability of pilosebaceous apparatus to
reepithelialize wound
-skin resurfacing delayed 6 months to 2 years after discontinuation of medication
-active infection
-physical examination:
-dynamic (present in animation) vs static (present in animation and repose) rhytids
-dynamic rhytids:
-attached to facial musculature - not very responsive to laser resurfacing
-horizontal forehead lines, glabellar frown lines, periorbital crow’s feet, nasolabial folds
-static rhytids:
-correctable with laser
resurfacing
FITZPATRICK CLASSIFICATION OF SUN-REACTIVE SKIN
-classification systems of skin: TYPES
-Glogau classification
-Fitzpatrick: Skin Type Skin Color Sunburn Tan
-light skin (Type I) to dark I White Yes No
skin (Type VI)
-types I-III will tolerate II White Yes Minimal
resurfacing without
III White Yes Yes
significant risk of
pigmentation changes IV White No Yes
-types IV-VI at increased
V Brown No Yes
risk
VI Black No Yes
1339
PREOPERATIVE PREPARATION
TECHNIQUE
POSTOPERATIVE CARE
1340
-complications:
-milia:
-epithelial inclusion cysts from follicular plugging with occlusive dressings during
reepithelialization
-resolve spontaneously
-contact dermatitis:
-d/t decreased barrier function of de-epithelialized skin
-antibiotic-containing ointments, soaps, moisturizers and cosmetics
-tx: low-potency topical steroid ointments
-HSV infections:
-most common infections seen as consequence of laser resurfacing
-vesicles usually absent dx based on high clinical suspicion
-failure to treat with antivirals lead to scarring or disseminated infection
-bacterial and fungal infections:
-less common
-usually d/t Staph aureus and Pseudomonas aeruginosa
-hyperpigmentation:
-common following skin resurfacing in patients with Fitzpatrick skin type III or higher
-pts with darker skin types are treated prophylactically with hydroquinone in preoperative
period
-postop hyperpigmentation also tx with hydroquinone
-hypopigmentation:
-delayed; may be observed up to 1 year
-permanent and few treatments available
-can occur with any skin type
-scarring:
-increased if: isotretinoin use, keloid tendency or previous resurfacing procedures
-also from excessive tissue ablation into deep reticular dermis
-regional variations: perioral, mandibular and neck areas
-tx: topical and intralesional steroids, silicone dressings and pulsed dye laser
-ectropion:
-previous lower blepharoplasty at increased risk
-lower lid laxity
-requires surgical repair
-CO2 Laser:
-invisible beam
-primarily absorbed by water
-excellent for cutting, coagulation, or ablating (depending on area of focus)
-Nd:YAG Laser:
-near-infrared beam, invisible
-primarily absorbed by pigmented tissues
-deeper penetration
-more scatter than CO2 lasers
-indicated for cutaneous lesions (port-wine stains, telangiectasia, hemangiomas, etc.)
1341
-KTP Laser:
-visible laser, primarily absorbed by oxyhaemoglobin
-may use a fiberoptic carrier
-indicated for cutaneous lesions and as a cutting tool
-Argon Laser:
-visible, broad-band blue light
-primarily absorbed by oxyhaemoglobin
-depth of penetration between CO2 and Nd:YAG lasers
ERBIUM LASER
1342
TISSUE EXPANDERS
-advantages:
-avoids distant flaps, allows for hair-bearing skin
-disadvantages:
-requires multiple procedures, deformity from expansion device
-common uses:
-face and neck, scalp (alopecia), preauricular region (otoplasty), concurrent procedure with serial
excisions
Biomechanical Properties:
-collagen: stores strain energy applied during deformation of skin
-elastin: most linearly elastic biosolid known determines elastic property
-glycosaminoglycans: binds collagen and elastin fibers
-hyaluronate: type of GAG that binds fluid to form a gel
-Biological Creep:
-property of conventional tissue expanders
-permanent changes in microanatomy
-increases epithelial mitotic activity and subdermal vasculature
-results in net increase in surface area
-Mechanical Creep:
-no change in microanatomy
-displaces fluid and extracellular substances
-realigns collagen fibers by breaking bonds with GAGs and elastin fibers
-no net increase in surface area
-Stress Relaxation:
-decrease in stress when skin is held under constant pressure
Techniques:
-base should be 2.5 times area of defect
-rectangle expander has best expander volume-to-skin area
-most expanders used in head, face, and neck are from 1-250 ml
-Conventional tissue expansion technique:
-expand over 4-6 weeks of use
-relies on biological creep
-Rapid intraoperative tissue expansion:
-expansion and deflation of prosthesis in operating room over 3 minute intervals (typically 3
cycles)
-no true net gain of skin surface area
-relies on mechanical creep
-important to match expander to geometric configuration of the expansion site
-serial injections of saline performed weekly
-W-shaped or V-shaped incision recommended as universal incision for insertion of a tissue expander
Scalp
-used to correct male-pattern baldness
-used to close defects after tumour excision or to repair scar tissue
-implant placed in loose subgaleal connective tissue, superficial to periosteum
1343
Auricle
-postauricular skin, which lies over a bony prominence and is thinner than scalp, can become necrotic at
pressure points can expose the implant
-this skin is expanded more slowly than is the more flexible skin of the face and neck
Face
-expander inserted extraperiosteally beneath frontalis muscle
-expanded forehead flap can be used repeatedly for nasal reconstruction
-cheek can provide enough tissue by means of expansion to resurface almost one third of ipsilateral face
-for traumatic and burn scars, after Mohs tumour excision, or for congenital skin lesion
-expander placed through preauricular face-lift incision
Neck
-skin of neck amenable to expansion, although not used as much as skin of scalp and face
Complications:
-current rate is 5-7%
-infection
-extrusion and leakage
-neuropraxia or vascular compromise
-bone resorption
-skin necrosis
-hematoma
1344
OTOLARYNGOLOGY FACTS AND POINTS
1. The temporalis muscle attaches to the squamosa portion of the temporal bone.
2. The anterior boundary of the tympanic cavity is the carotid wall, eustachian tube, tensor tympani.
3. Meckel’s cave is a concavity in the superior part of the temporal bone.
4. Gradenigo syndrome is associated with inflammation of the following cranial nerve in the Dorello canal:
VI
5. Trautmann triangle is determined by the sigmoid sinus, bony labyrinth and superior petrosal sinus or dura.
6. The upper limit of normal for the diameter of the internal auditory canal in an adult male is 8 mm.
7. The posterior semicircular canal and saccule are innervated by the inferior vestibular nerve
8. The inferior tympanic artery to the middle ear is a branch of the ascending pharyngeal artery.
9. The superior portions of the utricle and saccule and the superior and horizontal semicircular canals are
supplied by the anterior vestibular artery.
10. The lobule of the ear has sensory innervation from C2,3 via lesser occipital nerve.
11. The average size of the footplate is 1.41 x 2.99 mm.
12. The scala vestibular and scala media are separated by the Reissner membrane.
13. In the adult, the eustachian tube is approximately 35 mm.
14. The auricle of the ear has reached adult shape by the following week of gestation: 20th.
15. Congenital microtia occurs in 1:20,000.
Audiology
16. The human ear is capable of hearing the frequency range form 20-20,000 Hz.
17. In audiology, speech noise is white noise with the following frequencies filtered out: below 300 Hz and
above 3000 Hz
18. The decibel scale is logarithmic and incorporates a ratio. All of the following are used for reference levels:
intensity, sound pressure, hearing, sensation level.
19. The effective vibrating part of the tympanic membrane is approximately 55 mm2.
20. The transformer ratio of the middle ear is about 22:1. This translates into approximately 25 dB.
21. In 1960, Bekesy outlined his theory of hearing. He stated that when the stapes footplate moves in and out
of the oval window, there is a resulting upward and downward movement of the basilar membrane, which
causes distortion of the endolymph. This theory is called the Travelling Wave Theory of Hearing.
22. A saucer shaped (SNHL) audiogram is most indicative of congenital hearing loss.
23. A double peaked impedance audiometry pattern can be seen in the use of a high frequency probe tone in a
“B” tympanogram.
24. A type As tympanogram is consistent with otosclerosis.
25. The above tympanogram is a type Ad.
26. During a Carhart Tone Decay Test, one presents a tone at the threshold for the following number of
seconds: 60.
-a tone is presented for 60 seconds. If the tone disappears, raise the stimulus level and continue
until the patient can hear for 60 seconds. If this last level is 20 dB or more above threshold, the
test is positive for retrocochlear pathology.
27. The following test is similar to the Carhart test but it incorporates rest periods during the testing. It is the
Owen Test.
-test to help rule out retrocochlear pathology.
28. In Bekesy Audiometry when there is a continuous tracing above the pulsed tracing, this is indicative of a
functional hearing loss. This is called a Bekesy type V.
29. In acoustic reflex testing, the reflex will likely be an absent if there is conductive pathology or a
sensorineural hearing loss greater than 60 dB.
30. In high resk neonates, the following percentage of the screen group will have hearing loss using BERA: 3-
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4%.
31. The audiometric test that is based on the principle that one increases the volume of one’s voice in the
presence of background noise due to the fact that the noise is heard and interferes with self-monitoring is
called the Lombard test.
32. A positive Bing test is indicative of normal hearing.
-it is a tuning fork test in which the tone is louder with the ear canal occluded.
33. The tuning fork test in which the tuning fork is placed against the mastoid and then, when it is no longer
heard, is placed against the tragus while the examiner gently occludes the meatus is called the Lewis test.
-no a good test, and interpretation of the test is neither simple nor consistent.
34. According to OSHA, Permissible Noise Exposure over an 8-hour day should not exceed 90 dB.
35. Earmuffs, custom-fitted earplugs, or disposable earplugs each provide the following amount of sound
attenuation: 20-40 dB.
36. The origin of the summating potential is the hair cells and is a direct current shift of the baseline of the
recording.
37. The generator site for wave V of the ABR is thought to be the inferior colliculus.
38. The ABR generated by a broad-band click stimulus has its major contribution from the following
frequency range: 3000 to 4000 Hz.
39. A patient has a 60 dB hearing level at 4000 Hz in the suspect ear. To correct the latency of the ABR for
this patient, the following time interval should be deducted: 0.1 ms.
-for responses to a standard 80 dB nHL broadband click, deduction of 0.1 ms for each 10 dB that
the 4 kHz hearing loss exceeds 50 dB.
40. The least interaural latency difference considered suspicious for an acoustic tumour is 0.2 ms.
-the interaural difference in wave V latency (IT5) will normally be 0.2 ms. Greater than 0.2 ms
seen in more than 96% of acoustic tumours
41. The cochlear microphonic originates from the hair cells.
42. The most accurate non-invasive test for acoustic tumour diagnosis is MRI.
43. The normal latency of the fifth wave of the ABR is in the range of 5-6 ms.
44. The origin of wave I of the ABR is the auditory nerve.
45. The normal value of the wave III-V interval is approximately 2 ms.
46. The kinocilia are located at the end of each hair cell nearest the tallest stereocilia.
47. The utricle is primarily sensitive to linear movement.
48. A 40 year old patient is having a caloric test done. Stimulating the right ear with water warmer than body
temperature results in the following directional movement of endolymph: ampullofugal.
49. The endolymphatic potential across the membrane separating the endolymph from the peilymph is 80 mV
50. In electronystagmography testing (ENG), investigators use the following percentage difference between
right-beating and left-beating nystagmus to be significant in the Jongkee formula for directional
preponderance: 25-30%.
51. A 50 year old male presents with vertigo. During his ENG testing, he has a right-beating nystagmus with
left ear down and a left-beating nystagmus with right ear down. This is suspicious of positional alcohol
nystagmus.
-cupula is rendered a floating object by alcohol diffusion. It becomes gravity dependent and
produces a peripheral vestibular abnormality secondary to the prior 24- to 48-hour ingestion of
alcohol.
52. Simultaneous binaural bithermal stimulus testing produces diagnostic information and is what percentage
more sensitive than the alternate binaural bithermal method done? 55%
53. A 60 year old male is suspected of having a central lesion. One of the most reliable sings would be failure
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of ocular fixation.
54. Alternate bithermal caloric responses may reveal an abnormality about 50% of the time while simultaneous
bithermal caloric responses increase the yield to 80% in the following condition: Meniere disease
55. On ENG testing of a 23 year old female with symptoms of unsteadiness, it was noted that there was
evidence of anterior internuclear ophthalmoplegia on testing eye movements. This is indicative of multiple
sclerosis.
56. Nystagmus present when gazing in the direction of the fast component and in straight gaze is termed
second-degree nystagmus.
-suggests a central origin. Also, vertical or diagonal nystagmus suggests a central origin.
57. Positional nystagmus, when the direction of the nystagmus remains fixed regardless of the position of the
head during the positional testing although it may be stronger in a particular direction, is termed Nylen type
II nystagmus.
-this implies either a peripheral lesions or a central lesion.
58. Aschan type I nystagmus is when the nystagmus is nonfatigable and persistent: its direction changes with
head position.
59. The Kobrak test is a simple caloric test that is done with the patient in the upright position and the head
tilted back at 60o angle.
60. The directional preponderance test is a standardized test to measure canal paresis and directional
preponderance and in this test the patient is placed in supine and the head is elevated at a 30o angle.
61. The principle of ENG is based on the difference in electrical potential between the retina and the cornea.
62. In a positive fistula test, stimulation of the ear with positive pressure results in nystagmus to the same side.
63. The Charcot triad (nystagmus, scanning speech, intention tremor) may be associated with multiple
sclerosis.
64. The rare variant of Meniere disease in which there is a dramatic restoration of hearing after an acute attack
of vertigo is called Lermoyez syndrome.
65. Internuclear ophthalmoplegia is a disturbance of the lateral movements of the eyes characterized by a
paralysis of the internal rectus on one side and weakness of the external rectus on the other, and if it is
bilateral it is pathognomonic of multiple sclerosis.
66. A speech impairment that occurs with CVA or another neurologic problem in which substitutions and
additions of sounds in words is termed apraxia.
-dysarthria is a central or peripheral nervous system deficit resulting in muscle slowness,
weakness, or incoordination.
67. When a child tends to repeat what is said to him or her it is termed echolalic.
68. The frequency of voice that is considered optimal for adult men is at 125 Hz. For women: 225 Hz.
69. A 40 year old male presents to his MD with a voice disorder. He is diagnosed as having flaccid dysarthria.
His most likely diagnosis contributing to this is myasthenia gravis.
-flaccid dysarthria is a voice disorder that occursn in lower motor neuron or primary muscle
disorders such as MG and tumours and strokes involving the brainstem nuclei.
70. Amyotrophic lateral sclerosis is a condition in which a voice disorder may present as mixed dysarthria.
71. One of the most important tests in detecting vibratory asymmetries and submucosa scars is
strobovideolaryngoscopy.
72. The region of the intermediate and deep layers of the lamina propria is called the vocal ligament.
73. The volume of air remaining in the lungs at the end of expiration during normal breathing, which may be
divided into expiratory reserve volume and residual volume, is called functional residual capacity.
74. This medication has been used in treatment of performance anxiety but can produce thrombocytopenic
purpura, mental depression, and bronchospasms among other adverse reactions: Beta blockers.
75. The theory of speech that suggests that the contribution of a particular speech manoeuver to the spectrum
depends on its relation to the nodes or antinodes of the standing waves is called the perturbation theory.
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Congenital Deafness
76. Hereditary deafness occurs in the following incidence of live births: 1:4000
77. The Mondini-Alexander classification of inner ear developmental anomalies is incomplete development of
the bony and membranous labyrinth. The cochlea may be represented by a single curved tube and the
vestibular labyrinth is not developed.
78. If a mother is infected with rubella druing the first trimester, the percentage of children with deafness at
birth is 5-10%.
79. In a congenital syphilis patient, when there is vertigo and nystagmus on stimulation with high intensity
sound such as the Barany noise box, it is called Tullio phenomenon.
80. Leopard syndrome is a form of hereditary congenital deafness associated with variable SNHL, pulmonary
stenosis, hypogonadism, and ocular hypertelorism.
81. Tietze syndrome is a hereditary congenital deafness associated with profound deafness, absent eyebrows,
blue irides, and albinism.
82. the autosomal dominant hereditary congenital deafness syndrome associated with widely spaced medial
canthi, flat nasal root in 75% of cases, confluent eyebrows, white forelock, and coloured irides is
Waardenburg disease.
83. Achondroplasia is associated with saddle nose, frontal and mandibular prominence, mixed hearing loss and
dwarfism.
84. The hereditary congenital deafness syndrome associated with syndactylia, craniofacial dysostosis,
hypoplastic maxilla, exophthalmos, and a flat conductive hearing loss is Apert syndrome.
85. The hereditary congenital deafness syndrome associated with cranial synostosis, parrot-beaked nose, short
upper lip, mandibular prognathism, and premature closure of the cranial suture lines is Crouzon syndrome.
86. Klippel-Feil syndrome is a hereditary congenital deafness associated with SNHL, short neck due to fused
cervical vertebrae, external auditory canal atresia, and spina bifida.
87. The syndrome of congenital deafness, pigeon breast, scoliosis, thin elongated individuals with long spidery
fingers and hammer toes is Marfan.
88. A 6 month old male presents with hearing loss, optic atrophy, sclerotic brittle bone, choanal atresia, and
fluctuating facial nerve paralysis. The most likely diagnosis is Albers-Schonberg disease.
89. Treacher Collins syndrome is associated with malformation of ossicles, antimongoloid palebral fissure,
mandibular hypoplasia and a normal IQ.
90. A 1 year old male presents with micrognathia, cleft palate, mixed hearing loss, hypoplastic mandible,
mental retardation, and breathing difficulties when sleeping. The most likely diagnosis is Pierre Robin
syndrome.
91. Vander Hoeve syndrome or osteogenesis imperfecta is an AD congenital hearing loss syndrome associated
with fragile bones, loose ligaments, hearing loss, and 60% have blue sclera.
92. Alport syndrome is suspected in a 4 month old baby. One of the most helpful tests in making the diagnosis
would be a urinalysis.
93. Fanconi anemia syndrome, Alstrom syndrome, Van Buchem syndrome, and Mohr syndrome all share the
same trait of autosomal recessive inheritance.
94. Hallgren syndrome, Alstrom syndrome, and Cockayne syndrome all share the same trait of associated
visual loss.
95. Hurler syndrome (gargoylism) is a hereditary congenital deafness syndrome associated with mental
retardation, dwarfism, mixed hearing loss, forehead prominence, and abnormal mucopolysaccharides are
deposited in tissues.
96. Laurence-Moon-Bardet-Biedl syndrome is associated with congenital deafness, obesity, dwarfism, mental
retardation, and retinitis pigmentosa.
97. Pendred syndrome is a hereditary congenital deafness syndrome associated with a “U”-shaped audiogram,
diffuse goiter development at puberty, and a normal IQ. This syndrome constitutes the following
percentage of hereditary deafness syndromes: 10%.
98. The syndrome associated with retinitis pigmentosa, polyneuropathy, ataxia, and SNHL is Refsum
syndrome.
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99. With regard to congenital abnormalities of the middle and external ear, when one has microtia, atretic
canals, and abnormal ossicles it is termed a class III abnormality.
100. The hereditary congenital deafness syndrome that is autosomal recessive and is associated with retinitis
pigmentosa, ataxia, and vestibular dysfunction is Usher syndrome.
Cochlear Implants
101. The F0 (fundamental frequency) is mainly responsible for pitch in cochlear implant technology. This is a
frequency range from 100-200 Hz.
102. The most prominent cell in the matrix of the spiral ligament are type I fibroblast cells.
103. The nucleus multichannel cochlear implant is 25 mm long and contains approximately 22 electrodes.
104. There are 13 to 16 million people in the US with hearing loss. Of these, there are approximately how many
thousand with severe to profound hearing loss: 150,000-200,000
105. One notable exception to having cochlear implant is Michel deformity.
106. The current minimum age limit for implantation of a cochlear implant is age 1 year.
107. A 4 year old child has had a cochlear implant inserted in her right ear at age 3. She presents with
longstanding (4 months) bilateral noninfected middle ear effusions. The next step is to suggest no
treatment at present and observe for infection
108. A 5 year old female had a cochlear implant inserted successfully. The parents are told that if she has any
further surgery she should avoid monopolar cautery.
109. Several factors are involved in predicting a more rapid or greater improvement in speech reception and
production in children after cochlear implant surgery. This indicates: postlingual onset of deafness,
implantation during the preschool years, a shorter period of auditory deprivation, participation in an oral
communication therapy program.
110. The children who have been the most obvious candidates for a cochlear implant are those who have
demonstrated no response to warble tones in the sound field with appropriate hearing aids or responses
suggestive of vibrotactile rather than auditory sensation. This aided response is with no response above
1000 Hz but in the lower frequency having responses at levels greater than 40-50 dB HL.
111. The anterior margin of the foramen magnum os formed by the basioccipital synostosis.
112. All of the following are characteristisc os neurofibromas associated with Von Reckinghausen disease:
multiple, nonencapsulated, incorporate axons, malignant degneration.
113. In performing a translabyrinthine removal of an acoustic neuroma, spinal fluid may be decompressed by
opening the cochlear aqueduct.
114. In performing a middle fossa procedure to remove an acoustic neurma, generally the anterior limit of the
dissection is the middle meningeal artery.
115. Transposition of the following nerve routinely occurs during a transcochlear approach: CN VII
116. The greater and lesser wings of the sphenoid bone are separated by the superior orbital fissure.
117. the trigeminal ganglion lies in the Meckel cave.
118. Anterior to the jugular foramen lies the carotid canal.
119. For large lesions of the cerebellopontine angle, the following approach will allow the surgeon to obtain the
widest field of view: suboccipital.
120. Characteristics of glomus tumours include all the following: multicentric origin, metastatic change is rare,
familial tendency, associated with neuropeptide secretion
121. A 40 year old male presents at your office with an acute facial nerve paralysis. The differential diagnosis
should include all the following: Lyme disease, herpes zoster, sarcoidosis.
122. The facial nerve is not fully developed until a child is 4 years old.
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123. The incidence of Bell’s palsy per 100,000 population is 20-30.
124. A family history of Bell’s palsy is present in 8%.
125. The labyrinthine segment of the facial nerve extends from the fundus of the IAC to the facial hiatus, where
the fallopian is narrowest. This segment is approximately 3 to 5 mm.
126. The facial nerve has thousands of fibers. Seventy percent are myelinated and 30% sensory and
secretomotor. The total number of fibers is approximately 10, 000.
127. A 60 year old male presents to your office with 24 hour history of right otalgia, dysgeusia, and hyperacusis.
You should expect in 48 hours he may develop Bell palsy.
128. On testing the facial nerve in a 40 year old male with facial nerve paralysis, there is a difference between
the two sides in minimal nerve excitability testing. A difference of how many mA suggest nerve
deprivation: 3.5 mA.
129. The incidence of severe degeneration in facial nerve paralysis with herpes zoster is approximately 40%.
130. Which of the following tests is used to predict facial nerve function ro return 6-12 weeks before clinical
evidence of return of function: electromyography.
131. A 24 year old male presents with blistering of his right conchal bowl, facial nerve paralysis, and pain.
Viral testing would show rising titers to the following virus: varicella-zoster.
132. The incidence of facial paralysis in newborns is the following: 0.25% of live births.
133. A newborn child has on examination facial diplegia, bilateral loss of abductors of the eye, extremity
anomalies, and aplasia of the brachial and thoracic muscles. The most likely diagnosis is Mobius
syndrome.
134. A large children’s hospital in the midwest did a retrospective analysis of facial nerve paralysis in newborns
over a 20 year period. Their study showed the following percentage of facial nerve paralysis was due to
birth trauma: 80%.
135. a 14 year old female was involved in an incident during which she sustained a knife wound to the central
left cheek. she had a facial nerve paralysis and repair was carried out within 24 hours. She most likely had
the following repair: epineural repair
136. A 60 year old male presents with a peripheral facial nerve paralysis. He has a firm 2x3 cm parotid mass.
Needle aspiration indicates a malignant tumour. The most common diagnosis is adenoid cystic carcinoma.
137. The following is disruption of the nerve trunk: neuropraxia.
138. A survey, at a large New York hospital, of temporal bone fractures revealed the following percentage of
fractures involved the facial nerve: 20%.
139. A 30 year old female presents to your office with recurrent orofacial edema, recurrent facial palsy, and
lingua plicata (fissured tongue). The most likely diagnosis is Melkersson-Rosenthal syndrome.
140. An 18 year old male form Connecticut presents to your office with a facial nerve paralysis, generalized
malaise, an erythematous skin lesion, regional lymphadenopathy, and a history of having camped outdoors
the previous week. The most likely diagnosis is Lyme disease.
141. Auriculotemporal syndrome (Frey syndrome) is associated with aberrant innervation of the sweat glands by
parasympathetic fibers of the IXth cranial nerve.
142. A 35 year old male presents to your office with indolent ulcers of the mucous membranes and skin with
stomatitis as well as anogenital ulceration, iritis, and conjunctivitis. He has Behcet syndrome.
143. A 45 year old female presents to your office with a history of crocodile tears characterized by residual
facial paralysis with profuse lacrimation during eating. She has Bogorad syndrome.
144. The symptom complex that occurs in individuals working in high pressure when they are returned too
suddenly to normal pressure is called Caisson disease
145. Cavernous sinus syndrome is caused by thrombosis of the cavernous intracranial sinus and is associated
with involvement of the following nerves: II, III, IV and V1
146. The syndrome of nonsyphilitis interstitial keratitis associated with vertigo, tinnitus, ataxia and progressive
SNHL is called Cogan syndrome.
147. Costen syndrome is a symptom complex involving an abnormality of the TMJ - impaired bite and is
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characterized by tinnitus, vertigo and pain in the frontal, parietal, and occipital areas.
148. DiGeorge syndrome involves cardiovascular and craniofacial anomalies and abnormalities of the thymus
gland.
149. The syndrome associated with leukopenia, arthritis, and enlarged lymph nodes and spleen is termed Felty
syndrome.
150. A 50 year old male presents to your office with a symptom complex of acute suppurative otitis, pain in the
eye and temporal area, abducens paralysis and diplopia. He has Gradenigo syndrome.
151. A 40 year old man presents to the office with Horner syndrome. He has paralysis of the cervical
sympathetic nerves and therefore has ptosis, mosis, anhidrosis and enophalmosis.
152. Vernet syndrome (jugular foramen syndrome) is associated with involvement of cranial nerves IX, X and
XI.
153. Multiple endocrine adenomatosis type IIA (Sipple syndrome) is associated with hyperparathyroidism,
pheochromocytoma and medullary carcinoma of the thyroid.
154. Rollet syndrome is associated with involvement of cranial nerves III, IV, and VI.
155. One of the most reliable clinical tests for hypocalcemia is the facial twitch obtained by tapping the
distribution of the facial nerve. This is called Chvostek sign.
156. In the embryology of the fetus, the derivatives of the five arches (pharyngeal or branchial) are of a
combination of mesodermal origin.
157. During the course of embryonic development, the third arch artery is the precursor of the carotid artery.
158. The thymus gland is derived from the ventral aspect of the third pouch.
159. The second branchial arch gives rise to the geniculate ganglion VII.
160. The cartilage bar of the fourth branchial arch forms thyroid cartilage and cuneiform cartilage.
161. The ventral (thyroid) diverticulum that descends between the first and second arches can forma a
thyroglossal duct cyst but usually it atrophies by the sixth week of gestation.
162. In the fetus, the tongue is fully developed by the 20th week.
163. The hard palate is formed in the fetus by the ninth week.
164. The incidence of esophageal atresia in cases of tracheoesophageal fistulas is slightly greater than 90%.
165. The hyoid bone is usually calcified by age 2. The thyroid cartilage starts to calcify at age 20.
166. The muscle that is the primary elevator of the soft palate is the levator veli palatini.
167. An incomplete cleft lip involves a portion of the lip and may form a muscular diastasis with intact
underlying skin to a large cleft with only a small band of residual tissue connecting the two sides of the lip.
This band is call the Simonart bar.
168. The embryologic development of the lip and palate occurs between 4 and 7 weeks.
169. a newborn child is noted to have an incomplete cleft of the palate. This probably occurred at the following
point in embryologic development: 7 to 12 weeks.
170. In your office, you have a mother who had a cleft palate repaired as a child. She has one child without
congenital deformities but she is 12 weeks pregnant. You can advise her that the chance of this child
having a cleft palate alone is 6%.
171. The incidence of a cleft deformity per live births is 1:680.
172. A child is seen in the neonatal nursery with a cleft palate deformity. The parents are very anxious to have
this repaired. You suggest they should wait until 10 to 12 months.
173. You are asked to see a child in the newborn nursery with a cleft lip deformity only. The parents want an
idea of when this can be surgically repaired. You tell the parents this can usually be done at 10 weeks.
174. Lip adhesion is a preliminary procedure used in the therapy of cleft lip repair. In the procedure, there are
usually laterally based flaps obtained from the lip itself. The procedure is usually done at 1 to 4 weeks.
175. One of the palatoplasties done for a soft palate deformity using posteriorly and anteriorly based unipedicle
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microperiosteal flaps is called an Oxford palatoplasty.
176. The procedure used to close the soft palate cleft with closure of the hard palate at a later date is called
Schweckendick procedure.
177. The most common complication of palatoplasty procedures is hypernasal speech (30%). Fistula formation
is from 10-21%.
178. The Dibbell technique is a procedure to correct the nasal ala, the lateral alar margin and the lip.
179. The technique used to lengthen the columella in cleft lip repair is the Bardach.
180. The primary complication of a pharyngeal flap initially is hemorrhage.
181. Type I is an IgE mediated reaction via mast cells, type II is a cytotoxic reaction, type III is an immune
complex-mediated reaction, and type IV is a cell-mediated reaction.
182. The third most abundant serum immunoglobulin that inhibits the adherence of microorganisms and alien
macromolecules is IgA. IgG is the major antibody of secondary responses, IgM is the predominant
antibody in early immune response, IgD is found in large quantities in circulatory B cells, and IgE is found
in basophil and mast cells. IgA is the predominant Ig in seromucous secretions.
183. Tests of B-cell function include measurement of serum levels of immunoglobulins, antibody response
following immunization, and the presence of plasma cells
184. The principle organs that serve as sites for proliferation and development of cells involved in immune
responses include all the following: bone marrow, Peyer patches, lymph nodes, spleen.
185. Cellular hypersensitivity occurs 24-72 hours after antigen introduction.
186. Tests of T-cell function: lymphocyte count and morphology, E-rosette assay, allogenic skin graft rejection,
delayed hypersensitivity skin tests.
187. Corticosteroids affect the sodium pump, reduce capillary permeability, and stabilize lysosomal membranes.
188. In chemotaxis, there is a very organized movement of cells.
189. 13-20% of US population suffers from allergic disease.
190. An allergen is an antigen that causes allergic reaction.
The Chest
191. The volume of gas that is either inspired or expired during each normal respiratory cycle is called the tidal
volume.
192. One of the most useful tests for asthmatics to monitor the severity of an asthmatic attack is the forced
expiratory volume.
193. A flow volume loop demonstrating decreased expiration and inspiratory curves is indicative of pulmonary
COPD.
194. A flow volume loop demonstrating decreased inspiratory curve is indicative of extrathoracic obstruction.
195. A measure of the distensibility of the lung parenchyma is called the compliance.
196. Decreased compliance is indicative of pulmonary fibrosis.
197. Normal lung function is considered to have an alveolar-arterial gradient of less than 20 mmHg.
198. FEV1 should be the following percentage or greater of the predicted volume from a normative chart: 80%
199. Total lung capacity for males is 6L; 4.2L for females.
200. A class I congenital genesis of the lung has been classified by Schneider as total genesis of the lung
201. A methemoglobin level of this degree produces cyanosis: 75 mg/dL
202. The leading primary pulmonary carcinoma in women is squamous cell carcinoma.
203. The triad of apical lung tumour, vocal cord paralysis and Horner syndrome is called Pancoast syndrome.
204. The thyroidea ima artery is present in the following percentage of the population: 10%.
205. The following percentage of mediastinal tumours are malignant: 30%.
206. A 6-month old child is taken to the operating room to have a peanut removed from her right main stem
bronchus. The size of the bronchoscope you would most likely choose would be 3.5 mm.
207. In the adult male, the average distance from the incisor teeth to the hiatus is 38 cm.
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208. The most common cause of hemoptysis related to the lung is bronchiectasis.
209. The most common cause of dysphagia lusoria is an abnormal subclavian artery
210. The ligamentum arteriosus is an abnormality of the following branchial arch: 4th.
Related Ophthalmology
211. The floor of the orbit is formed by the orbital plate of the maxilla, orbital surface of the zygoma, and the
orbital process of the palatine bone.
212. A 20 year old male sustained eye trauma and ti was determined he had a displaced trochlea. The physical
exam would have revealed diplopia on downward gaze.
213. A 35-year old male presents to your office with proptosis, excessive lacrimation, periorbital edema and
photophobia. one test that would be helpful in making a diagnosis would be a TSH assay
214. The superior orbital fissure transmits the superior orbital vein, ophthalmic vein, orbital branch of the
middle meningeal artery, recurrent branch of the lacrimal artery, and cranial nerves III, IV, VI, V1
215. The usual causative organism in cavernous sinus thrombosis is coagulase-positive S. aureus.
216. The orbital decompression procedure in which the floor and the medial wall of the orbit are removed to
allow expansion into the ethmoid and maxillary sinuses was first described by Ogura.
217. The lateral rectus muscle is innervated by the following cranial nerve: VI nerve.
218. The muscles involved with movement of the eyes down and to the right are right inferior rectus and left
superior oblique.
219. The procedure for decompression for malignant exophthalmos in which an ethmoidectomy is done and the
floor of the frontal sinus is removed is described by Sewell.
Related Neurology
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cardiac manifestations.
232. Refsum syndrome is a familial disorder that is believed to be inherited in an autosomal recessive fashion.
Patients have retinitis pigmentosa, cerebral ataxia, and SNHL. Serum analysis would reveal elevated
phytanic acid.
233. The second most common cerebral pontine angle mass lesion is a meningioma.
234. The incidence of accessary ostia from the maxillary sinus is approximately: 20-30%
235. The Onodi cell is the most posterior of the posterior ethmoid cells.
236. A clinical bony dehiscence of the c cavernous portion of the carotid canal is present in 22% of patients.
237. As a landmark, one uses the anterior ethmoid artery. It is important to know that this can be absent
unilaterally in the following percentage of patients: 14%; bilaterally absent in 2% of patients.
238. The range of bacteria involved in acute sinusitis include S. pneumoniae, S. aureus, H. influenzae and
Streptococcus pyogenes.
239. The most common fungal sinus infection in an otherwise healthy patient is Aspergillus niger.
240. Woodworkers have an increased incidence of this type of tumour in the maxillary sinus: adenocarcinoma
241. An anatomic variation of the ethmoidal infundibulum can be related to the following cells: Haller cell
242. The most common sinus involved in inflammatory sinus disease is the ethmoid sinus.
243. A 30 year old immunosuppressed female had a CT scan that showed metallic densities within the maxillary
sinus. Another test that may be helpful would be a T2-weighted MRI will demonstrate reduced signal
intensity in a patient with fungal sinusitis.
244. Squamous cell carcinoma is the most common true neoplasm of the paranasal sinus. The incidence is
approximately 1:200000.
245. The incidence of CSF rhinorrhea in patients who suffer serious head trauma is 2-3%. Accidental trauma is
the cause of 80% of the patients with CSF rhinorrhea.
246. The most common postoperative complication of endoscopic sinus surgery is synechia.
247. Only 20% of patients with CSF rhinorrhea develop meningitis as their initial symptom.
248. In the general population, the incidence of anaphylaxis as a result of the use of penicillin-based antibiotics
is 1:10,000
249. Staph aureus has a high resistance to ampicillin
250. One of the major side effects of long-term isoniazid treatment is peripheral neuropathy.
251. Cephalexin has very poor coverage against: hemophilus, pseudomonas, and bacteroides
252. Cefuroxime has poor coverage against bacteroides and pseudomonas.
253. Erythromycin can significantly elevate theophylline levels in the bloodstream.
254. Tetracycline antibiotic suspension has been helpful against aphthous stomatitis.
255. Ciprofloxacin has poor activity against anaerobes.
256. Erythromycine is very effective against Legionella pneumophilia.
257. Ciprofloxacin exerts its antibacterial activity via the inhibition of bacterial topoisomerase II.
258. With long-term amphotericin administration, one should monitor renal function
259. Vancomycin can be ototoxic in high doses.
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REVIEW QUESTIONS IN FACIAL PLASTICS
AND RECONSTRUCTIVE SURGERY
1. What are the advantages (3) and disadvantages (3) of local flaps?
2. What types of vessels are the basis of musculocutaneous flaps? Axial-pattern flaps?
Random-pattern flaps?
3. What is an angiosome?
4. What are four axial-pattern flaps and their supplying arteries?
5. What is the delay phenomenon?
6. What is “skin creep”? What is “stress relaxation”?
7. What is the significance of relaxed skin tension lines?
8. What are some of the causes of skin flap failure (8)?
9. How do you construct a Rhomboid flap? A Dufourmental flap? A bilobed flap?
10. What are the three types of advancement flaps?
11. What are the steps involved in survival of a STSG (5)?
12. What examples of regional cutaneous flaps (3)?
13. What are examples of regional myocutaneous flaps (4) and their blood supply?
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27. What are methods are used to close small to moderate defects of the cheek? Moderate
to large defects of the cheek (2)?
28. What method is used to close small thin defects of medial canthal region?
Mandibular Reconstruction
29. Which portion of the mandible, when missing, causes severe functional and cosmetic
deficits?
30. After how many treatments of hyperbaric oxygen does the vascular density plateau? At
what percentage does this plateau occur compared to normal non-irradiated tissue?
31. How is hyperbaric oxygen beneficial for the reconstruction of irradiated bone?
32. Which regional flap provides the largest area of tissue and has the greatest reach of any
regional pedicled flap?
33. What are the goals of primary oromandibular reconstruction?
34. What are the ideal qualities of the osseous component of a composite free flap (5)?
35. What are the ideal qualities of the soft-tissue component of a composite free flap (7)?
36. Which free flaps are able to accept osteointegrated implants (2)?
37. What is the blood supply of the following free flaps?
-iliac crest
-scapular
-fibular
-radial forearm
-lateral arm
38. Which flaps are capable of sensation (5)?
39. What is the maximum amount of bone that can be harvested from the radius without
severely compromising the residual radius?
Scar Camouflage
47. What are some excisional techniques for scar camouflage (4)?
48. A Z-plasty with angles of 60-, 45- and 30-degrees will increase the length of the scar by
what percentage?
49. What are other scar irregularization techniques (2)?
50. Which patients should not have dermabrasion or laser resurfacing (5)?
51. What are the complications of intralesional steroids for scar revision (3)?
Facial Reanimation
52. What are the four broad categories of facial reanimation methods?
53. In a patient with newly diagnosed facial nerve paralysis, what is the surgeon’s most
immediate concern?
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54. How long do you wait before attempting a surgical interruption that may result in
irreversible damage to the facial nerve?
55. List the different techniques used for facial reanimation (5).
56. What are common nerve grafts used for repair (2)?
57. What conditions are required before performing nerve crossover techniques (5)?
58. Which crossover technique is the most reliable?
59. What is Mobius syndrome?
60. When would muscle transposition techniques be employed (3)?
61. What are the two methods of muscle transposition? What is an advantage and
disadvantage of each technique?
Facial Analysis
79. What are “aesthetic subunits” of the nose? What do they consist of (5)?
80. In terms of dissection planes, what is the ideal plane of dissection over the upper and
lower lateral cartilages? Bony dorsum?
81. What are the elevator muscles of the nose (3)? The depressor muscles (2)? The
compressor muscles (2)? The dilatory muscles (1)?
82. What is the tip defining point?
83. What are the major tip support mechanisms of the nose (3)?
84. What are the minor tip support mechanisms of the nose (6)?
85. What are the legs of the nasal “tripod” (3)?
Introduction to Rhinoplasty
86. What is generally involved in at the initial consultation for rhinoplasty (5)?
87. What are the main points to evaluation for the nose (4)?
88. What is the maximum dose for cocaine in most adults? How long does it last?
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89. What is the maximum dose for lidocaine in adults, with or without epinephrine? How
long does it last?
90. What are the different types of incision in rhinoplasty (5)?
91. What is an “open roof” deformity?
92. Where do you begin a lateral osteotomy? What happens if this is done too low? What
happens if this is done too high?
93. What is an intermediate osteotomy?
94. What are the advantages (3) and disadvantages (3) of an external approach?
95. Which minor tip support mechanism is lost with external approach?
96. What are relative contraindications to external approach because of compromised blood
supply to the skin-soft tissue envelope (3)?
97. Where do the major arteries of the nose run in relation to the SMAS?
98. What are the arteries that supply the skin of the nose (3)?
99. Which two incision are used for the external approach?
100. What are the indications for the external approach?
101. What is the most common complication of an external approach?
102. What is the most important anatomical factor that is important in dictating the potential
surgical outcome of nasal tip refinement?
103. What is tip recoil and how is it important in the evaluation of the nasal tip?
104. What are the major (3) and minor (6) tip support mechanisms of the nose?
105. What are the different approaches to the nasal tip (3)?
106. When is a cartilage splitting technique used?
107. What incisions are used for a cartilage delivery approach (2)?
108. What technique is used when more significant cephalic tip rotation is required in more
severe tip deformities?
109. What technique is used to achieve narrowing refinement of the broad tip?
110. What are potential indications of the open rhinoplasty approach (7)?
111. What methods can be employed to enhance tip projection (5)?
112. What methods can be employed to enhance tip rotation (7)?
113. What methods are used to reduce the volume of the nasal tip (3)?
114. What are some of the features of a unilateral cleft-lip nose deformity (6)?
115. What are some of the features of a non-white nose (4)?
116. What materials can be used to augment a saddle-nose deformity (5)?
117. What are the disadvantages of alloplastic materials (2)?
118. What is the main disadvantage of demineralized bone and irradiated cartilage?
119. With regards to the orientation of the alar axis, when is it contraindicated to perform alar
resection and why?
120. For a twisted nose, what is the suggested order to perform the osteotomies? What can
be done if after performing the osteotomies, there is still a depression on the lateral side
of the nose?
121. When should cosmetic surgery be delayed in children?
122. What are some of the changes in the nose related to aging (3)?
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Revision Rhinoplasty
Blepharoplasty
137. What are the histological changes in the aging skin (5)?
138. What are two major extrinsic factors to aged skin?
139. What part of the face does rhytidectomy address?
140. What is the SMAS?
141. What are the four basic types of rhytidectomy?
142. What are two surgical adjuncts to rhytidectomy to address the lower 2/3 of the face?
143. What is the most common complication of rhytidectomy?
144. What is the most common nerve injured during rhytidectomy?
145. What is the most common branch of the facial nerve injured and why?
146. What are the complications of rhytidectomy (6)?
147. What is the ideal position of the hyoid for good results post-facelift?
148. What patient factor will increase the risk of skin slough approximately 12 times?
149. What are methods to address deep nasolabial folds (4)?
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Chin and Malar Augmentation
166. What is the approximate normal angle between the ear and the head?
167. Name the various landmarks of the external ear.
168. What is the blood supply to the pinna (3)?
169. What is the venous drainage of the pinna (4)?
170. What is the motor (2) and sensory (4) innervation of the pinna?
171. What are the two major deformities that cause outstanding ears and what are the
surgical techniques used to correct them?
172. What are the complications of otoplasty (4)?
173. What are the five stages involved in auricular reconstruction?
174. What are the alternatives to microtia reconstruction?
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REVIEW QUESTIONS IN GENERAL OTOLARYNGOLOGY
1. What are the three clinical forms of fibrous dysplasia? Which is the most common form?
2. What are the features of McCune-Albright syndrome (3)?
3. What is the typical radiographic appearance of fibrous dysplasia (1)?
4. What are the biochemical abnormalities seen in Paget’s disease (3)?
5. What is the medical treatment of Paget’s disease (3)?
6. What is the difference between Mikulicz disease and Mikulicz syndrome?
7. What are the sialographic features of autoimmune parotid disease (2)?
8. What are the features of Sjogren syndrome (3)?
9. Which autoantibodies are implicated in Sjogren syndrome (2)? Which other autoantibodies may
be elevated?
10. How is Sjogren syndrome diagnosed?
11. What are the treatments available for recurrent acute sialadenitis (3)?
12. What is the differential diagnosis of recurrent bilateral nontender parotid swelling (5)?
13. What are the three histologic features of Wegener’s?
14. What are the treatments available for Wegener’s (4)?
15. What is the typical histologic picture of T-cell lymphoma? What are the treatments available
(3)?
16. What are the features of Churg-Straus syndrome (3)?
17. What are four causes of non-neoplastic, non-traumatic subglottic stenosis?
18. What is amyloid composed of? What stain will identify it?
19. What is the histologic feature in sarcoidosis (1)?
20. In the head and neck, where do sarcoid deposits most frequently occur?
21. What two biochemical tests can be used to diagnose sarcoidosis?
22. What is the main medical treatment of sarcoidosis?
23. What are the clinical features of relapsing polychondritis?
24. What is the cause of Hashimoto thyroiditis? What is the test used to diagnosis this condition?
25. What is Riedel struma?
26. What are the autoantibodies associated with the following disorders?:
-SLE (2)
-RA (2)
-Sjogren (2)
-systemic sclerosis (2)
-polymyositis/dermatomyositis (1)
-mixed connective tissue disease (1)
-Wegener’s (1)
27. Which autoimmune disease is associated with skin and mucosa lesions, malar rash, nasal
septal perforation, pericarditis, arthritis, and renal failure?
28. Which autoimmune disease is associated with dysphagia, tight perioral skin and calcinosis?
29. What is the underlying pathophysiology of polyarteritis nodosa?
30. What are the laryngeal (1) and otologic (3) manifestations of Wegener’s granulomatosis?
31. What is the diagnosis of a patient presenting with temporal headaches, jaw claudication and an
elevated ESR?
32. What are the features of Behcet’s disease (2)?
33. What are the features of Cogan syndrome (3)?
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34. What are five clinical features of Kawasaki disease? What important investigation is required to
follow these patients?
35. What is the treatment of Kawasaki disease (2)?
41. Which pharyngeal pouch are the major salivary glands derived from?
42. What type of cells is predominantly seen in the parotid, submandibular and sublingual glands?
43. Which nerve carries postganglionic parasympathetic fibers from the otic ganglion to the parotid
gland? Aberrant innervation to skin can cause which syndrome?
44. What are the functions of saliva (7)?
45. Draw the secretory unit.
46. What is the parasympathetic innervation of the parotid gland: in terms of preganglionic nerve,
ganglion, postganglionic nerve?
47. What is the parasympathetic innervation of the submandibular and sublingual gland: in terms of
brainstem nuclei, preganglionic nerve, ganglion?
48. What is the primary neurotransmitter of the parasympathetic?
49. What is the composition of saliva (6)?
50. In the unstimulated state, which gland has the highest salivary flow? Which gland has the
highest salivary flow in the stimulated state?
51. For problems of hypersecretion, what surgical procedures can be done (4)?
52. What is the most common viral disorder involving the salivary gland? What other viruses can
affect the salivary glands (3)?
53. What organisms are usually seen in acute suppurative sialadenitis (3)?
54. What are three granulomatous diseases that can affect the salivary glands?
55. What is Heerfordt syndrome?
56. How is Sjogren syndrome diagnosed? What is seen on biopsy?
57. What percentage of calculi occur in the submandibular vs. parotid vs. sublingual glands?
58. What are the treatment options of a submandibular calculi?
59. What are some causes of non-inflammatory nonneoplastic enlargement of the salivary glands
(sialadenosis) (6)?
60. What is the accuracy of FNAB in determining malignant versus benign tumours?
61. What percentage of salivary gland tumours are diagnosed as malignant on frozen section but
are found to be benign on permanent sections?
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62. What percentage of salivary gland tumours are diagnosed as benign on frozen section but are
found to be malignant on permanent sections?
63. What test has the highest predictive value for recurrence in patients with adenoid cystic
carcinoma?
64. What is the incidence of cervical metastasis due to oral or major salivary gland adenoid cystic
carcinoma?
65. What is the 10 year survival rate for patients with adenoid cystic carcinoma who have cervical
metastasis?
66. List the six anatomic valves that are involved in deglutition.
67. List the four phases of swallowing and describe what occurs in each of the phase.
68. What are the two pressure generators during swallowing?
69. What effect does bolus volume have on both airway closure and cricopharyngeal opening
duration?
70. During the pharyngeal phase, which components can be exerted by voluntary control (2)?
71. What are two postural maneuvers that can be performed to decrease the risk of aspiration?
72. What is laryngeal penetration?
Taste
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92. What other nerves are involved in taste sensation (2)?
93. How can you clinically differentiate dysgeusia caused by a genuine stimulus versus a taste
phantom?
94. What are some of the causes of taste disorders?
Stomatitis
95. What are some infectious causes of stomatitis (4)? What are some noninfectious causes (6)?
96. What is the treatment of herpes gingivostomatitis in the immunocompetent and
immunocompromised patient?
97. What is Vincent’s gingivitis and what two organisms are usually implicated?
98. Which conditions are usually associated with desquamative gingivitis (5)? How is a diagnosis
made?
99. What is the pathophysiology of cicatricial pemphigoid and bullous pemphigoid? What is seen on
histopathology? How do these two diseases differ clinically and histopathologically? How are
these diseases treated?
100. What is a positive Nikolsky sign?
101. What condition is caused by autoantibodies directed against desmosome-monofilament
complexes, affects Ashkenazi Jews, with pathology that demonstrates intraepithelial clefting,
Tzank cells and acantholysis?
102. What condition is associated with target lesions, an rapid explosive onset of macules, papules,
vesicles, bullae or places? What are the severe forms of this condition that may require ICU
admission (2)?
103. What condition has a histology of hyperkeratosis, Civatte bodies, liquefactive degeneration of
basal cell layer and a sandlike lymphocytic infiltration in lamina propria?
104. What are the different clinical variants of lichen planus (5)?
105. What are the various clinical presentations of candidiasis (6)?
106. What are the three clinical presentations of aphthous ulcers?
107. What is the differential diagnosis of white lesions in the oral cavity (15)?
Pharyngitis
108. Tissues of the pharynx are prone to reactive changes because of which predominant tissue?
109. What is the differential diagnosis of pharyngitis (15)?
110. What are the complications of GABHS pharyngitis (3)?
111. A 9-year-old boy develops a paroxysmal cough and difficulty breathing. A throat culture reveals
a non-motile pleomorphic gram-negative coccobacillus. What is the most likely organism?
112. Which viruses can cause a mononucleosis like picture (3)?
Odontogenic Infections
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121. What are the complications of odontogenic infections (10)?
141. What are the neck spaces that involve the entire length of the neck (4)?
142. What are the suprahyoid neck spaces (4)?
143. What are the anterior, posterior, superior and inferior boundaries of the retropharyngeal space,
danger space and prevertebral spaces?
144. What are the boundaries of the parapharyngeal space (7)?
145. What are the contents of the prestyloid and poststyloid compartments of the parapharyngeal
space?
146. Which fascial layer(s) make up the carotid sheath?
147. What are the organisms seen in the majority of DNIs?
148. Which type of streptococci are commonly seen in pharyngeal infections?
149. Which type of streptococci are commonly seen in odontogenic infections?
150. What diagnostic test is required in DNIs to assess for a serious life-threatening complication? If
this complication is present, what needs to be done in addition to draining the deep neck
abscess and giving IV antibiotics.
151. What is the most common cause of a submandibular space infection?
152. Where do submandibular space infections gain access to the lateral pharyngeal space?
153. What is the treatment of submandibular space infections?
154. What are the other spaces that are in direct contact to the parapharyngeal space?
155. How does the presentation of infections involving the pre- and post-styloid space differ?
156. Which syndrome is associated with suppurative IJV thrombosis?
157. What are some signs of impending bleeding from carotid artery erosion?
158. What is the surgical approach for drainage of a parapharyngeal space abscess?
159. At what age do retropharyngeal lymph nodes usually involute?
160. What is the surgical approach for drainage of a retropharyngeal space abscess?
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161. What is a Pott’s abscess?
162. What is the most common organism involved in prevertebral space infections?
163. What are the complications of deep neck infections (10)?
164. What is the organism involved in Lemierre syndrome? What is the treatment?
Esophageal Disorders
165. What are the three regions of natural constriction in the esophagus and approximately what
level are they during rigid esophagoscopy in the adult male?
166. What are the layers of the esophagus (4)?
167. Define primary, secondary and tertiary peristalsis.
168. What decreases LES pressure (5)?
169. What are the advantages of rigid (5) and flexible (5) esophagoscopy?
170. What are common ENT manifestations of GERD?
171. What are the treatment options of GERD?
172. What are the complications of reflux (5)?
173. What are the four manometric findings of achalasia? What are the treatment options (3)?
174. What are the findings on barium swallow for diffuse esophageal spasm (1)? What are the
treatment options (3)?
175. What is the difference seen on barium swallow between achalasia and scleroderma?
176. What are the treatment options for cricopharyngeal dysfunction causing dysphagia (2)?
177. What are the features of Plummer-Vinson syndrome (6)?
178. Where does Zenker’s diverticulum occur? What are the treatment options (2)?
179. What is the most common organism infecting the esophagus in the immunocompromised host?
180. What is the most common benign tumour of the esophagus?
181. What are the two most common malignant tumours of the esophagus?
182. What is Boerhaave syndrome?
1366
REVIEW QUESTIONS IN HEAD AND NECK ONCOLOGY
8. What is brachytherapy?
9. How does radiation induce cell death?
10. What are the four R’s of radiation oncology?
11. Which phase in the cell cycle are tumour cells more radiosensitive? radioresistant?
12. What are the advantages and disadvantages of preoperative radiation therapy?
13. What are the advantages and disadvantages of postoperative radiation therapy?
14. What are the complications of radiation therapy?
15. What is hyperfractionation?
16. What is accelerated fractionation?
17. What is hypofractionation?
18. What dose of radiation is usually needed for subclinical disease? Microscopic disease?
Clinically palpable disease?
19. What are the indications for adjuvant radiation treatment?
20. What are the contraindications of radiation therapy?
Cutaneous Malignancy
21. In descending order of incidence, what are the three most common cutaneous malignancies?
22. What are some risk factors for developing cutaneous malignancies (8)?
23. Name a syndrome in which patients have a propensity to develop BCCs. What is the mode of
inheritance? What are other features of this syndrome (3)?
24. What are the five subtypes of BCC? Which is the most aggressive/dangerous and why?
25. What is the rate of metastasis for BCC?
26. What are the treatment options for BCC (5)?
27. What is the metastatic potential of cutaneous SCCa?
28. What are the factors associated with a high-risk SCCa?
29. What are some histological features of SCCa (5)?
30. What are the five histologic variations of cutaneous SCCa?
31. What is the most common premalignant lesion of the head and neck? What is the treatment of
this lesion (3)?
32. Briefly, what is Bowen’s disease?
33. What is the name of an epithelial tumour with a rapid growth within 2 months with involution that
occurs in males and older patients most commonly on the nose?
34. What margins should be taken for small BCC? What margins should be taken for aggressive
BCC and SCCa?
35. What are the indications for Moh’s surgery (4)?
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36. What is the treatment of the N0 and N+ neck in cutaneous SCCa?
37. Describe the TNM classification for skin carcinoma.
Malignant Melanoma
38. What are the risk factors for developing melanoma (6)?
39. What are the clinical characteristics of a lesion that is suspicious for melanoma (5)?
40. What are the four clinicopathologic types of melanoma?
41. Describe the Clarke and Breslow classification of melanomas.
42. When can elective neck dissection be offered in the management of melanoma?
43. What is sentinel node biopsy and when can it be used?
44. What is the primary modality of treatment?
45. What are the typical resection margins for lesions that are in situ, 1-2 mm, 2-4 mm and greater
than 4 mm thick?
46. When is a radical neck dissection advocated?
47. What other adjuvant treatments are available (3)? When are they used?
48. In general, what are the treatment options for superficial, intermediate and deep melanomas.
Include discussion for N0 and N+ disease.
49. What are the adverse effects of interferon?
50. What are the risk factors associated with nasal and paranasal sinus malignancies (7)?
51. What is the differential diagnosis of benign epithelial tumours (5), malignant epithelial tumours
(6), benign non-epithelial tumours (4), malignant non-epithelial tumours (8)?
52. What are the advantages and disadvantages of MRI and CT scan for evaluation of sinonasal
malignancies?
53. What are the three types of papilloma?
54. Which HPV types are more associated with benign disease? Which types are more associated
with malignant disease?
55. What is the rate of malignancy with inverted papilloma?
56. What are the top two common malignant tumours of the sinonasal tract? Which risk factors are
associated with each?
57. Describe the histology of an esthesioneuroblastoma (2).
58. What is the treatment modality for lymphoma and extramedullary plasmacytoma?
59. Describe the T staging for maxillary sinus tumours.
60. What is Ohngren’s line and what is its significance?
61. List the various surgical approaches to sinonasal tumours (6).
62. List in descending order the three most common sites of origin of sinonasal tumours.
63. What are the pathways to orbital invasion (3)?
64. What is the rate of cervical and distant metastasis? What is the recommended treatment for the
N0 neck?
65. What are absolute contraindications for craniofacial resection of sinonasal tumours (6)?
66. What are the complications of treatment for sinonasal cancers (10)?
67. What are the reconstructive options post-extirpation of sinonasal malignancies (3)?
Orbital Tumours
68. What is the most common primary intraconal orbital neoplasm in the adult?
69. What is the most common vascular tumour of the orbit and periocular tissue in infancy and
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childhood?
70. What is the most common malignant primary tumour of the orbit in children?
71. What is the most common epithelial neoplasm of the orbit?
72. What is the most common malignant epithelial neoplasm of the lacrimal gland?
73. What is the differential diagnosis of an orbital tumour (vascular, hematopoeitic, neural,
mesenchymal)?
74. What are the signs and symptoms of an orbital tumour (5)?
75. What is the most common metastatic orbital tumour?
76. What orbital condition is characterized by poorly localized orbital pain, eyelid swelling showing
multiple tissues in the orbit affected on CT?
77. What is the most common primary cyst of the orbit?
78. What is the most common eyelid malignancy?
79. Of the major salivary glands, neoplasms are found in which gland the majority of the time?
What is the percentage?
80. What is the proportion of benign vs malignant neoplasms in the parotid, submandibular and
sublingual glands?
81. What is the most common salivary gland neoplasm in children? What is the second most
common?
82. What is the most common malignant salivary gland neoplasm in children? What is the second
most common?
83. What is the most common benign neoplasm in adults? What is the second most common?
84. What is the most common malignant parotid neoplasm in adults?
85. What is the most common malignant submandibular gland neoplasm in adults? What is the
second most common?
86. Briefly, in terms of pathogenesis of salivary gland neoplasms, what is the multicellular theory?
What is the bicellular theory?
87. According to the multicellular theory, which cells of the salivary gland unit are the following
tumours derived from:
-mucoepidermoid carcinoma
-adenocarcinoma (2)
-oncocytic tumors
-acinic cell carcinoma (2)
-pleomorphic adenoma
-adenoid cystic carcinoma
88. For each of the pathologic descriptions, name the tumour:
-multiple cystic spaces with a double layer of oxyphilic granular cells and lymphoid
stroma projecting into the cystic spaces.
-chondromyxoid stroma, incomplete encapsulation with pseudopod extensions.
-serous acinar cells with clear cytoplasm arranged in a cystic, papillary, vacuolated or
follicular pattern.
-aggregates of mucoid cells separated by strands of epidermal cells; positive keratin and
mucous staining.
-glandular formation of cylindric cells of variable height forming papillae, acini or solid
masses.
-intracellular keratinization, intercellular bridges, keratin pearl formation.
-basaloid epithelium arranged in cylindric formations in an eosinophilic hyaline stroma
and perineural invasion.
-solid nests of epidermoid cells with few mucoid elements; positive stain for keratin and
mucin.
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89. What percentage of Warthin tumours are bilateral?
90. Histologically, how can one differentiate a high-grade MEC from SCCa?
91. Histologically, how can one differentiate a MEC from an adenocarcinoma?
92. Which salivary tumours have a propensity for perineural invasion (4)?
93. Which malignant salivary gland neoplasm shows the greatest propensity for distant metastasis?
94. What is the most important etiologic factor for the development of tumours of the major salivary
glands (esp. MEC)?
95. What normal structures can be mistaken for salivary gland neoplasms (3)?
96. In general, what is the treatment for malignant salivary tumours (include discussion of
histological grade, and the N0 and N+ neck) (4)?
97. Which malignant tumours are low-grade (2) and which are high-grade (5)? What is the
approximate 5 year survival for low- vs high-grade malignancies?
98. What are the five methods of locating the facial nerve?
99. What are the complications of parotidectomy (5)? Which is the most common complication?
100. Which branch of the facial nerve is most at risk for injury?
101. What is Frey syndrome? What is the cause? What are the treatment options (5)?
102. What are the poor prognostic indicators for salivary gland neoplasms (6)?
Lip Cancer
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127. Excluding lip cancer, what are the top three most common subsites of the oral cavity that
develop squamous cell carcinoma?
128. What are the risk factors for developing oral SCCa (6)?
129. What is the TNM staging for squamous cell carcinoma of the oral cavity?
130. What is the differential diagnosis of other oral cavity tumours (8)?
131. What are the three gross pathology forms of SCCa?
132. What are poor prognostic factors associated with SCCa of the oral cavity (6)?
133. What are the treatment options for early T1-T2 lesions? Late T3-T4 lesions?
134. For most oral cavity lesions, when is elective treatment of the N0 neck considered based on T
stage?
135. Which subsite of the oral cavity has a higher predilection for verrucous carcinoma? How does
this diagnosis affect treatment (2)?
136. Which subsite of the oral cavity has equal incidence of SCCa and salivary gland malignancies?
137. What is the preferable mode of therapy for early primary retromolar trigone SCCa?
138. Alveolar carcinoma is most commonly located where in the oral cavity?
139. Of oral cavity cancers treated primarily with radiotherapy for cure, what is the subsite with
highest complication rate?
140. What are some options for reconstruction of oral cavity defects (4)?
141. What is the differential diagnosis for a mass in the jaw (mandible or maxilla) (10)?
142. What are the two most common cystic lesions in the jaw? What is the pathogenesis and what is
their typical radiographic appearance?
143. Why is the differentiation of an odontogenic keratocyst from other cysts important?
144. Which syndrome is associated with multiple kertaocyts, BCC, bifid ribs, frontal bossing and
hypertelorism?
145. What is the most common epithelial odontogenic tumour? Where is it most commonly located?
What is its typical radiographic and histologic characteristic? How is it treated?
146. Name two other epithelial odontogenic tumours.
147. Which odontogenic tumour is common in young women and has benign self-limited growth?
148. How are odontogenic lesions diagnosed (ie. investigations etc..)
149. What are the basic treatment modalities and give an example of the type of lesion that the
treatment would be used for (3)?
150. What are the complications of odontogenic cysts, tumours and related jaw lesions (3)?
Neck Dissection
1371
Controversies in Management of N0 Neck in Squamous Cell Carcinoma of the Upper
Aerodigestive Tract
160. What are the three options in the management of the N0 neck in SCCa?
161. What are histologic features that may be predictors of cervical metastasis?
162. What are the disadvantages of elective neck irradiation?
163. What are the risk factors for the development of lymphomas (6)?
164. What are the sites and presenting symptoms of NHL in the head and neck (10)?
165. What is the major the limitation of FNA in the evaluation of lymphoma?
166. What immunohistochemical studies are used to differentiate lymphoma from other high grade
malignancies?
167. Describe the Working Formulation classification of NHL and list examples under each category.
168. Which type of NHL is the most common in the head and neck?
169. Which site of involvement of NHL has a higher propensity for CNS involvement?
170. What drugs are involved in the CVP and CHOP regimens?
171. In general, how are lymphomas treated (2)? What are the complications of these treatments?
172. What is the treatment for lymphoma causing an impending airway obstruction?
173. What are the features of tumour lysis syndrome (4)?
174. In terms of development, where does the thyroid gland originate from?
175. What is the lymphatic drainage of the thyroid gland (3)?
176. What biochemical marker is used to measure the completeness of thyroid ablation after surgery
or radioisotope therapy?
177. What is the most common benign thyroid neoplasm?
178. What is the limitation of FNAB when it comes to follicular neoplasms?
179. What are the four types of thyroid malignancies?
180. What are the histologic features of papillary thyroid carcinoma?
181. What are the histologic subtypes of papillary thyroid carcinoma (6)?
182. What is the main mode of spread for papillary thyroid cancers? What is the main mode of
spread for follicular carcinomas?
183. What tumours are involved in the MEN II syndromes?
184. From which cells do medullary thyroid carcinomas originate?
185. What is the typical histologic appearance of medullary thyroid carcinoma?
186. What is the most common site of metastasis of medullary thyroid carcinoma?
187. What is the significance of RET-proto-oncogene?
188. What is the treatment of medullary thyroid carcinoma (2)?
189. What is the risk of malignancy of a solitary thyroid nodule?
190. What are the prognostic factors in thyroid malignancies (4)?
191. How do high and low risk malignancies differ in terms of recurrence and mortality rates?
192. What is the rationale of radioactive iodine therapy? What are the risks of this type of therapy
(3)?
193. What are the complications of thyroidectomy (5)?
194. What are the manifestations of Graves disease (3)?
195. Which drugs are used in suppressive therapy for hyperthyroidism (4)? What treatments are
available if the patient fails suppressive therapy (2)?
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Parathyroid Disease and Surgery
Nasopharyngeal Cancer
Oropharyngeal Cancer
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230. What are the different types of cancer that can occur in the oropharynx (5)?
231. What is the most common malignancy of the palatine tonsil?
232. What is the most common presenting symptom?
233. What are the histologic variants of SCCa in the oropharynx (6)?
234. Describe the TNM staging of oropharyngeal cancers.
235. What are the treatment options for early (T1-T2) oropharyngeal cancers?
236. What are the treatment options for advanced (T3-T4) oropharyngeal cancers?
237. What features of the primary tumour will make it surgically unresectable (3)?
238. What are the different surgical approaches to the oropharynx (7)?
239. What are the indications for postoperative radiation?
240. What type of reconstruction is required for large surgical defects?
241. What are the complications of treatment (radiation and surgical)?
Hypopharyngeal Cancer
242. What are the superior and inferior limits of the hypopharynx?
243. What are the anatomic subsites of the hypopharynx?
244. What is the lymphatic drainage of the hypopharynx?
245. What is the most common malignancy of the hypopharynx? What are some other malignancies
that can affect this area?
246. What are the risk factors?
247. List some features of Plummer-Vinson syndrome. How is this related to hypopharyngeal
malignancy?
248. List the subsites in order of decreasing incidence of malignant involvement.
249. What is the incidence of occult lymph node metastasis in the N0 neck?
250. What is the incidence of distant metastasis?
251. What is the incidence of palpable nodal metastasis at presentation?
252. What is the incidence of coexisting primary malignancies in patients with one head and neck
cancer?
253. What is the risk of patients with primary head and neck cancers to develop a second primary
within 5 years?
254. Describe the TNM staging for hypopharyngeal cancers.
255. What are treatment options for early (T1-T2) hypopharyngeal cancers?
256. What are treatment options for late (T3-T4) hypopharyngeal cancers?
257. What are indications for partial laryngopharyngectomy (4)?
258. If radiation therapy is to be used primarily, generally what type fractionation scheme is used?
259. What levels must be addressed in the management of the N0 neck?
260. What levels must be addressed in the management of the N+ neck?
261. What are the options for surgical reconstruction (6)?
262. What is the mortality rate associated with gastric pull-up?
263. What is the superior and inferior limits of the cervical esophagus (2)?
264. What are the layers of the esophagus (4)?
265. What is the blood supply of the cervical esophagus (1)?
266. What is the nerve supply to the cervical esophagus (1)?
267. What is the lymphatic drainage of the cervical esophagus (2)?
268. What is the most common tumour of the cervical esophagus?
269. What are the major risk factors for cervical esophageal cancer (2)?
270. What is the most common abnormal finding? What other symptoms/signs are seen (3)?
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271. What investigations can be carried out to diagnose cervical esophageal cancer (3)?
272. Describe the T-staging of cervical esophageal cancer.
273. What is the general management of an early esophageal cancer with extension to the
postcricoid area and involvement of the thoracic esophagus?
274. What is the general management option for advanced esophageal cancer?
275. Overall, what is the prognosis for esophageal cancer (poor, moderate, or excellent)?
276. For gastric pull-up, what are the reasons one must perform a total esophagectomy (3)?
277. What is the operative mortality of the gastric pull-up?
278. In terms of laryngeal carcinoma, what percentage involves the glottis, supraglottis, and
subglottis?
279. For glottic cancers, what is the risk of nodal involvement for T1 and T2 lesions (1)? T3 lesions?
280. What are the various histologic stages of glottic lesions (5)?
281. What proportion of dysplastic lesions eventually progress to carcinoma?
282. What is “microinvasive” carcinoma?
283. What is Ackerman’s tumour? What features make it different from regular carcinoma (4)?
284. What are the treatment options for early glottic carcinoma (6)?
285. What are relative contraindications for laser microscopic excision (4)?
286. What are the general contraindications for open partial laryngectomy (5)?
287. What are the contraindications for cordectomy (2)?
288. What are the indications for VPL (5)?
289. What structures are removed in a VPL (4)? What other structure is removed in an extended
VPL (1)?
290. What is used to line the laryngeal lumen after VPL (1)? What can be used to add bulk if voice
quality is poor post-VPL?
291. For lesions involving only the anterior commissure what open partial technique can be used?
292. What are some complications of VPL (7)?
Supraglottic Laryngectomy
293. What are the patient selection criteria for supraglottic laryngectomy (5)?
294. What is the most common reason for local or regional recurrence after treatment of a T1 or T2
supraglottic cancer?
295. What is the risk of nodal metastasis for a T1, T2, T3 and T4 supraglottic carcinoma?
296. What are the indications and contraindications for supraglottic carcinoma?
297. What structures are removed (7)?
298. What are the main indications for supracricoid partial laryngectomy with cricohyoidopexy?
299. What are the contraindications of this procedure?
300. Cricohyoidepiglottopexy is used for what type of cancer?
301. What structures are removed (4)?
302. Describe the three anatomic regions of the larynx and their approximate levels.
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303. What are the tissue barriers to the spread of cancer (6)?
304. What are the boundaries of the pre-epiglottic space?
305. What are the boundaries of the paraglottic space?
306. What are the most common sites of cartilage invasion by cancer (5)?
307. Which (named) nodes do glottic cancers first spread to?
308. What is the differential diagnosis of a laryngeal lesion (7)?
309. Describe the TNM staging of supraglottic, glottic and subglottic cancers.
310. What are the surgical options for advanced supraglottic carcinomas (4)?
311. What are the treatment options for advanced glottic carcinoma?
312. What are the treatment options for subglottic carcinoma?
313. Which chemotherapeutic agents are commonly used for organ preservation (2)?
314. What are the complications of surgery and radiation for advanced laryngeal cancer?
Tracheal Tumours
337. What is the most common head and neck tumour in children?
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338. A child has a subglottic hemangioma, what percentage will have other cutaneous hemangioma?
339. What syndrome is associated with capillary malformations of the face?
340. Where do juvenile nasopharyngeal angiofibromas originate from?
341. What are the surgical approaches for the exenteration of JNAs (4)?
342. What are 3 malignant vascular tumours of the head and neck area?
343. What type of cells are paragangliomas derived from?
344. What two cell types are seen histologically in paraganglioma?
345. What are the anatomic locations of paraganglioma (5)?
346. What is the “rule of 10's” for carotid body tumours?
347. If a patient has a paraganglioma and is symptomatic with high blood pressure and tachycardia,
what tests should be done (3)?
348. How do you differentiate a carotid body tumour from a glomus vagale?
349. What is the Shamblin classification of carotid body tumours (3)?
350. What is the significance of Brown’s sign?
Cranial-Base Surgery
1377
REVIEW QUESTIONS IN LARYNGOLOGY
Laryngitis
20. What type of epithelium constitutes the mucosal layer of the vocal cords?
21. What are the 5 layers of the true vocal cord and what do they consist of?
22. Which muscles are the adductors (3), abductor (1) and tensor (1) of the vocal cords?
23. Which brainstem nucleus is responsible for the motor function of the larynx?
24. What clinical findings are seen with paralysis of the SLN (3)? What laryngoscopic findings are
seen (3)?
25. What should be elicited in the patients’ history in the evaluation of hoarseness (10)?
26. What investigations should/can be performed in the evaluation of hoarseness and/or vocal cord
paralysis (10)?
27. Classically, which nerve(s) is/are injured if the vocal cords are in a cadaveric position?
Paramedian position?
28. What are the top three causes of stridor in children (in order)?
29. What is the most common cause of vocal cord paralysis in children? What are other causes
(5)?
30. For children with unilateral vocal cord paralysis, what is the main modality of treatment?
31. What percentage of newborns with bilateral vocal cord paralysis require tracheotomy?
32. What is the most common cause of vocal cord paralysis in adults? What are other causes of
vocal cord paralysis (15)?
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33. What is the medical management of unilateral vocal cord paralysis?
34. How long should you wait before performing surgery for unilateral vocal cord paralysis?
35. What are the surgical options for unilateral vocal cord paralysis (4)?
36. For endoscopic medialization, what materials are available (4)? Which of these materials is
falling out of favour and why?
37. What are the surgical options for bilateral vocal cord paralysis (5)?
38. Which portion of the vocal folds are vocal cord nodules located? How do you manage them?
39. What is the most common benign lesion of the adult larynx?
40. What is the most common benign lesion of the child’s larynx?
41. What are the two types of vocal cord polyps?
42. Where are mucous retention cysts of the larynx most commonly found (2)? What is their
surgical management if involving the vocal cords?
43. What is the main causes of vocal cord granuloma (2)? How are they treated?
44. What is the risk of transmission of HPV in the birth canal?
45. Which subtype of HPV is responsible for more aggressive papillomatosis?
46. What are the two most common sites for laryngeal papillomatosis?
47. What are the non-surgical option for treatment of papillomatosis (4)?
48. Which type of cells do granular cell tumours originate from?
49. What is the most common site of a granular cell tumour?
50. If the larynx is involved, what are the most common site for a granular cell tumour?
51. What is the most common nerve of origin for neurogenic tumours?
52. Is laryngeal amyloid a localized or systemic problem?
53. What is the most common area affected in laryngeal amyloidosis?
54. What is seen on histology in laryngeal amyloidosis (2)?
55. What is the classic histology seen in sarcoidosis (1)?
56. What is the treatment of sarcoidosis?
57. What is capillary ectasia? In whom is it most commonly seen? What is the management?
58. What are the two histological types of intracordal cysts?
59. What is a glottic sulcus? What is seen on stroboscopic examination? What is the treatment?
60. What is a condition seen in middle-aged women who are chronic smokers causing a decreased
pitch in voice?
61. What is the pathophysiology of an intubation granuloma?
62. What are the two forms of laryngeal papillomatosis? Which is the more aggressive form?
63. Which type of patients are vocal cord nodules most often seen (2)?
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71. What is the voice cycle?
72. What is the “body-cover” concept of phonation?
Voice Analysis
81. What are some speech and swallowing symptoms suggestive of neuropathology (6)?
82. Which progressive disease can present with monotonous and raspy voice, velopharyngeal
incompetence, visible fasciculation in tongue, and difficulty with swallowing?
83. What disorder presents with easy fatigue with muscle use, ptosis, difficulty speaking, breathing
or swallowing with repetitive movements? Which test can confirm this condition?
84. Which condition consists of relapsing and remitting sensory and motor deficits, vertigo, tremor,
scanning speech and dysphagia?
85. What condition results from infarction of the central tegmental tract? How can this condition be
corrected?
86. Which condition is characterized by generalized bradykinesia with sluggish articulation and
monotone voice with decreased loudness?
87. What is adductor and abductor dysphonia? How can they be treated?
Phonosurgical Procedures
88. What are the laryngeal framework surgery classification according to Isshiki (4)?
89. What are the complications of vocal fold medialization by injection (5)?
90. What are the advantages and disadvantages of medialization thyroplasty over medialization by
injection (5)?
91. What are some surgical procedures to alter pitch (4)?
Controversies in Laryngology
1380
REVIEW QUESTIONS IN OTOLOGY AND NEUROTOLOGY
1. Which branchial arches is the pinna derived from? Which hillocks do these arches contribute
to? What part of the pinna do these hillocks eventually form?
2. What are the embryologic derivatives of the tympanic membrane?
3. What are the embryologic derivatives of the ossicles?
4. Where is the usual location of a congenital cholesteatoma?
5. What is the incidence and most common site for facial nerve dehiscence?
6. What is the incidence of coexisting middle/outer ear and inner ear abnormalities?
7. At what gestational age does the membranous labyrinth obtain adult shape? Adult size?
8. Which inner ear structure continues to grow into the third trimester?
9. Which structures develop from the pars superior and pars inferior portions of the developing
otocysts?
10. What are the classifications of inner ear maldevelopment and what are their approximate
incidences?
11. What is the most common histopathologic finding in congenital deafness?
12. What is Bing-Siebemann dysplasia?
13. Malformations of the cochlea are believed to be due to disruptions during the first 4 to 7 weeks
of development. What malformations are seen if this disruption occurs before 4 weeks GA? At 5
weeks GA? At 6 weeks GA? At 7 weeks GA?
14. What is the most common radiologically detectable abnormality of the inner ear?
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29. Briefly describe the central auditory pathway from cochlea to auditory cortex.
30. What is recruitment?
31. What is the significance of the tuning curve?
Electronystagmography
1382
67. What is the fixation index and what value is considered significant?
93. What are three methods that can be used to monitor the auditory system intraoperatively?
94. What is the most sensitive method? What is the least sensitive method?
95. Which method best senses changes in cochlear blood supply?
96. Which three surgeries place the facial nerve at risk?
97. Excluding operations for acoustic neuroma, which segment of the facial nerve is most commonly
injured?
98. What anaesthetic considerations should be made when monitoring the facial nerve?
99. In terms of tissue signal characteristics, what are the signal intensities for fat, CSF, nasal
mucosa, and soft tissue in a T1, T2 and contrast enhanced T1 MRI?
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100. What infectious condition of the external auditory canal can be mistaken for a malignancy?
101. What is coalescent mastoiditis?
102. What is a Bezold abscess?
103. What is a cholesterol granuloma? What are the MRI signal characteristics?
104. What are the MRI characteristics of a petrous apex cholesteatoma?
105. What is the most common site for labyrinthine fistula secondary to bony erosion from a
cholesteatoma?
106. What is the most common primary tumour of the middle ear?
107. What is the most common positive imaging finding in individuals with congenital SNHL? What
syndrome is this commonly associated with?
108. What are the MRI characteristics of an endolymphatic sac tumour?
109. What condition is associated with a “double ring sign” around the cochlea?
110. Where is the facial nerve most commonly injured in a longitudinal and transverse temporal bone
fracture?
111. What is the most common cause for objective pulsatile tinnitus and a vascular hypotympanic
mass?
112. What is the most common CPA tumour? Second most common? Third most common?
113. What are the MRI characteristics of an acoustic neuroma? A meningioma?
132. What is the most common true neoplasm of the middle ear?
133. Which tumours contain “zellballen” of chief cells containing norepinephrine and dopamine?
134. What is Brown’s sign?
135. What is Vernet syndrome? Villaret syndrome?
136. What investigations are required for glomus tumours (3)?
137. What surgical approaches are available for glomus tympanicum (2)? Glomus jugulare?
138. In which location of the temporal bone are hemangiomas most common?
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139. A chronic bloody draining ear is suggestive of what type of pathology?
140. Which type of lesion is characterized by a rim of palisading basaloid cells with central necrosis
and ulceration?
141. Name four glandular tumours of the EAC.
142. Which tumour is characterized by solitary cystic lesions originating from primitive hair matrix
cells?
143. Which disease is associated with endolymphatic sac tumours?
144. What are the three clinical types of Langerhans Cell Histiocytoses?
145. What are the three types of rhabdomyosarcoma?
146. What lesion is characterized by stellate, intermediate and vacuolated physaliphorus or soap-
bubble cells in mucoid matrix growing in nests, cords or trabeculae?
147. What is the pathogenesis of cholesterol granulosa (4)?
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management in the context of an acute otitis media and facial nerve paralysis?
176. What are some signs of sigmoid sinus thrombophlebitis? How is this diagnosed?
177. In cases of sigmoid sinus thrombophlebitis, when should a clot be removed? What else needs
to be done?
178. What are the four clinical stages of brain abscess?
179. What is the most common intracranial complication arising form middle ear infections?
180. What is otic hydrocephalus? What is the theory behind its development? How is this treated?
181. What are the potential routes of spread that can cause meningitis from otitis media (6)?
182. What are the three mechanisms for the development of a subdural abscess in the context of
otitis media?
183. What are the possible chief symptoms of a temporal bone fracture (5)?
184. How can temporal bone trauma cause vertigo (6)?
185. How can temporal bone trauma cause sensorineural hearing loss (5)?
186. How can temporal bone trauma cause conductive hearing loss (3)?
187. How can temporal bone trauma cause facial weakness or paralysis (4)?
188. Compare and contrast longitudinal versus transverse temporal bone fractures with regards to
location, frequency, type of hearing loss, incidence of facial nerve paralysis, and degree of
trauma associated.
189. What investigation is required for penetrating trauma to the temporal bone?
190. What are the suggested indications for early surgical exploration in patients with facial nerve
paralysis (3)?
191. What is the most common area of facial nerve injury in patients with longitudinal fractures?
Transverse fractures? Penetrating trauma?
192. If surgical exploration is required, what approach is used for longitudinal fractures if hearing is a
concern? In a transverse fracture where hearing is a concern? In a transverse fracture where
hearing is not a concern?
193. What are the complications of temporal bone trauma?
194. What long term complication is related to tissue entrapment from temporal bone trauma?
195. Which emergencies require immediate surgical intervention in temporal bone trauma (2)?
Cholesteatoma
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209. What are the two areas at risk for recurrences of a cholesteatoma?
210. What are the complications of cholesteatoma (5)?
211. Why is the inferior portion of a postauricular incision placed more posteriorly in children under 2
years of age?
212. What is the significance of the temporal line?
213. What are the indications for a simple mastoidectomy (4)?
214. What is Koerner’s septum? Where does it originate from?
215. What are the boundaries of the facial recess?
216. What are the landmarks of the facial nerve within the mastoid (6)?
217. Where is the most common area of dehiscence of the facial nerve?
218. What is the most common site of injury of the facial nerve?
219. What are the advantages and disadvantages of canal-wall-up versus canal-wall-down
mastoidectomy?
220. What are techniques used to minimize postoperative chronic infections following canal-wall-
down mastoidectomy (5)?
221. What is the Bondy procedure?
222. What percentage of petrous apices are pneumatized?
223. What are the air cell tracts to petrous apex (6)?
224. What are the complications mastoid surgery (8)?
225. What should be done in a patient who has total facial nerve paralysis in the postoperative
period?
Otosclerosis
234. What is the most common site for otosclerotic lesions? Where are other areas that they can
occur (5)?
235. What are three theories for the cause of sensorineural hearing loss in otosclerosis?
236. What is the mode of inheritance of otosclerosis?
237. Approximately what percentage of the population is affected by otosclerosis?
238. How does pregnancy affect hearing in otosclerosis?
239. What is Schwartze’s sign? In what percentage of patients with otosclerosis is it seen in?
240. What are the audiometric findings in otosclerosis?
241. What is Carhart’s notch?
242. What is the “on-off” effect?
243. What inherited, systemic disease is associated with otosclerosis?
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244. What is the maximal conductive loss in otosclerosis?
245. In general, what are the treatment options for otosclerosis?
246. What are the absolute contraindications to surgery?
247. What are the intraoperative, short term and long term risks and complications of stapedectomy?
248. What are the causes for failure of stapedectomy?
249. Describe the intratemporal segments of the facial nerve and their approximate lengths.
250. Where is the most common site of dehiscence of the facial nerve?
251. What does the extratemporal segment innervate (4)?
252. Which muscles are innervated by the frontal branch of the facial nerve (4)? The marginal
mandibular (4)?
253. What is the blood supply to the facial nerve (3)?
254. List the four different types of innervation of the facial nerve and their functions.
255. How is the facial nerve located in a middle cranial fossa approach?
256. What are three areas of dehiscence of the facial nerve?
257. What is the differential diagnosis of acute facial nerve paralysis (15)?
258. What is the differential diagnosis of bilateral facial nerve paralysis (6)?
259. What is Melkersson-Rosenthal syndrome?
260. Describe the 4 electrophysiologic tests for evaluation of facial nerve function. What do each
indicate and what are their limitations?
261. List the House-Brackmann classification for facial paralysis.
262. What is the most common cause of facial paralysis? What is the second most common?
263. What is the etiology, treatment and prognosis of Bell’s palsy?
264. What is Ramsay Hunt syndrome?
265. How do you decide when to explore a facial laceration?
266. What are the options for interpositional grafts for the facial nerve?
267. What is Mobius syndrome?
268. What are the conservative and surgical options for eye care in facial paralysis?
279. What structure is implicated in the spread of middle ear infections to the labyrinth?
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280. What is the arterial supply of the stria vascularis (2)?
281. What three organisms account for 70% of cases of bacterial meningitis?
282. Which organism is associated with hearing loss post meningitis?
283. What area of the labyrinth is affected by fungal meningitis?
284. Which congenital viral infections is associated with hearing loss?
285. What are some histologic findings associated with viral infections of the labyrinth?
286. How is CMV infection diagnosed (3)?
287. What are some features of congenital rubella infection?
288. What is three conditions are required for the diagnosis of idiopathic sudden sensorineural
hearing loss?
289. What are the treatments for SSNHL?
290. What symptom complex is seen in mumps (4)?
291. With regards to temporary threshold shifts, the magnitude of the shift is dependent on what three
factors?
292. Which are more hazardous, high-frequency or low-frequency sounds?
293. In terms of frequency, where do loud pure tones cause the greatest TTS.
294. How does NIHL differ with presbycusis in terms of progression?
295. What are some of the reasons for the 4-kHz notch in NIHL (4)?
296. If a person has a unilateral complete facial nerve paralysis and works in a dangerously loud
environment, how would his hearing compare in the ear on the paralysed side to the other?
297. What is the primary site of injury for NIHL?
298. What is the pathology of TTS vs PTS?
299. What is impulse noise? At what critical level is impulse noise most hazardous?
300. At what levels on the dBA scale does the risk grow rapidly for NIHL?
301. What is the most important non-occupational exposure for NIHL?
302. What are the key points in the diagnosis of occupational NIHL (8)?
303. How do you calculate the monaural impairment (MI) and the overall hearing handicap (HH)?
304. At what time weighted average exposure does the OSHA require hearing protection for
workers?
305. What is the 5 dB “trading rule”? What is an 8-h exposure to 90 dBA equivalent to at 4 hours, 2
hours, 1 hours?
Ototoxicity
1389
Cerebellopontine Angle Tumours
335. What are the risk factors that would prompt screening for sensorineural hearing loss (10)?
336. In a child with newly diagnosed sensorineural hearing loss, what non-audiological investigations
and consultations are ordered and why (12)?
337. What percentage of childhood SNHL is due to genetic factors, acquired factors and unknown
factors?
338. What percentage of genetic causes of SNHL is due to syndromes? What percentage are
autosomal recessive, autosomal dominant, X-linked, and mitochondrial?
339. What percentage of congenital hearing loss is due to membranous labyrinthine malformations
versus bony and membranous labyrinthine malformations?
340. What is Michel aplasia? At what gestational age does an insult cause this malformation?
341. What is Mondini aplasia? At what gestational age does an insult cause this malformation?
342. What is the most common form of inner ear aplasia?
343. What malformation is due to aplasia of the cochlear duct?
344. What malformation is due to complete membranous labyrinthine dysplasia?
345. What is the most common cause of congenital SNHL seen on radiographic evaluation? What
are the CT findings that make this diagnosis (2)?
346. What are the key features of Waardenburg syndrome?
347. What are the key features of Stickler syndrome?
348. What are the key features of Branchiotorenal syndrome?
349. What are the key features of Treacher Collins syndrome?
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350. Which type of neurofibromatosis is associated with bilateral acoustic neuromas?
351. What are the key features of Usher syndrome? How are Ush 1 and Ush 2 different clinically?
352. What are the key features of Pendred syndrome?
353. What ECG abnormality is seen in Jervell and Lange-Nielsen syndrome?
354. What are connexions? Which connexions can be tested for?
355. What is are the key features of Alport’s syndrome?
356. With regards to non-syndromic SNHL, how does autosomal dominant and recessive hearing
loss differ in terms of occurrence, degree of loss, familial variability, and audiogram
characteristics?
357. What percentage of sudden sensory hearing loss is defined versus idiopathic?
358. What are some of the defined causes of SSHL (10)?
359. What are the four theories of idiopathic SSHL?
360. What is seen on temporal bone histopathology following viral infection (1)?
361. What are some investigations in the workup of SSHL (6)?
362. What is the main treatment used for SSHL? What other proposed treatments have been
described (5)?
363. What proportion of patients recover spontaneously from SSHL?
364. What are the poor prognostic factors for SSHL (5)?
Tinnitus
377. What are the four types of presbycusis and what is the pathophysiology?
378. What are the age related changes seen in the auditory (3) and vestibular system (3)?
379. What are the five main classes of drugs used to control acute vestibular and autonomic
symptoms?
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Cochlear Implants and Other Implantable Auditory Prostheses
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411. Describe the three phases of nystagmus in Meniere’s disease.
412. What percentage of patients with Meniere will have profound hearing loss?
413. What are the conservative, medical and surgical treatment options for Meniere disease?
414. What is delayed endolymphatic hydrops? What are potential causes (4)?
415. What are the features of Cogan syndrome? What is the treatment?
416. What is recurrent vestibulopathy? What is the natural history of this condition?
417. What are the features of benign positional vertigo (6)?
418. What are the surgical treatment options for BPV (2)?
419. What is the fistula test? What is considered a positive fistula test?
420. What is the treatment of an inner ear fistula (5)?
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REVIEW QUESTIONS IN PEDIATRIC OTOLARYNGOLOGY
1. In children with croup, what is seen in the hypopharynx and subglottic area on inspiration and
expiration?
2. Where do subglottic hemangiomas most commonly occur?
3. Where are foreign body ingestions most commonly seen?
4. Under which circumstance can there be a false positive for retropharyngeal abscess on lateral
neck views?
5. What is the most common cause of neonatal nasal obstruction?
Laryngeal Stenosis
13. In terms of size, what proportion is the pediatric larynx compared to the adult?
14. What is the vocal process to vocal cord ratio in the pediatric larynx? in the adult?
15. At what level is the cricoid of an infant’s larynx compared to an adult’s?
16. What is the narrowest part of an infant’s airway?
17. Subglottic stenosis is considered when the diameter of the airway is less than ____?
18. Compare the signs and symptoms of supraglottic, glottic and subglottic obstruction in terms of
quality of voice, characteristic of stridor, feeding, and cough.
19. What is the most popular theory concerning the etiology of congenital subglottic stenosis?
20. What are the different types of congenital subglottic stenosis (3)?
21. What is the Cotton-Myer grading scale for subglottic stenosis (4)?
22. Where do laryngeal webs arise from?
23. What is the incidence of post-intubation subglottic stenosis?
24. What are the risk factors that predispose to subglottic stenosis post-intubation (5)?
25. What is the pathophysiology of post-intubation subglottic stenosis (4)?
26. What are the surgical treatment options for Grade I or II unilateral stenosis?
27. What are the surgical treatment options for failed extubation stenosis?
28. What are the surgical treatment options for Grade III and IV stenosis?
29. What are the criteria for anterior cricoid split (7)?
30. How does the phase of stridor help in determining the location of airway obstruction?
31. What is the most common cause of stridor in infancy?
32. What are the different types of laryngomalacia (6)?
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33. What are the indications for a supraglottoplasty (4)?
34. What are three different types of supraglottoplasty?
35. What is the most common cause of bilateral vocal cord paralysis in children?
36. What are some vascular anomalies that can cause tracheal compression?
37. What organism causes croup? What is the classic sign seen on x-ray? What is the treatment?
38. What is the organism that causes epiglottitis? What is the classic sign seen on x-ray? What is
the management for a child with epiglottitis and impending airway compromise?
39. What is the organism that causes bacterial tracheitis? What is the management?
Pediatric Tracheotomy
44. What are the different categories of agents that can cause injury to the esophagus if ingested
(3)?
45. Which of the above is the most worrisome and why?
46. When should endoscopy ideally be performed?
47. How are caustic esophageal injuries graded?
48. What is the management of caustic esophageal injuries based on this grading system?
49. What is the most common morbidity resulting from alkaline ingestion?
50. What are other complications of caustic ingestions (8)?
51. What type of radiographs should be done for suspected foreign body aspiration?
52. What are the different types of foreign body obstruction and what would their corresponding
radiographs look like (4)?
53. What medical management should be included in organic foreign body aspirations?
54. When performing bronchoscopy, what anaesthetic consideration is important to discuss with the
Anesthetist?
55. In adults, the right mainstem bronchi is the most common area for aspiration. Why (4)?
56. What is the most common type of foreign body aspirated in children?
57. What is the most common type of foreign body ingested in children?
58. What locations are foreign bodies in the esophagus most likely found (3)?
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69. Histologically, what is the make-up of a glioma (2)?
70. What are the three broad categories of encephaloceles? Which is the most common?
71. What are the types of sincipital encephaloceles (3)? Where are the masses located?
72. What are the types of basal encephaloceles (4)? Where are the masses located?
73. How can one clinically differentiate a intranasal encephaloceles from polyps based on location
within the nasal cavity?
76. List the congenital neck masses that are in the lateral neck (3), midline neck (5), and that involve
the entire neck (2).
77. What are the nerve, muscle, skeletal and artery derivatives of the branchial arches?
78. What are the derivatives of the pharyngeal pouches?
79. What is the most common type of branchial arch anomaly?
80. What is the most common type of first branchial arch anomaly? What is its course?
81. What is the course of a second branchial arch fistula?
82. What is the course of a third branchial arch fistula?
83. What is the course of a fourth branchial arch fistula?
84. What infectious condition may be diagnostic of a fourth branchial arch anomaly?
85. What is a pseudotumour of infancy? How is it diagnosed? How is it treated?
86. Describe the pathogenesis of a thyroglossal duct cyst.
87. What procedure is required for removal of a thyroglossal duct cyst?
88. What congenital neck mass causes immediate respiratory symptoms in the newborn period?
89. With regards to nasal embryology, what ruptures at 6 weeks to form the posterior choana?
90. Choanal atresia has a male or female preponderance?
91. Which is more common, unilateral or bilateral choanal atresia?
92. What percentage of bilateral choanal atresia is associated with CHARGE?
93. What other syndromes are associated with choanal atresia?
94. What are the frequency of bony versus membranous choanal atresia?
95. What are the CT findings for choanal atresia (3)?
96. What are the various theories of choanal atresia (4)?
97. Clinically, how do unilateral and bilateral atresias differ?
98. When are unilateral atresias repaired? Bilateral atresias?
99. What are the two main approaches for atresia repair? What are their advantages and
disadvantages?
100. What are the surgical approaches for repair of piriform aperture stenosis?
101. What is the significance of a single central incisor?
102. Briefly describe the prenasal space theory for the development of a nasal dermoid.
103. What are some signs of a nasolacrimal duct cyst (3)?
104. What are the indications for surgery of nasolacrimal duct cysts (3)
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Pediatric Rhinosinusitis
105. In terms of time frame of symptoms, how is sinusitis differentiated from URTI?
106. What are some of the signs and symptoms of pediatric rhinosinusitis (6)? Are these symptoms
diagnostic for sinusitis?
107. Nasal polyps in the pediatric population is associated with which condition?
108. What are the indications for CT scan in pediatric rhinosinusitis (4)?
109. What etiologic factors are responsible for the development of rhinosinusitis (5)?
110. What bacteria are involved in acute rhinosinusitis (3)?
111. What bacteria are involved in chronic rhinosinusitis (8)?
112. What are the potential routes for expansion of infection for the ethmoid to the orbit (4)?
113. Describe Chandler’s classification for orbital complications secondary to sinusitis (5)?
114. What are the intracranial complications of sinusitis (4)?
Cleft Lip and Palate: Evaluation and Treatment of the Primary Deformity
115. What is the incidence of CL(P)? With regards to ethnicity, which populations are most
susceptible and least susceptible? What is the M:F?
116. What is the incidence of CL? What is the M:F?
117. During development, which weeks are crucial for the development of the upper lip, nose and
primary palate? Which weeks are crucial for the development of the secondary palate?
118. What do the frontonasal process form (3)? What do the maxillary processes form (2)?
119. With regards to fusion of the secondary palate, in which direction does this occur?
120. What are the main features of a submucous cleft (3)? How is this best diagnosed?
121. What is the first priority in the management of cleft lip and palate deformities?
122. What are some of the anatomic deformities seen in a unilateral cleft lip (3)?
123. What are some of the anatomic deformities seen in a bilateral cleft lip (3)?
124. In a cleft palate, where do the muscle fibers run and where do they insert?
125. In terms of timing of surgery, when are the lip adhesion, lip repair and palatal repair performed?
126. What are some postoperative complications of cleft palate repair?
127. Why is middle ear disease common in children with cleft palate?
128. What are the treatment options for VPI (3)?
129. What are some causes of cleft lip palate (3)?
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144. What is the first line treatment of acute tonsillitis?
145. For chronic tonsillitis, what can obviate the need for tonsillectomy in 15% of children?
146. What are the absolute (5) and relative (5) indications for tonsillectomy?
147. What are the contraindications for tonsillectomy (3)?
148. What is the pathogenesis of a peritonsillar abscess?
149. What are complications of tonsillectomy (8)?
150. What is Grisel’s syndrome?
151. What are some indications for observation post-T+A (5)?
152. What are the risks in Down syndrome children with regards to tonsillectomies (2)?
153. List some common congenital anomalies affecting the nose/nasopharynx, oral/oropharynx,
larynx, trachea and esophagus.
154. A newborn infant with high-pitched inspiratory stridor is most likely to have a lesion in which
anatomic location?
155. A 3-week old infant presents with circumoral pallor and occasional cyanosis. In addition to a
thorough evaluation of the upper airway, what other investigation should be done?
156. What investigation should be done for a newborn that presents with severe respiratory distress
and bilateral vocal cord paralysis?
157. What percentage of subglottic hemangiomas are associated with cutaneous ones?
158. Describe the four types of laryngeal clefts.
159. What are the 5 types of tracheoesophageal fistulas?
160. List vascular anomalies that can cause airway and/or esophageal compression (5).
161. Which types of HPV are commonly implicated in laryngeal papillomatosis (2)?
162. What is the histology of papillomatosis?
163. Which are the common sites of involvement (6)?
164. What are the risk factors for developing laryngeal papillomatosis (5)?
165. What are the two clinical types of RRP? How do they differ?
166. What is the risk of transmission of HPV to an infant from a mother with condylomata?
167. What is the main treatment modality of RRP?
168. What protective precautions are required for laser treatment (8)?
169. Other than airway fire, what are the disadvantages of jet ventilation (7)?
170. What are some adjuvant treatment options for RRP (6)?
171. What are risk factors for malignant transformation of RRP (4)?
172. What are the adverse side effects of interferon-alpha treatment (6)?
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-almond shaped palpebral fissures, deficient nasal alae, tubular nose with bulbous nasal
tip, small mouth, VPI
-bilateral acoustic neuroma, meningioma, spinal cord schwannomas
-café-au-lait spots and cutaneous neurofibromas
-mental retardation, prominent ears, large jaw, long face, jocular speech
-preauricular pits, branchial cleft abnormalities, renal abnormalities
-craniosynostosis, hypertelorism, syndactyly, cervical vertebral fusion
-short-limb dwarfism
Pediatric Malignancies
175. Excluding retinoblastoma and neoplasms of the CNS, what is the most common pediatric
malignancy of the head and neck?
176. What is the most frequent soft-tissue malignancy of childhood?
177. What is the most common malignancy in infants under 1 year of age?
178. What is the most common presenting sign in Hodgkin disease?
179. What is a Reed-Sternberg cell?
180. What is the Ann Arbor staging system for lymphoma?
181. What is the treatment of early versus late stage Hodgkin disease?
182. What is the treatment for lymphoma causing airway, nervous or vascular compromise?
183. What are the top two locations for rhabdomyosarcoma in the head and neck?
184. What are the histologic types of rhabdomyosarcoma (3)? Which type is most common in
children? Adolescents? Adults?
185. What is the treatment of rhabdomyosarcoma?
186. What is the most common type of thyroid malignancy in children?
187. At what time should children with MEN IIA and IIB have thyroidectomies?
188. What are the late complications in the treatment of pediatric malignancies (4)?
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Eustachian Tube Function and Middle Ear Aeration
206. What are the differences between the ET of adult and child (4)?
207. Which muscle dilates the ET? What innervates this muscle?
208. What closes the ET?
209. What are the functions of the ET (3)?
210. What is the Polizter and Toynbee test?
211. Describe the 9-step tympanometric inflation-deflation test.
212. What are the indications for tympnoscentesis
213. What is the “watch and wait” method for treatment of AOM?
Pediatric Audiology
214. What are the risk indicators that would warrant further hearing investigations in children (11)?
215. What are the behavioural test techniques and approximately what age are they employed (4)?
216. ABR provides threshold estimate in what frequency range?
217. What is the frequency range tested in OAEs?
218. What is the definition of central auditory processing disorders?
219. What are the signs of CAPD (4)?
231. What are the clinical (2) and histological (2) differences between hemangioma and vascular
malformation?
232. What are the three clinical stages of hemangioma growth?
233. What are the three clinical types of hemangioma?
234. What is Kasabach-Merritt syndrome?
235. What are the indications for immediate treatment of hemangiomas (3)?
236. What are the treatment options for hemangiomas (4)?
237. Differentiate fast flow versus slow flow malformations.
238. What are potential complications of hemangiomas (5)?
239. What is the natural history of hemangiomas?
240. How are subglottic hemangiomas managed?
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241. What is the basic histology of capillary, venous and lymphatic malformations? How are they
treated?
242. What is Sturge-Weber syndrome?
243. Differentiate the two different types of lymphatic malformations based on location and ease of
resectability.
Velopharyngeal Insufficiency
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REVIEW QUESTIONS IN RHINOLOGY
1. List the six different cell types within the olfactory neuroepithelium?
2. Define anosmia, hyposmia and dysosmia.
3. What are some of the causes of olfactory loss?
4. What is the link between olfaction and neurodegenerative disease such as Alzheimer’s disease?
5. What is the UPSIT?
Nonallergic Rhinitis
Allergic Rhinosinusitis
Nasal Obstruction
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31. According to Poisseuille’s equation, what variable most contributes to resistance?
32. What are the boundaries of the nasal valve?
33. What is the Cottle maneuver?
34. What are the causes of nasal obstruction?
35. What is Samter’s triad?
36. What disease is suspected if one sees polyps in children?
37. What are the mechanisms of action of topical steroids?
38. What is the most common pathogen in a septal abscess?
39. What are the causes of septal perforation?
Sinus Imaging
68. What are some anatomic variations that can contribute to sinus disease (6)?
69. What is a radiographic hallmark of granulomatous involvement of the sinuses?
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70. What is the radiographic appearance of fungal sinusitis on CT scan? MRI?
71. What is the radiographic appearance of polyps on CT scan? MRI?
72. What is the radiographic appearance of an inverted papilloma?
73. What is the radiographic appearance of a juvenile nasopharyngeal angiofibroma?
Sinus Surgery
93. What are the indications for the Calwell-Luc operation (6)?
94. What are complications of the Calwell-Luc operation?
95. What are the indications for an external ethmoidectomy (4)?
96. What type of incision is used for external ethmoidectomy?
97. In relation to the lacrimal crest, how far back is the anterior ethmoid artery? posterior ethmoid
artery? optic nerve?
98. The anterior and posterior ethmoid arteries are important landmarks for what?
99. What are the complications of external ethmoidectomy?
100. What are two other non-endoscopic methods to surgically manage the ethmoid sinuses?
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106. What are the four consistent landmarks from anterior to posterior used in endoscopic surgery?
107. Where is the base of skull thinnest?
108. What are the three patterns of sphenoid pneumatization according to Congdon? Which pattern
is the most common?
109. What are the contents of the cavernous sinus?
110. Which nerve travels in close association with the carotid artery in the cavernous sinus?
111. What is the main contraindication to a transnasal intracranial procedure?
112. List the various approaches for transsphenoidal hypophysectomy (5).
113. List the various approaches for sphenoid inflammatory disease (3).
114. List the various approaches to access sphenoid tumours (4).
115. What are the possible complications of sphenoid surgery?
116. What are the risk factors for acute bacterial sphenoiditis (4)?
117. What organisms are involved in invasive fungal sinusitis (4)?
118. What are the boundaries of Bolger’s parallelogram? What is the safe entry point into the
sphenoid sinus in relations to this parallelogram?
Epistaxis
129. Which branch of the internal carotid artery supplies the nasal cavity (1)?
130. From this branch, which arteries arise (2)?
131. Which branches of the external carotid artery supplies the nasal cavity (2)?
132. What are the subsequent branches that supply the nasal cavity (6)?
133. There are two plexus of arteries within the nasal cavity, what are they?
134. Which arteries make up the anastomosis in Little’’s area (4)?
135. What are some local (10) and systemic (10) causes of epistaxis?
136. Name two autosomal dominant vascular disorders in which epistaxis is prominent.
137. What are the non-medical treatments of epistaxis (6)?
138. What are the surgical treatments of epistaxis (6)?
139. What are possible complications of nasal packing (10)?
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Manifestations of Systemic Diseases of the Nose
CSF Leaks
155. What are the two broad categories of CSF rhinorrhea? Which category is the most common?
156. What is the most common cause of CSF otorrhea?
157. Which type of temporal bone fracture results more frequently with CSF leaks?
158. Where do CSF rhinorrheas most commonly occur?
159. Which congenital anomalies are associated with CSF otorrhea (2)?
160. What are the signs and symptoms of CSF rhinorrhea (5) and otorrhea (5)?
161. What is the incidence of CSF otorhinorrhea after acoustic neuroma surgery?
162. What are the most common locations for spontaneous CSF otorrhea (3)?
163. List 5 methods that can be used to diagnose CSF leaks.
164. List 4 methods that can be used to localize CSF rhinorrhea.
165. Which tissue fluids is B2 transferrin found in (3)?
166. Which type of CSF leaks are likely to resolve with conservative management?
167. Which type is likely to require surgical exploration?
168. What is involved in the conservative management of CSF leaks (5)?
169. If using a lumbar drain to manage CSF leak, when is this instituted and how much fluid is
drained per day?
170. What are the surgical approaches for repair of CSF rhinorrhea (3)?
171. What material can be used to repair dura (4)?
172. For grafting, what materials are generally used and how?
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REVIEW QUESTIONS IN TRAUMA
Auricular Trauma
Laryngeal Trauma
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Mandibular Fractures
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75. What are the complications of nasoethmoidal fractures (5)?
76. What is the most common cause of frontal sinus fractures?
77. What are the surgical approaches to frontal sinus fractures (4)?
78. What is the management of non-displaced and displaced anterior table fractures?
79. What is the management of non-displaced and displaced posterior table fractures?
80. What is the treatment of comminuted, contaminated or through-and-through fractures (2)?
81. What are the options for frontonasal duct damage (2)?
82. What are the complications of frontal sinus fractures (8)?
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