10 Deep Neck and

Odontogenic Infections
James M. Christian | Adam C. Goddard | M. Boyd Gillespie

Key Points
■ Methicillin-resistant Staphylococcus aureus (MRSA) is currently the most common isolate in
community-acquired deep neck infections in children younger than 2 years.
■ Up to 10% of MRSA isolates are clindamycin resistant.
■ Conservative management without drainage is more likely to succeed with abscess pockets less
than 2.5 cm in diameter that involve a single neck space.

D eep neck infection (DNI) remains a frequent, potentially
life-threatening condition in both children and adults. Knowl-
edge of the complex spaces of the neck and how they commu-
nicate is necessary for appropriate surgical management. The
location of the infection may provide information about the
origin of the infection and the likely organisms that must be
covered when empiric therapy is instituted.
ETIOLOGY
Infectious and inflammatory conditions of the upper aerodiges-
tive tract are the primary cause of DNI. It is estimated that the
direct cost of DNIs in the United States exceeds $200 million
annually.1 Dental infections are the most common cause of
DNI in adults, whereas oropharyngeal infections are the most
common cause in children.2-5
Bacterial biofilms are estimated to cause 65% to 80% of
human infections, and they play a key role in the etiology of
odontogenic infections.6 Most dental-related infections are
localized, minor exacerbations from long-standing decay or
periodontal disease. Consequently, considerable attention has
been given to periodontitis—a chronic inflammatory disease of
the tooth-supporting structures, and by definition a chronic
low-grade infection as the result of a microbial biofilm—as a
potential risk factor in the morbidity and mortality of systemic
conditions such as cardiovascular disease, diabetes mellitus,
and premature birth. Epidemiologic studies have revealed an
association between periodontal disease and both cardiovascu-
lar disease and diabetes mellitus, but research is ongoing to
delve more deeply into these relationships.7-9
In the pediatric population, acute rhinosinusitis is a common
cause of retropharyngeal lymphadenitis. Oral surgical proce-
dures and endoscopic instrumentation may iatrogenically
incite an upper airway infection or traumatize the pharyngo-
esophageal lumen. Sialadenitis, with or without ductal obstruc-
tion, can precipitate infectious spread. Foreign bodies trapped
within the upper aerodigestive tract may initiate infections that
spread to the deep neck. Superficial infections, such as skin
cellulitis, may spread along fascial planes into deeper neck
compartments. Penetrating trauma, including needle injection
associated with intravenous (IV) drug use, may introduce
pathogens into the fascial planes. Congenital or acquired
lesions such as branchial cleft cysts, thyroglossal duct cysts, or
laryngoceles may become infected and result in spread of infec-
tion. Congenital cysts account for 10% to 15% of DNIs in the
pediatric population, and these should be suspected, especially
in the setting of recurrent DNI.10 Acute mastoiditis may prog-
ress to a Bezold abscess with spread to the upper neck through
bony fissures. Necrotic malignant lymph nodes can form
abscesses and demand a high degree of suspicion for cancer if
observed in adult patients older than 40 years, in whom approx-
imately 5% of cases of DNI are associated with malignant lymph
nodes.11 Immunocompromised patients may come to medical
attention with more virulent or atypical pathogens. Although
the etiologic factors are many, a thorough search for the cause
often reveals no clear source.
MICROBIOLOGY
The microbiology of DNI often yields a mixture of aerobic and
anaerobic organisms representative of oropharyngeal flora.
Studies have isolated approximately 280 species of bacteria in
the oral cavity, but less than 50% of the oral flora can be identi-
fied through traditional methods.12,13 Recent studies have uti-
lized cultivation-independent molecular methods (16rRNA
sequencing methods) to identify nearly 600 bacterial species.
Table 10-1 lists many of the common, normal aerobic, faculta-
tive, and anaerobic species of bacteria—several fungal species,
viruses, and even protozoans can also be found in the normal
oral flora. In most patients, these normal oral bacteria are the
cause of most odontogenic infections. Staphylococcus aureus in
particular is much more common in the nose and throat and
may participate in mixed odontogenic infections. Gram-
negative anaerobes comprise much of the rest of the mouth’s
normal flora, and these organisms can increase in numbers,
especially in patients with chronic periodontal disease.14
Several studies in the past have consistently shown a pre-
dominance of certain species associated with odontogenic
infections.15-21 These include the Streptococcus milleri group, Pre-
votella (Bacteroides), Peptostreptococcus, and Staphylococcus species.
In a recent study by Rega and colleagues15 that described the
microbiology of head and neck infections of odontogenic
origin, the most common bacteria isolated were viridans strep-
tococci, Prevotella, staphylococci, and Peptostreptococcus. This

164
 10 | DEEP NECK AND ODONTOGENIC INFECTIONS 165

The proportion of community-acquired methicillin-resistant

TABLE 10-1. Normal Oral Flora
Staphylococcus aureus (MRSA)–associated neck-space infections
Aerobic Bacteria Anaerobic Bacteria is significantly increasing worldwide, especially in the pediatric
Gram-Positive Cocci population.25-27 MRSA is more likely to infect younger patients
Streptococcus Streptococcus in lateral neck compartments.25 Another study found that
Peptococcus MRSA was the most common organism isolated in children
Peptostreptococcus younger than 16 months, with African-American children at
Gram-Negative Cocci even greater risk.26 Approximately 8% of MRSA isolates in that
study were clindamycin resistant.26
Neisseria Veillonella Atypical organisms are a relatively common cause of DNI.
Gram-Positive Bacilli Actinomyces are endogenous saprophytic organisms of the oral
Diphtheroids Clostridium cavity and tonsil. The most common site of cervicofacial acti-
Actinomyces nomycosis is in the vicinity of the angle of the mandible, and
Eubacterium this pathogen may cross fascial planes in its route of spread
Lactobacillus (Fig. 10-1). A granulomatous reaction with central abscess for-
Gram-Negative Bacilli mation and necrosis with “sulfur granules” is characteristic.
Patients with tuberculous and nontuberculous infections of the
Haemophilus Prevotella
head and neck most commonly come to medical attention with
Eikenella Bacteroides
Fusobacterium cervical lymphadenopathy. Histopathologically, caseating nec-
Porphyromonas rotizing granulomatous inflammation is present. Cat scratch
disease—caused by the pleomorphic, gram-negative bacillus
Modified from Peterson LJ. Odontogenic infections. In Cummings CW,
Bartonella henselae—manifests with swollen, tender cervical
ed: Otolaryngology—head and neck surgery, vol 2, ed 2. St Louis: Mosby;
19 9 3 . lymph nodes, and late lesions may form an abscess. Treatment
of atypical neck-space infections often leans toward nonsurgical
management, because incision and drainage procedures may
finding has been consistent for many years, even as name result in a chronic wound or fistulous tract.
changes, especially for Bacteroides, have taken place to better
reflect more recent genetic information.12-15 Recent studies that
used molecular methods to identify species from samples taken
ANATOMY
from odontogenic infections have found a greater prevalence Accurate diagnosis and application of timely treatment requires
of facultative or obligate anaerobes and a limited number of an understanding of the complex anatomic organization of the
streptococci.13 ,16,22 This difference in results may be influenced neck spaces. Fascial planes divide the neck into true and poten-
by the methods for determining speciation, where aerobic and tial spaces. A description of the neck spaces and contents are
anaerobic conventional cultures support the growth of certain summarized in Table 10-2. Common pathways of spread are
microbes over others. Further, as much as 60% of the oral flora outlined in Figure 10-2.
cannot be cultured by routine culture methods.23 Odontogenic infection from decaying teeth and poor oral
Almost all odontogenic infections are due to mixed flora. hygiene continue to be the most common source of DNI in the
Retrospective microbiologic analyses consistently demonstrate adult patient, and several additional spaces of note with regard
common oral pathogens and polymicrobial isolates.24 The to odontogenic infections must also be considered; these are
commonly cultured organisms, which often reflect the micro- covered below.
biology of odontogenic infections, are Streptococcus viridans;
Staphylococcus epidermidis and S. aureus; Group A β-hemolytic
Streptococcus (S. pyogenes); and Bacteroides, Fusobacterium, and Pep-
MAXILLARY SPACES
tostreptococcus species. Cultures occasionally reveal Neisseria, The two primary maxillary spaces that may be involved are the
Pseudomonas, Escherichia, and Haemophilus species. canine space and the buccal space. The canine space becomes

A B
FIGURE 10-1. A, Patient with onset on trismus 5 days after dental work. B, Computed tomography–guided needle biopsy of a left parapharyngeal space
mass showed actinomycosis.
166 PART II | GENERAL OTOLARYNGOLOGY

TABLE 10-2. Major Deep Neck Spaces and Their Contents

Neck Space Boundaries Contents Communicating Spaces
Peritonsillar • Medial-palatine tonsil • Loose connective tissue • Parapharyngeal
• Lateral superior constrictor muscle • Tonsillar branches of the lingual, facial,
and ascending pharyngeal vessels
Parapharyngeal • Superior: base of middle fossa Prestyloid • Peritonsillar
• Inferior: hyoid bone • Fat • Submandibular
• Anterior: pterygomandibular raphe • Lymph nodes • Visceral
• Posterior: prevertebral fascia • Internal maxillary artery • Retropharyngeal
• Medial: superior constrictor • Auriculotemporal, lingual, inferior • Carotid
• Lateral: deep lobe parotid, medial pterygoid alveolar nerves • Masticator
• Pterygoid muscles • Parotid
• Deep lobe parotid
Poststyloid
• Carotid
• Internal jugular
• Superior sympathetic nerve
• Cranial nerves IX, X, X, and XII
Infratemporal • Superior: sphenoid and temporal skull, fossa • Pterygoid muscles • Temporal fossa
fossa medial to zygomatic arch • Temporalis tendon • Pterygomaxillary fossa
• Anterior: infraorbital fissure, maxilla • Internal maxillary artery
• Lateral: ramus and coronoid of mandible • Pterygoid venous plexus
• Medial: lateral pterygoid plate with tensor • Mandibular nerve (V3 ) with otic
and levator palatine muscles ganglion
Pterygomaxillary • Superior: sphenoid body, palatine bone • Maxillary nerve (V2) • Infratemporal fossa
fossa • Anterior: posterior wall or maxillary antrum • Sphenopalatine ganglion • Parapharyngeal space
• Posterior: pterygoid process, greater wing of • Internal maxillary artery • Masticator space
sphenoid • Temporal fossa
• Medial: palatine bone
• Lateral: temporalis muscle via
pterygomaxillary fossa
Temporal fossa • Superior: temporal line of skull • Temporalis muscle • Infratemporal fossa
• Inferior: zygomatic arch • Temporal fat pad • Pterygomaxillary fossa
• Lateral: temporalis fascia
• Medial: pterion skull
Parotid • Medial: parapharyngeal space • Parotid gland • Parapharyngeal
• Lateral: parotid fascia • Facial nerve • Temporal fossa
• External carotid artery • Masticator
• Posterior facial vein
Masticator • Medial: fascia medial to pterygoid muscles • Masseter muscle • Parotid
• Lateral: fascia overlying masseter • Pterygoid muscles • Pterygomaxillary
• Ramus and posterior body of mandible • Parapharyngeal
• Inferior alveolar nerve
• Internal maxillary artery
Submandibular • Superior: floor of mouth • Sublingual and submandibular glands • Parapharyngeal
• Inferior: digastric muscle • Wharton duct • Visceral space
• Anterior: mylohyoid and anterior belly • Lingual nerve
digastric muscle • Lymph nodes
• Posterior: posterior belly of digastric and • Facial artery and vein
stylomandibular ligament • Marginal branch of cranial nerve VII
• Medial: hyoglossus and mylohyoid
• Lateral: skin, platysma, mandible
Visceral • Superior: hyoid bone • Pharynx • Submandibular
• Inferior: mediastinum • Esophagus • Parapharyngeal
• Anterior: superficial layer of deep cervical • Larynx • Retropharyngeal
fascia • Trachea
• Posterior: retropharyngeal space; • Thyroid gland
prevertebral fascia
• Lateral: parapharyngeal space
Carotid sheath • Anterior: sternocleidomastoid muscle • Carotid artery • Visceral space
• Posterior: prevertebral space • Internal jugular vein • Prevertebral
• Medial: visceral space • Vagus nerve • Parapharyngeal
• Lateral: sternocleidomastoid muscle • Ansa cervicalis nerve
Retropharyngeal • Superior: base of skull • Lymph nodes • Carotid sheath
• Inferior: superior mediastinum • Connective tissue • Superior mediastinum
• Anterior: pharynx, esophagus • Parapharyngeal space
• Posterior: alar fascia • Danger space
• Medial: midline raphe of superior constrictor
• Lateral: carotid sheath
 10 | DEEP NECK AND ODONTOGENIC INFECTIONS 167

TABLE 10-2. Major Deep Neck Spaces and Their Contents—Cont’d

Neck Space Boundaries Contents Communicating Spaces
Danger • Superior: base of skull • Loose areolar tissue • Retropharyngeal
• Inferior: diaphragm • Prevertebral
• Anterior: alar fascia of deep layer of deep • Mediastinum
cervical fascia
• Posterior: prevertebral fascia of the deep
layer of the deep cervical fascia
Prevertebral • Superior: base of skull • Dense areolar tissue • Danger space
• Inferior: coccyx • Paraspinous, prevertebral, and scalene
• Anterior: prevertebral fascia muscles
• Posterior: vertebral bodies • Vertebral artery and vein
• Lateral: transverse process of vertebrae • Brachial plexus
• Phrenic nerve

SCENARIO 1
Retroparapharyngeal Carotid sheath
space
Peritonsillar Parapharyngeal
Acute tonsillitis
abscess space
Submandibular
space Visceral space

SCENARIO 2
Parapharyngeal
space

Rhinosinusitis/ Retropharyngeal Retroparapharyngeal

upper pharyngitis lymph node space
Carotid sheath

SCENARIO 3
Masticator Pterygomaxillary Infratemporal
Upper jaw
space space fossa

Dental infection Parapharyngeal

space
Submandibular
2nd and 3rd molar
space

Lower jaw Visceral space

1st molar,
Sublingual space
anterior

SCENARIO 4

Parapharyngeal
Danger space
space
Esophagoscopy/
intubation/
trauma
Retropharyngeal Mediastinum
space

FIGURE 10-2. Common pathways of spread in deep neck infection.

168 PART II | GENERAL OTOLARYNGOLOGY

infected almost exclusively as a result of apical infection of the

root of the maxillary canine tooth. The root must be long
enough to ensure that the apex is superior to the insertion of
the levator anguli oris muscle. The canine space is located
between the anterior surface of the maxilla and the levator labii
superioris. When infected, swelling usually occurs lateral to the
nose, and loss of the ipsilateral nasolabial fold is often appar-
ent. Drainage is most often accomplished with an intraoral
stab incision.
The buccal space is an ovoid space below the zygomatic arch
and above the inferior border of the mandible. It becomes
involved when the infection of maxillary molar teeth breaks out
superior to the attachment of the buccinator muscle; the buccal
space lies between this muscle and the skin. All three maxillary
molars may cause infection in this space, which is dramatic in
appearance and may cause trismus.

MANDIBULAR SPACES
The primary mandibular spaces include the submental, sublin-
gual, and submandibular spaces. The primary spaces are those
into which infection spreads directly from the teeth through
bone. The submental space lies between the anterior bellies of
the digastric muscles and between the mylohyoid muscle and
the skin. This space is involved with infected mandibular inci-
sors, whose roots are long enough to allow erosion apically to
the attachment of the mentalis muscle. Isolated submental
space infections are not common.
The sublingual and submandibular spaces exit on the medial
aspect of the mandible. They are usually involved because of
lingual perforation of infection from the mandibular premo-
lars and molars. The factor that determines whether the sub-
lingual or submandibular space is involved is the location of
the perforation relative to the mylohyoid muscle attachment
(Fig. 10-3 ). If the location of the apex of the tooth is superior
(premolars, first molar), the sublingual space is involved; con-
versely, if the apices are inferior to the mylohyoid (second and
third molars), the submandibular space is involved.
The sublingual space lies between the lingual oral mucosa
and the mylohyoid muscle. Its posterior boundary is open, so
it communicates freely with the submandibular space and
the secondary spaces located more posteriorly and superi-
orly. Clinically, extraoral swelling is minimal, but intraoral
lingual swelling in the floor of the mouth can be marked,
and if bilateral, the tongue will be elevated, and swallowing
becomes difficult.
Mylohyoid line
FIGURE 10-3. The mylohyoid line is the attachment of the mylohyoid
muscle. Infections above this line affect the sublingual space, and infections
below this line affect the submandibular space.
The submandibular space lies between the mylohyoid muscle
and the skin. Like the sublingual space, it has an open posterior
boundary, so it can communicate easily with the secondary
spaces as well. When this space becomes infected, the swelling
begins at the inferior lateral border of the mandible and
extends medially to the digastric area and posteriorly to the
hyoid bone.
If all three primary mandibular spaces bilaterally become
infected, the infection is known as Ludwig angina, first described
by Wilhelm Friedrich von Ludwig28 in 183 6. Ludwig angina was
not uncommon in the preantibiotic era and was a significant
cause of death. It is characterized as a rapid, bilateral gangrenous
cellulitis of all three primary spaces. It can extend posteriorly to
involve the secondary spaces, where it causes gross swelling;
elevation and displacement of the tongue; and tense, brawny
induration of the submandibular region superior to the hyoid
bone (Fig. 10-4). If fluctuance is present, it is usually minimal
because of the rapidity of the cellulitic process. The patient
experiences severe trismus, drooling, and inability to swallow
along with tachypnea and dyspnea. Impending compromise of
the airway produces marked anxiety. If not treated, the cellulitis

A B
FIGURE 10-4. A patient with Ludwig angina with swelling of the bilateral upper neck (A) and bilateral sublingual spaces causing the tongue to obstruct the
upper airway (B).
 10 | DEEP NECK AND ODONTOGENIC INFECTIONS 169

can progress with alarming speed and can produce airway

obstruction and death. The usual cause is an odontogenic infec-
tion from a mandibular molar. Virulent streptococci are clearly
involved, but ultimately, the picture is mixed as usual.29 ,3 0

CLINICAL EVALUATION
HISTORY
The symptoms of DNI are determined by both the generalized
inflammatory process and localizing symptoms at the site of
infection. Inflammatory symptoms such as pain, fever, swelling,
and redness are common. Symptoms such as dysphagia, odyno-
phagia, drooling, “hot potato” voice, hoarseness, dyspnea,
trismus, and ear pain offer further clues about the location of
the inflammatory process as well as its potential severity. Infor-
mation about the onset and duration of symptoms should be
elicited. Recent events such as dental work, upper airway surgery
or intubation, IV drug use, sinusitis, pharyngitis, otitis, or blunt
or penetrating soft tissue trauma that preceded worsening
symptoms should be identified in order to formulate a differen-
tial of likely microorganisms and common pathways of spread.
The medical history should be reviewed to account for anti- FIGURE 10-5. Large right parotid stone causing parotid space inflammation
biotic allergies and immunodeficiency status. Patients with a and phlegmon.
history of human immunodeficiency virus (HIV), hepatitis, dia-
betes, collagen vascular diseases, hematologic malignancy, and cavity and oropharynx is facilitated by the use of a headlamp,
recent chemotherapy or steroid use are at increased risk of which will free up the hands for bimanual examination. Diffi-
atypical pathogens and rapidly progressive disease that may not culty with mouth opening indicates that inflammation has
display an acute inflammatory response. Even on appropriate already spread to the parapharyngeal, pterygoid, or masseteric
therapy, immunocompromised patients are at increased risk of spaces. An odontogenic source of infection should be consid-
DNI. In a large retrospective study, 10,000 HIV-infected indi- ered in the presence of alveolar swelling and decayed, loose,
viduals on standard retroviral therapy had a twofold risk of DNI tender, or broken teeth. The floor of the mouth should be
over 6 years of observation compared with 50,000 controls.3 1 assessed for visible edema, which may cause posterior deflec-
tion of the oral tongue. The Stensen and Wharton ducts should
be assessed for purulent discharge and should be palpated for
PHYSICAL EXAMINATION obstructing stones (Fig. 10-5).
A complete head and neck physical examination is required in Visualization of the oropharynx is necessary to assess for
all patients with potential DNI. Palpation of the neck and face asymmetric lateral or posterior wall swelling and/or deviation
may identify localizing tenderness or fluctuance and crepitus of the uvula. Unilateral pharyngeal wall swelling in the absence
caused by airway trauma or gas-producing organisms. Oto- of associated inflammatory symptoms, such as fever and mucosal
scopic examination of the ear and nasal passages can rapidly erythema, should raise the possibility of parapharyngeal tumors,
reveal edema, purulence, drainage, and tenderness, and it can which should not be biopsied or incised without further evalu-
rule out obstructing foreign bodies. Examination of the oral ation (Fig. 10-6). A unilaterally enlarged, irregular, or ulcerated

A B
FIGURE 10-6. Right peritonsillar swelling without pain or inflammation (A) is shown to be due to a right parapharyngeal space tumor on computed tomo-
graphic imaging (B).
170 PART II | GENERAL OTOLARYNGOLOGY
tonsil, especially in the setting of prolonged exposure to
tobacco and alcohol, may indicate the presence of a tonsillar
malignancy.
A complete cranial nerve examination is recommended.
Infections of the upper dentition, paranasal sinuses, facial soft
tissues, and parotid place the orbits at increased risk because
of retrograde flow through the facial and ophthalmic veins.
Edematous eyelids must be manually separated to assess the
underlying globe. Reduced mobility of the globe and/or an
absent papillary light reflex indicates orbital inflammation or
abscess, which will require urgent attention to save the eye.
Flexible fiberoptic evaluation of the upper airway in an
awake patient is indicated in most cases of suspected DNI,
especially if the patient has hoarseness, dyspnea, stridor, and/
or dysphagia or odynophagia without an obvious cause on oro-
pharyngeal examination. A normal pulse oximetry reading
does not eliminate the need for direct airway evaluation,
because the oxygen saturation is a poor proxy for airway status,
because it typically does not fall until the airway is completely
occluded. The presence of a patent, midline, nonedematous
airway should be documented before transport for radio-
graphic evaluation in order to prevent an airway emergency
while the patient is supine in the radiology suite. Direct evalu-
ation of the airway will identify patients who may be difficult to
intubate by standard technique, should surgery be required.
LABORATORY EVALUATION
BLOOD TESTS
An initial complete blood count typically demonstrates leuko-
cytosis in cases of DNI. A lack of a leukocytic response may
indicate viral illness, immunodeficiency, or a condition such as
tumor, which can be confused with DNI. Daily measures of the
white blood count may be helpful in monitoring a patient’s
response to treatments such as IV antibiotics and/or surgical
drainage. IV steroids are often necessary to reduce upper
airway inflammation in DNI and should not be withheld out of
concern that steroid-related leukocytosis will make it difficult
to monitor treatment response. A basic electrolyte panel should
be obtained to assess glucose level, bodily hydration, and renal
function in the event that general anesthesia becomes neces-
sary during treatment.
IMAGING STUDIES
Plain Film Radiography
Radiographic imaging plays a critical role in the evaluation of
suspected DNI. Plain film technology is inexpensive, rapid,
widely available, and provides excellent information in select
A B
FIGURE 10-7. A right neck lymphadenitis and abscess secondary to right hypopharyngeal squamous cell carcinoma.
circumstances. In cases of suspected dental origin, plain film
radiography or a panoramic view of the jaw can help to identify
dental sources of infection or salivary stones (>5 mm), if this is
not already obvious on physical examination. Translucencies at
the apex of the dental root are a common finding with dental-
related abscess. Lateral neck films are useful for a quick evalu-
ation of the upper aerodigestive tract in cases of suspected
retropharyngeal abscess or supraglottitis. Presence of an air-
fluid level or a thickening of the prevertebral tissue at C2 of
more than 5 mm in a child or more than 7 mm in an adult
indicate retropharyngeal infection. Thickening of the epiglot-
tis, commonly known as the thumbprint sign, or thickening of
the arytenoids indicates likely supraglottitis with urgent need
for direct airway evaluation in a controlled setting with trache-
otomy capabilities. Chest radiography is indicated in cases of
dyspnea, tachycardia, and/or cough to rule out aspiration and/
or mediastinitis.
Computed Tomography
Computed tomography (CT) scans of the head and neck
remain the standard radiographic technique for the evaluation
of DNI, because physical examination alone misidentifies the
involved space and the number of involved spaces in 70% of
cases.3 2 CT scans with IV contrast provide excellent visualization
of most bony and soft tissue structures of the head and neck.
The IV contrast allows visualization of the great neck vessels
and enhancement of areas of inflammation. CT scans are valu-
able in determining whether the infection is contained within
the lymph nodes, or if it has spread beyond that and into the
fascial planes of the head and neck. Although CT is excellent
for identifying the presence of DNI, it cannot reliably differenti-
ate between the generalized edema of phlegmon versus puru-
lent abscess, because both often commonly appear as hypodense
collections with peripheral enhancement. Therefore the deci-
sion to explore the neck should be made on clinical grounds
with the expectation that pus will not be found in up to 25%
of explorations.3 3 Metastatic adenopathy, most commonly from
a tonsillar primary, should be ruled out clinically, because this
may mimic neck abscess on CT, or it may contain abscess if
secondarily infected (Fig. 10-7).3 4 The CT provides the surgeon
with valuable information about which neck spaces require
exploration and drainage at the time of surgery. The use of IV
contrast is contraindicated in most patients with iodine or con-
trast dye allergy and in patients with compromised renal func-
tion; other imaging modalities are indicated in instances where
IV contrast cannot be used.
Magnetic Resonance Imaging
Magnetic resonance imaging (MRI) is not routinely used for
suspected DNI; however, it should be considered in select

circumstances in which it is superior to CT. In addition, MRI
scanning is time consuming, and it is less likely to be tolerated
by patients in pain or those having trouble swallowing or main-
taining their airway while supine. MRI scans may provide addi-
tional detail to CT in infections that involve the intracranial
cavity, parotid, and prevertebral space. Evaluation of the major
vessels of the head and neck is occasionally indicated if there
is a suspicion of suppurative thrombi of major head and neck
vessels—such as in the sigmoid sinus, internal jugular vein, or
cavernous sinus—or if infection followed trauma to the neck,
such as an IV needle stick. MR angiography with venous flow-
through provides excellent evaluation of thrombi and pseudoa-
neurysm, but invasive angiographic techniques may be needed
for stenting or balloon occlusion in rare cases of infected
pseudoaneuryms.
Ultrasonography
Ultrasonography is used extensively in the evaluation of both
benign and malignant lesions of the head and neck in Europe,
but it has been used in a more limited role in the United States.
Portable ultrasounds are becoming more available in emer-
gency rooms and outpatient clinics and may be used more
extensively for DNI with increasing experience. The noninva-
sive nature of ultrasound makes it an attractive imaging modal-
ity for pediatric patients, and the lack of radiation reduces
concerns about potential long-term harm. Most ultrasonogra-
phy practitioners are adept at using ultrasound to perform fine
needle aspiration, which may be helpful to obtain culture or
provide therapeutic drainage.3 5 Ultrasound may be limited in
cases of significant neck edema or phlegmon, and it may be
less sensitive for nonlateral neck spaces (e.g., parapharyngeal,
retropharyngeal), which may be beyond the focal range of the
technology. Although the fluid levels of an abscess can be seen
by ultrasound if they are large and superficial enough, lack of
visualization does not rule out the possibility of abscess because
of its limitations on serial evaluation of multiple cross-sectional
spaces better seen on CT. In a study of 210 children with DNI,
ultrasound provided sufficient information in 9 8% of patients;
however, CT better assessed the upper airway and neck spaces
in a minority of complicated cases of DNI.3 6
TREATMENT
MEDICAL MANAGEMENT
Airway Management
The initial management of any patient with known or suspected
DNI is securing the airway. Loss of airway has traditionally been
the major source of mortality from DNI.3 7 Airway complications
should be anticipated in all cases of DNI, especially in those
that involve the floor of the mouth and the parapharyngeal and
retropharyngeal spaces. Fiberoptic evaluation of the upper
airway at the time of initial evaluation will often identify an
evolving airway complication before it occurs. Pulse oximetry
monitoring is helpful if interpreted in the proper context, but
a normal oximetry should not provide false security if the
patient clinically displays airway distress. Patients with airway
compromise should not be transported out of an intensive care
suite for prolonged radiographic testing until the airway is
secure. IV access should be obtained to allow rapid administra-
tion of medications and anesthetic agents when needed. First-
line airway therapy includes use of an oxygenated face tent with
cool mist humidity, IV steroids, and epinephrine nebulizers. If
the patient has mild airway symptoms, and the examination
reveals mild edema with less than 50% obstruction at the glottic
or supraglottic level, the patient will often respond to medical
therapy alone while under direct observation in the emergency
suite or intensive care unit.
10 | DEEP NECK AND ODONTOGENIC INFECTIONS 171
Urgent airway intervention is necessary in the event of greater
levels of stridor and dyspnea, which are usually accompanied by
airway obstruction of more than 50%. Effective communication
between the consulting otolaryngolgist and critical care/
anesthesiology personnel is mandatory. The otolaryngologist
needs to convey the results of the initial airway evaluation with
the anesthesiologist and should be actively involved in intubation
planning. In general, an awake fiberoptic intubation can be suc-
cessfully performed if the airway is visualized to be large enough
to allow the passage of the average flexible bronchoscope (5 to
6 mm). Airway preparation with lidocaine nebulizers and lido-
caine jelly–lubricated nasal trumpets with or without light seda-
tion will allow most adult patients to be intubated comfortably
while awake. The patient should be sitting upright, and strong
suction should be available to clear airway secretions to improve
visualization. A tracheotomy set should be available in the room
in the event that a surgical airway is required. An elective trache-
otomy may be considered if extubation is not anticipated within
24 to 48 hours, or if surgical drainage procedures are likely to
result in significant or prolonged airway edema. In such situa-
tions, elective tracheotomy has been associated with reduced
hospital stays and reduced costs compared with prolonged intu-
bation.3 8 An awake tracheotomy should be planned in cases
where minimal or no airway lumen is visualized. Increasing peak
airway pressures and frothy airway secretions following success-
ful intubation may indicate the onset of postobstructive pulmo-
nary edema, which typically resolves with positive-pressure
mechanical ventilation and judicious use of IV diuretics.
Fluid Resuscitation
Poor fluid intake before presentation is common in cases where
neck infection causes significant dysphagia, odynophagia, or
trismus. Dehydration is especially common in infections of the
peritonsillar and retropharyngeal spaces, and it may be the
main etiology of sialadenitis-related infections of the parotid
space. Signs of fluid deficit include tachycardia, dry and pasty
mucous membranes, and decreased skin turgor. Regardless,
most patients benefit from timely infusion of 1 to 2 L of isotonic
IV fluids. Providing adequate fluid resuscitation before surgical
intervention will reduce the severity of anesthesia-related
hypotension.
Antibiotic Therapy
DNI requires timely treatment with IV antibiotics at the time of
diagnosis because of the rapidly progressive nature of these
infections. Culture is not required before empiric antibiotic
therapy; broad-spectrum coverage is usually mandatory, because
most cases involve mixed flora of gram-positive cocci and gram-
negative rods with or without anaerobes.15 As a result of increas-
ing rates of MRSA in the community, especially in children
younger than 2 years, clindamycin is the initial therapy of
choice in this patient population.3 9 Antibiotic coverage may
need to be expanded in cases of otologic or sinus infection or
nosocomial infections, in which Pseudomonas is common,
whereas expanded anaerobic coverage is often necessary for
fulminate odontogenic infections.
Fluids obtained from aspiration or incision and drainage
should be sent for culture and sensitivity because of the increas-
ing rate of resistant organisms in the at-large community.
Clindamycin resistance may be present in 5% to 10% of MRSA-
related pediatric DNIs.25 Culture and sensitivity information is
especially valuable in the setting of hospital-acquired infections
or in an immunocompromised host. A detailed history and
physical examination often identifies patients at risk for atypical
infections, which should be confirmed by staining and cultur-
ing aspirated fluids or tissue biopsy samples.
Overall, both penicillin with or without metronidazole and
clindamycin in the penicillin-allergic patient have proven to be
172 PART II | GENERAL OTOLARYNGOLOGY
effective in most cases. Ampicillin-sulbactam is recommended
as a first-line drug given the up to 20% resistance rate to peni-
cillin G and clindamycin in DNI.40 Penicillin resistance can be
related to the synthesis of β-lactamase by streptococci, Prevotella,
Porphyromonas, and Fusobacterium. The combined therapy of
penicillin with metronidazole provides for broad coverage
of both aerobic and anaerobic bacteria with the elimination of
β -lactamase–producing bacteria and with minimal side effects.
Eikenella corrodens is associated with some odontogenic
infections and is resistant to clindamycin, metronidazole, and
macrolides. Fluoroquinolones, specifically moxifloxacin, are
recommended for treatment of E. corrodens. Moxifloxacin is
effective against oral streptococci and anaerobes and can be
taken orally with the same bioavailability as with the parenteral
route; however, this drug should not be used in pregnant
women or children because of its toxic effects on growing car-
tilage. Third-generation cephalosporins, such as ceftriaxone,
are able to cross the blood-brain barrier and are effective
against oral streptococci and most oral anaerobes. Vancomycin
can be used when all other previously discussed antibiotics are
contraindicated. Its combined use with metronidazole is effec-
tive for gram-positive and obligate anaerobes.15 The choice of
antibiotic therapy is typically dictated by the clinical scenario
and the culture and sensitivity findings; first-line antibiotic
alternatives are shown in Box 10-1.
Prophylactic antibiotics before dental, oral, and head and
neck procedures may reduce the risk of DNI. Prophylaxis
should consist of an oral or IV dose of a β-lactamase–resistant
penicillin or clindamycin given within 3 0 minutes of proce-
dures on nonsterile body cavities; a first-generation cephalospo-
rin (e.g., cephalexin) or clindamycin can be given for neck
incisions in a sterile field. Prophylaxis is mandatory for any
patient with a history of heart murmur or rheumatic valve
disease and in those with vascular or joint prosthetic devices.
IV antibiotic therapy without surgical intervention may be
sufficient in select circumstances. Several large series have
shown resolution of DNI with antibiotic therapy alone in 60%
of cases.24,3 9 If the patient is clinically stable and otherwise
healthy with abscess cavities less than 2.5 cm in diameter and
involving a single neck space, a 48- to 72-hour trial of empiric
IV antibiotic therapy is appropriate.41 A trial of empiric antibiot-
ics is recommended in almost all stable pediatric cases, because
Box 10-1. FIRST-LINE ANTIBIOTIC ALTERNATIVES FOR
DEEP NECK INFECTION
Community-Acquired Infection (Gram-Positive Cocci,
Gram-Negative Rods, Anaerobes)
• Ampicillin-sulbactam 1.5-3.0 g IV q6h
• Clindamycin (if penicillin allergic) 600-900 mg IV q8h
• Moxifloxacin (if Eikenella is suspected) 400 mg daily
Compromised Patients/Nosocomial Infection (Pseudomonas;
MRSA): Pseudomonal and Gram-Negative Alternatives
• Ticarcillin-clavulanate 3.0 g IV q6h
• Pipercillin-tazobactam 3.0 g IV q6h
• Imipenem-cilastatin 500 mg IV q6h
• Ciprofloxacin (if penicillin allergic) 400 mg IV q12h
• Levofloxacin (if penicillin allergic) 750 mg IV q24h
MRSA
• Clindamycin 600-900 mg IV q8h plus vancomycin 1 g IV q12h
• Trimethoprim-sulfamethoxazole 10 mg/kg/day divided q8h
(if clindamycin-resistant) plus vancomycin 1g IV q12h
Necrotizing Fasciitis (Mixed Gram-Positive and Expanded
Anaerobes)
• Ceftriaxone 2 g IV q8h plus clindamycin 600-900 mg IV q8h plus
metronidazole 500 mg IV q6h
IV, intravenous; MRSA, methicillin-resistant Staphylococcus aureus.
even sizable collections may respond favorably to IV antibiotics
and steroids alone.42 In general, the patient should be kept on
a nothing-by-mouth status and should be closely monitored for
changes in clinical status and elevation in white blood cell
count. Repeat imaging and/or surgical intervention are neces-
sary in patients who fail to improve or who worsen during the
observation period. If significant clinical improvement is noted
with IV antibiotics after 48 to 72 hours, therapy is continued
for 24 hours beyond normalization of symptoms, followed by a
2-week course of an equivalent oral antibiotic. Patients who
require surgery usually need 48 to 72 hours of IV antibiotics
postoperatively before discharge home on oral therapy.
SURGICAL MANAGEMENT
Principles of Surgical Management
Several guiding principles should be heeded when surgical
therapy is considered for DNI.
1. Antibiotic availability in pus-filled spaces is limited by
poor vascularity.
2. Treatment of a fascial space infection depends on open
incision and dependent drainage.
3 . Fascial spaces are contiguous, and infection can spread
readily from one space to another, so it is important to
open all primary and secondary spaces; once opened,
spaces need to have drains and possibly irrigation cath-
eters placed.
4. Involved teeth should be extracted, ideally at the time of
incision and drainage, to ensure resolution of the infec-
tion; once a fascial space infection has occurred, it is
prudent to extract the involved teeth rather than to rely
on endodontic treatment.43
Surgical drainage is necessary under certain circumstances:
1) when an air-fluid level is present in the neck or when gas-
producing organisms are evident; 2) when airway compromise
is a threat from abscess or phlegmon; or 3 ) when the patient
fails to respond to 48 to 72 hours of empiric IV antibiotic
therapy. The main goals of surgical intervention include provid-
ing a fluid or tissue sample for tissue staining, culture, and
sensitivity testing; providing therapeutic irrigation of the
infected body cavity; and establishing a stable external drainage
pathway to prevent the reaccumulation of abscess.
Needle Aspiration
Needle aspiration without incision will often suffice for small
abscesses contained within the confines of a lymph node or
with acute infections caused by suspected congenital cysts or
fibrotic pseudocysts. Recurrent infection is common in head
and neck cysts; therefore complete surgical excision should be
planned after the acute inflammation subsides. Aspiration can
be performed at the bedside in the adult, when the neck mass
is palpable and the patient is cooperative. Young children typi-
cally require conscious sedation to prevent errant aspiration.
Applying lidocaine ointment to the skin surface for 15 minutes
before aspiration aids in patient comfort. Lidocaine injections
often hurt as much as the therapeutic aspiration itself and may
obliterate the palpable contours of the mass, making the aspira-
tion more difficult. Slow advancement of a 16- or 18-gauge IV
catheter on a control syringe while applying negative pressure
will usually allow localization of the abscess. The needle can be
removed from the catheter, and the catheter can be flushed
with 1 to 2 mL of sterile saline when the pus is too thick to fully
aspirate. Image-guided techniques that use ultrasound or CT
scan are being increasingly used in cases where initial unguided
fine needle aspiration is unsuccessful, or the mass is nonpal-
pable.44,45 Image guidance can also allow placement of small
pigtail catheters using a Seldinger technique for drainage and
flushing.

A B
FIGURE 10-8. A penetrating trauma introduced air and secretions into the retropharyngeal space as seen on sagittal (A) and axial (B) computed tomography
scan; the result was a deep neck infection.
Transoral Incision and Drainage
The peritonsillar space can be accessed transorally in a coop-
erative adult without significant trismus. The procedure is often
more likely to succeed and be more comfortable to the patient
if IV fluid rehydration, pain medication, antibiotics, and ste-
roids are administered at least an hour before the procedure.
Following application of topical anesthetic spray, 1 to 2 mL of
1% lidocaine with 1 : 100,000 epinephrine is injected into the
mucosa of the lateral soft palate. An initial attempt to drain the
space by aspiration is reasonable and helps to locate the abscess
pocket. If the space cannot be decompressed with aspiration
alone, a 1- to 2-cm incision is made through the mucosa and
submucosa along the normal curvature and 1 cm behind the
edge of the anterior tonsillar pillar. Gentle vertical spreading
of the incision with a hemostat will access the peritonsillar
space to allow egress of abscess. Irrigation with sterile saline
using a 20-mL syringe and an 18-gauge angiocatheter can easily
be performed through the incision. The patient can be dis-
charged home on oral pain medication and antibiotics with
outpatient follow-up arranged within 48 to 72 hours. Tonsil-
lectomy at a later date is an option for patients with a history
of peritonsillar abscess, recurrent or chronic tonsillitis, or
obstructive symptoms from tonsillar hypertrophy. Approxi-
mately 16% of adults and 7% of children will experience a
recurrent peritonsillar abscess at a later date after an initial
episode.5 Alternatively, acute “quinsy” tonsillectomy at the time
of presentation can be considered in cases of recurrent peri-
tonsillar abscess, recurrent acute tonsillitis, or if a general anes-
thetic is needed because of patient discomfort or poor exposure.
Acute tonsillectomy may be more difficult and bloody than
nonacute tonsillectomy because of the surrounding inflamma-
tion; therefore the surgeon should have access to adequate
lighting, suction, electrocautery, tonsil packs, and suture.
Transoral incision and drainage is also a preferred method
of surgery for select deep neck-space infections. Odontogenic
infections limited to the alveolus may respond to removal of
the offending tooth to drain the infected root, although neck
incision is necessary in cases where infection has spread beyond
the alveolar tissues. A neck incision with dependent drainage
of the bilateral floor of the mouth through the mylohyoid
muscle is mandatory in cases of Ludwig angina in order to
reduce the risk of airway obstruction. The buccal space can be
accessed via transoral incision of the buccal mucosa with blunt
dissection parallel to the facial nerve through the buccinators.
The masticator space can be entered by incision of the retro-
molar trigone with blunt dissection through the masseter. After
drainage and irrigation, a half-inch Penrose drain or gauze wick
10 | DEEP NECK AND ODONTOGENIC INFECTIONS 173
can be placed through the incision and secured with a silk
suture, if ongoing drainage is deemed necessary. Otherwise, the
wound can be left open to close secondarily, or it may be closed
loosely with interrupted Vicryl or chromic suture.
The retropharyngeal space is often best entered transorally,
especially because many infections in this space originate from
the adenoids and are located in the high oropharynx or naso-
pharynx, which is difficult to access through the neck (Fig.
10-8). After securing the airway and inserting a tonsil gag, trans-
mucosal needle aspiration of the likely site of infection is per-
formed. Once the abscess pocket is identified, the overlying
mucosa is incised, and blunt dissection is used to enter the
pocket. Caution should be exercised when dissecting beyond
the lateral pharyngeal walls in order to prevent inadvertent
injury to the carotid artery. Drains are typically not placed
because of the potential for drain aspiration and potential diffi-
culties with drain removal. If a drain or wick is placed, it can be
brought out through the mouth and taped securely to the face.
Alternatively, a small ellipse of mucosa and submucosa can be
excised at the site of incision in order to slow the healing process
and allow several days of drainage before wound contraction.
Transcervical Incision and Drainage
Transcervical incision and drainage is the traditional surgical
approach to deep neck-space infection. The location of the
incision is dictated by the neck spaces that require exploration.
If the skin above a neck abscess has become fluctuant, adequate
drainage can often be achieved under local anesthesia, with or
without sedation, via an incision oriented along the relaxed skin
tension lines. In general, the deep neck spaces can be accessed
by one of three potential incisions that provide both excellent
anatomic exposure and cosmetic healing: 1) the preauricular
parotid incision, 2) the horizontal neck incision, or 3 ) the
horizontal submental incision. The preauricular parotid inci-
sion with neck extension as necessary allows access to the
parotid and temporal spaces. A horizontal neck incision in a
natural skin crease provides access to the masticator, parapha-
ryngeal, pterygoid, submandibular, prevertebral, retropharyn-
geal, carotid, and lateral neck spaces. The parapharynegal and
pterygoid spaces are entered by retracting the submandibular
gland anteriorly while dissecting superior and medial to the
posterior belly of the digastric muscle along the medial surface
of the mandibular ramus. The prevertebral and retropharyn-
geal spaces are entered by first identifying the prevertebral
fascia by retraction of the strap muscles medially and the carotid
sheath laterally at a level inferior to the carotid bifurcation; the
space can then be bluntly dissected superiorly in the midline
174 PART II | GENERAL OTOLARYNGOLOGY
to the level of the abscess. The midline horizontal neck incision
can be made to access the region of the strap muscles, thyroid,
and trachea. A horizontal incision in the lower left neck with
dissection to the prevertebral fascia medial to the carotid sheath
provides a drainage conduit for the esophagus and upper medi-
astinum. A horizontal submental incision provides a direct
route to the bilateral submandibular spaces and floor of mouth.
After securing the airway by an awake fiberoptic intubation
or tracheotomy, the proposed incision site is marked on the
neck, injected with 1% lidocaine with 1 : 100,000 epinephrine,
and sterilely prepped and draped. In most cases, the patient
should not be paralyzed during the procedure in order to allow
monitoring of adjacent cranial nerves. The guiding principal
of surgery for DNI is obtaining adequate access and drainage
of the infected space while minimizing risk to normal struc-
tures. Following incision through the superficial cervical fascia,
blunt dissection with a small, curved hemostat and Kittner
sponge can help separate normal structures while creating a
pathway to the infected compartment. Finger dissection of
neck tissues should be avoided in patients with a history of
transcervical IV drug abuse because of the possibility of broken
needle fragments in the neck soft tissue. Access to the deep
neck often requires excision of enlarged lymph nodes that
block access to the infected space; however, care should be
exercised not to overdissect, because this may increase the risk
to normal nerves and vessels that may be displaced or obscured
by inflammation. Once the deep neck space is entered, any
fluid or pus should be cultured; this should be followed by
irrigation with copious amounts of isothermic normal saline.
External drainage is maintained by placement of a half-inch to
1-inch Penrose drain, which is brought out through the incision
and secured to the neck skin with a suture. The remainder of
the incision can be closed loosely with 4-0 nylon sutures.
Superior
ophthalmic
Cavernous
sinus
Emissary
vein
Retromandibular
vein
Internal
juglar vein
FIGURE 10-9. Infection can spread to the cavernous sinus from the jaw, facial soft tissues, and sinuses via the valveless inferior and superior ophthalmic
venous plexus.
SELECTED COMPLICATIONS OF
DEEP NECK INFECTIONS
VASCULAR COMPLICATIONS
Lemierre Syndrome
Lemierre syndrome is a rare thrombophlebitis of the internal
jugular vein most often caused by the anaerobic, gram-negative
bacillus Fusobacterium necrophorum.46 Although rare, awareness
of this syndrome is important given the characteristic presenta-
tion and potentially fatal outcome if it is not recognized and
treated. The syndrome typically follows a period of pharyngitis
before progressing to fever, lethargy, lateral neck tenderness
and edema, occasional trismus, and septic emboli most com-
monly seen as bilateral, nodular infiltrates on chest radiogra-
phy or as septic arthritis. The bacterium is thought to spread
via the tonsillar veins to the internal jugular system, where the
bacterial endotoxin induces platelet aggregation and septic
thrombus formation. Diagnosis is confirmed by a neck CT with
IV contrast, which demonstrates a filling defect in the internal
jugular system. First-line therapy includes IV β-lactamase–
resistant antibiotics with or without heparin anticoagulation.
Surgery to excise the jugular vein may be indicated in patients
with a worsening clinical course despite appropriate medical
therapy or in the event of neck abscess formation.
Cavernous Sinus Thrombosis
Cavernous sinus thrombosis is a life-threatening infection with
a mortality rate of 3 0% to 40% caused by retrograde spread
of infection from the upper dentition or paranasal sinuses via
the valveless ophthalmic venous system to the cavernous sinus
(Fig. 10-9 ).47 Symptoms include fever, lethargy, orbital pain,
proptosis, reduced extraocular mobility, and dilated pupil with
vein
Angular vein
Inferior
ophthalmic vein
Pterygoid plexus
Facial vein

FIGURE 10-10. Bacterial thyroiditis causing acute airway obstruction and
descending mediastinitis.
sluggish papillary light reflex. The diagnosis is best confirmed
by MRI of the brain with contrast that demonstrates dural
enhancement in the region of the cavernous sinus. Treatment
includes critical-care life support, broad-spectrum IV antibiot-
ics, and anticoagulation therapy.
Carotid Artery Pseudoaneurysm or Rupture
Rare cases of carotid artery pseudoaneuryms or rupture have
been reported after spread of infection from the retropharyn-
geal or parapharyngeal spaces to the carotid space.48 Hallmarks
of this complication include a pulsatile neck mass, Horner
syndrome, palsies of cranial nerves IX through XII, expanding
hematoma or neck ecchymosis, or bright red blood from the
nose or mouth in the setting of a DNI. The complication
requires immediate surgical ligation of the carotid artery.
Mediastinitis
Mediastinitis is a relatively rare complication of DNI caused by
spread of infection along the retropharyngeal and prevertebral
planes of the neck into the upper mediastinum; it has a mortal-
ity rate of 3 0% to 40%.49 ,50 Presentation includes diffuse neck
edema, dyspnea, pleuritic pain with deep breathing, tachycar-
dia, hypoxia, and pleural effusion or mediastinal widening on
chest radiography. Thoracic CT scan with IV contrast often
reveals the presence of fluid collection, air-fluid levels, or
stranding or infiltration of the mediastinal fat (Fig. 10-10). Risk
factors for mediastinitis in the pediatric population include age
younger than 2 years, retropharyngeal space involvement, and
MRSA.51 Broad-spectrum IV antibiotics are necessary because
of a high frequency of multiple pathogens that include both
gram-positive and gram-negative and aerobic and anaerobic
species. If limited to the anterior-superior mediastinum above
the carina, transcervical drainage via a bilateral cervicotomy
with blunt dissection along the prevertebral plane will often
10 | DEEP NECK AND ODONTOGENIC INFECTIONS 175
provide sufficient access for drainage, irrigation, and place-
ment of soft rubber drains. Thoracotomy should be strongly
considered in cases that extend beyond the upper mediastinum
or that involve more than one mediastinal compartment. In a
meta-analysis of 69 patients with mediastinitis from cervical
abscess, the mortality rate was 19 % among patients who under-
went both cervical and thoracic drainage and 47% among those
who underwent cervical drainage alone.52
Necrotizing Fasciitis
Necrotizing fasciitis is a severe form of DNI that occurs more
often in older adults (age >60 years) and immunocompromised
patients, especially in those with poorly controlled diabetes.53
The origin of the infection is commonly odontogenic and
involves mixed aerobic and anaerobic flora. Clinical presenta-
tion may consist of a rapidly progressive cellulitis with pitting
neck edema and orange-peel appearance from obstructed
dermal lymphatics with or without subcutaneous crepitus. Neck
CT with IV contrast reveals tissue gas in more than 50% of
cases and widespread, nonloculated hypodense areas without
peripheral enhancement, consistent with liquefaction necro-
sis. Treatment requires critical-care support, management of
immunocompromising conditions, broad-spectrum IV antibiot-
ics, and surgical exploration. Findings at surgery consistent
with necrotizing fasciitis include foul odor; brown, watery fluid
collections; and liquefied and grayish fat and muscle that pull
apart with minimal finger pressure. Debridement of dead tissue
until a bleeding, viable edge or vital nerves or vessels are
reached is recommended. The wound is thoroughly irrigated,
packed with moistened gauze, and left open for a second-look
procedure in 48 to 72 hours. Patients may require skin grafting
or flap reconstruction once the infection subsides, and adju-
vant hyperbaric oxygen therapy can be considered if readily
available.53 Mortality may be as high as 20% to 3 0% in treated
patients and is highest in patients with mediastinal extension.
For a complete list of references, see expertconsult.com.
SUGGESTED READINGS
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Duggal P, Naseri I, Sobol SE: The increased risk of community-acquired
methicillin-resistant Staphylococcus aureus neck abscesses in young
children. Laryngoscope 121:51–55, 2011.
Eisler L, Wearda K, Romatoski K, et al: Morbidity and cost of odonto-
genic infections. Otolaryngol Head Neck Surg 149 :84–88, 2013 .
Flynn R, Paster B, Stokes L, et al: Molecular methods of diagnosis of
odontogenic infections. J Oral Maxillofac Surg 70:1854–1859 , 2012.
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from molecular mechanisms to clinical cases: implication of peri-
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113 :103 –109 , 2010.
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aureus infections in children. Curr Opin Otolaryngol Head Neck Surg
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