15 Ed PDF

ED
CORNEA PBO
REVIEW
Raymond Nelson C. Regalado, MD DPBO
PBO Review Course 2015
St. Luke’s Medical Center
•  3 zones
–  1. Palpebral
•  Contains accessory lacrimal glands of Wolfring
•  Contains goblet cell-lined crypts of Henle
–  2. Forniceal
•  Contains accessory lacrimal gland of Krausse
–  3. Bulbar
•  Contains lymphocytes, Langerhans and goblet
cells
ED CORNEA OPEX REVIEW, SOJR-PGH Manila, 2014

•  Nonkeratinized squamous epithelium
•  With an underlying substantia propria
–  Lymphatic vessels, plasma cells, mast cells,
macrophages

•  Avascular
•  Transparent
–  Homogenous arrangement of collagen fibrils
–  Relative deturgescence (78% water content)
–  Measures 9-11 mm V and 11-12 mm H
–  Prolate
•  Steep center, flat peripheral (nasal>temporal)
–  Index of refraction 1.3375
•  Thicker peripherally (0.7-1mm) than centrally
(0.5-0.55mm)
•  Main refractive element (43D or 2/3 total)
•  Central 3-4 mm is nearly spherical
•  Nutrition via glucose diffusion from aqueous
•  Oxygen is from the tear film and limbus
•  Corneal sensation by ophthalmic division of
CN V
–  Radially into the stroma, anterior thru Bowmans
and terminates in the wing cell layer of the
epithelium

•  5 layers (!ABCDE!)
–  1. Anterior epithelium
•  Nonkeratinized stratified squamous epithelium
•  5-6 cell layers
–  Superficial cells (2-3): with tight junctions
–  Wing/polygonal cells (2-3)
–  Columnar basal cells (1): mitotic
•  Attached to its own basement membrane secretion by
hemidesmosomes
–  Anchoring fibrils regenerate in 6-8 weeks
–  Differentiation in 1-2 weeks
–  Desquamation in 5-7 days

–  2. Bowman’s (membrane) layer
•  Not a true membrane!
–  Modified region of the anterior stroma
•  Collagen type I and III
•  Does not regenerate, replaced by scar tissue

–  2. Corneal Stroma
•  90% of corneal thickness
•  78% water content
–  Maintained by the NA-K-ATPase endothelial pump
•  Collagen type I (70%), III, V, VI
•  Responsible for corneal transparency (collagen
arrangement)
•  Contains GAGs as majority of ECM
–  Keratan sulfate (65%), dermatan sulfate and chondroitin
sulfate

–  2. Descemet’s membrane
•  Basal lamina of the endothelium
•  True membrane, PAS-positive
•  Thickness increases with age (3-12 um)
•  Collagen type III, VIII
•  3 zones: nonbanded, anterior banded, posterior
amorphous nonbanded
•  Hassle-Henle warts: peripheral excrescences of
DM seen in the elderly
•  Guttae: central DM excrescences

–  2. Endothelium
•  Single layer of hexagonal cells
•  Cell density decreases with age (3500-2000 cells/
sq.mm.)
•  Does not regenerate
–  Polymegathism: increases in size, most sensitive index
of endothelial dysfunction
–  Pleomorphism: change in shape
•  Contains Na-K-ATPase pump to maintain
transparency of the stroma

•  Stains
–  1. Fluorescein
•  Stains exposed basement membrane
•  Creates positive (ulcers, abrasions) and negative (due
to elevated lesion) staining
•  Needs cobalt blue filter
–  2. Rose bengal and 3. Lissamine green
•  Stains dead and devitalized tissue, and those with
mucin disruption
•  Rose bengal has anti-viral properties but is more
irritating
•  Lissamine green better tolerated, used to delineate
extent of masses prior to excision (SCCA)

•  Typical patterns
–  Diffuse: conjunctivitis, trauma, toxicity
–  Superior: SLK, FB, trichiasis
–  Interpalpebral: DES, exposure, neurotrophic
–  Inferior: blepharitis, exposure, lagophthalmos
trichiasis
–  3 and 9 o’clock: contact lens

-- - --=- . Conjunctival epithelium
@ @ Iil
•  Papillae

Anchoring
septa
Blood
vessel
hir
--
Neutrophil s,
lymphocytes, and
other le ukocytes
–  Vascular changes Figure 2-7 Cross-sectional d iagram of conjunctival papilla with a central vasc
rounded by acute and chronic le ukocytes .
–  Raised lesions of edema and inflammation

with a vascular core and
A m ild papi fibrous
llary reactio n producesseptae
a smooth , velvety appearance (Fig 2-)!
or progressive changes result in enlarged vascular tufts that obscure the under
(PAPULA) vessels (Fig 2-SB). Connective tissue septae restrict inflammatory changes t
vascular core, producing the appearance of elevated, polygonal, hyperemic m
–  Nonspecific bral
papilla has a central red dot that represents a dilated capi llary viewed end-on
and forniceal conjunctiva beyond the tarsus is less helpful in revealing t
–  If anchoring septae break, may produce giant

an inflamm ato ry reaction because the anchoring septae become sparser towar
and permit und ulat ion of less adherent tissue. With prolonged. recurrent, or
or cobblestonejunctival
papillaein flammation , the anchoring fibers of the tarsal conjunctiva stretch
leading to confluent papillary hype rtrophy (F ig 2-SC). The furrows betwee
larged fi brovascular stru ctures collect mucus and pus.

•  Follicles t
Conjunctival
–  Raised round lesions blood vessels
of lymphocytic infiltration without a mononuclear

vascularcells ob-
Figure 2-9 Cross-secti onal diag ram of con-
junctival follicle with
F
W
core (FUTI) scuring conjunctival blood vessels.
–  Seen in (MoMoTHCABE)
•  Moraxella, Molluscum, Toxic, Herpetic, Chlamydia,
Adenoviral, Bartonella, EBV
A B
Figure 2-11 Follicular conjunctivitis . A, Inflammatio
ED CORNEA OPEX REVIEW, SOJR-PGH Manila, 2014 B, Right eye showi ng follicular conjunctivitis in the
•  Granuloma
–  Nodule of chronic inflammation
(mononuclears, giant cells) with fibrovascular
proliferation
–  Usually seen in Parinaud’s

•  Membrane/Pseudomembrane
–  Fibrinous sheet adherent to the conjunctiva
•  True: bleeds when peeled
•  Pseudo: easily removed
–  Seen in (COLDS CABAG)
•  Chemical burn, OCP, Ligneous, Diphteroid, SJS
•  Chlamydia, Adenoviral, B-hemolytic strep, Allergic,
Gonococcal

•  Measures corneal thickness
•  Thicker cornea may signify endothelial
dysfunction
–  Post-op edema occurs at thickness greater
than 650 um
•  Measured by
–  Optical
–  Ultrasonic (more accurate)
–  Laser, OCT, AS imaging, etc

•  Quantitative measurement of corneal
sensation
•  Uses a hand-held contact esthesiometer
with retractable filaments or a noncontact,
air-puff type

•  Cell density (CD)
–  NV: 2500 (1500-3000)
–  CD less than 1000 at surgical risk
•  Standard deviation
–  NV: less than 140
•  Coefficient of Variation(CV)
–  Measures cell area
–  NV: less than 0.3
–  CV of greater than 0.4 at surgical risk
•  Percent hexagonality (6A)
–  Percentage with 6 apices
–  NV: more than 50% (approaching 100%)
–  6A less than 50% at surgical risk

•  Estimates corneal power by reading 4
points of the central 2.8-4mm zone
•  Reported as
–  Radius of curvature (in mm, lower steeper)
–  Refracting power (in diopters, higher steeper)

•  Placido disk based for qualitative measure
of conreal curvature
–  Steep: mires are closer and thinner
–  Flat: mires are further and thicker

•  Measures corneal shape, curvature and
thickness
•  Uses Placido-based systems and
elevation-based systems
•  Color-coded
–  Red: steep (CLOSE TO THE SUN)
–  Blue: flat (CLOSE TO THE SEA)

•  Definition (DEWS 2007)
–  A mulJfactorial disease of the tears and ocular
surface that results in symptoms of discomfort,
visual disturbance, and tear-‐film instability with
potenJal damage to the ocular surface. It is
accompanied by increased osmolarity of the tear
film and inflammaJon of ocular surface.
•  Core mechanism: tear film instability and
hyperosmolarity

•  Major causes
–  Reduced tear flow and increased evaporation
–  Low humidity, high air flow
–  Advanced age, female, refractive surgery,
CTL wear, decreased sensation, radiation, low
androgens

•  Tear film evaluation
–  Layers:
•  1. Mucin (inner)
–  From conjunctival goblet cells
–  Creates a wettable surface
•  2. Aqueous (middle) – 90% of tear composition
–  From lacrimal gland, Krausse and Wolfring
–  For lubrication, nutrition, oxygenation, antimicrobial
•  3. Lipid (outer)
–  From Meibomian glands, Zeis
–  Retards evaporation

•  Tear Break Up Time (TBUT)
–  NV: 15 seconds (10-30)
–  Done prior to other manipulations or drops
–  Instill fluorescein with saline (NOT anesthetic)
–  Last blink to first dry spot

•  Basic Secretion Test (BST)
–  Basic tearing
–  Anesthesia, Schirmer strips, 5 minutes
–  NV: more than 10 mm
–  Less than 5 mm: aqueous tear deficient

•  Schirmer I
–  Basic and reflex tearing
–  BST without anesthetic
•  Schirmer II
–  Reflex tearing
–  Schirmer I with nasal stimulation
–  Less than 15 abnormal

•  Tear composition assays
–  Tear osmolarity: increased, pathognomonic
•  Tear lysozime and lactoferrin: decreased

•  1. Aqueous tear deficiency (ATD)
–  A. Sjogren
–  B. Non-Sjogren
•  Lacrimal gland or duct problem or neurotrophic
•  2. Evaporative tear dysfunction (ETD)
–  A. Intrinsic
•  MGD, lid disorders, low blink rate
–  B. Extrinsic
•  Vit A deficiency, topical drugs, CTL, ocular surface
disease

•  Sjogren Syndrome (SYOTA HARAna)
–  SJOGREN: Hypergammaglobulinemia, ATD,
Rheumatoid arthritis, Ana positive
–  Primary: without CTD
–  Secondary: with CTD, usually RA
–  Due to T-cell inflammatory destruction of the
lacrimal gland or peripheral efferent nerve
dysfunction

tending thro ugh the gland ular orifice. They also may become posterio rl y di splaced on
eyelid margin. Meibomian secretions in active disease may be turbid and have increas
viscos ity. Followi ng yea rs of meibomian gland infla mmatio n, extensive atro phy of
meibomian gland acini may develop and eyelid compression no longer express the
m ian secretions. Atrophy of meibomian gland acini and derangement of glandular arc
tecture can be shown by transillumination of the eyelid as well as in frared photograph
Foam may appear in th e tear meniscus along the lower eyeLid. Patients frequen
have an unstable tear film with rapid TBUTs, particularly in long-standi ng d isease w
meibomia n gland atrop hy an d reduced lipid production. Mi ld to severe ocular surf
inflammat ion may accompany MG D, which may include th e foll owing manifestations
•  Meibomian gland dysfunction (MGD) • bulbar and tarsal conj unctival inj ection
pap illary reaction on the inferior tarsus
episcleritis
–  Lid margin brush marks, inspissation,

punctate epithelia l erosions in the infer ior cornea
marginal epith elial and sub epithelial infiltrates
corneal neovascul ari zation and scarring (pannus)
posterior lid margin sign using lissamine

corneal thi nn in g
Patients with MGD are frequently noted as havi ng one or more manifestations of
green sacea) including facial telangiec tasia in an axial distri bution (forehead, cheeks> nose, a
–  Management
•  Eyelid hygiene
•  Doxycycline, tetracycline
•  Short-course steroids
Figure 3-12 Meibom ian gland dysfunction.

•  Rosacea
–  Acneiform disorder of face, neck and
shoudlers
–  Malar rash, recurrent papules and pustules,
rhinophyma
–  Management
•  Tetracyline, doxycycline
•  Topical metronidazole cream for skin lesions

•  Seborrheic blepharitis
–  Oily/greasy crusts (SEBUM=SCURFS)
–  SPKs in the inferior third
–  Treatment:
•  Eyelid hygiene are the mainstay
•  Antibiotics, steroids

•  Chalazion
–  Chronic, painless lipogranulomatous
inflammation of Meibomian or Zeis
–  If recurrent, consider malignancy
–  Management
•  Warm compress + massage
•  Small: intralesional steroid
•  Large: I&C (internal:vertical, external:horizontal)

•  Hordeolum
–  Inflammatory or infectious nodules
–  External: Zeis or lash follicles
–  Internal: inspissated MGs
–  Usually caused by Staph
–  Self-limited (1-2 weeks)
–  Warm compress + massage

•  Sarcoidosis
–  Noncasseating granulomatous inflammation
–  Calcific band keratopathy, posterior fundus
periphlebitis, granulomatous uveitis
–  Mikulicz: DES, enlarged lacrimal and salivary
glands
–  Lofgren: iridocylitis with erythema nodosum
and hilar lymphadenopathy
–  Heerdfort: uveitis, fever, facial nerve palsy
(uveoparotid fever)

•  Vitamin A deficiency
–  Xerosis, ulcers, keratomalacia, nyctalopia
(earliest symptom)
–  Bitot spot: superficial foamy elevation on the
bulbar interpalpebral conjunctiva
–  Systemic deficiency has a 50% mortality rate
–  Treat with vit A and protein-calorie
supplements and lubricants

•  Exposure keratopathy
–  Due to lagophthalmos or proptosis
–  SPKs in the interpalpebral or inferior third
–  Management
•  Lubricants
•  Taping lids at bedtime
•  Surgical (tarsorrhaphy, lid weights)
•  Treat ocular conditions

treatment of superior limbic keratoconju nctivitis. Am I Ophthalmol. 1997;124(1) :80-87.
A ......_ _ B
Figure 3-19 A, Superior li m bic keratoconjunct iv itis . B, Ro se be ngal dye sta inin g patte rn in
•  Superior limbic keratoconjunctivitis (SLK)

superior limbic ke ratoconjunct ivitis. (Courtesy of Vincent P deL uise, MD.)
–  Mechanical trauma from upper eyelid on the

superior bulbar and palpebral conjunctiva
–  Fine papillary reaction of palpebral conj
–  Dye staining of the superior cornea and/or
bulbar conjunctiva
–  Treatment
•  Lubricants, anti-inflammatory, BCL
•  Cautery or fixation of superior bulbar conj

•  Recurrent corneal erosion
–  Usually due to abrading or shearing injury (not
lacerating) with a pre-existing EMB dystrophy
–  Recurrent pain especially at night or upon
awakening, without precipitating event
–  Check other eye to differentiate post-traumatic
from dystrophic
–  Frequent lubrication, saline drops, ointments
at bedtime
–  Oral doxycycline and topical steroids

•  Persistent corneal epithelial defect
–  Usually due to
•  Herpetic, chemical burn, toxicity, neurotrophic,
DES
–  Typically inferonasal (due to Bell’s)
–  Always ask for medication history (look for
preservatives)

•  Neurotrophic keratopathy
–  Damaged CN 5
•  Surgical (LASIK, PKP), MS, herpes, toxicity, DM
–  Riley-Day syndrome
•  Ashkenazi Jews, alacrima, dec DTR, impaired
taste, pain and temperature sensations

•  Trichiasis and Distichiasis
–  Trichiasis (Turned in): inward curving of
lashes
–  Distichiasis (Double): extra row of lashes

•  Dellen
–  Saucer-shaped depression and thinning
adjacent to an elevated lesion (pterygium,
bleb)
–  Due to ocular dryness

•  Limbal stem cell deficiency (LSCD)
–  Located at the limbus, and scattered in the
bulbar and forniceal conjunctiva
–  25-33% needed for normal ocular surface
healing
–  Usually shows wavelike irregularity during
staining, with a pale limbus
–  Treat with LSC transplant

•  Normal ocular flora
–  Eyelid margin (CAMPED)
•  Corynebacterium, S. Aureus, Micrococcus, P. acnes, S.
Epidermidis, Demodex
–  Conjunctiva (CAPE)
•  Corynebacterium, S. Aureus, P. Acnes, S. Epidermides
•  Invasive bacteria (can penetrate an intact
epithelium) (CHaNeLS)
–  Corynebacterium, Haemophilus, Neisseria,
Listeria, Shigella

•  Indications for culture
–  Sight-threatening ulcers (>1-2 mm)
–  Atypical history and/or appearance
–  Unresponsive to therapy

•  Culture media
–  Aerobes
•  BAP, CAP, Thioglycolate
–  Anaerobes
•  BAP (anaerobic), Thioglycolate
–  Mycobacterium
•  LJ agar
–  Fungi
•  Sabouraud, BHI
–  Acanthamoeba
•  Nonnutrient agar with E. coli overlay
–  Neisseria
•  Thayer-Martin agar

•  Nearly 100% of older than 60 y/o have
HSV in the trigeminal ganglion
•  HSV1: orofacial ocular
•  HSV 2: genital
•  Acquired more commonly by
asymptomatic viral shedding than with
direct contact with lesions

Figure 4·2 Skin vesicles of HSV dermato-
blepha rit is. (Courtesy of James Chodosh. MD.)
•  Manifests as:
–  1. Blepharoconjunctivitis
CHAPTER 4: Infecti ou s Diseases/ Exte rna l Eye: Basic Concepts and Viral Infecti ons
•  Follicular, preauricular lymph node, skin vesicles

–  2. Epithelial keratitis
•  Dendritic ulcers with terminal bulbs or coalesce to
become geographic ulcers
Fi gure 4-4 Rose bengal staining of herpetic epi thelial keratitis out lin es a typical dendr
•  Always test for corneal hyposthesia tesy of James Chodosh, MD.)

•  Other dendritiform epithelial ulcers
–  (RAVENS)
–  Regeneration lines, Adenovirus, VZV, EBV,
Neurotrophic K, HSV

•  Manifests as:
–  3. Stromal keratitis
•  Most common cause of infection-related blindness
in the US
•  3 forms: interstitial, disciform, necrotizing
–  4. Others
•  Iridocylcitis (unilateral IOP elevation withfocal iris
transillumination defects)
•  Neurotrophic K, topical antiviral medication
epitheliopathy

•  Herpetic Eye Disease Study (HEDS)
–  Answers YES to the following:
•  Topical steroids for stromal keratitis
•  Prophylactic acyclovir to minimize recurrent HSV
•  Primary HSV is self-limited
•  Treat with
–  Acyclovir 400 5x for 10 days (Fam, Val, Gan)
–  Add topical steroids if stromal

•  Manifests as maculopapular, vesicular
then pustular dermatitis in ipsilateral CN 5
distribution
•  Hutchinson’s sign
–  Signifies increased risk for ophthalmicus
because of affectation of the nasociliary
branch of the ophthalmic division of CN 5

•  Causes
–  Pseudodendritic epithelial keratopathy, iris
Figure 4-12 Nummular keratitis of herpes zoster ophthalmicus. (Courresyof Rhea L. Siatkow
atrophy, lipid k, choroiditis, etc

–  Nummular stromal keratitis is characteristic
•  Management
–  Oral antivirals
•  Acyclovir 800 mg 5x for 7-10 days
•  For postherpetic neuralgia, add gabapentin or
pregabalin

•  Usually by close contact (close quarters),
swimming pools, ophthalmic equipment
•  Manifests as
–  1. Follicular conjunctivitis
•  Self-limited
–  2. Pharyngoconjunctival fever (PCF)
•  Serotypes 3 or 7
•  Fever, pharyngitis, conjunctivitis, preauricular
lymphadenopathy

•  Manifests as Figure 4-16 Subepithelial corneal infiltrates in a patient
–  3. Epidemic keratoconjunctivitis (EKC) specific signs, but laboratory diagnos is is only rare
•  Serotypes 8, 11, 19, 37 (8+11 is 19 not 37) readily diffe rentiate ade novi rus from HSV infection
or resolves before resu lts become ava ilable. A rapid
Detector [Rapid Pathogen Screening; South Willia
•  Often bilateral, preceded by URTI tige ns in the conjunctiva is now ava ilable. Paired s
confirmation of acute adenovirus infection, but thi
•  Classic diffuse, small subepithelial infiltrates which
Therapy fo r adenoviral ocular infect
MANAGEMENT
may persist for months to years indicated

presses and artificial tears may provide symptom
only when the clinical signs, such as muco
•  Treatment
ated bacterial infection or when a viral cause is less
For patients wi th conjunctival membranes due
cian with force ps or a cotton swab every 2- 3 days, c
–  Mainly supportive corticosteroids, may speed resolution and prevent

reduce photophobia and improve vision impaired
Because corticosteroids may prolong viral sheddi
–  May use steroids only if there is BOV due to
subepithelial infiltrates and if with membranes

•  Staphylococcal blepharitis
•  Eyelid matting and crusting and collarettes
•  May be associated with angular blepharitis
–  Chronic condition caused by Moraxella
–  Lateral canthal maceration
•  May also cause phlyctenulosis
–  Type IV hypersensitivity
–  Small elevated nodules at 10-2-4-8 positions
–  Also caused by TB
•  Management
–  Antibiotic ointment
•  Erythromycin, bacitracin, moxifloxacin
•  Lid hygiene
•  With or without steroids
•  Review of blepharitis
–  Collarettes, matting: Staph
–  Scurfs: Seborrheic
–  Sleeves, cylinders: Demodex

•  Explosive, hyperacute, purulent
•  Preauricular lymphadenopahty,
membranous conjunctivitis
•  Management
–  IM ceftriaxone 1 g IM (w/o ulcers)
–  IV ceftriaxone 1g q12 x 3 days (w/ ulcers)

•  3 types
Fi gure 5-14 Trachoma exhibiting Herbert pits of the superior limbus (round to oval, re
–  1. Trachoma lucen t areas within pannus) .
and superficial fibrovascular pann us, which is most prominent in the superior third
cornea but may extend cent rally into the visual axis (Fig 5- 15).
•  Serotype A-C Clinical diagnosis of trachoma requires at least 2 of the following clinical featu
conjunctival follicles on the upper tarsal conjuncti va
•  Follicular conjunctivitis
limbal foll icles and thei r sequelae (Herbert pits)
typical tarsal conjunctival scarring
vascular pannus most marked on the superior limbus
•  Art line: linear scarring on superior tarsus

Severe conjunctival and lacrimal gland duct scarring from chronic trachoma can r
aqueous tear defici ency, tear drainage obstruction, trichiasis, and entropion.
•  Herbert pits: limbal depressions from necrosed

limbal follicles
•  Topical erythro ointment, oral tetracycline, or single
dose azithro

•  3 types
–  2. Inclusion conjunctivitis
•  Serotypes D-K
•  Sexually transmitted
•  Follicular conjunctivitis 1-2 weeks after inoculation
•  Mucopurulent discharge with lymphadeopahty
•  Azithro single dose, doxy, tetray, erythro (all oral)
–  3. Lyphogranuloma venereum
•  Serotypes L1-L3

•  Caused by (in descending frequency)
–  Chlamydia, Strep, Staph, Haemoph, group D
strep, Morax, E. coli, N gono
•  Gonococcal
–  2-4 days (1-7 days) after birth
•  Chlamydia
–  5-7 days (up to 19 days)

•  Most commons
–  Pseudomonas for CTL wearers
–  Gram positive bacteria (Staph)
–  Moraxella for Gram negative
–  Predisposing factors
•  CTL wear
•  Trauma
•  Eye drops
•  Impaired defense mechanism (neurotrophic)
•  Ocular surface disease
•  Systemic conditions (DM)

•  Typical features
–  Staph: distinct borders, clear surrounding,
marginal infiltrates
–  Strep: serpiginous, advancing borders,
hypopyon, crystalline (by S. viridans in post-
op eyes)
–  Pseudomonas: fast-course, ground-glass,
mucopurulent, AC reaction, corneal
perforation in 48 hours, brush borders,
scalloped borders, CTL wear

–  Neisseria: opthalmia neonatorum 2-4 days,
quick perforation
–  Moraxella: chronic, slowly progressive,
advancing border
–  HSV: dendrites, hyposthesia
–  VZV: pseudodentrites
–  Mycobacterium: delayed onset, crystalline

–  Neisseria: opthalmia neonatorum 2-4 days,
quick perforation
–  Moraxella: chronic, slowly progressive,
advancing border
–  HSV: dendrites, hyposthesia
–  VZV: pseudodentrites
–  Mycobacterium: delayed onset, crystalline

•  Management
–  Start with broad-spectrum antibiotics
•  Fluoroquinolones (besi, moxi, gati, oflox)
–  Wait for clinical response or results of GS/CS
–  Starts steroids if
•  Organism identified, test results present, favorable
response for 2-3 days, frequent follow ups
–  Also start cycloplegics

–  Slow course
–  History of vegetable matter and previous
treatment failure
–  CTL wearer, history of excessive steroid use
–  Fern-like or brush-like border
–  Epithelial plaque
–  Immune ring, satellite lesions

•  Treatment
–  Natamycin for filamentous fungi (fusarium)
–  Amphotericin B for yeasts (candida) or
filaments (aspergillus)
–  Corneal debridement

–  Ring infiltrate, pseudodendrites, radial
perineuritis, scleritis
–  History of washing with well water, CTL wear
–  Pain disproportionate to clinical appearance
•  Treatment
–  Biguanides (PHMB) or clorhexidine

•  Review of ring infiltrates
–  (PAMFAH)
–  Pseudomonas, Acanthamoeba,
Mycobacterium, Fungi, Anesthesia, Herpes

•  Type 1
–  Anaphylactic, allergic
–  Allergic conjunctivitis
•  Type 2
–  Cytotoxic
–  OCP
•  Type 3
–  Immune complex, antigen-antibody
–  Scleritis, PUK, SJS
•  Type 4
–  Delayed, cell-mediated
–  Phlycten, contact dermatitis, graft rejection

•  Hay-fever/seasonal
–  Type 1, associated with atopy
–  Prominent itching, chemosis, lid swelling,
watery or mucoid discharge
–  Treatment
•  Avoid allergen
•  Antihistamines, mast cell stabilizers

•  Vernal keratoconjunctivitis (VKC)
–  Type 1 and 4
–  Male children, atopy, itching, blepharospasm
–  Palpebral and limbal type
–  Diffuse papillary hypertrophy (cobblestone or
giant papillae)
–  Horner-Trantas dots: degenerated eosinophils
and epithelial cells on the limbus
–  May cause shield ulcers, PSC, pannus
•  Vernal keratoconjunctivitis (VKC)
–  Treatment
•  Antihistamines, aircon, relocation
•  Mast cell stabilizers
•  Cyclosporine, pulse steroid therapy
•  Supratarsal steroid injection

•  Atopic keratoconjunctivitis (AKC)
–  Type 4 hypersensitivity
–  Similar to VKC except
•  Usually year-round, older patients
•  Smaller papillary reaction (boggy)
•  More severe vascularization, symblepharon

Figure 7-9 Giant papillary conjunctivit is. (Courtesy of Kirk R. Wi/he/mus, MD.)
•  Giant papillary conjunctivitis (GPC)

–  Type 1 and 4 from chronic mechanical trauma
•  CTL, sutures, prosthesis
–  Papillae greater than 0.3 mm with destruction
of anchoring septae
–  Treatment
•  Discard offending agent
•  Patient education
•  Mast cell stabilizers

•  Stevens-Johnson Syndrome (SJS)
–  Type 3 caused by
•  Medications (sulfonamides, penicillins,
tetracyclines, anticonvulsants, isoniazid, thiazide
diuretics)
•  Infectious (strep, HSV, adenovirus, mycoplasma)
–  Produces target lesions (red lesions with a
pale ring and outer red ring
–  Bullous eruptions of mucous membranes

•  Stevens-Johnson Syndrome (SJS)
–  Main differentials
•  OCP: slower
•  TEN: overdrive
–  Management
•  Supportive
•  Prevent symblepharon by membrane peeling
•  Antibiotics, steroids

•  Ocular cicatricial pemphigoid (OCP)
–  Type 2
–  Classic features
•  Trichiasis is an early finding
•  4S: Subepithelial fibrosis, shortening of fornix,
symblepharon, stuck eye (frozen globe)
–  Management
•  Multi-specialty (dentist, derma, ENT, OB, IM)
•  Dapsone, cyclophosphamide, prednisone

•  Thygeson SPK
–  Multiple slightly elevated corneal epithelial
lesions in a quiet eye
–  Supportive, steroids, BCL
•  Cogan syndrome
–  Stromal K, vertigo, hearing loss 1-2 weeks
after URTI
–  Diagnosis of exclusion
–  Steroids

•  Peripheral ulcerative keratitis (PUK)
–  Usually with rheumatic disease (RA, SLE)
–  Peripheral epithelial loss with stromal thinning
which may ulcerate and melt
–  May have adjacent scleritis
–  Treament
•  Profuse lubrication
•  Conjunctival resection
•  IV cyclophosphamide, steroid therapy

•  Mooren Ulcer
–  History of trauma, surgery or infection
–  Cause is usually unknown
•  Those with known local or systemic disease are termed
PUK
–  Chronic, progressive, painful (Mooren=Masakit),
idiopathic
–  Circumferential then central spread
–  May perforate with minor trauma
–  Purely corneal (unlike PUK with scleral)
–  Treat with steroids, BCL, cyclosporine,
conjunctival excision, immunosuppressives

•  Episcleritis
–  Self-limited, benign, bilateral
–  Blanches after phenylephrine
–  Simple, diffuse, nodular
•  Sleritis
–  Underlying autoimmune or CTD (RA, SLE)
–  Boring pain with violaceous sclera
–  May produce necrotizing scleritis

•  Papilloma
–  HPV 6 (children) or 16 (adults)
–  Pedunculated (inferior fornix) or sessile
(limbus)
–  Most regress spontaneously
–  Excise if questionable

•  Conjunctival intraepithelial neoplasia (CIN)
–  Exposed bulbar conj, older male smokers,
light complexion, prolonged sun exposure
–  Papilliform, gelatinous, leukoplakic
–  Excise with a 3-4mm margin
–  Adjunctive cry0therapy and topical mitomycin

•  Squamous cell CA (SCCA)
–  Secondary to UV radiation
–  Broad-based with sharp borders, superficial,
with feeder vessels
–  Wide excision, absolute alcohol on slceral
bed, cryotherapy

•  Melanoma
–  Over-all mortality rate of 25%
–  Rare in blacks and Asians
–  May arise from PAM (70%), de novo (10%), nevi
(2%)
–  Usually at the bulbar conj or limbal area
–  25% are amelanotic
–  Poor prognosis
•  Palpebral, caruncular, forniceal
•  Deep, thick, eyelid margin, lymphatic invasion, mixed
cell type

CHAPTER 8: Clinical Approach to Neoplastic Disorders ofthe Conjunctiva and Cornea •
•  Lymphoma
Figure 8-16 Conj unctival lymphoma .
–  Neoplastic lymphoid proliferation of

Metastatic Tumors
monoclonal B cell lymphocytes Metastatic tumors to the conjunctiva are much less common than those to the uveal
and orbit, but such tumors have arisen from cancer of the breast, lung, kidney, and
where, including cutaneous melanoma. Metastatic lesions to the uveal tract, orbit, or
–  Unilateral salmon pink mobile mass

nasal sinuses can extend into the conjunctiva. Metastases or leukemic infiltrates t
limbus or cornea also occur.
–  Incisional biopsy needed, excisional if small

Epibulbar Choristoma
Epibulbar Dermoid
–  Local RT if confined to conj, systemic chemo if

The congenital epibulbar dermoid typ ically occurs on the inferotemporal globe or
porallimbus as a smooth, elevated, solid mass embedded in the superficial sclera a
cornea (Fig 8-17). About 1 in 10,000 individuals is affected.
with spread PATHOGENESIS An epibulbar dermoid results from faulty development of the eyelid
and consists of displaced embryonic tissue that was destined to become skin. Derm
are composed of fibrous tissue and occasionally hair with sebaceous glands; they are
ered by conjunctival epithelium. Epibulbar dermoids are solid rather than cystic an
not fully entrapped beneath the surface, unlike derm oid cysts.
CLI NICAL FIND INGS Dermoids are well circumscribed, porcelain white, round to ov
sions that occur most often at the inferotemporal limbus, but they can also be f
on the central cornea, in the subconjunctival space, or in the orbit. Fine hairs may
trude from some dermoids. A limbal dermoid often has an arcuslike deposition of
along its anterior corneal border. Corneal astigmatism caused by a dermoid can le

•  Dermoid
–  Inferotemporal globe or limbus
–  Goldenhar syndrome
•  Oculoauriculovertebral dysplasia
•  Epibulbar dermoid, preauricular skin tag, aural
fistulae, vertebral anomalies
–  May cause flattening of the adjacent meridian
and secondary anisometropic amblyopia

•  Anomalies of the Globe
–  Cryptothalmos
•  Bilateral
•  Ablepharon: eyelids and adnexae fail to form, AS
structures unformed or absent
•  Pseudocryptothalmos: only ankyloblepharon with a
formed eyeball

•  Anomalies of the Globe
–  Microphthalmos
•  Small disrognaized globe (Micro=Magulo)
•  Associated with colobomas
–  Nanophthalmos
•  Small but functional eye (Nano=Unano)
•  High hyperope, AS crowding

•  Anomalies of the Anterior Segment
–  Microcornea
•  Less than 10 mm in adults (or 9mm in newborn)
•  Flat cornea, hyperope, angle-closure
•  Associated with PFV, cataracts, AS dysgenesis, ONH
–  Megalocornea
•  More than 13 mm
•  Associated with iris translucency, miosis, cataract,
arcus, mosaic corneal dystrophy (of Francois)
•  Vs Buphahtlmos: high IOP, long axial length

•  Anomalies of the Cornea
–  Posterior embryotoxon
•  Thickened and anteriorly displaced Schwalbe’s line
(junction of the TM and Descemet’s)

•  Anomalies of the Cornea Fi gure 9-5 Axenfeld-Rieger syndrome exh ibiting iris atrophy, corectopia, and pseudopolyc
(Counesy of V!'ncent P deLUise, MD.)
–  Axenfeld-Rieger syndrome to the border of the opacity (Fig 9-6). Approximately 60% of cases are bilateral. Ass
ated ocular ab normalities are present in approximately 50% of cases. Ocular abnormal
•  Axenfeld anomaly: post embryotoxon + PAS

include keratolenticular touch, cataract, congenital gla ucoma, microcornea, aniridia,
PFY. Characteristic histopathologic findin gs in Peters anomaly include a localized
sence of the corneal endothelium and Descemet's membrane beneath the area of opac
Peters an o maly has been associated with systemic malformations in up to 60%
•  Axenfeld syndrome: + glaucoma

patients. These abnorm alities include developmental delay, heart defec ts, external
abnormalities, hearing loss, CNS deficits, spinal defects, gastrointestinal and genito
nary defects, facial clefts, and skeletal anomalies. Although systemic malformations
•  Axenfeld-Rieger anomaly: + iris hypoplasia,

corectopia, polycoria
•  Axenfeld-Rieger syndrome: + dental or skeletal
malformations
Figure 9-6 Peters anomaly.

The image cannot be displayed. Your computer may not have enough memory to open the image, or the
image may have been corrupted. Restart your computer, and then open the file again. If the red x still
appears, you may have to delete the image and then insert it again.

–  Peters anomaly
•  Central corneal opacity at birth associated with
central iridocorneal adhesions
•  Usually bilateral
•  Associated with cataracts, glaucoma, microcornea,
aniridia, PFV and systemic abnormalities
•  Absent endothelium and Descemet’s membrane
underneath opacity

–  Congenital Hereditary Endothelial Dystrophy
(CHED)
•  Bilateral corneal edema at birth
•  CHED 1: AD
–  First 2 years, slowly progressive, diffuse, bluish gray ground
glass corneal opacity
–  Degeneration of endothelial cells at 5 mos AOG
–  Pain, photophobia, tearing, no nystagmus
•  CHED 2: AR
–  Present at birth, stable
–  No tearing or photophobia but with nystagmus

•  Epithelial Basement Membrane Dystrophy
(EBMD)
–  MDF, Cogan microcystic epithelial dystrophy,
Anterior BMD
–  Thickened basement membrane with
epithelial micocysts
–  Bilateral, women, 50s
–  Produces recurrent corneal erosions
–  Stromal micropuncture, diamond burr, PTK

•  Meesman Corneal Dystrophy
–  Contains peculiar substance of granular and
filamentary material
–  Seen as microcysts in the interpalpebral zone
extending to the limbus with clear surrounding
epithelium
–  No treatment needed

•  Reis-Buckler (CDB 1)
–  Disrupted/absent Bowman
–  Appears in first few years of life
•  Thiel-Behnke (CDB 2)
–  Saw-tooth fibrocellular pattern
–  First or second decade

•  Lattice Dystrophy
–  Biber-Haab-Dimmer Figure 10-8 Lattice corneal dystrophy. (Courtesy of Vincent P deLuise, MD.)
–  Amyloid deposit, Congo red stain

–  Glass-like stromal branching
–  Meretoja syndrome: lattice plus systemic
amyloidosis (facie, lagophthalmos,
blepharoptosis, pendulous ears, nerve
palsies, dry skin)

•  Granular Dystrophy
–  Groenouw type 1
Figure 10-10 Granular dystrophy type 1.
–  Hyaline deposits, Masson trichome

–  Ground-glass deposits with clear spaces
–  Avellino dystrophy
•  Granular + Lattice
•  With stellate and snowflake corneal opacities

284 • External Dise ase and Cornea
•  Macular Dystrophy
–  Groenouw type 2
Figure 10-12 Macular dystrophy, showing involvement to the limbus with diffus
MANAGEMENT Recurrent erosions are treated as for other stromal dystrophies,
–  Autosomal Recessive!
tophobia may be reduced with tinted contact lenses. PTK may be used for sym
anterior macular dystrophy. Definitive treatment requires penetrating corneal t
tation, altho ugh recurrences may be seen .
–  Mucopolysacharide (or GAG) deposits, Alcian

Schnyder corneal dystrophy (SeD)
Alternative names Schnyder crystalline corneal dystrophy (SCCD), Schnyder c
blue
dystrophy si ne crystals, hereditary crystalline stromal dyst rophy of Schnyder, c
stromal dystrophy, central stromal crystalline corneal dystrophy, corneal crysta
trophy of Schnyder, Schnyder corneal crystaUine of dystrophy
–  Significant BOV! Due to lack of clear

Inheritance Autosomal dominant
Genetics Loc us Ip36; gene: UbiA prenyltransferase domain-containing p
intervening spaces with involvement of the

(UBIADl)
Category
corneal periphery PATHOLOGY This condition is thought to be a local disorder of corneal lipid me
Pathologically, the opacities are accumulations of unesterified and esterified ch
and phospholipids. Oil red 0 stains the phospholipids red. In the normal proce
bedding tiss ue in paraffin, cholesterol and other fatty substances are dissolved;
the pathologist must be made aware of the requirements for special stains. Electro
copy shows ab normal accumulation of lipid and dissolved cholesterol in the ep
in Bowman layer, and throughout the stroma. Confocal microscopy reveals d
of the basal epithelial/subepithelial nerve plexus, with highly reflective intrace
extracellular deposits.

•  Schnyder crystalline dystrophy
–  Cholesterol in the stroma
–  Central opacification, arcus lipoides,
midperipheral opacification, decreased
corneal sensation
•  Fleck corneal dystrophy
–  Dandruff-like material in the stroma
•  Central cloudy dystrophy of Francois
–  Polygonal lipid-like deposits with clear spaces

•  Marilyn Monroe Always / Goes HoMe to /
LA California
–  Macular, Mucopolysaccharide, Alcian blue
–  Granular Hyaline Masson trichome
–  Lattice, Amyloid, Congo red

•  Fuchs Endothelial Dystrophy (FED)
–  Primary endothelial dysfunction causing
corneal edema and DM thickening due to lack
of NA-K-ATPase pumps
–  Corneal guttae, DM thickening and folding,
stromal edema
–  Pain in the morning
–  PKP or DSEK

•  Posterior Polymorphous Dystrophy
(PPMD)
–  Abnormal multi-layered endothelial cells that
behave like epithelial cells
–  With microvilli, positive for keratin, proliferative
tendencies
–  Mostly asymptomatic

•  Keratoconus (KC)
–  Central/paracentral corneal ectasia with apical Figure 10-25 Kera tocon us.
thinning but positive family histories have been reported in 6%- 8% of cases. Clinically un
first-degree relatives have a higher chance of showing subclinical topographic ab
ties associated with keratoconus than does the general population. Multiple chrom
–  Fragmented Bowmans, epithelial and stromal

loci have been reported, but the identification of specific genes remains elusive. T
bination of genetic and environmental risk factors such as eye rubbing, inflamma
thinning, Descemet breaks, diffuse scarring

oxidative stress all playa role in the onset and progression of keratoconus.
McMonnies CWo Abnormal rubbing and keractectasia. Eye Contact Lens. 2007;33(6 P
265 - 271.
–  Bilateral, young to early adults

PATHOLOGY Histopathologically, keratoconus shows the following:
fragmentation of Bowman layer
–  Earliest sign: scissoring of the red reflex

thinn ing of the stroma and overlying epithelium
folds or breaks in Descemet's membrane
variable amounts of diffuse scarring
CLINICAL FINDINGS Nearly all cases are bilateral, but I eye may be much more sev
volved. Sometimes the less affected eye shows only high astigmatism, which may
sidered the minimal manifestation of keratoconus. Alternatively, videokeratosc
show enantiomorphism (a mirror image) and reveal some mild steepening in t
eye. The disease tends to progress during the adolescent years and into the mid
30s, although progression can occur at any time. Early biomicroscopic and his
logic findings include fibrillation of Bowman layer, leading to breaks and follow
brous growth and dysplasia through the break. As progression occurs, the apical
of the central cornea worsens, and extreme degrees of irregular astigmatism can
No associated inflammation occurs.
–  Other signs:
•  Rizzuti: conical reflection on the nasal cornea from
illumination on the temporal side
•  Munson: protrusion of lower lid on down gaze
•  Fleischer ring: iron deposits on cone base
•  Vogt striae: posterior stromal stress lines

–  Acute hyrdrops: sudden rupture of the DM usually
caused by repetitive rubbing
•  Posterior stroma may heal in 6-12 weeks but with
resultant scarring
–  Increased incidence in Downs, atopy, Marfan
–  Management
•  EOR correction
•  PKP (CTL intolerance, scarring, progressive thinning)
•  Intrastromal rings, collagen cross linking

•  Pellucid marginal degeneration (PMD)
Figure 10-30 Pellucid ma rgina l degeneration. (Courtesy of Vincent P deLuise, MD.)
–  Corneal protrusion with inferior peripheral

thinning
–  20-40 y/o, bilateral, rare Figure 10-31 Topography of pellucid margina l degeneration. Note the inferior steepen ing and
"lobster claw" pattern.
–  Hydrops may occur but perforation is rare

–  Correct EOR
–  PKP more difficult, may do wedge resection or
lamellar tectonic grafts

•  Keratoglobus
–  Corneal protrusion with generalized thinning
in the midperiphery
–  Only ectatic condition present at birth
–  Associated with blue sclera and Ehlers-
Danlos
–  Prone to perforation with minimal trauma

CHAPTER 10: Corneal Dystrophies and Ectasias • 303
,,
,,
,
A B c
Figure 10-32 The presence of cornea l thinning and the type of co ntour abnorma li ty can be
•  Pinguecula
–  Yellow white AMORPHOUS deposits at the
limbal interpalpebral conjunctiva
–  Secondary to UV exposure
–  Excise only if cosmetically unacceptable,
interferes with CTL wear, persistent
inflammation

•  Pterygium
–  WING-SHAPED fold of conj and fibrovascular
tissue invading the superficial cornea
–  Elastotic degeneration
–  Stocker line: pigment deposition at the pterygium
head
–  Excise if: persistent discomfort, significant
astigmatism, DES, encroaching on visual axis,
cosmetically unacceptable
–  Variable techniques: bare sclera (NO), simple
closure, mitomycin, autograft

•  Degeneration vs Dystrophy
–  Degeneration
•  Peripheral, asymmetric, late in life
–  Dystrophy
•  Central, symmetric, early in life

•  Coats white ring
–  Small (<1mm) gray white dot, remnant of
metallic FB
•  Spheroidal degeneration
–  Climatic droplet K, Bietti nodular dystrophy,
Labrador K
–  Common, bilateral, interpalpebral, males
–  Translucent brown spheroidal deposits

•  Iron lines
–  Fleisher ring: KC base
–  Hudson-Stahli line: junction of upper 2/3 and
lower 1/3 of aging cornea
–  Kayser-Fleisher ring (copper): peripheral
Descemet’s in Wilson’s
–  Stocker line: pterygium head
–  Ferry line: filtering bleb head

•  Crocodile Shagreen
–  Mosaic gray opacities at Bowmans, with clear spaces
•  White limbal girdle of Vogt
–  Narrow concentric superficial band along the
interpalpebral limbus with clear interval
•  Corneal arcus
–  Lipid deposition in the limbus with clear space
–  Indicative of elevated serum cholesterol and LDL
especially in younger than 40
–  Always bilateral; if unilateral, suspect contralateral
carotid artery disease or ocular hypotony

•  Terrien marginal degeneration Figure 12-9 Terrien margina l degeneration wi th superior thinning . (Courtes yofJ.
–  Quiet, slowly progressive, usually unilateral

gradually. The epithelium remains intact, and a fine vascular pannus travers
stromal thinning. A line of lipid deposits appears at the leading edge of the
tral edge of the furrow) (Fig 12-9). Spontaneous perforation is rare, althoug
–  Starts superiorly then spreads

can easily occur with minor trauma. Corneal topography reveals flattening
eral thinned cornea, with steepening of the corneal surface approximately 9
the midpoint of the th inned area. This pattern usually results in high again
oblique astigmatism. Spontaneous ruptures in Descemet's membrane can re
circumferentially, rarely involving the inferior

mellar fluid or even a corneal cyst.
An inflammatory condition of the peripheral cornea that may resemble
ginal degeneration occurs, in rare instances, in children and young adults
limbus as Fuchs superficial marginal keratitis, it features progressive thinning with

ulceration and can lead to perforation.
Surgical correction is indicated when perforation is imminent due to pro
ning or when marked astigmatism Significantly limits visual acuity. Cresce
–  Steep wall with intact epithelium

mellar or full-thickness corneoscleral patch grafts may be used and have bee
arrest the progression of severe against-the-rule astigmatism for up to 20 year
mellar keratoplasty grafts may be required in severe cases of 360" marginal
–  Spontaneous perforation is rare Postinflammatory changes

Salzmann nodular degeneration Salzmann nodular degeneration is a non
corneal degeneration that sometimes occurs as a late sequela to old, long-st
–  (Terrien=Tahimik, Taas, Tibay)

tis, or it may often be idiopathic. Causes include phlyctenulosis, trachoma, a
keratitis. The degeneration may not appear until years after the active ker
sided. It can be bilateral and is more common in middle-aged and older wom
ules are gray-white or blue-white and elevated (Fig 12-10), and they may be a
recurrent erosion. They often develop in a roughly circular configuration
or paracentral cornea and at the ends of vessels of a pannus. Histopathologi

•  Salzmann nodular degeneration
–  Post-inflammatory or idiopathic
–  Grayish nodules on the corneal periphery or
adjacent to a pannus
–  Localized replacement of Bowmans with
hyaline and fibrillar material

•  Calcific band keratopathy
–  Calcium hydroxyapatite deposits in the Bowmans
layer
–  Usually idiopathic; other causes
•  Chronic ocular disease, hypercalcemia, hereditary,
silicone oil in aphakics
–  Horizontal band of dense plaques with clear
peripheral zone
–  Swiss-cheese appearance due to corneal nerve
channels
–  Remove by EDTA chelation

•  ICE syndrome
–  Iridocorneal endothelial syndrome
–  Common in middle aged females
–  Spectrum of disorders with unilateral corneal
edema, glaucoma and iris abnormalities
–  3 variants
•  Chandler: mainly corneal edema
•  Essential iris atrophy: with corectopia, polycoria
•  Iris nevus (Cogan Reese): pigmeneted iris nodules
–  Definitive management: PKP with glaucoma
management

•  Peripheral corneal guttae
–  Hassall-Henle bodies
–  DM excrescences in the periphery that appear
with aging
–  If central, may be pathologic (corneal guttae)

•  Corneal verticillata
–  Vortex keratopathy
–  Whorl-like pattern of brown or gray deposits in
the inferior interpalpebral corneal epithelium
–  Most commonly from
•  Amiodarone, chloroquine, indomethacine,
phenothiazines
–  Resolves with discontinuation of offending
agent

•  Chemical injuries
–  Alkali burn more severe than acid burn
because of saponification and cellular
disruption with rapid corneal penetration
–  Management
•  Immediate and copious irrigation with water or
BSS (at least 2L) until pH normalizes
•  Steroids, cycloplegics, oral tetracyclines, vitamin
C, lubrication

•  Traumatic hyphema
–  May be spontaneous (look for rubeosis, clotting
problems, herpetic disease, IOL related, RB,
leukemia)
–  Rebleeding occurs 2-5 days after injury due to
lysis and clot retraction
–  Corneal staining caused by endothelial uptake of
hemoglobin
–  General treatment:
•  Protect eye, restrict activity, head elevation, observation
•  Analgesics, cycloplegics, steroids, antifibrinolytics

•  Traumatic hyphema

•  Penetrating injuries
–  Central: shorter and closer
–  Peripheral: further and longer
–  Suture corneal component first
–  Suture depth at least 90%
•  Look for tenting of the DM

•  Conjunctival flaps
–  Indicated for
•  Chronic sterile epithelial ulcers
•  Closed but unstable corneal wounds
•  Painful bullous keratopathy
•  Phthisis for prosthesis
–  NOT indicated for
•  Infectious ulcers
•  Corneal perforations
•  Tectonic support for thin corneas

•  PKP
–  Full-thickness
–  For any corneal pathology
•  DSAEK/DSEK
–  Selective, posterior stroma-endothelium
–  For endothelial dystrophy, PBK, ICE or failed corneal
grafts
•  DALK
–  Selective, anterior stroma to epithelium
–  For KC, stromal dystrophy, anterior scars/opacities
•  DMEK
–  Selective, only Descemet and endothelium, no stroma

•  Group 1: excellent prognosis (90%)
–  Avascular, central location, healthy periphery
–  KC, central scars, lattice/granular dystrophy,
early Fuchs
•  Group 2: very good prognosis (80-90%)
–  Extending to periphery with less than 2
quadrants vascularity
–  Advanced Fuchs, PBK, herpetic, ICE, macular
dystrophy, IK

•  Group 3: fair prognosis (50-80%)
–  Extremes of corneal thickness, perforations,
active infections, inflammations
–  Active keratitis, CHED, young children, mild
chemical injury, moderate sicca
•  Group 4: poor prognosis (less than 50%)
–  Severe fibrovascularization, conjunctival
ischemia, advanced dry eye
–  Severe chemical/radiation injury, SJS, OCP,
congenital glaucoma, multiple graft failures

•  Control IOP prior to surgery
•  Donor cornea usually 0.25-0.5 mm larger
than host bed
–  For KC, use same size
•  Fleiringa ring to prevent collapse of scleral
shell, usually 2-3 mm larger than cornea
–  Aphakia, pseudophakia, planned lens
removal, pediatric, post-vitrectomized

•  Goal of suturing is watertight closure
•  Second cardinal suture is the most
important
•  Small leaks with a formed chamber will
close spontaneously
–  Leaks lasting for more than 3 days should be
resutured

•  Rejection rare in the first 2 weeks, but may
occur as late as 20 years after
•  Warning signs: decreased VA, redness,
pain
•  Endothelial rejection most common and
most devastating
–  Khodadoust line: inflammatory precipitates in
a linear and clumping fashion

Thank you and good luck!

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ED CORNEA OPEX REVIEW, SOJR-PGH Manila, 2014

ED CORNEA OPEX REVIEW, SOJR-PGH Manila, 2014

ED CORNEA OPEX REVIEW, SOJR-PGH Manila, 2014

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– Raised lesions of edema and inflammation

– If anchoring septae break, may produce giant

ED CORNEA OPEX REVIEW, SOJR-PGH Manila, 2014

of lymphocytic infiltration without a mononuclear

core (FUTI) scuring conjunctival blood vessels.

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ED CORNEA OPEX REVIEW, SOJR-PGH Manila, 2014

ED CORNEA OPEX REVIEW, SOJR-PGH Manila, 2014

ED CORNEA OPEX REVIEW, SOJR-PGH Manila, 2014

ED CORNEA OPEX REVIEW, SOJR-PGH Manila, 2014

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– Lid margin brush marks, inspissation,

posterior lid margin sign using lissamine

Figure 3-12 Meibom ian gland dysfunction.

ED CORNEA OPEX REVIEW, SOJR-PGH Manila, 2014

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ED CORNEA OPEX REVIEW, SOJR-PGH Manila, 2014

ED CORNEA OPEX REVIEW, SOJR-PGH Manila, 2014

ED CORNEA OPEX REVIEW, SOJR-PGH Manila, 2014

• Superior limbic keratoconjunctivitis (SLK)

– Mechanical trauma from upper eyelid on the

ED CORNEA OPEX REVIEW, SOJR-PGH Manila, 2014

ED CORNEA OPEX REVIEW, SOJR-PGH Manila, 2014

ED CORNEA OPEX REVIEW, SOJR-PGH Manila, 2014

ED CORNEA OPEX REVIEW, SOJR-PGH Manila, 2014

ED CORNEA OPEX REVIEW, SOJR-PGH Manila, 2014

ED CORNEA OPEX REVIEW, SOJR-PGH Manila, 2014

ED CORNEA OPEX REVIEW, SOJR-PGH Manila, 2014

ED CORNEA OPEX REVIEW, SOJR-PGH Manila, 2014

ED CORNEA OPEX REVIEW, SOJR-PGH Manila, 2014

ED CORNEA OPEX REVIEW, SOJR-PGH Manila, 2014

ED CORNEA OPEX REVIEW, SOJR-PGH Manila, 2014

• Follicular, preauricular lymph node, skin vesicles

• Always test for corneal hyposthesia tesy of James Chodosh, MD.)

ED CORNEA OPEX REVIEW, SOJR-PGH Manila, 2014

ED CORNEA OPEX REVIEW, SOJR-PGH Manila, 2014

ED CORNEA OPEX REVIEW, SOJR-PGH Manila, 2014

–  Raised lesions of edema and inflammation

–  If anchoring septae break, may produce giant

–  Lid margin brush marks, inspissation,

•  Superior limbic keratoconjunctivitis (SLK)

–  Mechanical trauma from upper eyelid on the

•  Follicular, preauricular lymph node, skin vesicles

•  Always test for corneal hyposthesia tesy of James Chodosh, MD.)

–  Mainly supportive corticosteroids, may speed resolution and prevent

–  1. Trachoma lucen t areas within pannus) .

•  Art line: linear scarring on superior tarsus

•  Herbert pits: limbal depressions from necrosed

•  Giant papillary conjunctivitis (GPC)

–  Neoplastic lymphoid proliferation of

–  Unilateral salmon pink mobile mass

–  Incisional biopsy needed, excisional if small

–  Local RT if confined to conj, systemic chemo if

•  Axenfeld anomaly: post embryotoxon + PAS

•  Axenfeld syndrome: + glaucoma

•  Axenfeld-Rieger anomaly: + iris hypoplasia,

•  Anomalies of the Cornea

–  Amyloid deposit, Congo red stain

–  Hyaline deposits, Masson trichome

–  Mucopolysacharide (or GAG) deposits, Alcian