(From Kaiser PK, Friedman NJ, Pineda II, R: Massachusetts Eye and Ear Infirmary Illustrated Manual of Ophthalmology, 2nd edn. Philadelphia, WB Saunders, 2004.)

Pathology

necrosis occurs from virally induced cytolysis, arteriolar and choriocapillaris occlusion; necrotic cells slough into vitreous, leaving large areas devoid of retina

FA

focal areas of choroidal hypoperfusion early; late staining

Treatment

acyclovir (IV × 5–10 days, then oral × 6 weeks; decreases risk of development of ARN in fellow eye by approximately 50%; ganciclovir is an alternative); oral steroids; aspirin to inhibit vascular thrombosis

Prognosis

watch fellow eye closely (usually develops ARN within 4 weeks)

65–90% develop rhegmatogenous RD (usually within 3 months)

Progressive Outer Retinal Necrosis (PORN)

Variant of ARN in AIDS but painless with minimal intraocular inflammation

Often have history of cutaneous zoster

74% unilateral at presentation, 70% become bilateral

Findings: multiple discrete peripheral or central areas of retinal opacification/infiltrates (deep with very rapid progression), ‘cracked mud’ appearance after resolution; vasculitis is not prominent (Figure 8-8)

Figure 8-8 Progressive outer retinal necrosis, early stage.

(From Hudson HL, Boyer DS, Martin DF, et al: Viral posterior uveitis. In Yanoff M, Duker JS [eds]: Ophthalmology, London, Mosby, 1999.)

Treatment: combination of foscarnet and ganciclovir; poor response to antivirals

Prognosis: 67% become NLP within 4 weeks; RD in 90%

Herpes Zoster

Uveitis typically develops during convalescence from acute Varicella infection

Reactivated uveitis (anterior and/or posterior), may have keratitis (epithelial or stromal)

May require chronic topical steroid treatment to prevent recurrence

Rubella

Sensorineural hearing loss, salt and pepper retinopathy; may develop cataract or glaucoma (rare to have both) (Figure 8-9)

Figure 8-9 Rubella retinopathy.

(Courtesy of George S. Novalis, MD. From Hudson HL, Boyer DS, Martin DF, et al: Viral posterior uveitis. In Yanoff M, Duker JS [eds]: Ophthalmology, London, Mosby, 1999.)

Vision and electrophysiologic testing are usually normal

Live virus in an infant is found in the lens, as well as conjunctival swab, pharyngeal swab, and urine cultures

Pneumocystis Choroiditis

Due to Pneumocystis carinii

Choroiditis with multifocal orange nummular lesions; lesions contain cysts of Pneumocystis carinii (Figure 8-10)

Figure 8-10 Multiple choroidal lesions in Pneumocystis choroiditis.

(From Cowan CL: Sarcoidosis. In Yanoff M, Duker JS [eds]: Ophthalmology, London, Mosby, 1999.)

Associated with use of inhaled pentamidine (which is prophylaxis for pulmonary Pneumocystis only)

Cysticercosis

Due to infection with pork tapeworm Taenia solium or T. saginata; humans are definitive host, pigs are intermediate host

Adult worm lives in small intestine; larvae travel to eye, producing cystic subretinal or intravitreal lesion (cysticercus)

Findings

mass lesion or exudative RD (Figure 8-11)

Figure 8-11 Cysticercus in the eye.

(From Cowan CL: Sarcoidosis. In Yanoff M, Duker JS [eds]: Ophthalmology, London, Mosby, 1999.)

Treatment

vitrectomy required for posterior segment disease

Diffuse Unilateral Subacute Neuroretinitis (DUSN)

Due to infection with small roundworm in subretinal space: dog hookworm (Ancylostoma caninum) or racoon nematode (Baylisascaris procyonis)

Findings

deep, gray-white retinal lesions; optic nerve swelling; vitreous cells; late findings include retinal vascular narrowing, diffuse RPE pigmentary changes, optic atrophy; results in unilateral ‘wipe-out’ syndrome

ERG

decreased

Treatment

laser nematode

Cat-Scratch Disease

Due to Bartonella henselae (also causes oculoglandular syndrome)

Findings

retinal granuloma or neuroretinitis

Treatment

oral antibiotics (doxycycline 100 mg bid, and rifampin 300 mg bid × 4–6 weeks)

Onchocerciasis (River Blindness)

Due to Onchocerca volvulus; larvae mature in humans, forming adult worms that live in fibrous, subcutaneous nodules (usually in joints); female worms (100 cm long, live for up to 20 years) and male worms (5 cm long, live for much shorter time) reproduce sexually, females give birth to ~2000 microfilariae/day; microfilariae (300 µm long, live for 1–2 years) migrate all over body by direct invasion and hematogenous spread, prefer skin and eyes; live microfilariae induce little or no inflammation; death of organism causes severe granulomatous inflammation and scarring

Transmitted by black fly: breeds along fast-moving streams; bites infected host and acquires microfilariae, which mature into infectious larvae; transmits larvae to humans with bite; 17 million infected; 1–2 million blind (Africa and Latin America)

Second leading cause of corneal blindness in world (trachoma is first)

Findings

intraocular microfilariae (in AC), anterior uveitis, SPK, sclerosing keratitis, scleritis, chorioretinitis, optic neuritis and atrophy; may develop cataract, PAS, and glaucoma (Figure 8-12)

Figure 8-12 Sclerosing keratitis as a result of onchocerciasis.

(Courtesy of Professor HR Taylor. From Cowan CL: Sarcoidosis. In Yanoff M, Duker JS [eds]: Ophthalmology, London, Mosby, 1999.)

Other findings

pruritus, pigmentary changes (leopard-skin appearance), chronic inflammation, scarring, maculopapular rash, subcutaneous nodules

Diagnosis

skin snip (place piece of skin in tissue media, 20–100 microfilariae emerge)

Treatment

ivermectin, suramin, diethylcarbamazine (DEC)

Propionibacterium Acnes

Gram-positive rod; anaerobic

May become sequestered in capsular bag following cataract surgery

Findings

delayed onset, chronic granulomatous uveitis, often with fibrin or hypopyon; white plaque on posterior capsule is characteristic

Treatment

intravitreal antibiotics (vancomycin, cephalosporins; resistant to aminoglycosides); usually also requires partial or total removal of capsular bag with/without IOL removal/exchange

Ophthalmomyiasis

Due to direct ocular invasion by fly larvae (maggots) that can invade AC, posterior segment, or subretinal space

Subretinal invasion

larvae travel through fundus, leaving criss-crossing tracks of atrophied RPE; death of organism causes ocular inflammation

Inflammations ( Table 8-1)

Acute Posterior Multifocal Placoid Pigment Epitheliopathy (APMPPE)

Occurs in young, healthy adults; female = male; usually bilateral

Table 8-1 White Dot Syndrome

Acute, self-limited; may be nonspecific choroidal hypersensitivity reaction

Possible HLA-B7 association

Associated with cerebral vasculitis

Flu-like prodrome (33%) followed by decreased vision

Findings

multiple creamy yellow-white plaque-like lesions (usually <1 DD) at level of RPE or choriocapillaris (possibly due to choroidal hypoperfusion); lesions fade over 2–6 weeks, leaving geographically shaped RPE changes (hypopigmentation and hyperpigmentation); may have vitreous cells, mild AC reaction; rarely vascular sheathing, disc edema, CNV (Figures 8-13)

Figure 8-13 Acute posterior multifocal placoid pigment epitheliopathy demonstrating multiple posterior pole lesions.

(From Kaiser PK, Friedman NJ, Pineda II R: Massachusetts Eye and Ear Infirmary Illustrated Manual of Ophthalmology, 2nd edn. Philadelphia, WB Saunders, 2004.)

Other findings

thyroiditis, erythema nodosum, cerebral vasculitis, regional enteritis

FA

initial blockage with late hyperfluorescence; window defects in old cases (Figures 8-14, 8-15)

Figure 8-14 Fluorescein angiogram of same patient as shown in Figure 8-13 demonstrating early hypofluorescence of the lesions.

(From Kaiser PK, Friedman NJ, Pineda II, R: Massachusetts Eye and Ear Infirmary Illustrated Manual of Ophthalmology, 2nd edn. Philadelphia, WB Saunders, 2004.)

Figure 8-15 Fluorescein angiogram of same patient as shown in Figure 8-14 demonstrating late staining of the lesions.

(From Kaiser PK, Friedman NJ, Pineda II, R: Massachusetts Eye and Ear Infirmary Illustrated Manual of Ophthalmology, 2nd edn. Philadelphia, WB Saunders, 2004.)

Treatment

none

Prognosis

vision recovers in most patients to >20/40; rarely recurs

Multiple Evanescent White Dot Syndrome (MEWDS)

Onset between age 14 and 50; female > male; unilateral > bilateral

Symptoms

decreased vision, dark spots in the periphery (peripheral scotomas), shimmering photopsias

Findings

granular retinal appearance with small (100–200 µm) white spots in posterior pole at level of RPE; may have vitreous cells, positive RAPD, mild optic disc swelling (Figure 8-16)

Figure 8-16 Multiple evanescent white dot syndrome demonstrating faint white spots.

(From Kaiser PK, Friedman NJ, Pineda II, R: Massachusetts Eye and Ear Infirmary Illustrated Manual of Ophthalmology, 2nd edn. Philadelphia, WB Saunders, 2004.)

VF

enlarged blind spot

FA

early hyperfluorescence in wreath-like configuration; late staining of lesions and optic nerve (Figure 8-17)

Figure 8-17 Same patient as shown in Figure 8–16 demonstrating early fluorescein angiogram appearance.

(From Kaiser PK, Friedman NJ, Pineda II, R: Massachusetts Eye and Ear Infirmary Illustrated Manual of Ophthalmology, 2nd edn. Philadelphia, WB Saunders, 2004.)

ERG

reduced a wave (involvement of RPE and outer retina)

Prognosis

vision recovers over weeks but may be permanently decreased due to pigmentary changes in fovea; 10% have recurrent episodes in same or fellow eye

Serpiginous Choroidopathy

Chronic, recurrent, indolent disease of unknown etiology

Onset between age 40–60; female = male; usually bilateral

Affects inner chorioretinal pigment epithelium

Symptoms

painless loss of vision

Findings

geographic (map-like) pattern of scars with active edges (yellow-gray, edematous), usually beginning in posterior pole (often extending from disc); active areas become atrophic over weeks to months; new lesions occur contiguously or elsewhere (often in snake-like pattern); may have mild AC reaction, vitritis, vascular sheathing, RPE detachment, NVD, CNV (rare) (Figure 8-18)

Figure 8-18 Fundus view of the right eye of a 57-year-old woman with early serpiginous choroiditis.

(From Moorthy RS, Jampol LM: Posterior uveitis of unknown cause. In Yanoff M, Duker JS [eds]: Ophthalmology, London, Mosby, 1999.)

VF

absolute scotomas corresponding to atrophic scars

FA

acute lesions stain

Treatment

may respond to oral steroids, immunosuppressive drugs

Prognosis

fair to poor; commonly recurs months to years later

Birdshot Choroidopathy (Vitiliginous Chorioretinitis)

Occurs after 4th decade of life; female > male; usually bilateral

Associated with HLA-A29 (90%)

Symptoms

decreased vision, nyctalopia, decreased color vision, peripheral visual field loss

Findings

cream-colored depigmented spots scattered throughout fundus; may have mild AC reaction, vitritis, retinal vasculitis, disc edema, optic atrophy, CME, epiretinal membrane, CNV (Figure 8-19)

Figure 8-19 Birdshot retinochoroidopathy.

(From Moorthy RS, Jampol LM: Posterior uveitis of unknown cause. In Yanoff M, Duker JS [eds]: Ophthalmology, London, Mosby, 1999.)

FA

pronounced perifoveal capillary leakage with CME

ERG

diminished scotopic response (rod dysfunction)

Punctate Inner Choroidopathy (PIC)

Onset between age 20 and 40; healthy, moderately myopic women

Symptoms

acute scotomas and photopsias

Findings

small (100–300 µm) yellow or gray inner choroidal lesions; resolve over weeks to form atrophic scars that may enlarge and become pigmented; new lesions do not appear; may have serous RDs; 40% risk of CNV; no AC or vitreous cells (Figure 8-21)

Figure 8-21 Punctate inner choroidopathy.

(From Moorthy RS, Jampol LM: Posterior uveitis of unknown cause. In Yanoff M, Duker JS [eds]: Ophthalmology, London, Mosby, 1999.)

Treatment

none

Acute Retinal Pigment Epitheliitis (Krill’s Disease)

Rare, occurs in young adults; usually unilateral

Symptoms

sudden decrease in vision

Findings

clusters of hyperpigmented spots (300–400 µm) in macula surrounded by yellow-white halos; with resolution, the spots lighten or darken, but halos remain; no vitritis (Figure 8-22)

Figure 8-22 Retinal pigment epitheliitis.

(From Moorthy RS, Jampol LM: Posterior uveitis of unknown cause. In Yanoff M, Duker JS [eds]: Ophthalmology, London, Mosby, 1999.)

DDx

central serous retinopathy, acute macular neuroretinopathy (wedge-shaped or cloverleaf dark red perifoveal dots; paracentral scotoma; normal ERG)

FA

blockage of spots with halos of hyperfluorescence

Treatment

none

Prognosis

resolves completely in 6–12 weeks

Frosted Branch Angiitis

White spots along retinal arterioles (Figure 8-23)

Figure 8-23 ‘Frosted branch angiitis’ secondary to cytomegalovirus retinitis.

(From Hudson HL, Boyer DS, Martin DF, et al: Viral posterior uveitis. In Yanoff M, Duker JS [eds]: Ophthalmology, London, Mosby, 1999.)

DDx: CMV retinitis, toxoplasmosis (Kyrieleis’ plaques)

Endophthalmitis

Inflammation involving 1 or more coats of the eye and adjacent ocular cavities

Etiology

infectious or sterile; must rule out infection

Symptoms

pain, decreased vision

Findings

lid edema, chemosis, AC reaction, hypopyon (pink hypopyon = Serratia), vitritis

Classification

Acute postoperative (<6 weeks after surgery; 90% in 1st week):

RISK FACTORS: blepharitis, wound leak, iris prolapse, vitreous loss, contaminated IOL, diabetes, chronic alcoholism

ORGANISMS: S. epidermidis, S. aureus, Streptococci, Pseudomonas

INCIDENCE:

Extracapsular extraction (ECCE) or intracapsular cataract extraction (ICCE) (with or without IOL): 0.072%

Secondary IOL: 0.3%

PPV: 0.51%

PK: 0.11%

Glaucoma filter: 0.061% (Streptococcus [Enterococcus] faecalis, Streptococci [57%], H. influenzae [23%])

PREVENTION:

TREAT BLEPHARITIS: 85% of responsible organisms (S. epidermidis and S. aureus) are found on lids; hot compresses, lid hygiene, Polysporin ointment × 1 week preop; add doxycycline 100 mg bid × 1 week for acne rosacea or seborrheic dermatitis

STERILIZE OPERATIVE FIELD: 5% povidine iodine (Betadine); preoperative topical antibiotics (fluoroquinolone)

AVOID INOCULATION: drape eyelashes

ANTIBIOTICS: intracameral (injection or in irrigating solution); topical preop for 1–3 days and postop for 7–10 days; consider subconjunctival antibiotics with broken posterior capsule or vitreous loss

Delayed postoperative:

Propionibacterium acnes (anaerobic gram + rod) or fungal

Trauma:

Incidence of 2%–7% after penetrating trauma

RISK FACTORS: retained intraocular FB, delayed surgery (>24 hours), rural setting (soil contamination), and disruption of the crystalline lens

25% CULTURE POSITIVE: Bacillus (30%), S. epidermidis (25%), Streptococci (13%), S. aureus (8%), Gram-negative and mixed flora

Poor visual outcome

Endogenous:

RISK FACTORS: immunosuppression, indwelling venous catheters, IVDA, following intra-abdominal surgery

30% of patients with Candida septicemia develop endophthalmitis

Sterile: culture negative

Treatment

rule out infection (AC and vitreous taps)

Intravitreal antibiotics: vancomycin 1 mg/0.1 mL, ceftazidime 2.25 mg/0.1 mL (consider intravitreal dexamethasone 400 µg/0.1 mL)

Systemic antibiotics: in severe cases, most traumatic cases, and endogenous bacterial cases; vancomycin 1 g IV q12 hours or cefazolin 1 g IV q8 hours; ceftazidime 1 g IV q12 hours

Topical fortified antibiotics: vancomycin 25–50 mg/mL, ceftazidime 50 mg/mL q1 hour

Topical steroids and cycloplegics

Major Clinical Study

Endophthalmitis Vitrectomy Study (EVS)

Objective: to evaluate the treatment of acute (<6 weeks) postoperative (cataract or secondary IOL surgery) endophthalmitis with immediate vitrectomy vs ‘tap and inject,’ and whether intravenous antibiotics (ceftazidime and amikacin) are necessary

Methods: patients with clinical evidence of acute (<6 weeks) postoperative (cataract or secondary IOL surgery) endophthalmitis and visual acuity of LP or better, and sufficient clarity to see at least some part of the iris were randomly assigned to emergent AC and vitreous taps alone or with vitrectomy and with injection of intravitreal antibiotics (0.4 mg amikacin and 1.0 mg vancomycin). Patients were also given subconjunctival injections of antibiotics (25 mg vancomycin, 100 mg ceftazidime, and steroid [6 mg dexamethasone phosphate]), topical fortified antibiotics (50 mg/mL vancomycin and 20 mg/mL amikacin) and steroid (prednisolone acetate), and oral steroid (prednisone 30 mg bid × 5–10 days). Patients were also randomly assigned to receive systemic IV antibiotics (2 g ceftazidime IV q8h and 7.5 mg/kg amikacin IV followed by 6 mg/kg q12h) or no systemic antibiotics. Intravitreal steroids were not used

Results

420 patients enrolled

On average, signs and symptoms occurred 6 days after surgery (75% presented within 2 weeks of surgery)

69% had positive cultures; 94% were Gram-positive bacteria (70% coagulase-negative Staphylococcus, 10% S. aureus, 9% Streptococci species)

IV antibiotics were of no benefit

Immediate vitrectomy had significant benefits only when patients presented with light perception vision or worse

Conclusions

For endopthalmitis after cataract or secondary IOL surgery, perform emergent treatment with AC tap and injection of intravitreal antibiotics when vision is better than LP

Vitrectomy should be reserved for patients presenting with light perception vision or worse

IV antibiotics do not improve the outcome

Panuveitis

Sarcoidosis

Multisystem granulomatous disease characterized by noncaseating granulomas; unknown etiology

Females > males; more common among African Americans (10 : 1)

25–50% have systemic sarcoidosis

Ocular disease: 30% unilateral, 70% bilateral; 40% acute, 60% chronic

Findings (25–30%)

uveitis in 60% of patients with ocular involvement; 66% of uveitis is anterior (2 forms: acute granulomatous [responds well to corticosteroids] and chronic recurrent [difficult to control with corticosteroids]), KP, iris nodules, lacrimal gland infiltration (25%; painless bilateral enlargement), conjunctival follicles, keratoconjunctivitis sicca, episcleritis and scleritis with nodules, choroiditis with yellow or white nodules, retinal periphlebitis with candlewax drippings (granulomas along retinal venules), pars planitis, vitritis, retinal neovascularization, optic nerve granuloma; secondary cataracts, glaucoma, and band keratopathy

Pathology

noncaseating granulomas (caseating granulomas occur in TB) with Langhans’ multinucleated giant cells (Figure 8-24)

Figure 8-24 Sarcoidosis demonstrating conjunctival granuloma with giant cells surrounded by lymphocytes and plasma cells.

(From Yanoff M, Fine BS: Ocular Pathology, 5th edn, St Louis, Mosby, 2002.)

Diagnosis

Lab tests: angiotensin-converting enzyme (ACE; elevated in any diffuse granulomatous disease affecting the lung), serum lysozyme (more sensitive than ACE, but less specific)

Chest X-ray or chest CT: hilar adenopathy (Figure 8-25)

Gallium scan: look for parotid, lacrimal, or pulmonary involvement

Biopsy: skin lesion, conjunctival nodule, lymph node, salivary or lacrimal gland, lung; if elevated ACE and positive CXR, 60–70% of blind conjunctival biopsies will be positive

Figure 8-25 Bilateral hilar adenopathy in a patient without pulmonary symptoms.

(From Cowan CL: Sarcoidosis. In Yanoff M, Duker JS [eds]: Ophthalmology, London, Mosby, 1999.)

Treatment

topical, periocular, and systemic steroids, immunosuppressive therapy

Lofgren’s Syndrome

Hilar lymphadenopathy, erythema nodosum, anterior uveitis, arthralgia

Mikulicz’s Syndrome

Lacrimal and parotid gland swelling, sicca syndrome

Etiology

sarcoidosis, TB, lymphoma/leukemia

Heerfordt’s Syndrome

Fever, parotid gland enlargement, anterior uveitis, facial nerve palsy

Behçet’s Disease

Chronic recurrent multisystem condition characterized by relapsing inflammation and occlusive vasculitis

Triad of oral ulcers, genital ulcers, and inflammatory eye disease

Associated with HLA-B51; males > females, usually young adults; more common in Japan and Mediterranean countries

Findings (75%)

recurrent, explosive inflammatory episodes with active episodes lasting 2–4 weeks

Uveitis (posterior more common than anterior); can present with nongranulomatous anterior uveitis (usually bilateral; may have transient hypopyon); occasionally, conjunctivitis, episcleritis, or keratitis can occur; posterior involvement with recurrent vascular occlusions, retinal hemorrhages, exudates, CME, vitritis, traction RD, ischemic optic neuropathy; may develop glaucoma and cataract (Figure 8-26)

Figure 8-26 Fundus view of a patient who has Behçet’s disease.

(From Yanoff M, Fine BS: Ocular Pathology, 5th edn, St Louis, Mosby, 2002.)

Other findings

oral (aphthous) ulcers, genital ulcers, skin lesions (erythema nodosum, acne-like lesions, folliculitis), arthritis (50%; especially wrists and ankles), thrombophlebitis, large vessel occlusion; GI pain, diarrhea, constipation; CNS involvement (25%; meningoencephalitis, strokes, palsies, confusional states)

Pathology

obliterative vasculitis with activation of both cellular and humoral limbs of immune system; circulating immune complexes in >50%

Diagnosis

Clinical: (see Box 8-2)

Behcetine skin test (cutaneous hypersensitivity): intradermal puncture; positive test = pustule formation within minutes

HLA-B51

Treatment

systemic steroids, cytotoxic agents (chlorambucil most effective for retinal vasculitis, meningoencephalitis), colchicine (prevents recurrences), cyclosporine (ciclosporin); plasmapheresis

Vogt-Koyanagi-Harada Syndrome (VKH)

Uveoencephalitis: bilateral diffuse granulomatous panuveitis, serous RDs, disc edema, meningeal irritation, skin pigmentary changes, and auditory disturbance

Harada’s disease

if only eye findings

Presumed autoimmune process against melanocytes

Typically occurs in Asians, American Indians, and Hispanics between ages 30 and 50 years; female > male

Associated with HLA-DR4

Symptoms

decreased vision, pain, redness, photophobia, stiff neck, headache, deafness, tinnitus, vertigo

Findings

bilateral diffuse granulomatous panuveitis, serous RDs, vitritis, exudative choroiditis, CB detachment, CME, ON hyperemia and edema, poliosis; later develop perilimbal vitiligo (Sugiura’s sign), Dalen-Fuchs nodules (yellow-white retinal spots), sunset fundus (RPE disturbance with focal areas of atrophy and hyperpigmentation [healing phase])

Other findings

temporary deafness, tinnitis, vertigo, meningeal irritation, skin changes (30%; alopecia, vitiligo, poliosis)

Clinical course

Prodrome: headache, meningismus, seizures, bilateral decreased vision with pain, redness, photophobia

Syndrome: uveitis with serous RDs

Chronic stage: sunset fundus, Dalen-Fuchs nodules, perilimbal vitiligo

Recurrent stage: AC reaction, pigment changes; 60% retain vision >20/30

Pathology

inflammation of choriocapillaris and retina; Dalen-Fuchs nodules (epithelioid cells between Bruch’s membrane and RPE) (Figure 8-27)

Figure 8-27 VKH demonstrating granulomatous inflammation in choroid extending into choriocapillaris and through RPE.

(From Yanoff M, Fine BS: Ocular Pathology, 5th edn, St Louis, Mosby, 2002.)

DDx

sympathetic ophthalmia, posterior scleritis, syphilis, lupus choroiditis, hypotony, uveal effusion syndrome

Diagnosis

LP: CSF pleocytosis

FA: multiple focal areas of subretinal leakage (‘1000 points of light’)

Treatment

steroids (6 months), cycloplegic, immunosuppressive agents

Prognosis

60% retain vision >20/30

Complications

cataracts (25%), glaucoma (33%), CNV (10%)

Sympathetic Ophthalmia

Bilateral granulomatous panuveitis following penetrating eye trauma

Due to immune sensitization to melanin or melanin-associated proteins in uveal tissues; T-cell mediated (delayed hypersensitivity reaction); latency of 10 days to 50 years after injury

Incidence: 0.1–0.3% of penetrating injuries; 0.015% of intraocular surgery

Findings

Koeppe nodules, mutton fat KP, retinal edema, Dalen-Fuchs nodules; may have disc edema (Figure 8-28)

Figure 8-28 Dalen-Fuchs nodules in a patient with sympathetic ophthalmia.

(From Kaiser PK, Friedman NJ, Pineda II, R: Massachusetts Eye and Ear Infirmary Illustrated Manual of Ophthalmology, 2nd edn, Philadelphia, WB Saunders, 2004.)