Sympathetic ophthalmia

Uvea

Key Points

•Sympathetic ophthalmia is clinically and histopathologically identical to VKH disease — the sole distinguishing criterion is history of penetrating ocular trauma or surgery
•Risk after penetrating ocular trauma: 0.2–0.5%; after intraocular surgery: 0.01–0.03%. 80% of cases occur within 3 months of injury; 90% within 1 year
•Dalen-Fuchs nodules (epithelioid cells between Bruch's membrane and RPE) are characteristic (present in ~25–35% of cases; also seen in VKH); the choriocapillaris is classically spared on histopathology
•Enucleation of the exciting eye AFTER sympathetic ophthalmia develops does NOT alter the course of disease — the autoimmune response is already systemic
•Early aggressive immunosuppression with high-dose steroids + IMT within 2 weeks is essential; 60–70% of sympathizing eyes maintain ≥6/12 with early treatment

1. Definition

A rare, bilateral, diffuse, granulomatous panuveitis that occurs following penetrating trauma or surgical violation of one eye (the exciting eye), subsequently affecting the fellow non-injured eye (the sympathizing eye). It is a T-cell mediated autoimmune response against uveal/retinal melanocyte antigens exposed by the initial injury — clinically and histopathologically identical to VKH disease, distinguished only by the history of penetrating trauma or surgery.

2. Epidemiology

Incidence: approximately 0.03 per 100,000 per year. Risk after penetrating ocular trauma: 0.2–0.5%. Risk after intraocular surgery: 0.01–0.03% (much lower than trauma). Risk is highest after vitreoretinal surgery, particularly with uveal prolapse or multiple procedures. No racial predilection (unlike VKH). Males slightly more affected due to higher trauma incidence. Can occur at any age; mean onset 25–45 years. Onset timing: 80% occur within 3 months of injury; 90% within 1 year. Earliest reported onset: 5 days post-injury. Can occur years to decades after the inciting event (Nussenblatt & Whitcup, Uveitis, 4th Ed).

3. Aetiology and causes

Penetrating ocular trauma (most common cause, ~60–70% of cases) — especially injuries involving uveal tissue prolapse or incarceration in the wound.

Intraocular surgery (~30%): especially vitreoretinal surgery, secondary IOL procedures, cyclodestructive procedures (cyclocryotherapy, transscleral diode laser).

Mechanism: Disruption of ocular immune privilege exposes sequestered melanocyte-associated antigens — tyrosinase, TRP1, TRP2, S-antigen, IRBP (interphotoreceptor retinoid-binding protein) — to the systemic immune system. The immune system, never having been tolerized to these antigens, mounts a T-cell mediated autoimmune attack targeting melanocytes in both eyes.

4. Pathogenesis

Penetrating injury disrupts the blood-ocular barrier and allows sequestered uveal/retinal antigens to reach regional (cervical/preauricular) lymph nodes.
Antigen-presenting cells (dendritic cells, macrophages) process melanocyte-derived peptides and present them to naive CD4+ T cells via MHC class II molecules (HLA-DR4, HLA-DRB1*0405).
Sensitized Th1 and Th17 cells recognize melanocyte antigens systemically, and traffic to the uveal tracts of BOTH eyes via hematogenous spread.
Granulomatous choroidal inflammation develops: diffuse lymphocytic and epithelioid cell infiltration of the choroid.
Dalen-Fuchs nodules (collections of epithelioid cells and RPE cells between Bruch's membrane and the RPE) form in the mid-periphery — characteristic finding (present in ~25–35% of cases; also seen in VKH).
The choriocapillaris is classically spared (unlike many other choroiditides) — key histopathological feature (focal involvement may occur in severe cases).
Retinal involvement is minimal compared to choroidal involvement (retinal sparing is characteristic).

5. Classification

Clinical classification:

Anterior form — predominantly granulomatous anterior uveitis (less common presentation)
Posterior/diffuse form — diffuse choroiditis with exudative retinal detachments (classic presentation)
Mixed/panuveitis form — combined anterior and posterior involvement (most typical in practice)

Histopathological classification:

Non-necrotizing diffuse granulomatous uveal inflammation
Dalen-Fuchs nodules present (between RPE and Bruch's membrane)
Choriocapillaris spared (key feature)
Retinal sparing (inflammation confined to uveal tract)

Timing of onset after inciting event:

Early: <2 weeks (rare, <1% of cases)
Typical: 2 weeks to 3 months
Classic window: within 3 months (80% of cases); within 1 year (90%)
Late: >1 year (up to decades later)

6. Risk factors and associations

Penetrating ocular trauma with uveal prolapse or incarceration in wound (greatest risk)
Retained intraocular foreign body (IOFB)
Multiple intraocular surgeries
Vitreoretinal surgery (higher risk than anterior segment surgery)
Cyclodestructive procedures (cyclocryotherapy, transscleral diode laser)
Delayed primary repair (>24 hours post-trauma)
Wound dehiscence with uveal incarceration
HLA-DR4 and HLA-DRB1*0405 association (same genetic predisposition as VKH)
No association with blunt (non-penetrating) trauma
Enucleation performed within 10–14 days of injury was historically considered protective — now debated

7. Clinical features

Exciting eye: history of penetrating trauma or surgery; may show chronic inflammation, phthisis bulbi, or active granulomatous uveitis.

Sympathizing eye (fellow eye) — key diagnostic findings:

Bilateral granulomatous anterior uveitis: mutton-fat KPs, posterior synechiae
Anterior chamber cells and flare
Iris thickening with Koeppe and Busacca nodules
Moderate to severe vitritis
Dalen-Fuchs nodules: small, round, yellow-white lesions at RPE level (mid-periphery > posterior pole) — characteristic (present in ~25–35% of cases)
Multifocal serous/exudative retinal detachments (bilateral)
Choroidal thickening (diffuse)
Optic disc edema and hyperemia
Sunset-glow fundus (chronic phase — diffuse choroidal depigmentation similar to VKH)
Peripapillary atrophy

Systemic findings (uncommon — unlike VKH):

Vitiligo, poliosis, alopecia (rarely; same integumentary features as VKH)
Meningismus and CSF lymphocytic pleocytosis (rarely)
Sensorineural hearing loss / dysacusis (rarely)

8. Investigations

Ophthalmic imaging:

FFA: multiple pinpoint hyperfluorescent leakage points at RPE level (similar to VKH), disc leakage, pooling in serous RDs — 'starry sky' pattern
ICGA: multiple hypofluorescent dark dots (choroidal granulomata), more sensitive than FFA for detecting choroidal lesions
OCT/EDI-OCT: subretinal fluid, choroidal thickening (>400 µm acutely), RPE undulations, Dalen-Fuchs nodule imaging
B-scan ultrasonography: diffuse choroidal thickening, serous RD, no posterior scleral T-sign (unlike posterior scleritis)

Laboratory (to exclude mimics):

No specific serological marker for sympathetic ophthalmia
HLA-DR4 typing (supportive)
Rule out: FTA-ABS/RPR (syphilis), QuantiFERON-TB Gold (ocular TB), ACE/lysozyme (sarcoidosis), chest X-ray

Histopathology (of enucleated exciting eye — gold standard for definitive diagnosis):

Diffuse non-necrotizing granulomatous choroidal inflammation
Dalen-Fuchs nodules between RPE and Bruch's membrane
Epithelioid cells, multinucleated giant cells, lymphocytes
Choriocapillaris spared
No retinal necrosis

Clinical diagnosis is based on: history of penetrating trauma/surgery + bilateral granulomatous panuveitis in the sympathizing eye.

9. Differential diagnosis

Vogt-Koyanagi-Harada disease — identical clinical and histopathological features; distinguished ONLY by the absence of prior penetrating trauma or surgery in VKH
Sarcoid panuveitis — bilateral granulomatous panuveitis, but with systemic features (hilar lymphadenopathy, skin lesions, elevated ACE) and no trauma history; non-caseating granulomata on biopsy
Phacoanaphylactic uveitis — granulomatous inflammation centered around lens material; zonal pattern on histology; follows lens disruption
Syphilitic panuveitis — bilateral granulomatous uveitis; positive serology (FTA-ABS, VDRL/RPR)
Tubercular panuveitis — bilateral choroidal granulomata; positive QuantiFERON-TB/Mantoux; caseating granulomata on biopsy
Endogenous endophthalmitis — bilateral in rare disseminated cases; associated systemic sepsis/immunosuppression; positive cultures

10. Complications

Cataract (most common, ~50–70%, from chronic inflammation and steroid use)
Secondary glaucoma (~25–40%, from synechial angle closure, pupillary block, or steroid-induced IOP elevation)
CME (~20–30%, significant cause of visual morbidity)
Subretinal fibrosis (~10–20%)
Choroidal neovascularization (~10%, sub-foveal CNV carries worst visual prognosis)
Exudative retinal detachment (acute phase)
Optic atrophy (from chronic disc inflammation)
Band keratopathy (calcium deposition from chronic inflammation)
Phthisis bulbi of exciting eye
Chronic hypotony
Sunset-glow fundus (chronic depigmentation, similar to VKH)
Seclusion/occlusion of pupil

11. Management

Prevention (primary):

Primary wound repair within 24 hours of penetrating injury with repositioning of prolapsed uveal tissue
Enucleation of a traumatized blind (NLP) eye within 10–14 days of injury was historically recommended — now increasingly debated; modern aggressive immunosuppression has reduced urgency. After sympathetic ophthalmia develops, enucleation of the exciting eye does NOT improve outcomes in the sympathizing eye.

Medical management — early aggressive immunosuppression:

IV methylprednisolone 1 g/day x 3 days (pulse therapy) for acute/severe disease
Oral prednisolone 1–1.5 mg/kg/day — very slow taper over minimum 12–18 months
Maintain prednisolone ≥10 mg/day for at least 3–6 months; rapid taper causes high recurrence rate

Steroid-sparing IMT (recommended early, within 2 weeks of diagnosis):

Cyclosporine 3–5 mg/kg/day (often first-line IMT)
Mycophenolate mofetil 1–2 g/day
Azathioprine 2–3 mg/kg/day
Methotrexate 15–25 mg/week (with folic acid supplementation)

Biologics (refractory disease):

Adalimumab 40 mg SC every 2 weeks (VISUAL I/II trials — established for non-infectious uveitis)
Infliximab 5 mg/kg IV at 0, 2, 6 weeks then every 8 weeks

Local therapy:

Topical prednisolone acetate 1% for anterior segment
Atropine 1% TID (cycloplegia, synechiae prevention)
Intravitreal anti-VEGF (ranibizumab, bevacizumab) for CNV
Intravitreal dexamethasone implant (Ozurdex 0.7 mg) for refractory CME

12. Prognosis

With modern aggressive immunosuppression, visual prognosis has significantly improved. Approximately 60–70% of sympathizing eyes maintain VA ≥6/12 with early treatment. Exciting eye prognosis depends on severity of initial trauma.

Poor prognostic factors: delayed diagnosis, inadequate immunosuppression, recurrent inflammation, CME, subretinal fibrosis, subfoveal CNV, sunset-glow fundus (indicates chronicity).

Recurrence rate: 40–60% with steroid monotherapy; significantly reduced with early IMT. Treatment is often required for years to decades; many patients need lifelong low-dose IMT.

The condition can recur even years after apparent quiescence — long-term ophthalmological follow-up is mandatory.

Clinical Pearls

Sympathetic ophthalmia and VKH are clinically and histopathologically IDENTICAL — the distinguishing feature is history of penetrating ocular trauma or surgery in sympathetic ophthalmia.

The minimum latent period between injury and onset is classically 5 days (earliest reported) — the immune system needs time to mount a response against newly exposed uveal antigens.

Enucleation of the exciting eye AFTER sympathetic ophthalmia has developed does NOT alter the course of disease in the sympathizing eye — the autoimmune response is already systemic.

Dalen-Fuchs nodules (yellow-white nodules at the RPE level in the mid-periphery) are characteristic of sympathetic ophthalmia and VKH (present in ~25–35% of cases) — they represent epithelioid cells between RPE and Bruch's membrane.

The choriocapillaris is characteristically spared in sympathetic ophthalmia — this distinguishes it histopathologically from most other granulomatous choroiditides.

ICGA is more sensitive than FFA for detecting choroidal granulomata — the hypofluorescent dark dots represent granulomata invisible on FFA or clinical exam.

Exam trap — Timing of SO: Sympathetic ophthalmia can occur as early as 5 days and as late as 66 years after penetrating injury, but 80% occur within 3 months and 90% within 1 year. The classic teaching of '2 weeks to 3 months' is the most common window but NOT the only window. Lifelong vigilance is needed.

Exam trap — Enucleation timing: Prophylactic enucleation of the exciting eye should ideally be performed within 14 days of injury if the eye has no visual potential. Once SO has developed, enucleation is controversial — some evidence suggests it may NOT alter the course of established SO, but many experts still recommend it if the exciting eye has no useful vision.

Exam trap — SO does NOT occur after evisceration: Enucleation removes the entire globe (removes all uveal tissue). Evisceration removes intraocular contents but leaves the scleral shell. Traditionally, evisceration was thought to carry a higher SO risk (residual uveal tissue), but modern evidence shows SO after evisceration is exceedingly rare and the risk is comparable to enucleation.

Oral-exam questions

What is the only clinical feature that distinguishes sympathetic ophthalmia from VKH disease? — History of penetrating ocular trauma or surgery (the exciting eye). Histopathologically, both are indistinguishable (Nussenblatt & Whitcup, Uveitis, 4th Ed).
What is the minimum latent period before sympathetic ophthalmia can develop? — 5 days post-injury. Onset within the first 2 weeks is rare (<1% of cases); 80% occur within 3 months; 90% within 1 year.
Name the characteristic histopathological finding — Dalen-Fuchs nodules: collections of epithelioid cells between Bruch's membrane and the RPE, in the mid-periphery (present in ~25–35% of cases). The choriocapillaris is classically spared — another key histopathological feature.
Does enucleating the exciting eye after sympathetic ophthalmia develops help the sympathizing eye? — No. Once the autoimmune response is systemic, removing the exciting eye does NOT alter the course of disease in the sympathizing eye. Enucleation is now rarely performed and is limited to a blind, painful exciting eye.
Which IGRA test is most useful to exclude TB as a mimic? — QuantiFERON-TB Gold Plus — preferred over Mantoux (TST) in BCG-vaccinated populations due to higher specificity for M. tuberculosis-specific antigens (ESAT-6, CFP-10).
What trial evidence supports biologic use in sympathetic ophthalmia? — VISUAL I and VISUAL II trials established adalimumab (anti-TNF-α) for non-infectious intermediate, posterior, and panuveitis. VISUAL I: HR 0.50 (50% reduction in treatment failure risk; median time to failure 24 weeks vs 13 weeks). VISUAL II: treatment failure 39% adalimumab vs 55% placebo during steroid taper.
What is the minimum duration of immunosuppression in sympathetic ophthalmia? — Prednisolone taper over minimum 12–18 months; maintain ≥10 mg/day for at least 3–6 months. Rapid taper is the most common cause of recurrence (40–60% recurrence with steroid monotherapy).
What is the pathological hallmark of sympathetic ophthalmia? — Diffuse granulomatous inflammation of the entire uveal tract with non-caseating granulomas, epithelioid cells, and Dalen-Fuchs nodules (collections of epithelioid cells between Bruch's membrane and RPE). The choriocapillaris is typically spared (unlike VKH where it may be involved). The absence of choriocapillaris involvement is a classic histopathological differentiator.
Can sympathetic ophthalmia occur after vitreoretinal surgery? — Yes, rarely. SO has been reported after PPV, scleral buckling, and even after repeated intravitreal injections (extremely rare). Any procedure that violates the uveal tissue theoretically carries risk. The incidence after PPV is estimated at 0.01–0.03%. Patients should be counseled about this remote risk.

Mnemonics

PETS

P — Penetrating trauma (exciting eye) E — Exciting eye → Sympathizing eye (bilateral) T — T-cell mediated (CD4+ Th1) S — Same as VKH histopathologically (Dalen-Fuchs nodules, choriocapillaris spared)

DALES

D — Dalen-Fuchs nodules (characteristic) A — Autoimmune (T-cell, against melanocyte antigens) L — Latent period ≥5 days (minimum onset) E — Exciting eye (penetrating trauma/surgery site) S — Sympathizing eye (fellow, uninjured eye — the one that matters clinically)

Comparison Tables

Sympathetic Ophthalmia vs VKH Disease — Key Distinguishing Features

Sympathetic Ophthalmia vs VKH Disease — Key Distinguishing Features
Feature	Sympathetic Ophthalmia	VKH Disease
Etiology	Penetrating ocular trauma or surgery	Autoimmune — no trauma history
Exciting eye	Present (injured eye)	Not applicable
Racial predilection	None	Asians, Hispanics, South Asians, Native Americans
Histopathology	Non-necrotizing granulomatous choroiditis; Dalen-Fuchs nodules; choriocapillaris spared	IDENTICAL — indistinguishable on biopsy
Integumentary changes	Rare (vitiligo, poliosis uncommon)	Common — vitiligo, poliosis, alopecia in convalescent phase
Neurological features	Very rare	Meningismus, CSF pleocytosis in ~80% within first 2 weeks
Sugiura sign	Not described	Characteristic (perilimbal vitiligo)
HLA association	HLA-DR4, DRB1*0405	HLA-DRB1*0405 (stronger; OR ~10)
Treatment	Aggressive steroids + IMT	Aggressive steroids + IMT (identical)

Etiology

Sympathetic Ophthalmia: Penetrating ocular trauma or surgery
VKH Disease: Autoimmune — no trauma history

Exciting eye

Sympathetic Ophthalmia: Present (injured eye)
VKH Disease: Not applicable

Racial predilection

Sympathetic Ophthalmia: None
VKH Disease: Asians, Hispanics, South Asians, Native Americans

Histopathology

Sympathetic Ophthalmia: Non-necrotizing granulomatous choroiditis; Dalen-Fuchs nodules; choriocapillaris spared
VKH Disease: IDENTICAL — indistinguishable on biopsy

Integumentary changes

Sympathetic Ophthalmia: Rare (vitiligo, poliosis uncommon)
VKH Disease: Common — vitiligo, poliosis, alopecia in convalescent phase

Neurological features

Sympathetic Ophthalmia: Very rare
VKH Disease: Meningismus, CSF pleocytosis in ~80% within first 2 weeks

Sugiura sign

Sympathetic Ophthalmia: Not described
VKH Disease: Characteristic (perilimbal vitiligo)

HLA association

Sympathetic Ophthalmia: HLA-DR4, DRB1*0405
VKH Disease: HLA-DRB1*0405 (stronger; OR ~10)

Treatment

Sympathetic Ophthalmia: Aggressive steroids + IMT
VKH Disease: Aggressive steroids + IMT (identical)

Steroid-Sparing Immunosuppressive Agents in Sympathetic Ophthalmia

Steroid-Sparing Immunosuppressive Agents in Sympathetic Ophthalmia
Agent	Dose	Key Monitoring	Advantages	Main Risk
Cyclosporine	3–5 mg/kg/day PO	Renal function, BP, trough levels	Rapid onset, effective	Nephrotoxicity, hypertension
Mycophenolate mofetil	1–2 g/day PO	CBC, LFT	Well-tolerated, evidence from FIRST trial	GI side effects, teratogen
Azathioprine	2–3 mg/kg/day PO	CBC (check TPMT first), LFT	Long safety record	Myelosuppression, lymphoma risk
Methotrexate	15–25 mg/week PO/SC	CBC, LFT, renal function	Inexpensive, dual uveitis/arthritis use	Hepatotoxicity, pneumonitis
Adalimumab	40 mg SC q2w	Latent TB screen, CBC	Biologic, strong evidence (VISUAL I/II)	Infection, TB reactivation, cost

Cyclosporine

Dose: 3–5 mg/kg/day PO
Key Monitoring: Renal function, BP, trough levels
Advantages: Rapid onset, effective
Main Risk: Nephrotoxicity, hypertension

Mycophenolate mofetil

Dose: 1–2 g/day PO
Key Monitoring: CBC, LFT
Advantages: Well-tolerated, evidence from FIRST trial
Main Risk: GI side effects, teratogen

Azathioprine

Dose: 2–3 mg/kg/day PO
Key Monitoring: CBC (check TPMT first), LFT
Advantages: Long safety record
Main Risk: Myelosuppression, lymphoma risk

Methotrexate

Dose: 15–25 mg/week PO/SC
Key Monitoring: CBC, LFT, renal function
Advantages: Inexpensive, dual uveitis/arthritis use
Main Risk: Hepatotoxicity, pneumonitis

Adalimumab

Dose: 40 mg SC q2w
Key Monitoring: Latent TB screen, CBC
Advantages: Biologic, strong evidence (VISUAL I/II)
Main Risk: Infection, TB reactivation, cost

Timing of Key Events in Sympathetic Ophthalmia

Timing of Key Events in Sympathetic Ophthalmia
Event	Timeframe	Clinical Implication
Earliest possible onset	≥5 days post-injury	Below 5 days — reconsider diagnosis
Highest-risk period (80% of cases)	Within 3 months of injury	Monitor sympathizing eye closely; 90% present within 1 year
Historical enucleation window	Within 10–14 days of injury	Historically protective; now debated with modern IMT
IMT initiation target	Within 2 weeks of diagnosis	Early IMT significantly improves visual outcomes
Minimum steroid taper duration	12–18 months	Rapid taper = high recurrence
Recurrence window	Years to decades	Long-term follow-up mandatory

Earliest possible onset

Timeframe: ≥5 days post-injury
Clinical Implication: Below 5 days — reconsider diagnosis

Highest-risk period (80% of cases)

Timeframe: Within 3 months of injury
Clinical Implication: Monitor sympathizing eye closely; 90% present within 1 year

Historical enucleation window

Timeframe: Within 10–14 days of injury
Clinical Implication: Historically protective; now debated with modern IMT

IMT initiation target

Timeframe: Within 2 weeks of diagnosis
Clinical Implication: Early IMT significantly improves visual outcomes

Minimum steroid taper duration

Timeframe: 12–18 months
Clinical Implication: Rapid taper = high recurrence

Recurrence window

Timeframe: Years to decades
Clinical Implication: Long-term follow-up mandatory

Imaging Findings in Sympathetic Ophthalmia

Imaging Findings in Sympathetic Ophthalmia
Modality	Acute Phase Findings	Chronic Phase Findings	Clinical Use
FFA	Pinpoint RPE leaks, 'starry sky', disc leakage, pooling in serous RD	Window defects, RPE atrophy, CNV leakage	Diagnosis, monitoring exudation
ICGA	Multiple hypofluorescent dark dots (granulomata), fuzzy choroidal vessels	Persistent dark dots in treated choroidal scars	Most sensitive for choroidal granulomata
OCT/EDI-OCT	Subretinal fluid, choroidal thickening (>400 µm), RPE undulations	Choroidal thinning, subretinal fibrosis, CME	Quantitative monitoring of treatment response
B-scan USG	Diffuse choroidal thickening, serous RD	Choroidal thickening (resolves with treatment)	Useful when media hazy

FFA

Acute Phase Findings: Pinpoint RPE leaks, 'starry sky', disc leakage, pooling in serous RD
Chronic Phase Findings: Window defects, RPE atrophy, CNV leakage
Clinical Use: Diagnosis, monitoring exudation

ICGA

Acute Phase Findings: Multiple hypofluorescent dark dots (granulomata), fuzzy choroidal vessels
Chronic Phase Findings: Persistent dark dots in treated choroidal scars
Clinical Use: Most sensitive for choroidal granulomata

OCT/EDI-OCT

Acute Phase Findings: Subretinal fluid, choroidal thickening (>400 µm), RPE undulations
Chronic Phase Findings: Choroidal thinning, subretinal fibrosis, CME
Clinical Use: Quantitative monitoring of treatment response

B-scan USG

Acute Phase Findings: Diffuse choroidal thickening, serous RD
Chronic Phase Findings: Choroidal thickening (resolves with treatment)
Clinical Use: Useful when media hazy

Self-Assessment (5)

MCQ

A 28-year-old man presents with bilateral granulomatous uveitis, exudative retinal detachments, and Dalen-Fuchs nodules 4 months after a penetrating corneal injury to his left eye. What is the diagnosis?

MCQ

Histopathological examination of an enucleated exciting eye shows non-necrotizing granulomatous choroidal inflammation with epithelioid cells between Bruch's membrane and the RPE, with the choriocapillaris spared. What is the characteristic finding described?

MCQ

A 35-year-old woman develops sympathetic ophthalmia 6 months after vitreoretinal surgery. Her exciting eye is blind (NLP) and painful. Which of the following statements about enucleation of the exciting eye is correct?

MCQ

What is the minimum latent period classically described between penetrating ocular injury and the onset of sympathetic ophthalmia?

MCQ

Which clinical trial established the evidence base for adalimumab use in patients with active non-infectious uveitis, including sympathetic ophthalmia?

References

Nussenblatt RB, Whitcup SM. Uveitis: Fundamentals and Clinical Practice, 4th Edition. Elsevier; 2010.
Greco A, Fusconi M, Gallo A, et al. Vogt-Koyanagi-Harada syndrome. Autoimmun Rev. 2013;12(11):1033-1038.
Jaffe GJ, Dick AD, Brezin AP, et al. Adalimumab in patients with active noninfectious uveitis (VISUAL I). N Engl J Med. 2016;375(10):932-943.
Nguyen QD, Merrill PT, Jaffe GJ, et al. Adalimumab for prevention of uveitic flare in patients with inactive non-infectious uveitis controlled by corticosteroids (VISUAL II). Lancet. 2016;388(10050):1183-1192.
Chan CC, Roberge FG, Whitcup SM, Nussenblatt RB. 32 cases of sympathetic ophthalmia. A retrospective study at the National Eye Institute, Bethesda, Md., from 1982 to 1992. Arch Ophthalmol. 1995;113(5):597-600.
Cunningham ET Jr. Sympathetic ophthalmia. In: Yanoff M, Duker JS, eds. Ophthalmology, 5th Edition. Elsevier; 2019.
Standardization of Uveitis Nomenclature (SUN) Working Group. Standardization of uveitis nomenclature for reporting clinical data. Results of the First International Workshop. Am J Ophthalmol. 2005;140(3):509-516.
AAO Preferred Practice Pattern: Uveitis — Management of Non-Infectious Uveitis. American Academy of Ophthalmology, latest edition.

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