Posterior Uveitis
Definition
Inflammation of the choroid, retina, or both (chorioretinitis), with diverse infectious and non-infectious etiologies including toxoplasmosis, sarcoidosis, Behçet disease, and birdshot chorioretinopathy.
Clinical Snapshot
Posterior uveitis (PU) encompasses inflammation of the choroid, retina, or both (chorioretinitis), with primary involvement of the posterior segment. It is the most etiologically diverse form of uveitis — infectious causes (toxoplasmosis, CMV, syphilis, tuberculosis) must be systematically excluded before initiating immunosuppressive therapy, as corticosteroids can catastrophically worsen infectious disease. Non-infectious PU includes sarcoidosis, Behçet disease, birdshot chorioretinopathy, Vogt-Koyanagi-Harada (VKH) disease, and sympathetic ophthalmia.
Epidemiology
PU accounts for approximately 15–20% of uveitis cases. Toxoplasmosis is the most common cause of infectious PU worldwide. Sarcoidosis is the most common cause of non-infectious PU in the United States. Geographic variation is significant — tuberculosis-associated uveitis is more common in endemic regions.
Pathophysiology
The pathophysiology varies by etiology. Infectious PU: direct invasion of retinal or choroidal tissue by the pathogen (toxoplasmosis, CMV) or immune-mediated inflammation triggered by the pathogen (tuberculosis, syphilis). Non-infectious PU: T-cell–mediated autoimmunity directed against retinal or choroidal antigens (birdshot — anti-retinal antibodies; VKH — anti-melanocyte T cells). Behçet disease involves neutrophil-mediated vasculitis of retinal vessels.
Risk Factors
- Prior toxoplasma infection (reactivation)
- Immunosuppression (CMV retinitis)
- Systemic sarcoidosis
- Behçet disease (HLA-B51 association)
- VKH disease (Asian, Hispanic, Native American ancestry)
- Geographic exposure (tuberculosis, histoplasmosis)
Clinical Presentation
Floaters, blurred vision, and visual field defects. Fundoscopy: focal or multifocal chorioretinal lesions, retinal vasculitis, disc edema, and vitreous cells. The pattern of lesions guides the differential diagnosis: focal necrotizing lesion adjacent to a scar (toxoplasmosis); perivascular sheathing and occlusive vasculitis (Behçet); multifocal cream-colored choroidal lesions (sarcoidosis, birdshot); diffuse choroidal thickening with exudative retinal detachment (VKH).
Diagnostic Pearls
- Infectious causes must be excluded before initiating immunosuppression — syphilis serology (RPR/FTA-ABS) is mandatory in all PU patients.
- Fluorescein angiography characterizes retinal vasculitis and identifies areas of non-perfusion.
- Indocyanine green angiography (ICGA) is superior for evaluating choroidal involvement — it is particularly useful in VKH and birdshot.
- Aqueous or vitreous humor PCR/cytology is indicated for atypical or refractory cases — it can identify infectious organisms and masquerade syndromes (lymphoma).
Differential Diagnosis
- Ocular lymphoma (masquerade — vitritis, subretinal infiltrates, older patients)
- Retinal detachment (exudative — VKH, posterior scleritis)
- Diabetic retinopathy (bilateral, microaneurysms)
Evidence-Based Management
Infectious PU: pathogen-specific antimicrobial therapy (see Ocular Toxoplasmosis, CMV Retinitis). Non-infectious PU: topical corticosteroids have limited utility for posterior disease. Systemic corticosteroids (prednisone 1 mg/kg/day) are first-line for non-infectious PU. Steroid-sparing immunosuppression (methotrexate, mycophenolate, azathioprine, cyclosporine) for chronic or steroid-dependent disease. Biologics (adalimumab — FDA-approved for non-infectious uveitis; infliximab) for refractory disease.
Monitoring & Follow-Up
OCT at every visit for CME and subretinal fluid. Fluorescein angiography to monitor vasculitis activity. Visual field testing for optic nerve and retinal function.
Clinical Pearls
- Never start immunosuppression without excluding syphilis — syphilitic uveitis can mimic virtually any form of uveitis and is treatable.
- Behçet disease uveitis is occlusive and can cause rapid, irreversible vision loss — aggressive immunosuppression (often biologics) is warranted.
- VKH disease has a prodromal phase (headache, tinnitus, dysacusis) before ocular involvement — a thorough history may reveal it.
- Adalimumab (Humira®) is FDA-approved for non-infectious intermediate, posterior, and panuveitis — it is an important option for refractory disease.
Related Therapeutics — Clinician's Companion
- Oral Therapeutics — Oral Prednisone, Methotrexate (Clinician's Companion)
- Anti-inflammatory Rescue — Pred Forte®, Durezol® (Clinician's Companion)
Key References
- 1.Jabs DA, et al. Standardization of uveitis nomenclature for reporting clinical data. Am J Ophthalmol. 2005.
- 2.Jaffe GJ, et al. Adalimumab in patients with active noninfectious uveitis. N Engl J Med. 2016.
This entry is an educational reference designed to support clinical reasoning and awareness. It does not constitute medical advice, establish a standard of care, or replace individualized patient assessment. Clinicians should consult current guidelines and applicable clinical resources when making patient care decisions.