Posterior Uveitis & Panuveitis: Overview

The uveal tract consists of the iris, ciliary body, and choroid. Posterior uveitis involves inflammation predominantly of the choroid and/or retina, while panuveitis involves the anterior chamber, vitreous, and posterior segment simultaneously without one site clearly predominating. These anatomic categories are frequent, visually significant, and etiologically diverse — spanning infectious, autoimmune, and idiopathic causes.

Pathophysiology varies fundamentally by cause. Infectious forms (HTLV-1-associated uveitis, viral retinitis, toxoplasmosis) reflect direct pathogen-driven inflammation or pathogen-triggered immune response. Autoimmune/systemic forms have distinct mechanisms: VKH disease involves T-cell-mediated autoimmunity against shared melanocyte antigens (eye, inner ear, meninges, skin), producing granulomatous panuveitis; sarcoidosis produces non-caseating granulomatous inflammation of any uveal segment; Behçet's disease produces occlusive retinal vasculitis as part of systemic vasculitis. This diversity demands a more systemic diagnostic approach than anterior uveitis alone.

Presentation depends on etiology but commonly includes blurred vision, floaters, and sometimes photopsias/scotomas from chorioretinal lesions; panuveitis adds anterior segment symptoms (pain, redness, photophobia). VKH classically presents with bilateral panuveitis, sometimes with a meningismus-like prodrome (headache, tinnitus, hearing changes) and later integumentary changes (vitiligo, poliosis).

Key differentials: infectious posterior uveitis (toxoplasmosis, viral retinitis, TB, syphilis, HTLV-1), VKH disease, sarcoidosis-associated uveitis, Behçet's disease (occlusive vasculitis, oral/genital ulcers), and masquerade syndromes (intraocular lymphoma).

Diagnosis combines standardized anatomic classification, etiologic workup (targeted serology, imaging, intraocular fluid analysis where indicated), and recognition of systemic associations. In a large HTLV-1 endemic-area cohort, panuveitis was the most frequent anatomic category (47.1%), and HTLV-1-associated uveitis the most common single etiology (10.5%), followed by sarcoidosis (10.4%) and VKH disease (8.7%) — illustrating the breadth of etiologies to consider, with relative frequencies varying by region.¹

Visual acuity at onset is worse in posterior uveitis/panuveitis than anterior/intermediate uveitis, but shows significant improvement by 1 year with treatment, faster than the roughly 3-year course for anterior/intermediate uveitis. Behçet's disease carries the worst 10-year visual prognosis among major etiologies, reinforcing the need for early, aggressive treatment.¹ Treatment is etiology-directed: infectious causes need targeted antimicrobials plus corticosteroids; autoimmune/idiopathic forms need systemic corticosteroids and, for chronic/severe disease, steroid-sparing or biologic therapy. In chronic-recurrent VKH, ongoing surveillance for inflammatory CNVM is warranted; anti-VEGF combined with systemic inflammation control achieves good outcomes despite frequent reactivation.² Glaucoma requiring treatment occurred in roughly a third of eyes and cataract surgery in nearly 40% over the study period, underscoring the complication burden across etiologies.¹

• Posterior uveitis/panuveitis have worse baseline VA than anterior/intermediate uveitis but often improve faster with treatment¹
• Behçet's disease has the worst long-term visual prognosis among major etiologies¹
• A systemic prodrome followed by skin/hair changes should raise suspicion for VKH disease
• Actively screen for CNVM in chronic-recurrent VKH disease²
• Common pitfall: treating posterior uveitis/panuveitis as one disease rather than pursuing etiology-specific workup
• Common pitfall: missing an infectious cause by starting corticosteroids without adequate exclusionary workup