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Anterior Uveitis Clinical Features

Clinical Presentation

Acute anterior uveitis classically presents with a symptom triad of ocular pain, photophobia, and redness, specifically a perilimbal (ciliary) flush, reflecting inflammation near the sensory-rich anterior segment. On slit-lamp exam, the hallmark confirmatory finding is cell and flare in the anterior chamber: inflammatory cells and protein leakage from a disrupted blood-aqueous barrier, visible as illuminated particles suspended within a narrow, bright slit beam used to optically section the anterior segment.

Iritis describes inflammation confined to the iris and is often used interchangeably with "anterior uveitis" in everyday practice. Iridocyclitis is the more specific term when the anterior (pars plicata) portion of the ciliary body is involved along with the iris.

Posterior Synechiae and Seclusio Pupillae

Recurrent or chronic anterior uveitis causes fibrinous adhesions between the iris and the underlying lens capsule. These posterior synechiae produce an irregular pupil margin, tethered in place instead of reacting normally to light. When the adhesions extend the full 360 degrees around the pupillary margin, the result is seclusio pupillae, and it is clinically dangerous: aqueous can no longer flow from the posterior to the anterior chamber, so the iris bows forward (iris bombé) and pupillary block glaucoma develops, an acute angle-closure mechanism.

Posterior synechiae are not the only route to elevated pressure in anterior uveitis. The trabecular meshwork itself can become inflamed, a process called trabeculitis, in which swollen meshwork tissue and accumulated fibrin and inflammatory cells obstruct aqueous outflow directly. Unlike the pupillary block mechanism above, this produces an open, unobstructed angle on gonioscopy: the pressure rise comes from the drainage tissue's own inflammation rather than a mechanically closed angle. Because the angle is open, management leans on aqueous suppressants and control of the underlying inflammation instead of a peripheral iridotomy.

Keratic Precipitates: Granulomatous vs. Nongranulomatous

Mutton-fat keratic precipitates (KP) are large, greasy-appearing, yellow-white aggregates of epithelioid cells and macrophages deposited on the corneal endothelium. They are the classic KP of granulomatous uveitis and should prompt a workup directed at the granulomatous causes: sarcoidosis, tuberculosis, syphilis, and Vogt-Koyanagi-Harada disease.

Fine, dust-like or stellate KP with mild flare and no nodules instead point toward a nongranulomatous process, the pattern typically seen with the HLA-B27-associated disease discussed below.

Fuchs heterochromic iridocyclitis belongs in the nongranulomatous group, but it behaves differently from HLA-B27 disease and is worth knowing by name. It is a chronic, mild inflammation with fine, stellate KP scattered diffusely across the whole corneal endothelium. Posterior synechiae do not form, even after years of inflammation, and the iris develops heterochromia. That combination identifies it on exam without the extensive systemic workup other chronic uveitides require.

Common Pitfall: Granulomatous vs. Nongranulomatous KP

Don't lump all keratic precipitates together. The combination of large mutton-fat KP, iris (Koeppe/Busacca) nodules, and thick posterior synechiae is what supports a granulomatous etiology on exam. Fine or stellate KP with no nodules supports a nongranulomatous one, and that includes Fuchs heterochromic iridocyclitis despite its chronic course.

Iris Nodules: Koeppe and Busacca

Iris nodules are another marker of granulomatous inflammation, found on careful slit-lamp exam. Koeppe nodules occur at the pupillary border, while Busacca nodules occur on the iris stroma away from the margin. Both are small but specific findings. Alongside mutton-fat KP and thick synechiae, they weight the differential firmly toward a granulomatous cause.

HLA-B27 and the Spondyloarthropathies

HLA-B27 is the classic genetic risk factor for anterior uveitis, and it is a major driver of the seronegative spondyloarthropathies. A patient with acute, painful, unilateral anterior uveitis that alternates sides between episodes, combined with chronic low back pain and morning stiffness, should raise suspicion for an HLA-B27-associated spondyloarthropathy such as ankylosing spondylitis. That pattern alone warrants a targeted rheumatologic and spinal history.

Two other seronegative spondyloarthropathies round out the classic associations. In a young man presenting with urethral discharge, asymmetric joint pain, and conjunctivitis before developing anterior uveitis, the triad of urethritis, arthritis, and conjunctivitis (historically called Reiter syndrome) points to reactive arthritis. A patient with anterior uveitis and well-demarcated silvery skin plaques on the elbows and scalp should be evaluated for psoriatic arthritis, another seronegative spondyloarthropathy that can present with anterior, and occasionally posterior, uveitis, making a dermatologic history a routine part of the workup.

High-Yield
  • Symptom triad of acute anterior uveitis: pain, photophobia, and redness (perilimbal flush).
  • Mutton-fat KP + Koeppe/Busacca nodules + thick synechiae = granulomatous pattern; fine/stellate KP with no nodules = nongranulomatous pattern.
  • 360° posterior synechiae (seclusio pupillae) → iris bombé → pupillary block glaucoma, a direct complication of uncontrolled anterior uveitis.
  • HLA-B27 disease: recurrent, unilateral, side-alternating anterior uveitis + inflammatory back pain. Reactive arthritis adds urethritis + conjunctivitis; psoriatic arthritis adds silvery skin plaques.
  • Fuchs heterochromic iridocyclitis is nongranulomatous: diffuse stellate KP, no posterior synechiae, heterochromia.

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