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Summary Table

Feature	Detail
Risk Factors	Young to middle-aged adults (20-50 years), HLA-B27 positivity, autoimmune diseases (ankylosing spondylitis, reactive arthritis, inflammatory bowel disease, psoriatic arthritis), sarcoidosis, Behcet disease, infections (HSV, VZV, syphilis, tuberculosis)
Etiology	Immune-mediated inflammation of the iris (iritis) and/or ciliary body (iridocyclitis); may be idiopathic in up to 50% of cases
Patient Presentation	Unilateral eye pain, photophobia, tearing, blurred vision; symptoms develop over hours to days
Classic Physical Exam	Ciliary flush (perilimbal injection), miotic pupil, cells and flare in the anterior chamber on slit-lamp exam, consensual photophobia (pain in the affected eye when light is shone into the contralateral eye)
Key Diagnostic Results	Slit-lamp examination showing anterior chamber cells and flare; keratic precipitates on the corneal endothelium; hypopyon in severe cases
Management	Topical corticosteroids (prednisolone acetate 1%) + cycloplegic agents (cyclopentolate or homatropine); treat underlying systemic cause
Keywords	"Ciliary flush," "cells and flare," "consensual photophobia," "perilimbal injection," "miotic pupil," "hypopyon," "HLA-B27"

1. Pathophysiology

Anterior uveitis refers to inflammation of the uveal tract limited to the anterior segment, involving the iris (iritis), the ciliary body (iridocyclitis), or both. The uveal tract is a highly vascular structure, making it particularly susceptible to immune-mediated inflammatory processes.

The underlying mechanism in most non-infectious cases involves a T-cell-mediated autoimmune response directed against uveal antigens. In genetically predisposed individuals, particularly those carrying HLA-B27, molecular mimicry between microbial antigens and self-antigens is thought to trigger this inflammatory cascade. Activated T-cells and macrophages infiltrate the iris and ciliary body, releasing cytokines that increase vascular permeability. This causes protein leakage (flare) and white blood cell migration (cells) into the anterior chamber, which are the hallmark findings on slit-lamp examination.

The inflammation of the ciliary body leads to spasm of the ciliary muscle, which is responsible for the deep, aching eye pain. Ciliary spasm also causes the pupil to constrict (miosis), distinguishing this from acute angle-closure glaucoma, which presents with a mid-dilated, fixed pupil. The concept of consensual photophobia is a high-yield discriminator: when light is directed into the unaffected eye, the consensual pupillary constriction in the inflamed eye triggers ciliary spasm and pain. This finding is nearly pathognomonic for anterior uveitis and is frequently tested.

The ciliary flush (also called perilimbal injection) results from dilation of the deep episcleral and ciliary vessels that encircle the limbus. This pattern of redness is distinct from the diffuse conjunctival injection seen in conjunctivitis, where the redness is most prominent in the fornices and fades toward the limbus.

In severe or prolonged inflammation, inflammatory cells can layer dependently in the anterior chamber, forming a hypopyon, a visible white fluid level. This is classically associated with Behcet disease and HLA-B27-associated uveitis, though it can occur in endophthalmitis as well.

Chronic or recurrent anterior uveitis can lead to posterior synechiae, which are adhesions between the iris and the anterior lens capsule. These adhesions can cause an irregular, poorly dilating pupil and, if circumferential (seclusio pupillae), can block aqueous humor outflow and precipitate secondary angle-closure glaucoma.

2. Classification and Clinical Manifestation

Classification	Anatomical Location	Key Features
Anterior uveitis (iritis/iridocyclitis)	Iris and ciliary body	Most common form (~50-60% of all uveitis); pain, photophobia, miosis, ciliary flush, cells and flare
Intermediate uveitis (pars planitis)	Vitreous and peripheral retina	"Floaters" and blurred vision predominate; minimal pain; snowbanking on pars plana; associated with multiple sclerosis
Posterior uveitis (choroiditis/retinitis)	Choroid and retina	Painless vision loss, floaters; associated with toxoplasmosis (most common infectious cause), CMV retinitis in immunocompromised
Panuveitis	All segments involved	Most severe; associated with sarcoidosis, Behcet disease, Vogt-Koyanagi-Harada syndrome, sympathetic ophthalmia

Duration and Course:

Pattern	Definition	Clinical Relevance
Acute	Sudden onset, limited duration (< 3 months)	Most common pattern; typical HLA-B27-associated uveitis
Chronic	Persistent > 3 months	Think sarcoidosis, juvenile idiopathic arthritis (JIA), Fuchs heterochromic iridocyclitis
Recurrent	Repeated episodes separated by periods of inactivity	Characteristic of HLA-B27-positive spondyloarthropathies

Systemic Associations

Association	Distinguishing Clue
Ankylosing spondylitis	Young male, chronic low back pain worse in the morning, improved with exercise, HLA-B27 positive, bilateral sacroiliitis on imaging
Reactive arthritis	Classic triad: urethritis, conjunctivitis/uveitis, arthritis; follows GI or GU infection
Inflammatory bowel disease	Bloody diarrhea, abdominal pain; uveitis may flare independently of bowel disease activity
Sarcoidosis	Bilateral hilar lymphadenopathy, non-caseating granulomas, elevated ACE level; can cause chronic granulomatous uveitis with "mutton-fat" keratic precipitates
Behcet disease	Recurrent oral and genital ulcers, hypopyon uveitis, pathergy test positive
Juvenile idiopathic arthritis	Young girl, ANA-positive, oligoarticular subtype; asymptomatic chronic uveitis (can cause vision loss without overt symptoms, requiring routine screening)

3. Diagnostic Workup

Test	Role	Key Findings
Slit-lamp biomicroscopy	Best initial and most important test	Anterior chamber cells and flare, keratic precipitates, posterior synechiae, hypopyon
Intraocular pressure measurement	Rule out secondary glaucoma	May be low (ciliary body shutdown), normal, or elevated (trabeculitis or synechiae blocking outflow)
HLA-B27 testing	Systemic workup for recurrent/bilateral cases	Positive in ankylosing spondylitis, reactive arthritis
Chest X-ray	Screen for sarcoidosis and tuberculosis	Bilateral hilar lymphadenopathy (sarcoidosis), apical infiltrates or calcified granulomas (TB)
Serum ACE level	Sarcoidosis evaluation	Elevated in approximately 60% of active sarcoidosis
RPR/VDRL and FTA-ABS	Rule out syphilis	Syphilis is "the great imitator" and can cause any form of uveitis
PPD or interferon-gamma release assay	Screen for tuberculosis	Latent or active TB can present with granulomatous uveitis

The slit-lamp examination is the cornerstone of diagnosis. It allows direct visualization of inflammatory cells floating in the aqueous humor and the protein-rich haze called flare. The grading of cells (0 to 4+) determines disease severity and guides treatment intensity.

Keratic precipitates (KPs) are clumps of inflammatory cells deposited on the corneal endothelium. Their morphology provides a diagnostic clue. Fine, small KPs suggest a non-granulomatous process (typical of HLA-B27-associated disease), while large, greasy "mutton-fat" KPs suggest a granulomatous etiology such as sarcoidosis, tuberculosis, or syphilis.

For a first episode of mild, unilateral acute anterior uveitis in a young patient, extensive laboratory workup is generally not required. However, when the uveitis is recurrent, bilateral, chronic, granulomatous, or associated with posterior segment involvement, a directed systemic workup becomes necessary. The minimum panel typically includes HLA-B27, chest X-ray, syphilis serologies, and tuberculosis screening.

The examiner may present a vignette where the patient has recurrent anterior uveitis and then ask what additional evaluation is needed. In that scenario, the answer is to look for an underlying systemic condition, and HLA-B27 testing combined with a thorough review of systems for spondyloarthropathy is the best next step.

4. Management and Treatment

Setting	Treatment	Details
First-line (acute episode)	Topical corticosteroids	Prednisolone acetate 1%, initially every 1-2 hours while awake, then tapered over 2-6 weeks based on response
Adjunct (acute episode)	Cycloplegic/mydriatic agent	Cyclopentolate 1% TID or homatropine 5% BID-TID to relieve ciliary spasm and prevent posterior synechiae formation
Refractory/chronic disease	Systemic immunosuppression	Oral corticosteroids as a bridge; steroid-sparing agents (methotrexate, azathioprine, mycophenolate) for long-term control
Infectious etiology	Targeted antimicrobial therapy	Antiviral for HSV/VZV (oral acyclovir/valacyclovir); treat syphilis and TB per standard protocols before or concurrent with anti-inflammatory therapy
Complications	Secondary glaucoma management	Topical IOP-lowering agents; may require surgical intervention for refractory cases

Topical prednisolone acetate 1% is the drug of choice. It is preferred over prednisolone sodium phosphate because the acetate formulation penetrates the cornea more effectively. Aggressive initial dosing (every 1-2 hours) followed by a gradual taper is critical. A common exam pitfall involves abruptly stopping corticosteroids, which leads to rebound inflammation.

Cycloplegic agents serve two purposes. First, they paralyze the ciliary muscle, providing pain relief by eliminating the spasm responsible for the aching discomfort and photophobia. Second, they dilate the pupil and keep the iris mobile, preventing the formation of posterior synechiae. Atropine 1% (longest-acting) is reserved for severe cases; cyclopentolate or homatropine is preferred for moderate cases because their shorter duration allows more frequent reassessment of pupillary function.

For patients with chronic or recurrent disease requiring prolonged corticosteroid use, steroid-sparing immunosuppressive agents are introduced. Methotrexate is the most commonly used first-line steroid-sparing agent. This is particularly important in JIA-associated uveitis, where chronic low-grade inflammation can silently damage the eye.

When an infectious cause is identified, treating the infection takes priority. Initiating corticosteroids without antimicrobial coverage in herpetic or syphilitic uveitis can worsen the infection.

5. Differential Diagnosis and Distractors

Differential Diagnosis	Why It Is Similar	Key Discriminator
Acute angle-closure glaucoma	Acute unilateral red, painful eye with vision changes	Mid-dilated fixed pupil, markedly elevated IOP, corneal edema, halos around lights; pupil in uveitis is miotic, not mid-dilated
Conjunctivitis	Red eye with tearing	No photophobia, no pain (itching or burning instead), diffuse conjunctival injection worst at fornices, no ciliary flush, no cells and flare, vision is normal
Episcleritis/Scleritis	Eye redness and discomfort	Episcleritis: sectoral redness, mild discomfort, blanches with phenylephrine. Scleritis: severe boring pain, violaceous hue, scleral edema, may not blanch with phenylephrine. Neither shows anterior chamber cells
Keratitis	Eye pain, photophobia, tearing, ciliary flush	Corneal findings predominate (fluorescein uptake, dendritic ulcer in HSV, corneal infiltrate); anterior chamber reaction may be present but secondary to corneal pathology
Endophthalmitis	Hypopyon, severe pain, vision loss	History of recent ocular surgery or penetrating trauma; vitreous involvement with severe vitritis; more fulminant course
Traumatic iritis	Cells and flare in anterior chamber after blunt trauma	Clear history of ocular trauma; look for associated hyphema (layered blood in anterior chamber), which distinguishes it from inflammatory hypopyon

6. Traps and High-Yield Pearls

The most common way students lose points on anterior uveitis questions is by confusing the pattern of eye redness. The vignette will describe perilimbal (ciliary) injection and test whether you can distinguish this from the diffuse conjunctival injection of conjunctivitis or the sectoral redness of episcleritis. If the redness is concentrated around the corneal limbus, think uveitis or keratitis, not conjunctivitis.

The second major trap involves consensual photophobia. If the vignette states that shining a light into the unaffected eye causes pain in the affected eye, this essentially confirms anterior uveitis. This finding is tested because it demonstrates an understanding of the consensual pupillary reflex triggering ciliary spasm in the inflamed eye.

Do not forget the JIA-uveitis connection. A young girl with oligoarticular JIA and a positive ANA requires routine ophthalmologic screening even in the absence of eye symptoms, because her uveitis is characteristically chronic and asymptomatic until complications (band keratopathy, cataracts, glaucoma) have already developed. The exam tests whether you know to screen proactively.

Another frequently tested concept is the association between HLA-B27 and recurrent acute anterior uveitis. When a patient with known ankylosing spondylitis or reactive arthritis presents with a red, painful eye and photophobia, anterior uveitis should be the leading diagnosis. The test-writer is evaluating your ability to link systemic autoimmune disease to ocular manifestations.

Finally, always remember that syphilis can mimic any form of uveitis. In any atypical or treatment-refractory case, syphilis serologies should be checked. Missing syphilis as a cause of uveitis is a classic diagnostic error that exam writers exploit.

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