Anterior Uveitis & Iridocyclitis

Anterior uveitis is inflammation of the iris (iritis) and/or ciliary body (cyclitis), together iridocyclitis — the commonest form of intraocular inflammation. It is a recurring NEET PG favourite because of its rich clinical signs (KPs, flare, synechiae, hypopyon) and its tight links to systemic disease (HLA-B27, ankylosing spondylitis, JIA, sarcoidosis).

Anatomy & terminology refresher

The uvea is the middle vascular coat of the eye, with three parts: iris (anterior), ciliary body (intermediate), and choroid (posterior). The blood supply explains inflammation patterns — the iris and ciliary body share the major arterial circle of the iris (from anterior ciliary + long posterior ciliary arteries), so they inflame together as iridocyclitis.

• Iritis = inflammation limited to iris.
• Cyclitis = inflammation of ciliary body.
• Iridocyclitis / anterior uveitis = both (the usual clinical reality).

High-yield: The primary site of inflammation defines the anatomical class. Anterior uveitis = AC the main site; intermediate uveitis = vitreous; posterior uveitis = retina/choroid; panuveitis = all three.

Classification

SUN (Standardisation of Uveitis Nomenclature) — anatomical

Type	Primary site of inflammation	Examples
Anterior uveitis	Anterior chamber (iris/ciliary body)	HLA-B27, JIA, Fuchs, herpetic
Intermediate uveitis	Vitreous / pars plana	Pars planitis, sarcoid, MS
Posterior uveitis	Retina or choroid	Toxoplasma, CMV, Behçet
Panuveitis	All three combined	VKH, sarcoid, sympathetic ophthalmia

By onset, duration & course (SUN)

• Onset: sudden vs insidious.
• Duration: limited (≤3 months) vs persistent (>3 months).
• Course: acute (sudden, limited), recurrent (repeated episodes with ≥3 months of inactivity off treatment), chronic (persistent, relapsing within <3 months of stopping therapy).

Granulomatous vs non-granulomatous (most tested clinical split)

Feature	Non-granulomatous	Granulomatous
Onset	Acute	Insidious
Pain/redness	Marked	Mild / minimal
KPs	Fine, small, white	Mutton-fat (large, greasy)
Iris nodules	Absent	Koeppe (pupil margin), Busacca (iris surface)
Course	Acute, self-limiting	Chronic
Classic causes	HLA-B27, trauma, post-op	Sarcoidosis, TB, syphilis, VKH, sympathetic ophthalmia, lepra

High-yield: Mutton-fat KPs + iris nodules = granulomatous uveitis → think sarcoid, TB, syphilis, VKH, sympathetic ophthalmia.

Mnemonic for granulomatous causes — "STeLViS": Sarcoid, TB, Leprosy, VKH/sympathetic ophthalmia, Syphilis.

Aetiology & associations

• Idiopathic — still the single largest group (~50%).
• HLA-B27 spondyloarthropathies — ankylosing spondylitis, reactive arthritis (Reiter), psoriatic arthritis, IBD-associated. Cause acute, recurrent, non-granulomatous, often unilateral or alternating, frequently with hypopyon and fibrinous exudate.
• JIA (pauciarticular, ANA-positive young girls) — chronic, bilateral, white (non-red), painless, asymptomatic anterior uveitis → high risk of band keratopathy, cataract, glaucoma. Needs slit-lamp screening.
• Sarcoidosis — granulomatous, mutton-fat KPs, "candle-wax" retinal vessels if posterior.
• Infective — herpes simplex/zoster (with raised IOP + patchy iris atrophy), TB, syphilis, leprosy, toxoplasma (posterior).
• Fuchs heterochromic iridocyclitis — chronic low-grade, iris heterochromia (affected eye lighter), diffuse stellate KPs all over endothelium, no synechiae, cataract + glaucoma; quiet white eye.
• Posner-Schlossman (glaucomatocyclitic crisis) — recurrent unilateral mild uveitis with markedly raised IOP, few KPs, open angle.
• Lens-induced (phacoanaphylactic/phacolytic), post-surgical, traumatic.

High-yield: Unilateral acute hypopyon uveitis in a young man with low backache → HLA-B27 / ankylosing spondylitis. Hypopyon here is mobile and sterile (shifts with head position).

Pathophysiology

Breakdown of the blood–aqueous barrier (tight junctions of non-pigmented ciliary epithelium and iris vessels) allows protein and cells to leak into the aqueous:

• Flare = light-scattering by leaked protein (Tyndall effect).
• Cells = inflammatory leukocytes floating in the AC.

Both immune (Type III/IV hypersensitivity, HLA-B27 molecular mimicry) and infectious mechanisms operate. Chronic inflammation → adhesions (synechiae), fibrosis, neovascularisation, and tissue damage producing the complications below.

The HLA-B27 association deserves a closer mechanistic note because it is so frequently examined. HLA-B27 is a class I MHC molecule; molecular mimicry between certain bacterial peptides (Klebsiella, Yersinia, Shigella, Salmonella, Chlamydia — the reactive-arthritis triggers) and self antigens, together with misfolding of the HLA-B27 heavy chain and a resulting pro-inflammatory unfolded-protein response, drives a Th17-skewed autoimmune attack. This is why HLA-B27 uveitis travels with the seronegative spondyloarthropathies and tends to be acute, recurrent, often alternating between eyes, and heavily fibrinous (plasmoid aqueous, fibrin clot, mobile hypopyon). In contrast, JIA-associated uveitis is an antibody-linked (ANA-positive) chronic smouldering process with minimal external signs, which is exactly why it is dangerous — the eye stays white while synechiae, band keratopathy, cataract and glaucoma silently accumulate. Recognising these two opposite behavioural patterns — noisy/acute (HLA-B27) versus quiet/chronic (JIA) — answers a large share of NEET stems.

Clinical features

Symptoms (acute non-granulomatous): pain, photophobia, lacrimation, redness, mild blurring of vision (NOT marked early). Granulomatous and JIA-associated forms can be strikingly asymptomatic.

Signs — stepwise on slit-lamp:

1. Circumcorneal (ciliary) congestion — deep, pinkish-violet flush around the limbus (vs superficial brick-red conjunctival congestion of conjunctivitis).
2. Keratic precipitates (KPs) — cellular deposits on corneal endothelium, classically in Arlt's triangle (inferior, gravity-dependent). Fine = non-granulomatous; mutton-fat = granulomatous; diffuse stellate = Fuchs/herpetic.
3. Aqueous flare & cells — graded by SUN.
4. Miosis — sphincter spasm; small, sluggish pupil.
5. Posterior synechiae — adhesions between iris and anterior lens capsule → irregular/festooned pupil on dilation; if 360° = seclusio pupillae → iris bombé → secondary angle-closure glaucoma.
6. Anterior synechiae — iris to cornea/angle.
7. Iris nodules — Koeppe (margin), Busacca (surface) in granulomatous disease.
8. Hypopyon — sterile pus layering inferiorly (HLA-B27, Behçet — in Behçet it is often shifting and "cold" without much redness).
9. Low IOP early (ciliary shutdown) but may rise later.

SUN grading

Grade	AC cells (field 1×1 mm)	Flare
0	<1	None
0.5+	1–5	—
1+	6–15	Faint
2+	16–25	Moderate (iris/lens clear)
3+	26–50	Marked (hazy)
4+	>50	Intense (fibrin/plasmoid aqueous)

High-yield: Posterior synechiae → festooned pupil on dilation; complete seclusio pupillae → aqueous trapped behind iris → iris bombé → secondary angle-closure glaucoma. Prevent with early cycloplegics.

Diagnosis & investigation of choice

Diagnosis is primarily clinical via slit-lamp biomicroscopy demonstrating cells and flare in the AC. The key NEET point is the targeted, tailored work-up based on pattern — NOT a blind battery in every case.

Approach: History & exam → classify (anterior, granulomatous?, unilateral/bilateral, acute/chronic) → directed investigations.

• First-episode, mild, unilateral, non-granulomatous, acute → often treat without extensive work-up.
• Recurrent / bilateral / granulomatous / chronic → investigate.

Suspected cause	Best/confirmatory test
HLA-B27 spondyloarthropathy	HLA-B27, sacroiliac joint X-ray (bamboo spine)
Sarcoidosis	Serum ACE, chest X-ray/CT (hilar lymphadenopathy), biopsy
TB	Mantoux/IGRA, chest X-ray
Syphilis	VDRL + TPHA/FTA-ABS
JIA	ANA, RF, joint exam, regular slit-lamp screening
Toxoplasma (posterior)	IgG/IgM serology
Behçet	Clinical (oral+genital ulcers, pathergy), HLA-B51

High-yield: Serum ACE + chest imaging is the classic screen for sarcoid uveitis. For granulomatous bilateral uveitis, always rule out TB, sarcoid, syphilis.

Management

Aims: relieve pain, suppress inflammation, prevent synechiae and complications, treat underlying cause.

Stepwise treatment flow

Topical cycloplegic (atropine/homatropine) → Topical corticosteroid (prednisolone acetate 1%) → Periocular/oral steroid if severe → Immunosuppressants/biologics for refractory or sight-threatening disease → Treat systemic cause.

1. Cycloplegics/mydriatics — atropine 1% / homatropine 2% / cyclopentolate. Two crucial roles:
   • Relieve pain & photophobia by paralysing the inflamed ciliary muscle and iris sphincter.
   • Prevent posterior synechiae by keeping the pupil mobile/dilated; can break fresh synechiae (add phenylephrine for synergistic dilation).
2. Corticosteroids — topical prednisolone acetate 1% is the mainstay/drug of choice for anterior uveitis. Frequent dosing initially (hourly), then taper. Periocular (sub-Tenon triamcinolone) or systemic steroids for severe/bilateral/posterior involvement.
3. NSAIDs — adjunct for pain.
4. Steroid-sparing immunomodulators — methotrexate, azathioprine, mycophenolate, ciclosporin for chronic/recurrent steroid-dependent disease (esp. JIA).
5. Biologics — anti-TNF (adalimumab/infliximab) for refractory uveitis (JIA, Behçet, HLA-B27). Adalimumab is FDA-approved for non-infectious uveitis.
6. Treat infective cause — antiviral (aciclovir) for herpetic, antibiotics for TB/syphilis, with steroid cover.

High-yield: Topical prednisolone acetate 1% is the drug of choice for anterior uveitis; atropine is given first to relieve pain and prevent synechiae.

High-yield: Before starting steroids in a "red eye with KPs", exclude herpetic/infective keratouveitis — steroids alone can worsen dendritic herpetic disease. Check corneal sensation and stain.

Complications

• Complicated cataract — classically posterior subcapsular.
• Secondary glaucoma — angle-closure (seclusio → iris bombé), trabeculitis, steroid-induced, or peripheral anterior synechiae.
• Hypotony & phthisis bulbi — from ciliary body shutdown in chronic disease.
• Cystoid macular oedema (CMO) — major cause of vision loss in chronic uveitis.
• Band-shaped keratopathy — calcium deposition; classic in JIA-associated chronic uveitis.
• Posterior synechiae, seclusio/occlusio pupillae.
• Choroiditis/retinitis if spread posteriorly.

High-yield: Triad of chronic JIA uveitis complications — band keratopathy + complicated cataract + secondary glaucoma.

Key differentials

The classic NEET differentiation is the acute red eye:

Feature	Acute anterior uveitis	Acute congestive glaucoma	Acute conjunctivitis	Keratitis
Pain	Moderate, aching	Severe + headache, vomiting	Gritty, mild	Sharp, FB sensation
Congestion	Circumcorneal (ciliary)	Mixed	Conjunctival (superficial)	Circumcorneal
Pupil	Small, sluggish (miosis)	Mid-dilated, fixed, oval	Normal	Normal/small
IOP	Usually low/normal (may rise)	Markedly high	Normal	Normal
Cornea	Clear (KPs on endothelium)	Hazy/oedematous	Clear	Ulcer/infiltrate, stains
AC	Cells + flare	Shallow	Clear	May have hypopyon
Discharge	Watery (reflex)	Watery	Purulent/mucoid	Watery/purulent
Vision	Slightly blurred	Markedly reduced, halos	Normal	Reduced

High-yield: Miosis = uveitis; mid-dilated fixed pupil = acute angle-closure glaucoma. This single sign frequently distinguishes the two in exam stems.

Other differentials by entity: Endophthalmitis (severe pain, marked hypopyon, vitritis, post-op/post-trauma — an emergency), masquerade syndromes (intraocular lymphoma, retinoblastoma, leukaemia in atypical/non-responsive cases).

A practical bedside rule: any uveitis that is bilateral, granulomatous, recurrent, posterior, or unresponsive to standard topical steroid mandates a systemic work-up, whereas a first, mild, acute, unilateral, non-granulomatous episode in an otherwise well patient can be treated empirically and observed. Atypical features that should raise suspicion of a masquerade or sinister cause include a hypopyon that does not respond to steroids, a unilateral chronic uveitis in an older patient (think lymphoma), spontaneous hyphaema with uveitis, and uveitis with a retinal mass in a child (retinoblastoma). When in doubt, refer for vitreous sampling rather than escalating immunosuppression blindly.

Recently asked / exam angle

• Mutton-fat KPs → granulomatous uveitis (sarcoid/TB) — repeated single-best-answer.
• HLA-B27 is the most asked association of acute anterior uveitis with hypopyon + ankylosing spondylitis.
• JIA uveitis characteristics: pauciarticular, ANA-positive young girl, bilateral, chronic, white quiet eye, asymptomatic → needs screening; complication = band keratopathy.
• Drug of choice questions: cycloplegic (atropine) for pain/synechiae; topical steroid (prednisolone acetate) for inflammation.
• Fuchs heterochromic iridocyclitis — heterochromia, no synechiae, stellate KPs, glaucoma/cataract — appears in "no posterior synechiae despite chronic uveitis" stems.
• Koeppe vs Busacca nodules location (margin vs surface).
• Arlt's triangle as the site of KP deposition.
• Iris bombé / seclusio pupillae mechanism of secondary glaucoma.
• Behçet — recurrent shifting hypopyon + oral/genital ulcers, HLA-B51, treated with steroids + immunosuppressants/biologics.
• SUN classification — anatomical site definitions and cell-grading cut-offs.

Rapid revision

1. Iridocyclitis = anterior uveitis; iris + ciliary body inflame together via the major iris arterial circle.
2. Cardinal AC signs: cells (leukocytes) + flare (protein/Tyndall) = blood–aqueous barrier breakdown.
3. Circumcorneal (ciliary) congestion + miosis distinguish uveitis from conjunctivitis and angle-closure glaucoma.
4. Mutton-fat KPs + Koeppe/Busacca nodules = granulomatous → sarcoid, TB, syphilis, VKH, sympathetic ophthalmia, leprosy.
5. KPs deposit in Arlt's triangle (inferior cornea, gravity-dependent).
6. HLA-B27 = acute, recurrent, non-granulomatous uveitis with mobile sterile hypopyon + ankylosing spondylitis.
7. JIA uveitis = ANA+ young girl, chronic, bilateral, white painless eye → band keratopathy, cataract, glaucoma; needs slit-lamp screening.
8. Fuchs heterochromic iridocyclitis = heterochromia, stellate KPs, no synechiae, cataract + glaucoma.
9. Posner-Schlossman = recurrent mild uveitis with markedly raised IOP, open angle.
10. Atropine/cycloplegic first — relieves pain and prevents/breaks posterior synechiae; prednisolone acetate 1% is the drug of choice for inflammation.
11. Seclusio pupillae → iris bombé → secondary angle-closure glaucoma; complicated cataract is posterior subcapsular.
12. Exclude herpetic keratouveitis before steroids; sarcoid screen = serum ACE + chest X-ray; refractory disease → anti-TNF (adalimumab).