Glaucoma and Anterior Uveitis

Anterior Uveitis — Overview

• Acute anterior uveitis (AAU) — rapid onset, usually unilateral; HLA-B27-related and idiopathic forms predominate
• Chronic anterior uveitis (CAU) — more likely bilateral, associated with systemic disease, often granulomatous

Systemic Associations (Table 12.1)

Clinical Features

• Miosis — pupillary sphincter spasm; predisposes to posterior synechiae
• Anterior chamber cells — graded per SUN Working Group (1×1 mm slit beam)
• Aqueous flare — protein leakage through breakdown of blood-aqueous barrier; even without cells, persistent flare indicates active inflammation and higher complication risk
• Hypopyon — horizontal layering of cells; immobile/fibrin-rich in HLA-B27; shifts with head position in Behçet disease
• Keratic precipitates (KP) — inferior Arlt triangle distribution
  • Small KP — non-granulomatous (AAU)
  • Mutton-fat KP — large, greasy; granulomatous (sarcoid, TB)
  • Stellate KP — Fuchs uveitis syndrome
• Iris nodules: Busacca (stromal, granulomatous) and Koeppe (pupillary margin, site of posterior synechiae)
• Fibrinous exudate — severe AAU, especially HLA-B27
• Posterior synechiae (PS) — adhesions between iris and anterior lens capsule; may progress to seclusio pupillae (360° PS)

Mutton-fat KP in granulomatous anterior uveitis

Iris nodules: Busacca and Koeppe types

Treatment of Anterior Uveitis

1. Topical corticosteroids — mainstay (e.g., prednisolone acetate 1%), tapered as inflammation resolves
2. Cycloplegics (e.g., cyclopentolate, atropine) — relieve ciliary spasm, prevent posterior synechiae, reduce pain
3. Periocular depot steroids — rule out infectious aetiology before use
4. Systemic steroids — for severe/refractory cases or bilateral disease
5. Systemic management per underlying condition (see below)
6. Treat secondary glaucoma — see next section; avoid pilocarpine

• Ankylosing spondylitis/HLA-B27: systemic NSAIDs (naproxen), rheumatology referral
• JIA: minimize topical steroids long-term (↑ risk of cataract and glaucoma in children); systemic steroids risk growth suppression
• Herpetic uveitis (HSV/VZV): oral antivirals (acyclovir, valacyclovir, famciclovir) + topical steroids; topical antivirals are insufficient for uveitis due to poor intraocular penetration
• IBD: systemic steroids, sulfadiazine, or other immunosuppressives

Secondary Glaucoma in Anterior Uveitis

Mechanisms

1. Open-Angle Mechanisms

2. Angle-Closure Mechanisms

Iris bombé secondary to seclusio pupillae

Diagnostic Dilemmas

• IOP fluctuation can be dramatic — phasing is helpful in borderline cases
• Ciliary body shutdown during acute uveitis flares lowers IOP, masking underlying glaucoma; as inflammation subsides and ciliary body function returns, IOP may spike
• Even eyes with IOP of 30–35 mmHg may become hypotonous during acute exacerbations
• Intermittent topical steroids cause fluctuating IOP
• Iris vessels can mimic neovascular glaucoma
• Glaucomatous damage may be hard to assess with small pupils or media opacities

Medical Treatment of Uveitic Glaucoma

Key clinical pearl: If the patient is on topical steroids and IOP rises from multiple possible causes, stop the steroid for 2 days and remeasure. Long-acting depot preparations are contraindicated in known steroid-responders.

Surgical Treatment

• Control of uveitis for minimum 3 months before surgery
• Pre-operative topical (and possibly oral prednisolone 0.5 mg/kg/day for labile disease) steroids
• Post-operative steroids tapered more slowly than in non-inflammatory glaucoma

Special Syndromes

• Rare condition; recurrent attacks of acute secondary open-angle glaucoma with mild anterior uveitis
• IOP markedly elevated during attacks (50–70 mmHg) but normalizes between episodes

• Chronic, low-grade, unilateral anterior uveitis; stellate KP diffusely distributed
• High risk of secondary glaucoma; medical control often inadequate; drainage devices offer best IOP control

Summary: Glaucoma Mechanisms in Anterior Uveitis at a Glance

Anterior Uveitis
        │
        ├── Trabecular obstruction (cells, debris, trabeculitis)
        │         └── Open-angle glaucoma
        │
        ├── Posterior synechiae → Seclusio pupillae
        │         └── Iris bombé → Angle-closure glaucoma (with pupillary block)
        │
        ├── PAS from inflammatory angle deposits
        │         └── Angle-closure glaucoma (without pupillary block)
        │
        ├── Steroid response
        │         └── Open-angle glaucoma
        │
        └── Neovascularization of iris/angle
                  └── Neovascular glaucoma