Uveitic Glaucoma

Uveitic glaucoma is raised intraocular pressure and optic nerve damage occurring in association with intraocular inflammation. Raised pressure complicates about 10 to 20 percent of uveitis cases, and glaucoma occurs in 5 to 10 percent.

• Mechanisms:
  • Open angle: trabecular obstruction by inflammatory cells and proteins, trabeculitis (herpetic, Posner-Schlossman syndrome, Fuchs uveitis), scarring of the meshwork, and steroid response.
  • Angle closure: posterior synechiae with iris bombe (seclusio and occlusio pupillae), peripheral anterior synechiae, neovascularisation, and swollen ciliary body with anterior rotation.
• Commonly associated uveitis: juvenile idiopathic arthritis, HLA-B27 anterior uveitis, sarcoidosis, herpetic (HSV, VZV and CMV) uveitis, Fuchs heterochromic uveitis, Behçet disease, and chronic anterior uveitis of any cause.
• Inflammation can also lower pressure (ciliary body shutdown), so pressure may rise when inflammation is treated.

• Painful red eye, photophobia, keratic precipitates, anterior chamber cells and flare, posterior synechiae with irregular pupil, iris nodules, with high pressure (often 30 to 60 mmHg in herpetic and Posner-Schlossman disease).
• Posner-Schlossman syndrome: recurrent episodes of mild inflammation (few keratic precipitates) with marked pressure rise (40 to 60 mmHg), open angle, in young adults.
• Chronic disease: optic disc cupping, field loss, cataract, band keratopathy, peripheral anterior synechiae.
• Systemic features of the underlying disease.

• Slit lamp for inflammation grade, keratic precipitates, synechiae; tonometry (repeated, because pressure fluctuates).
• Gonioscopy (open versus synechial closure, neovascular vessels, nodules).
• Anterior chamber paracentesis with polymerase chain reaction for herpes simplex, varicella zoster, and cytomegalovirus in unilateral hypertensive uveitis.
• Etiologic investigation: HLA-B27, ACE and chest imaging, interferon gamma release assay, syphilis serology, antinuclear antibodies, as indicated.
• Optic nerve imaging and perimetry.

• Control inflammation as the priority: topical prednisolone acetate 1 percent every 1 to 2 hours, tapered slowly; cycloplegia (cyclopentolate 1 percent three times daily or atropine 1 percent daily) to prevent synechiae and relieve pain; periocular or oral steroids (prednisolone 0.5 to 1 mg/kg daily) for severe disease; steroid sparing agents for chronic cases (methotrexate 15 to 25 mg weekly, adalimumab 40 mg every 2 weeks, mycophenolate 1 g twice daily).
• Herpetic uveitis: oral valaciclovir 1 g three times daily or aciclovir 800 mg five times daily for 2 to 6 weeks, then long term prophylaxis (valaciclovir 500 mg once or twice daily or aciclovir 400 mg twice daily).
• Pressure lowering: timolol 0.5 percent twice daily, brimonidine 0.2 percent twice daily (risk of follicular conjunctivitis), dorzolamide 2 percent three times daily, oral acetazolamide 250 to 500 mg if needed. Prostaglandin analogues can be used with caution when inflammation is controlled (they may reactivate herpes and may increase inflammation or macular oedema). Avoid pilocarpine (breaks blood aqueous barrier, forms synechiae).
• Steroid induced rise: switch to lower risk steroid (fluorometholone 0.1 percent, loteprednol 0.5 percent) or steroid sparing therapy.
• Laser peripheral iridotomy for iris bombe. Laser trabeculoplasty is generally avoided.
• Surgery for uncontrolled pressure after inflammation is controlled for at least 3 months: trabeculectomy with mitomycin C 0.4 mg/mL (higher failure rate), glaucoma drainage devices (preferred in children and active disease), goniotomy, and cyclophotocoagulation.
• Combined cataract and glaucoma procedures should be undertaken only when inflammation is quiet; perioperative steroid cover (prednisolone 0.5 to 1 mg/kg for 1 week before and after).
• Follow closely, because pressure often rises when steroids are tapered.