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Symptoms ⬇

Pain, photophobia, and decreased vision; symptoms may be minimal.

Signs ⬆ ⬇

Critical

Elevated IOP with a significant amount of anterior chamber inflammation; open angle on gonioscopy; white blood cells, macrophages, and proteins cause outflow blockage and trabeculitis resulting in elevated IOP. Characteristic glaucomatous optic nerve changes occur late in the disease course.

Other

Miotic pupil, KP, conjunctival injection, ciliary flush, posterior synechiae, and increased TM pigmentation, especially inferiorly. Angle closure glaucoma may occur from progressive PAS formation.

NOTE:

Acute IOP increase from any etiology is distinguished from chronic IOP increase by the presence of corneal edema, pain, and visual symptoms.

Differential Diagnosis ⬆ ⬇

  • Steroid-response glaucoma: Open angle. Patient on steroid medications (including for uveitis). Can be difficult to differentiate from inflammatory open-angle glaucoma. If significant inflammation is present, pressure elevation should be assumed inflammatory in nature and goal should be to quiet the eye with steroids. See 9.9, STEROID-RESPONSE GLAUCOMA.
  • Pigmentary glaucoma: Open angle. Acute increase in IOP, often after exercise or pupillary dilation; pigmented cells in the anterior chamber; 3+ to 4+ trabecular pigmentation; often endopigment in the form of a Krukenberg spindle. Radial iris TIDs are common. See 9.10, PIGMENT DISPERSION SYNDROME/PIGMENTARY GLAUCOMA.
  • Neovascular glaucoma. Nonradial, misdirected blood vessels along the pupillary margin, the TM, or both. See 9.14, NEOVASCULAR GLAUCOMA.
  • Pseudoexfoliation syndrome: Open angle. Grayish-white flaky material deposited throughout anterior segment structures. Classically in patients of European descent, but not always. Occasionally exfoliative material on cornea can be mistaken for KP. Deposits are more angular, less round than inflammatory KP. See 9.11, PSEUDOEXFOLIATION SYNDROME/EXFOLIATIVE GLAUCOMA.
  • Fuchs heterochromic iridocyclitis: Unilateral, more common in middle-aged women. Low-grade inflammation with loss of iris pigmented epithelium causing heterochromia (affected eye typically lighter). Fine bridging vessels in the angle are present and may bleed (Amsler sign). Not neovascular. No PAS. See 12.1, ANTERIOR UVEITIS (IRITIS/IRIDOCYCLITIS).
  • Glaucomatocyclitic crisis (Posner–Schlossman syndrome): Open angle and absence of synechiae on gonioscopy. Dramatic IOP elevation with minimal inflammation. Unilateral with recurrent attacks. See 9.8, GLAUCOMATOCYCLITIC CRISIS/POSNER–SCHLOSSMAN SYNDROME.

Etiology ⬆ ⬇

  • Uveitis: Anterior, intermediate, posterior, or panuveitis.
  • Keratouveitis: Herpetic infections are classically associated with elevated IOP in the setting of early/acute inflammation, whereas other etiologies may cause low IOP from ciliary body shutdown and hyposecretion.
  • After trauma or intraocular surgery.

Work Up ⬆ ⬇

Workup
  1. History: Previous attacks? Systemic disease (e.g., juvenile idiopathic arthritis, ankylosing spondylitis, sarcoidosis, acquired immunodeficiency syndrome [AIDS], V1 distribution varicella zoster, toxoplasmosis)? Previous corneal disease, especially herpetic keratitis?
  2. Slit lamp examination: Assess the degree of conjunctival injection and aqueous cell and flare. Posterior synechiae present?
  3. Complete baseline glaucoma evaluation. See 9.1, PRIMARY OPEN-ANGLE GLAUCOMA.

Treatment ⬆ ⬇

  1. Topical steroid (e.g., prednisolone acetate 1%) q1–6h, depending on the severity of the anterior chamber inflammation.
  2. Mydriatic/cycloplegic (e.g., cyclopentolate 1% t.i.d.).
  3. One or more of the following pressure-reducing agents can be used in addition to the other treatments, depending on the IOP and status of the optic nerve:
    • Topical β-blocker (e.g., timolol 0.5% daily or b.i.d.) if not contraindicated (e.g., asthma, COPD, bradycardia).
    • Topical α2 agonist (e.g., brimonidine 0.1% to 0.2% b.i.d. to t.i.d.).
    • Topical CAI (e.g., dorzolamide 2% t.i.d.) or oral CAI (e.g., methazolamide 25 to 50 mg p.o. b.i.d. to t.i.d. or acetazolamide 500 mg sequel p.o. b.i.d.) if renal function tolerates.
    • Hyperosmotic agent when IOP is acutely increased (e.g., mannitol 20% 1 to 2 g/kg i.v. over 45 minutes) if cardiopulmonary function permits.
    • Anterior chamber paracentesis if reduction in IOP is urgent or if IOP is refractory to topical therapy (see Appendix 13, ANTERIOR CHAMBER PARACENTESIS).
  4. Manage the underlying problem.
  5. If IOP remains dangerously elevated despite maximal medical therapy, glaucoma filtering surgery may be indicated. Trabeculectomy surgery has high rates of failure in cases of inflammatory glaucoma. Tube shunt is often the preferred alternative.
  6. If HSV suspected, start antiviral coveragse (e.g., acyclovir 400 mg p.o. 5× daily or valacyclovir 500 mg p.o. t.i.d. for 7 to 14 days).
NOTE:

Topical steroids are not used, or are used with extreme caution, in patients with an infectious process.

NOTE:

Prostaglandin agonists (e.g., latanoprost 0.005%) and miotics (e.g., pilocarpine) should be used with caution in active inflammatory glaucoma, but may be considered once the eye is quiet or if the benefits outweigh the risks.

Follow Up ⬆

  1. Patients are seen every 1 to 7 days at first. Higher IOP and more advanced glaucomatous cupping warrant more frequent follow up.
  2. Antiglaucoma medications are tapered as IOP returns to normal.
  3. Steroid-response glaucoma should always be considered if IOP remains high when inflammation has subsided (see 9.9, STEROID-RESPONSE GLAUCOMA). IOP elevation in the presence of significant uveitis suggests the need for more, not less, steroid and additional or alternative pressure lowering therapy.