Acute angle-closure glaucoma

Background

File:Eye angle anatomy.png

Eye angle anatomy.

File:Acute angle closure mechanism.png

Mechanism of acute angle closure.

• Sudden increase in intraocular pressure (IOP) due to obstruction of aqueous humor outflow through the trabecular meshwork
• Ophthalmologic emergency — permanent vision loss can occur within hours
• Normal IOP: 10-21 mmHg; in acute attack: typically 40-80 mmHg
• Pathophysiology:
  • Pupillary dilation → peripheral iris contacts trabecular meshwork → blocks aqueous outflow
  • Increased posterior chamber pressure → iris bows forward (iris bombe) → further obstruction
• Risk factors:
  • Hyperopia (farsightedness — smaller anterior chamber)
  • Asian and Inuit descent (anatomically shallow anterior chambers)
  • Female sex, age >40
  • Family history
• Precipitants: dim lighting, medications causing mydriasis (anticholinergics, sympathomimetics, topiramate), emotional stress

Clinical Features

File:Ciliary flush acute angle closure.jpg

Ciliary/circumcorneal flush and hazy cornea characteristic of acute angle closure glaucoma.

File:Acute angle closure pupil.jpg

Right eye with mid-sized, fixed pupil and ciliary flush.

• Sudden onset, severe unilateral eye pain
• Blurred vision with "halos" around lights (corneal edema)
• Frontal or supraorbital headache
• Nausea and vomiting (may be prominent → misdiagnosed as GI illness)
• Fixed, mid-dilated pupil (oval or irregular)
• Hazy, edematous cornea (steamy appearance)
• Ciliary flush (conjunctival injection most prominent at limbus)
• Rock-hard globe on palpation (elevated IOP)
• Decreased visual acuity

Differential Diagnosis

• Acute anterior uveitis/iritis (photophobia, small pupil, no corneal haze)
• Conjunctivitis (no visual changes, normal IOP)
• Corneal abrasion / corneal ulcer
• Endophthalmitis
• Migraine / cluster headache
• Orbital cellulitis

Unilateral red eye

• Nontraumatic
  • Acute angle-closure glaucoma^
  • Anterior uveitis
  • Conjunctivitis
  • Corneal erosion
  • Corneal ulcer^
  • Endophthalmitis^
  • Episcleritis
  • Herpes zoster ophthalmicus
  • Inflamed pinguecula
  • Inflamed pterygium
  • Keratoconjunctivitis
  • Keratoconus
  • Nontraumatic iritis
  • Scleritis^
  • Subconjunctival hemorrhage
• Orbital trauma
  • Caustic keratoconjunctivitis^^
  • Corneal abrasion, Corneal laceration
  • Conjunctival hemorrhage
  • Conjunctival laceration
  • Globe rupture^
  • Hemorrhagic chemosis
  • Lens dislocation
  • Ocular foreign body
  • Posterior vitreous detachment
  • Retinal detachment
  • Retrobulbar hemorrhage
    • Ocular compartment syndrome
  • Traumatic hyphema
  • Traumatic iritis
  • Traumatic mydriasis
  • Traumatic optic neuropathy
  • Vitreous detachment
  • Vitreous hemorrhage
  • Ultraviolet keratitis

^Emergent diagnoses
^^Critical diagnoses

Evaluation

• IOP measurement (Tono-Pen or Goldmann):
  • IOP >21 mmHg (typically >40 mmHg in acute attack)
• Slit lamp exam:
  • Shallow anterior chamber
  • Corneal edema
  • Cell and flare (inflammatory reaction)
  • Mid-dilated, fixed pupil

Diagnostic Criteria: 3 Signs + 2 Symptoms

• At least 3 signs: IOP >21 mmHg, conjunctival injection, corneal epithelial edema, mid-dilated nonreactive pupil, shallow anterior chamber
• At least 2 symptoms: ocular pain, nausea/vomiting, history of intermittent blurring with halos

Management

• Goal: rapidly lower IOP to prepare for definitive laser iridotomy
• Emergent ophthalmology consult
• Recheck IOP at least hourly
• Position: elevate head of bed, keep room well-lit (promotes miosis)
• Start simultaneously with topical beta-blocker, alpha-2 agonist, and systemic carbonic anhydrase inhibitor

Decrease Aqueous Humor Production

• Timolol 0.5%: 1 drop in affected eye; repeat in 1 hour if needed
  • Contraindicated in severe asthma/COPD, bradycardia, heart block
• Acetazolamide 500 mg IV or PO (PO preferred unless nauseated)
  • Contraindicated in sickle cell disease (promotes sickling in acidic environment)
  • Substitute methazolamide 100 mg if renal failure
• Dorzolamide 2%: topical carbonic anhydrase inhibitor — 1 drop affected eye

Alpha-2 Agonist

• Brimonidine 0.2% OR apraclonidine 1%: 1 drop affected eye
  • Reduces aqueous production and increases trabecular outflow

Facilitate Aqueous Outflow

• Pilocarpine 1-2%: 1 drop affected eye every 15 min x 2-4 doses, then q4-6h
  • Parasympathomimetic → miosis → pulls iris away from trabecular meshwork
  • Likely ineffective until IOP drops below 40-50 mmHg (ischemic sphincter muscle) — give immediately anyway
  • Do NOT use pilocarpine >4% (causes forward iris-lens displacement)
  • Note: miosis makes fundoscopic exam more difficult for ophthalmologist

Reduce Vitreous Volume (Refractory Cases)

• Mannitol 1-2 g/kg IV over 45 minutes (most common hyperosmotic agent)
  • Contraindicated in renal failure; can cause hypotension
• 50% glycerin or 45% isosorbide 1.5 mL/kg PO (rarely used)

Topical Steroids

• Prednisolone acetate 1%: 1 drop q15-30min x 4, then q1h
  • Not during acute attack; consider after IOP controlled to reduce inflammation

Disposition

• Admit for definitive treatment with laser peripheral iridotomy (definitive cure)
• Prophylactic iridotomy of the fellow (unaffected) eye is standard practice
• Ophthalmology follow-up within 24 hours

See Also

• Eye emergencies
• Open-angle glaucoma
• Tono-Pen use
• Anterior uveitis

References

• Prum BE Jr, et al. Primary angle closure — Preferred Practice Pattern. Ophthalmology. 2016;123(1):P1-P40. PMID 26581557
• Ah-Kee EY, et al. A review of drug-induced acute angle closure glaucoma. J Ophthalmol. 2015;2015:737053. PMID 25861463
• Sng CC, Ang M, Barton K. Acute angle closure glaucoma. In: Ophthalmology. 5th ed. Elsevier; 2019.