Acute angle-closure glaucoma

Background

Pathophysiology

• Obstructed aqueous outflow tract → aqueous humor builds up → increased intraocular pressure (IOP) → optic nerve damage → vision loss
• Increased posterior chamber pressure causes iris to bulge forward (iris bombé) → further obstruction of outflow tract → further increase IOP
• Acute attack is usually precipitated by pupillary dilation

Clinical Features

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

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

• Abrupt onset of severe (usually unilateral) eye pain
• Blurred vision
• Frontal or supraorbital headache
• Nausea / vomiting / abdominal pain

Differential Diagnosis

Unilateral Red Eye

• Acute angle-closure glaucoma^
• Anterior uveitis
• Caustic keratoconjunctivitis^^
• Conjunctival laceration
• Conjunctivitis
• Corneal abrasion
• Corneal erosion
• Ocular foreign body
• Corneal ulcer^
• Endophthalmitis^
• Episcleritis
• Globe rupture^
• Herpes zoster ophthalmicus
• Intraocular foreign body
• Inflamed pingueculum
• Inflamed Pterygium
• Keratoconjunctivitis
• Keratoconus
• Lens dislocation
• Nontraumatic iritis
• Scleritis^
• Subconjunctival hemorrhage
• Traumatic hyphema
• Traumatic iritis
• Ultraviolet keratitis

^Emergent diagnoses

^^Critical diagnoses

Evaluation

• Fixed, midposition pupil
• Hazy cornea
• Conjunctival injection most prominent at limbus (ciliary flush)
• Rock-hard globe
• IOP >20 mm Hg
• Slit lamp exam shows shallow anterior chamber and cell and flare

Definition: 3 signs + 2 symptoms

• At least 3 of these signs:
  • IOP >21 mm Hg
  • Conjunctival injection
  • Corneal epithelial edema
  • Mid-dilated nonreactive pupil
  • Shallow anterior chamber with occlusion
• At least 2 of these symptoms:
  • Ocular pain
  • Nausea/vomiting
  • History of intermittent blurring of vision with halos

Management

Goal of medical therapy is to 'break the attack' in order to prepare the patient for laser iridotomy.

1. Emergent ophthalmology consult
2. Recheck IOP at least hourly
3. Supine position to decrease IOP
4. Place patient in a well lit room (prevent pupillary dilation)
5. Start with a topical beta-blocker, alpha blocker and PO acetazolamide if no contraindications

Decrease production of aqueous humor

Timolol 0.5%:

• Blocks beta receptors on ciliary epithelium
• 1 drop in affected eye, repeat in 1 hour if needed.

Acetazolamide:

• Blocks productions of HCO3-, which draws Na+ into the eye; water follows by osmosis to form aqueous humour
• 500mg IV or PO (PO preferred unless patient is nauseated)
• Can substitute methazolamide 100mg if patient has renal failure.
• Contraindicated in sickle cell patients

Dorzolamide (Trusopt) 2%:

• topical carbonic anhydrase inhibitor
• 1 drop in affected eye

Alpha agonist

Brimonidine ophthalmic (Alphagan) 0.2% OR Apraclonidine ophthalmic 1%:

• Alpha agonist will increase trabecular outflow
• 1 drop in affected eye

Facilitate outflow of aqueous humor

Pilocarpine 1%–2%:

• Parasympatholytic alkaloid acts on muscarinic receptors found on iris sphincter muscle → causes muscle to contract → miosis → pulls iris away from trabecular network
• 1 drop in affected eye every 15 minutes x 2-4 doses, then every 4 to 6 hours
• Likely does not work until IOP drops below 40-50 mmHg, but still give immediately upon diagnosis
• Note: may make fundoscopic evaluation more difficult for ophtho consultant due to miosis

Reduce volume of aqueous humor

These therapies are usually resolved for failure of other treatments. Hyper osmotic agents such as mannitol are effective but are contraindicated in renal failure and can cause hypotension in the volume depleted patient.

• Mannitol: 1-2 g/kg IV (most common)
• 50% glycerin (Osmoglyn) OR 45% isosorbide (Ismotic): 1.5 mL/kg PO (rarely used)

Steriods

Topical steroids not indicated during acute attack, but may help inflammation after IOP under control.

See Also

• Eye Algorithm (Main)
• Tono-Pen use

References

Authors

Ross Donaldson