Acute angle-closure glaucoma

Background

Mechanism of acute angle closure.

A. Slit lamp exam of the right eye demonstrating diffusely shallow AC, large pupil, and slightly injected conjunctiva. B. Normal slit lamp photograph of the right eye after resolution of acute angle closure C. Anterior segment of the right eye demonstrating abnormal anterior iris convexity, iridocorneal apposition at the angle, and an anterior lens vault D. Normal anterior segment of the right eye demonstrating horizontal iris, no iridocorneal apposition, anterior iris convexity, or anterior lens vault.

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.

Acute angle-closure glaucoma with mid-dilated pupil and an intraocular pressure of 50 mmHg.

• Abrupt onset of severe (usually unilateral) eye pain
• Blurred vision
• Halos around lights
• Frontal or supraorbital headache
• Nausea / vomiting / abdominal pain
• Fixed, midposition pupil
• Hazy cornea
• Conjunctival injection most prominent at limbus (ciliary flush)
• Rock-hard globe

Differential Diagnosis

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

(A) shallow anterior chamber at presentation (B) closed iridocorneal angles on gonioscopy.

• 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. Elevate head of bed to decrease IOP
4. Place patient in a well lit room (prevent pupillary dilation)
5. Start with a topical beta-blocker, α-agonist 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

α2 agonist

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

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

Facilitate outflow of aqueous humor

Pilocarpine 1%–2%:

• Parasympathomimetic 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
• High-concentration pilocarpine (4%) should NOT be given because it can cause forward displacement of the iris-lens diaphragm.
• Note: may make fundoscopic evaluation more difficult for ophtho consultant due to miosis

Reduce volume of aqueous humor

These therapies are usually reserved 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 given over 45 minutes to minimize cerebral effecfts (most common)
• 50% glycerin (Osmoglyn) OR 45% isosorbide (Ismotic): 1.5 mL/kg PO (rarely used)

Steroids

• Topical steroids not indicated during acute attack, but may help inflammation after IOP under control.
  • Prednisolone acetate 1% 1 gtt every 15 to 30 minutes four times, then q1h

Disposition

• Admit for definitive therapy with iridotomy

See Also

• Eye Algorithm (Main)
• Tono-Pen use
• Open-angle glaucoma