Acute Closed-Angle Glaucoma

Pathology of Raised Intraocular Pressure

• Mechanism: Resulting from the failure of the aqueous humor drainage system.
• Angle Closure: Due to sudden blockage of the trabecular meshwork by the iris.
• Impact: Causes loss of vision by compression of the optic disc.
• IOP Levels: Intraocular pressure (IOP) > 21 mmHg.
• Aqueous Humor Flow:
  • Produced by the ciliary bodies in the posterior segment.
  • Flows to the anterior chamber (AC).
  • Resorbed through the trabecular meshwork into the canal of Schlemm.
  • Drains into episcleral veins.

Primary Causes:

1. Pupillary Block:
   • Occurs when the posterior iris contacts the lens.
   • Blocks the flow of aqueous humor from the posterior to the anterior chamber.
   • Increased posterior chamber pressure pushes the iris forward, blocking the trabecular meshwork.
2. Angle Crowding:
   • Abnormally configured iris (e.g., plateau iris) obstructs the angle during pupillary dilatation.

Precipitating Factors:

• Topical mydriatics.
• Anticholinergic and sympathomimetic drugs.
• Emotional stimuli.
• Accommodation (e.g., reading).
• Dim light.

Secondary Causes:

• Peripheral anterior synechiae (PAS), e.g., chronic uveitis.
• Neovascular glaucoma, e.g., diabetes mellitus.
• Membranous obstruction, e.g., iridocorneal endothelial syndrome.
• Lens-induced, e.g., large lens or small eye.
• Drugs, e.g., topiramate and sulfonamides (cause ciliary body swelling).
• Choroidal swelling, e.g., central retinal vein occlusion (CRVO) or post-op/laser treatment.
• Posterior segment tumor.
• Hemorrhagic choroidal detachment.
• Aqueous misdirection syndrome.

Risk Factors:

• Age: Typically affects individuals over 55 years.
• Gender: Higher prevalence in females.
• Ethnicity: More common in Southeast Asian, Chinese, and Inuit populations.
• Family History: Genetic predisposition.
• Hyperopia: Farsightedness with shallower anterior chamber depth.
• Medications: Certain drugs can precipitate or exacerbate ACAG.

History:

• Classic triad of symptoms:
  • Severe eye pain.
  • Headache.
  • Nausea/vomiting.
• Often rapid onset.
• Additional symptoms:
  • Blurred vision.
  • Halos around lights.

Examination:

• Decreased visual acuity.
• Injected conjunctiva.
• Fixed dilated pupil.
• Corneal microcystic edema.
• Tonometry: Elevated IOP typically ranging from 50 to 80 mm Hg (normal range 10-21 mm Hg).
• Fundoscopy: Pronounced cupping.

Management

• Urgent ophthalmology referral — severe and permanent damage may occur within hours.
• head up — at least 30 degrees
• topical b-blocker
  • timolol 0.5% 1-2 drops as a single dose (caution if bronchospasm or heart failure)
• topical cholinergic (miotic)
  •  pilocarpine 2 or 4 % eyedrops — one-two drops q15min until pupillary constriction occurs (a 2% solution may be better in blue-eyed patients and a 4% solution in brown-eyed patients); especially if angle crowding is suspected.
• topical alpha2-agonist
  • apraclonidine 1% 1-2 drops as a single dose.
• carbonic anhydrase inhibitor
  • acetazolamide 500mg IV, or PO if IV not available (not if topiramate or sulfonamide-induced acute closed angle glaucoma)
• Additional treatments:
  • symptomatic treatment of pain and nausea/ vomiting
  • if IOP and visual acuity have not improved in 1 hour, consider mannitol (e.g. 1-2 g/kg IV over 45 minutes)
  • topical steroid — e.g., prednisolone acetate 1%