Acute Angle-Closure Glaucoma vs Primary Open-Angle Glaucoma
Acute Angle-Closure Glaucoma and Primary Open-Angle Glaucoma are easy to mix up on the boards. Here's a side-by-side comparison — presentation, workup, imaging, and first-line treatment — drawn from our full outlines.
Acute Angle-Closure Glaucoma vs Primary Open-Angle Glaucoma at a glance
- Acute Angle-Closure Glaucoma: Ophthalmologic emergency — sudden IOP elevation from blocked aqueous outflow; vision loss if not treated within hours.
- Primary Open-Angle Glaucoma: Chronic painless optic neuropathy with progressive visual field loss — leading cause of irreversible blindness worldwide.
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Side-by-side comparison
| Feature | Acute Angle-Closure Glaucoma | Primary Open-Angle Glaucoma |
|---|---|---|
| At a glance | Ophthalmologic emergency — sudden IOP elevation from blocked aqueous outflow; vision loss if not treated within hours. | Chronic painless optic neuropathy with progressive visual field loss — leading cause of irreversible blindness worldwide. |
| Classic presentation | Steamy cornea + mid-dilated fixed pupil + rock-hard eye with severe pain in a hyperopic older woman.; Sudden severe unilateral eye pain and headache; Blurred vision and halos around lights (corneal edema); Nausea and vomiting (vagal response) — often misdiagnosed as abdominal/GI process; Photophobia; Symptoms may follow dim-light… | Progressive optic disc cupping with corresponding nerve fiber bundle visual field defects in a patient with elevated IOP.; Asymptomatic in early disease — vision loss is painless and gradual; Patients rarely notice peripheral field defects until advanced; Trouble with night driving, missing steps, or bumping into things; Central vision… |
| Workup / key labs | Clinical triad: acute pain + corneal edema + IOP >30 mmHg with closed angle on gonioscopy.; No labs delay treatment — clinical diagnosis | Characteristic optic disc and/or nerve fiber layer damage with corresponding visual field defect in an eye with open angle, after exclusion of secondary causes.; Not routinely indicated for diagnosis; Targeted workup (B12, ESR, ACE, syphilis, etc.) if optic neuropathy appears non-glaucomatous |
| Imaging | Goldmann or Tono-Pen IOP measurement — primary objective; Slit-lamp examination: shallow anterior chamber, corneal edema, mid-dilated pupil; Gonioscopy after IOP control — confirms closed angle, evaluates fellow eye; Anterior segment OCT or ultrasound biomicroscopy in equivocal cases | Goldmann applanation tonometry (gold standard) — multiple readings, diurnal variation; Pachymetry — central corneal thickness influences IOP measurement and is an independent risk factor (OHTS); Gonioscopy — confirms open angle and rules out angle closure and secondary causes; Dilated fundus exam and stereoscopic optic disc photography;… |
| First-line treatment | IMMEDIATE ophthalmology consult — vision is time-dependent; Position patient supine to allow lens to fall posteriorly; Topical aqueous suppressants in rapid succession (every minute × 3 then standard dosing):; • Topical beta-blocker — timolol 0.5%; • Topical alpha-2 agonist — apraclonidine 1% or brimonidine 0.2%; • Topical carbonic… | Target IOP reduction of 20-30% from baseline; lower targets for advanced disease (EMGT, AGIS data); Prostaglandin analog (POAG) — latanoprost, bimatoprost, travoprost, tafluprost — once daily at bedtime; most effective IOP-lowering class; side effects: iris darkening, periorbital pigmentation/atrophy, lash growth, conjunctival… |
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