Chronic, progressive optic neuropathy characterized by irreversible loss of retinal ganglion cells
Aetiology
Primary Open-Angle Glaucoma (POAG)
- Idiopathic dysfunction of aqueous humor outflow through the trabecular meshwork
Secondary Open-Angle Glaucoma
- Pseudoexfoliation syndrome
- Pigment dispersion syndrome
Risk Factors
- Family history of glaucoma
- Elevated intraocular pressure
- African or Asian ancestry
- Thin central corneal thickness
- Systemic vascular disease (e.g., hypertension, diabetes mellitus)
Clinical presentation
Symptoms
- Typically asymptomatic in early stages
- Gradual, painless loss of peripheral vision
- Central vision affected only in advanced disease
Signs
- Open anterior chamber angle on gonioscopy
- Increased cup-to-disc ratio and asymmetry
- Neuroretinal rim thinning (inferior and superior first)
- Retinal nerve fiber layer defects
Investigations
Clinical Examination
- Measurement of intraocular pressure (tonometry)
- Gonioscopy (after acute attack resolution)
- Funduscopy (often limited during acute phase)
- Nasalization
- Bayonetting
- C/D ratio > 0.5
- Exposed lamina cribrosa
Management
Medical Therapy (First-Line)
- Beta-adrenergic blockers (first line DOC)
- Timolol maleate 0.25-0.5% ED 1-2x/day
- Betaxolol HCl 0.25% ED 2x/day
- Levobunolol 0.25-0.5% ED 1-2x/day
- Carteolol 1% ED 1-2x/day
- Prostaglandin analogues
- Latanoprost 0.005% ED 1x/day
- Bimatoprost 0.03% ED 1x/day
- Alpha-adrenergic agonists
- Carbonic anhydrase inhibitors
- Acetazolamide 250mg PO 3-4x/day
- Dorzolamide 2% ED 3x/day
- Combination therapy when required
Laser Therapy
- Selective laser trabeculoplasty (SLT)
- Argon laser trabeculoplasty (ALT)
Surgical Therapy
- Glaucoma drainage devices
- Minimally invasive glaucoma surgery (MIGS)