Primary Open Angle Glaucoma

Primary open angle glaucoma (POAG) is a chronic, progressive, bilateral (often asymmetric) optic neuropathy with characteristic optic disc cupping and visual field loss, an open and normal appearing anterior chamber angle, and no secondary cause.

• The leading cause of irreversible blindness worldwide after cataract. Prevalence about 2 to 3 percent over age 40, rising to above 10 percent in the oldest age groups; about 4 to 5 times higher in people of African descent, with earlier onset and more rapid progression.
• Risk factors: raised intraocular pressure (the only modifiable factor), age, African ancestry, family history (first degree relative increases risk 4 to 9 times), thin central corneal thickness (under 540 micrometres), high myopia, low ocular perfusion pressure, diabetes, and disc haemorrhage.
• Mechanism: raised resistance to aqueous outflow in the trabecular meshwork, pressure related and vascular damage to retinal ganglion cell axons at the lamina cribrosa.

• Asymptomatic until late; central acuity is preserved until advanced disease, and the patient may notice only missed steps, bumping into objects, or tunnel vision.
• Intraocular pressure often above 21 mmHg (but up to one third of patients have normal pressure on a single measurement).
• Optic disc: increased vertical cup to disc ratio (over 0.6 or asymmetry over 0.2 between eyes), focal or diffuse neuroretinal rim thinning (inferior and superior poles first, violating the ISNT rule), notching, disc haemorrhage (Drance haemorrhage), bayoneting of vessels, peripapillary atrophy, retinal nerve fibre layer defects.
• Visual field defects: paracentral scotoma, arcuate (Bjerrum) scotoma, nasal step, then tunnel vision with preserved central island and temporal crescent.
• Normal anterior chamber depth and open angle on gonioscopy, a relative afferent pupillary defect in asymmetric advanced disease.

• Tonometry (Goldmann applanation, with central corneal thickness correction), diurnal variation if needed.
• Gonioscopy to confirm open angle and exclude secondary causes (pigment, recession, neovascularisation).
• Dilated optic disc examination with stereoscopic assessment and photography.
• Optical coherence tomography of the retinal nerve fibre layer, ganglion cell complex and optic nerve head, which detects loss before field defects.
• Standard automated perimetry (24-2 and 10-2 programmes): reproducible glaucomatous defects, mean deviation, pattern standard deviation, with confirmation on repeat testing.
• Pachymetry. Exclude non-glaucomatous optic neuropathy if pallor exceeds cupping, if field defects respect the vertical meridian, or onset is young (consider MRI).
• Diagnosis rests on disc and field changes, not on pressure alone.

• Goal: slow progression to preserve vision for the patient's lifetime. Set a target intraocular pressure: for early disease about 20 to 30 percent reduction from baseline (for example, below 18 mmHg), for moderate disease about 30 to 40 percent reduction (below 15 mmHg), and for advanced disease or fast progression about 40 to 50 percent reduction (12 mmHg or below). Each 1 mmHg reduction lowers the risk of progression by about 10 percent.
• First line topical therapy (start with one drug in one eye to assess response, review pressure at 4 to 6 weeks):
  • Prostaglandin analogues: latanoprost 0.005 percent, travoprost 0.004 percent, bimatoprost 0.01 or 0.03 percent, or tafluprost 0.0015 percent, one drop at night (reduction 25 to 33 percent). Side effects: hyperaemia, lash growth, iris and periocular pigmentation, periorbital fat atrophy, macular oedema (aphakia, pseudophakia), reactivation of herpes keratitis.
  • Beta blockers: timolol 0.25 or 0.5 percent twice daily (or gel once daily), betaxolol 0.25 or 0.5 percent twice daily (cardioselective). Contraindicated in asthma, severe COPD, bradycardia, heart block.
  • Alpha agonist: brimonidine 0.15 or 0.2 percent twice or three times daily (allergy, fatigue; avoid in infants).
  • Carbonic anhydrase inhibitors: dorzolamide 2 percent or brinzolamide 1 percent three times daily; oral acetazolamide 250 mg two to four times daily or 500 mg slow release twice daily for short term use (avoid in sulphonamide allergy and renal stones).
  • Rho kinase inhibitor: netarsudil 0.02 percent once daily at night; nitric oxide donating latanoprostene bunod 0.024 percent once daily.
  • Fixed dose combinations (timolol with dorzolamide, brimonidine or latanoprost) improve adherence.
• Laser: selective laser trabeculoplasty (360 degrees, about 100 spots, 0.6 to 1.2 mJ), a first line alternative or adjunct to drops, lowering pressure by about 20 to 30 percent with effect lasting 1 to 5 years; repeatable.
• Surgery when pressure is uncontrolled, progression continues, or adherence fails: trabeculectomy with mitomycin C 0.2 to 0.4 mg/mL for 1 to 3 minutes, glaucoma drainage devices (Ahmed, Baerveldt) and minimally invasive glaucoma surgery (trabecular micro bypass, canaloplasty, goniotomy, subconjunctival gel stent) with cataract surgery.
• Review: pressure every 3 to 6 months, visual fields every 6 to 12 months (more frequently in the first 2 years, 3 fields a year), OCT every 6 to 12 months; counsel about adherence (instillation technique, punctal occlusion), screening of first degree relatives, and driving.