Primary Open-Angle Glaucoma (POAG)

📖 Overview

• 🟢 POAG accounts for ~90% of all glaucoma cases.
• 😶 Silent disease: gradual, painless rise in intraocular pressure (IOP), often unnoticed until late.
• ⚠️ Typically asymptomatic until significant optic nerve damage and visual field loss occur → importance of early screening.

🧬 Aetiology

• 📈 Progressive rise in IOP (often 20–30 mmHg) damages the optic nerve head over years.
• 🚱 Due to impaired aqueous humor drainage through the trabecular meshwork, despite an “open” anterior chamber angle.

⚡ Risk Factors

• 👴 Age > 40 years
• 👨‍👩‍👦 Family history of glaucoma
• 🏿 Black ethnicity (higher risk and earlier onset)
• 👓 High myopia (short-sightedness)
• 🩸 Systemic conditions: diabetes, hypertension, thyroid disease

🔍 Clinical Presentation

• ❌ Usually asymptomatic until late disease.
• 🔴 Optic Disc Cupping: cup-to-disc ratio > 0.7, often asymmetric.
• 👁️‍🗨️ Visual Field Defects: classically nasal step, arcuate scotoma → progressing to tunnel vision.
• ⏳ Progression: peripheral vision lost first, central vision threatened later → untreated cases risk total blindness.

💊 Management (Target IOP < 21 mmHg)

• Topical Medications:
  • 💧 Beta-Blockers (Timolol, Betaxolol): ↓ aqueous humor production. ⚠️ Avoid in asthma, COPD, bradycardia.
  • 🌿 Prostaglandin Analogs (Latanoprost): ↑ aqueous outflow. Once daily; can cause iris darkening.
  • 🌊 Pilocarpine: miotic agent ↑ trabecular outflow, but causes miosis → ↓ night vision & brow ache.
  • 💊 Carbonic Anhydrase Inhibitors (Acetazolamide, Dorzolamide): ↓ aqueous humor production; oral forms reserved for acute/short-term use.
• Procedures:
  • 🔦 Laser Trabeculoplasty (e.g., Argon): improves outflow via trabecular meshwork.
  • 🔧 Trabeculectomy: creates a drainage fistula → lowers IOP. Gold standard for refractory disease.
  • 🌀 Minimally Invasive Glaucoma Surgery (MIGS): newer safer options (stents, shunts) for moderate disease.

📈 Prognosis

• 🔎 With regular screening + treatment, most patients preserve useful vision for life.
• ⚠️ Untreated → progressive field loss and irreversible blindness.
• 👓 Regular monitoring of IOP, visual fields, and optic disc is essential.

📚 References

• NHS – Glaucoma
• Glaucoma Research Foundation

Cases - Primary Open-Angle Glaucoma (POAG)

• Case 1 - Asymptomatic detection 👓: A 62-year-old man attends a routine optician’s appointment. Intraocular pressure (IOP) 28 mmHg, optic disc shows increased cup-to-disc ratio, and visual field test reveals arcuate scotoma. He has no symptoms. Diagnosis: POAG detected on screening. Managed with topical prostaglandin analogue (latanoprost) and referral to ophthalmology.
• Case 2 - Gradual visual loss 🕶️: A 70-year-old woman reports difficulty with peripheral vision and frequent tripping. Central vision is preserved. Exam: elevated IOP, optic disc cupping, bilateral peripheral visual field loss. Diagnosis: established POAG. Managed with topical therapy (beta-blocker, prostaglandin analogue), laser trabeculoplasty if uncontrolled.
• Case 3 - Strong family history 🧬: A 55-year-old man with a father blinded by glaucoma attends for review. He is asymptomatic but has borderline raised IOP, enlarged cup-to-disc ratio, and thinning of retinal nerve fibre layer on OCT. Diagnosis: early POAG in high-risk patient. Managed with prophylactic IOP-lowering drops and lifelong surveillance.

Teaching Point 🩺: Primary open-angle glaucoma = chronic, progressive optic neuropathy due to impaired aqueous outflow → optic nerve cupping and visual field loss. Key risk factors: age, family history, African/Caribbean ethnicity, myopia, diabetes, hypertension. Insidious onset: patients often unaware until late. Management: prostaglandin analogues first-line, then beta-blockers, carbonic anhydrase inhibitors, or surgical/laser trabeculoplasty if progression.