Primary Open-Angle & Normal-Tension Glaucoma

Glaucoma is best understood as a progressive optic neuropathy, with intraocular pressure (IOP) a modifiable risk factor rather than the disease itself. It is the second leading cause of irreversible blindness in Australia in people over 55, and 50–60% of Australian cases remain undiagnosed — the economic cost was $4.3 billion in 2025 (up from $1.9 billion in 2005).

Glaucoma causes irreversible retinal nerve fibre loss, seen as optic disc “cupping” — an increased vertical cup-to-disc ratio.

Classification

Type	Presentation	Urgency
Primary open-angle glaucoma (POAG)	Insidious, asymptomatic, disc cupping ± raised IOP	Routine ophthalmology
Normal-tension glaucoma (NTG)	Glaucomatous disc/field change with normal IOP	Routine ophthalmology
Primary angle-closure glaucoma (chronic)	Progressive peripheral field loss, shallow anterior chamber	Routine ophthalmology
Secondary glaucomas	Steroid-induced, pseudo-exfoliative, uveitic, pigmentary, traumatic, neovascular	As per underlying cause

See acute-glaucoma.md for the acute angle-closure emergency.

Epidemiology and risk factors

• Commonest cause of irreversible blindness in middle age; ~1 in 8 people over 80
• Family history: a first-degree relative confers roughly a 2.5-fold increased risk
• Age: risk rises ~7% per year; those aged 60–69 have roughly triple the risk of those 40–49
• Ethnicity: African and Asian ancestry carry disproportionately higher risk than European ancestry
• Other risk factors: diabetes, myopia (also raises hypermetropia-related angle-closure risk), long-term corticosteroid use, migraine/peripheral vasospasm, abnormal blood pressure, prior eye trauma
• Ocular hypertension remains the single strongest modifiable risk factor — risk rises with each 1 mmHg increment
• Male sex is associated with higher POAG risk; angle-closure glaucoma is more frequent in females

Presentation

• Early: asymptomatic
• Late: insidious peripheral visual field loss; central vision preserved until advanced

Screening (RACGP Red Book-style risk-based approach)

Screen those at higher risk (which is most people over 50):

• First-degree relative with glaucoma → refer for ocular examination 5–10 years earlier than the relative’s age of onset
• Caucasian/Asian patients ≥50 years; patients of African descent ≥40 years
• Any age with: diabetes, myopia, long-term steroid use, migraine/peripheral vasospasm, abnormal BP, prior eye trauma

Refer for optic nerve head examination (ophthalmoscopy), tonometry, and visual field assessment (perimetry) — by an ophthalmologist or optometrist. Follow-up frequency is individualised; no fixed consensus interval exists.

GP-relevant referral thresholds (2026 AJGP framework)

Finding	Likely condition	Action
Sudden VA drop, new field loss, fresh optic-disc (Drance) haemorrhage, or vertical cup-to-disc ratio ≥0.8/asymmetry ≥0.3	Rapidly progressive open-angle glaucoma	Urgent referral ≤1 week
IOP ≥35 mmHg (even asymptomatic), or IOP 25–34 mmHg with a suspicious disc or reproducible visual field defect	Sight-threatening ocular hypertension	Urgent referral ≤48 hours
IOP 22–25 mmHg without other risk factors; or a high-risk patient (age >60, FHx, diabetes, steroid use) even with normal IOP	Possible early POAG/NTG	Routine referral 1–3 months

Formal visual field testing and OCT imaging (used to confirm progression) are outside GP scope — performed by optometrists/ophthalmologists. Direct ophthalmoscopy in an undilated pupil gives only a rough cup-to-disc estimate; interpret cautiously, but marked inter-eye asymmetry or a clearly enlarged cup still warrants referral. Tonometry is not routinely available in general practice and is not required to trigger a referral decision.

Management

Managed by ophthalmology. Treatment cannot restore lost vision but slows disease progression — lifelong therapy aimed at reducing IOP:

Line	Class	Mechanism	Example	Notable adverse effects
First	Prostaglandin analogues	↑ uveoscleral outflow	Latanoprost	Iris/lash pigmentation, local irritation
Second	β-blockers	↓ aqueous production	Timolol	Systemic: bradycardia, hypotension, bronchospasm (caution in cardiac/respiratory disease)
Third	α-agonists	↓ production + ↑ outflow	—	Fatigue, dry mouth, drowsiness, delayed allergic conjunctivitis
Third	Carbonic anhydrase inhibitors	↓ production	—	Paraesthesia, GI upset, electrolyte disturbance, metabolic acidosis (oral agents especially)

PBS note: the 60-day dispensing model now allows up to 12 months’ supply for some glaucoma medications, alongside typically annual ophthalmology review — reinforcing drop technique, monitoring for the adverse effects above, and timely script renewal are the key GP contributions to preventing avoidable progression.

The GP’s coordinating role

• Coordinate and manage — ensure continuity of topical therapy, address comorbidities, arrange timely review
• Refer rather than defer — any suspected glaucoma (elevated IOP, suspicious disc, relevant symptoms/risk factors) goes to an eye care specialist for baseline assessment; go directly to ophthalmology when red-flag criteria (table above) are met
• Shared records — copy referral correspondence to both optometrist and ophthalmologist where a shared-care model is in place