Glaucoma management in adults: an update

Glaucoma management in adults: an update

Keywords

• eye drops
• glaucoma
• ocular hypertension
• prostaglandin analogues
• vision loss

Aust Prescr 2026:49:182-7

https://doi.org/10.18773/austprescr.2026.038

 

SUMMARY

Glaucoma is a group of progressive optic neuropathies that cause optic nerve damage and visual field defects. It is typically asymptomatic until irreversible vision loss has occurred. Early detection relies on regular comprehensive eye examinations, with targeted case finding particularly important for people at increased risk.

Lowering intraocular pressure is the only proven strategy to slow disease progression, and treatment should be individualised. Topical prostaglandin analogues (eye drops) are commonly used as first-line medical therapy, with once-daily dosing associated with improved adherence. Topical beta blockers may be added if the target intraocular pressure is not achieved or disease progression occurs. Patient adherence, eye drop technique and adverse effects should be reviewed regularly.

Selective laser trabeculoplasty (a laser treatment that helps fluid drain out of the eye, thereby lowering intraocular pressure) is an effective first-line alternative to eye drops.

Urgent referral to an ophthalmologist or emergency department is required for a suspected acute angle-closure attack. Symptoms include severe eye pain, headache, blurred vision, halos around lights, nausea and vomiting.

 

Introduction

Glaucoma is a group of progressive optic neuropathies characterised by retinal ganglion cell loss, resulting in structural optic nerve damage and corresponding visual field defects. Although commonly associated with elevated intraocular pressure (IOP), glaucoma may occur at normal IOP, and diagnosis is based on characteristic structural and functional changes. Although early diagnosis and appropriate management can prevent vision loss, glaucoma remains a leading cause of irreversible blindness worldwide because it is typically gradual and asymptomatic in the early stages, often resulting in delayed diagnosis.^1,2

In Australia, an estimated 300,000 to 380,000 people are affected by glaucoma, and prevalence increases with age. Importantly, approximately half of affected individuals are unaware they have the condition.³ Early identification, timely referral and appropriate management are therefore essential to prevent avoidable vision loss.

General practitioners, pharmacists, nurse practitioners and optometrists, play an important role in recognising individuals at risk, supporting treatment adherence, monitoring adverse effects, reinforcing patient education and facilitating timely referral to an optometrist or ophthalmologist when indicated.

This article provides an update on glaucoma management in adults, focusing on pharmacological therapy and primary care management.

 

Types of glaucoma

Glaucoma is broadly classified into primary and secondary types.

Primary glaucoma

Primary open-angle glaucoma is the most common form of glaucoma. It is characterised by a structurally open anterior chamber angle and progressive optic neuropathy, leading to characteristic visual field loss. This condition is typically chronic, painless and asymptomatic in its early stages, with visual impairment often developing only in advanced disease. IOP may be elevated or remain within the population reference range.^1,2

A subtype, often referred to as normal-tension glaucoma, occurs despite IOP measurements within the ‘normal’ range, a statistical construct defined as 2 standard deviations from the mean IOP in large population-based surveys. This subtype has been associated with vascular risk factors such as migraine, Raynaud phenomenon, systemic hypotension and obstructive sleep apnoea, and may be more prevalent in some Asian populations.^1,2

Primary angle-closure glaucoma is characterised by closure of the anterior chamber angle and impaired aqueous humour outflow with associated optic neuropathy. Anterior chamber angle closure may develop gradually or suddenly. Acute angle closure typically presents with sudden onset of severe eye pain, headache, blurred vision, halos around lights, nausea and vomiting. Examination findings may include a red eye (conjunctival hyperaemia), corneal oedema, a mid-dilated fixed pupil and markedly elevated IOP. This is an ophthalmic emergency requiring urgent (same-day) ophthalmology assessment; if an ophthalmologist is not accessible, the patient should be referred to an emergency department.¹

Secondary glaucoma

Secondary glaucoma results from identifiable ocular or systemic conditions that impair aqueous humour outflow or increase resistance to drainage, leading to elevated IOP and optic nerve damage. Common subtypes include:^1,2

• neovascular glaucoma – caused by abnormal blood vessel growth on the iris and drainage angle, most commonly secondary to retinal ischaemia such as proliferative diabetic retinopathy or retinal vein occlusion
• pigmentary glaucoma – caused by dispersion of pigment from the iris, which accumulates within the eye’s drainage system and impairs aqueous humour outflow
• pseudoexfoliative glaucoma – caused by deposition of fibrillar extracellular material within the anterior segment of the eye, resulting in obstruction of aqueous humour drainage. It is often associated with higher IOP, faster disease progression and greater treatment complexity than primary open-angle glaucoma
• uveitic glaucoma – associated with intraocular inflammation, which may impair aqueous humour drainage through inflammatory debris, structural changes or corticosteroid treatment used to manage uveitis.

 

Screening and risk factors

Glaucoma is often asymptomatic until irreversible vision loss has occurred. Although population-wide screening is not currently recommended in Australia, targeted case finding in individuals with recognised risk factors (Box 1) is encouraged. Glaucoma Australia recommends a comprehensive eye examination with an optometrist every 2 years from the age of 50 years, or from the age of 40 years for people with a family history of glaucoma or with Asian or African ancestry.⁴ More frequent review may be appropriate according to risk profile and previous examination findings; an ophthalmologist may also provide surveillance when clinically indicated.⁵

 

Diagnosis

A diagnosis of glaucoma is typically made by an optometrist or ophthalmologist using a combination of structural and functional assessments. Glaucoma assessment may include:^1,6

• direct visualisation of the optic disc to assess disc size and shape, neuroretinal rim thinning and cup-to-disc ratio, Drance haemorrhage, retinal nerve fibre layer dropout and peripapillary atrophy
• Goldmann applanation tonometry (the gold standard) to measure IOP
• direct visualisation of the anterior chamber angle using gonioscopy
• optical coherence tomography to identify focal or generalised neuroretinal rim or retinal nerve fibre layer thinning
• standard automated perimetry (e.g. Humphrey visual field analysis; the gold standard) to assess optic nerve function.

 

Management

The primary goal of glaucoma treatment is to reduce IOP to an individualised target in order to slow or prevent progressive optic nerve damage and visual field loss. Target IOP should be individualised according to baseline IOP, disease severity, risk factors, rate of progression and the lifetime risk of functional visual impairment. Although lowering IOP is the cornerstone of treatment for most glaucoma subtypes, management strategies may differ according to the underlying glaucoma type, disease severity and patient factors. Acute angle closure requires urgent specialist management.^1,2

Regular follow-up with an optometrist or ophthalmologist is essential to monitor IOP, optic nerve structure and visual function, and to adjust treatment if disease progression occurs.

Pharmacological treatment

Pharmacological treatment primarily consists of topical ocular hypotensive drugs (eye drops), with systemic medications reserved for select situations, such as acute or severe IOP elevation. The main topical drug classes include prostaglandin analogues, beta blockers, alpha₂-agonists, carbonic anhydrase inhibitors and cholinergic agents (Table 1). Topical therapy is typically introduced in a stepwise manner, guided by target IOP, disease severity and patient-specific factors. Treatment is generally long term and often lifelong because glaucoma is a chronic progressive condition.

Table 1 Pharmacological treatments for glaucoma^6,7

Drug class	Mechanism of action	Efficacy (IOP reduction)	Dosage frequency	Place in therapy	Adverse effects	Contraindications and precautions (including drug interactions)	PBS status8
Prostaglandin analogues (topical) Latanoprost Travoprost Bimatoprost	Increase uveoscleral outflow	25 to 33% (most effective)	Once daily at night	First line	Red eye, iris pigmentation (irreversible), eyelash growth and prostaglandin-associated periorbitopathy; consider switching drug if intolerable	Use with caution in uveitis (may worsen inflammation) and history of herpetic keratitis (may increase risk of reinfection) No clinically significant drug interactions	PBS listed
Beta blockers (topical) Timolol Betaxolol (restricted availability; rarely used)	Decrease aqueous humour production	20 to 25%	Once or twice daily	Second line or adjunct to topical prostaglandin analogues	Dry eye (use preservative-free if needed), bradycardia, hypotension, bronchospasm	Contraindicated in asthma, COPD and heart block Additive bradycardia with systemic beta blockers, calcium channel blockers and digoxin	Timolol: PBS listed Betaxolol: not PBS listed
Alpha2-agonists (topical) Brimonidine Apraclonidine	Decrease aqueous humour production and increase uveoscleral outflow	15 to 20%	2 to 3 times daily	Adjunct or short term (apraclonidine)	Allergic conjunctivitis (discontinue if severe), dry mouth, sedation	Brimonidine: contraindicated in patients receiving MAO inhibitors; use with caution with other CNS depressants (additive sedation) and in older adults (greater susceptibility to CNS effects) Apraclonidine: short-term use only (usually in a clinical setting), because tachyphylaxis is common	Brimonidine: PBS listed Apraclonidine: not PBS listed
Carbonic anhydrase inhibitors (topical) Dorzolamide Brinzolamide	Decrease aqueous humour production	15 to 20%	2 to 3 times daily	Adjunct	Ocular irritation, bitter taste	Use with caution in sulfonamide allergy (rare cross-reactivity) Systemic drug interactions minimal	PBS listed
Carbonic anhydrase inhibitors (oral) Acetazolamide	Decrease aqueous humour production	20 to 30%	As needed for acute IOP reduction, or 2 to 4 times daily	Acute or short term	Paraesthesia, fatigue, metabolic acidosis, electrolyte disturbance	Contraindicated in patients with creatinine clearance less than 10 mL/min or sulfonamide allergy Interacts with diuretics (electrolyte imbalance), lithium (reduced concentrations) and high-dose salicylates (toxicity)	PBS listed
Cholinergic agents (miotics) (topical) Pilocarpine	Increase trabecular outflow	15 to 25%	Up to 4 times daily	Limited use	Pupil constriction (miosis), brow ache, reduced vision in low light	Contraindicated in uveitis; use with caution in patients susceptible to retinal detachment, including those with previous retinal detachment, pre-existing retinal damage or high myopia Systemic drug interactions rare	PBS listed
CNS = central nervous system; COPD = chronic obstructive pulmonary disease; IOP = intraocular pressure; MAO = monoamine oxidase; PBS = Pharmaceutical Benefits Scheme (Australia)

Topical prostaglandin analogues are generally recommended as first-line therapy because they provide substantial IOP reduction, require once-daily dosing and have minimal systemic adverse effects (Table 1). Common adverse effects include red eye, eyelash growth, increased iris pigmentation and prostaglandin-associated periorbitopathy (deepening of the upper eyelid sulcus, eyelid tightening or drooping and a sunken-eye appearance). If adverse effects are problematic, switching to an alternative prostaglandin analogue, a different medication class or a preservative-free formulation may improve tolerability.¹

If target IOP is not achieved or disease progression occurs, a second drug may be added, commonly a topical beta blocker such as timolol, provided there are no contraindications (Table 1). Beta blockers may cause ocular surface dryness and systemic adverse effects including bradycardia, hypotension and bronchospasm. They should generally be avoided in patients with asthma, chronic obstructive pulmonary disease, heart block or symptomatic bradycardia.¹

Other drugs may be used as adjunctive therapy, including alpha₂-agonists (e.g. brimonidine) and topical carbonic anhydrase inhibitors (e.g. dorzolamide, brinzolamide) (Table 1). Brimonidine may cause allergic conjunctivitis, dry mouth, fatigue or sedation, whereas topical carbonic anhydrase inhibitors are commonly associated with transient ocular discomfort and a bitter taste. Fixed-combination preparations may simplify treatment regimens, improve adherence and reduce preservative exposure.¹

Systemic carbonic anhydrase inhibitors, such as acetazolamide, are generally reserved for short-term use in acute situations requiring rapid IOP reduction, including acute angle closure or markedly elevated IOP while awaiting definitive treatment.¹

Patient adherence is a major determinant of treatment success. Ocular surface disease and irritation are common and may impair quality of life and treatment adherence. Patients with persistent symptoms should be reviewed by their optometrist or ophthalmologist, and a switch to preservative-free lubricants or glaucoma medication formulations may be considered. Patients should be counselled on correct eye drop administration technique, including hand hygiene, avoiding contact between the bottle tip and the eye, and adherence to prescribed dosing schedules. When multiple eye drops are required, at least 5 minutes should be allowed between administration to minimise washout. Nasolacrimal occlusion (blockage of the tear ducts by gently pressing the inner corner of the eye) for 1 to 2 minutes after instillation may reduce systemic absorption and minimise adverse effects. Patients can also be directed to Glaucoma Australia for free education and support.

Nonpharmacological treatment

Nonpharmacological treatment options may be considered when target IOP is not achieved with pharmacological therapy, medications are poorly tolerated, adherence is problematic or as first-line treatment in select patients. Referral to an ophthalmologist is required for consideration of these interventions.

Selective laser trabeculoplasty (SLT) is a laser procedure that improves aqueous humour drainage through the trabecular meshwork, thereby reducing IOP. Increasing evidence supports SLT as an effective first-line alternative to topical medications in select patients with open-angle glaucoma or ocular hypertension, as well as an adjunctive treatment when further IOP reduction is required. The effect may diminish over time, but SLT can be repeated when clinically appropriate.⁹

Laser peripheral iridotomy creates a small opening in the peripheral iris to improve aqueous humour flow between the posterior and anterior chambers of the eye. It is indicated for primary angle-closure glaucoma and eyes considered at risk of angle closure.¹

Surgical interventions may be considered when glaucoma progresses despite maximally tolerated pharmacological therapy, adherence is poor, medications are not well tolerated or substantial IOP reduction is required. Minimally invasive glaucoma surgery, a group of procedures designed to minimise ocular tissue trauma, may be appropriate for select patients because of its favourable safety profile and rapid recovery, although its IOP-lowering effect is generally modest. More invasive procedures, such as trabeculectomy and glaucoma drainage device implantation, are generally reserved for advanced or refractory disease.¹

Newer and emerging therapies

Several newer glaucoma medications that provide additional IOP lowering are available internationally but not in Australia. Rho-kinase inhibitors, such as netarsudil and ripasudil, increase aqueous humour outflow through the trabecular meshwork; nitric oxide–donating prostaglandin analogues, such as latanoprostene bunod, combine prostaglandin activity with nitric oxide–mediated enhancement of trabecular outflow.¹

Emerging therapies aim to address limitations of conventional topical treatment, particularly poor adherence and limited ocular bioavailability. These emerging therapies include sustained-release intraocular implants, drug-eluting punctal plugs and contact lens–based drug-delivery systems. By reducing dosing frequency and improving drug delivery, these technologies may improve long-term treatment adherence and clinical outcomes. However, their availability and role in routine clinical practice remain limited at present.^1,2

 

When to refer

Appropriate referral pathways depend on the healthcare professional involved and the urgency of the clinical situation. General practitioners, pharmacists and nurse practitioners may refer patients to an optometrist for assessment of glaucoma risk or suspected disease, whereas optometrists may refer to an ophthalmologist when glaucoma is suspected, confirmed or progressing (Box 2). Effective communication between healthcare professionals helps optimise treatment and facilitate timely escalation of care when required.¹⁰

 

Conclusion

Glaucoma is a chronic, progressive optic neuropathy and a leading cause of irreversible vision loss. Early identification of at-risk individuals and timely referral are essential to prevent disease progression. Management is centred on reducing IOP to an individualised target, most commonly through long-term topical pharmacological therapy. Primary care clinicians play an important role in promoting regular eye examinations, making timely referrals, supporting ongoing management and treatment adherence, recognising adverse effects and reinforcing the need for regular follow-up.

 

Key practice points

This article was finalised on 28 August 2026.

Conflicts of interest: The authors declared no conflicts of interest.

This article is peer reviewed.

 

References

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7. Australian Medicines Handbook Pty Ltd. Australian Medicines Handbook. 2026. https://amhonline.amh.net.au/auth [cited 2026 Aug 11]
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10. Eiselen C, Chong EW, Tse J, Atik A. Glaucoma in general practice: An updated framework for Australian general practitioners. Aust J Gen Pract 2026;55:443–8.