Medicine – Glaucoma

Glaucoma is a group of progressive optic neuropathies characterised by damage to the optic nerve and retinal nerve fibre layer, producing characteristic visual-field loss. Raised intraocular pressure (IOP) is the most important modifiable risk factor, but glaucoma can occur even when IOP is within the statistically normal range.

The two major forms considered here are acute angle-closure glaucoma and primary open-angle glaucoma. They differ substantially in their presentation, mechanism, urgency, and treatment.

1. Acute Angle-Closure Glaucoma

Acute angle-closure glaucoma is an ophthalmic emergency in which the drainage angle between the iris and cornea suddenly closes, causing a rapid rise in intraocular pressure.

It usually affects one eye during an acute attack, although the fellow eye is often anatomically predisposed and therefore also at future risk.

2. Normal Aqueous Humour Drainage

Aqueous humour is produced by the ciliary body in the posterior chamber.

It normally passes through the pupil into the anterior chamber and then drains mainly through the:

Trabecular meshwork → Schlemm canal → episcleral venous circulation.

A smaller proportion leaves through the uveoscleral pathway.

3. Mechanism of Acute Angle Closure

In susceptible eyes, the peripheral iris can obstruct the trabecular meshwork, preventing normal aqueous humour drainage.

Aqueous humour continues to be produced while its outflow is severely reduced.

The result is:

Blocked aqueous outflow → rapid rise in IOP → corneal oedema + iris ischaemia + optic nerve damage.

Without rapid treatment, permanent visual loss can occur.

4. Effect of Pupil Dilatation

An acute attack is particularly likely when the pupil becomes mid-dilated, because this anatomical position can increase contact between the iris and lens and promote pupillary block in susceptible eyes.

Attacks may therefore occur in dim or dark environments, where physiological pupil dilatation occurs.

Certain medications capable of causing mydriasis may also precipitate angle closure in anatomically predisposed individuals.

Clinical Features of Acute Angle-Closure Glaucoma

5. Painful Red Eye

The classic presentation is a sudden, intensely painful red eye.

The pain can be severe and may radiate around the eye or into the forehead.

6. Reduced Vision

Patients develop rapidly reduced or blurred vision.

They may describe coloured halos around lights, particularly because corneal oedema alters the passage of light through the cornea.

7. Mid-Dilated Pupil

The pupil is classically mid-dilated and poorly reactive or fixed.

Therefore, the traditional description of simply a “dilated pupil” is better remembered as:

Mid-dilated + fixed/sluggish pupil.

8. Hazy Cornea

Markedly elevated intraocular pressure causes corneal oedema, producing a characteristic cloudy or hazy appearance.

The hazy cornea contributes to the patient’s reduced vision and halos around lights.

9. Other Symptoms

The severe autonomic response to acute angle closure may cause headache, nausea, and vomiting.

This is clinically important because patients can occasionally be mistaken for having a neurological or gastrointestinal illness rather than an ophthalmic emergency.

Treatment of Acute Angle-Closure Glaucoma

The immediate objective is to rapidly reduce intraocular pressure, followed by definitive treatment to prevent recurrence.

Urgent ophthalmological assessment is required.

10. Acetazolamide

Acetazolamide is a carbonic anhydrase inhibitor that reduces aqueous humour production by the ciliary body.

It can be given systemically during an acute attack and helps rapidly lower intraocular pressure.

11. Topical β-Blockers

A topical β-blocker such as timolol can reduce aqueous humour production.

This provides an additional mechanism for lowering intraocular pressure.

Systemic absorption can occur, so β-blockers require caution in patients with conditions such as asthma, significant bradycardia, or heart block.

12. Other Pressure-Lowering Treatment

Additional topical pressure-lowering agents may be used according to the clinical situation, including α₂-adrenergic agonists.

In very severe cases, an osmotic agent may occasionally be required when the intraocular pressure remains extremely high.

13. Pilocarpine

Pilocarpine is a muscarinic agonist that causes pupillary constriction (miosis).

This can pull the peripheral iris away from the drainage angle and improve aqueous outflow once the intraocular pressure has started to fall.

A useful correction to the original wording is that pilocarpine does not literally “open the canal of Schlemm.” Its main effect is to alter iris configuration and improve access to the trabecular drainage angle.

It may initially be ineffective when the IOP is extremely high because the ischaemic iris sphincter may not respond.

14. Laser Peripheral Iridotomy

The definitive treatment for pupillary-block angle closure is usually laser peripheral iridotomy.

A small opening is created in the peripheral iris, providing an alternative pathway for aqueous humour to move from the posterior to the anterior chamber.

This equalises pressure across the iris and helps prevent recurrent pupillary block.

The fellow eye frequently receives prophylactic laser iridotomy because it may have similar anatomical risk.

15. Surgical Iridectomy

Surgical peripheral iridectomy can achieve a similar result but is now generally reserved for situations in which laser treatment cannot be performed or is unsuccessful.

Therefore, the modern term to remember first is laser peripheral iridotomy, rather than routine surgical iridectomy.

16. Primary Open-Angle Glaucoma

Primary open-angle glaucoma (POAG) is a chronic progressive optic neuropathy in which the anterior chamber angle remains anatomically open, but aqueous humour drainage through the trabecular pathway is impaired.

Unlike acute angle closure, the disease usually develops slowly and painlessly over many years.

17. Intraocular Pressure

Raised intraocular pressure is an important risk factor.

Historically, an IOP above 21 mmHg was used as an important threshold.

However, this should not be treated as the definition of glaucoma.

Some people have:

IOP >21 mmHg without optic nerve damage → ocular hypertension.

Others develop:

Glaucomatous optic nerve damage despite IOP ≤21 mmHg → normal-tension glaucoma.

Therefore, glaucoma is fundamentally an optic neuropathy, not simply an elevated pressure measurement.

18. Insidious and Asymptomatic Onset

Primary open-angle glaucoma typically develops gradually and without pain.

Central visual acuity may remain normal until relatively late, so patients can have substantial optic nerve damage before noticing symptoms.

This is why screening of at-risk individuals and routine eye examinations are important.

19. Optic Disc Cupping

Progressive loss of retinal ganglion cell axons produces characteristic cupping of the optic disc.

The cup-to-disc ratio may increase, and progressive neuroretinal rim thinning can occur.

The important relationship is:

Retinal ganglion cell loss → optic nerve damage → increased disc cupping → visual-field loss.

Visual-Field Defects

20. Arcuate Scotoma

Glaucoma produces characteristic visual-field abnormalities because damage follows the distribution of retinal nerve fibres.

An arcuate scotoma is a classic defect.

It may extend from the region of the blind spot in an arc toward the nasal visual field.

21. Other Visual-Field Changes

Early abnormalities may include paracentral defects and nasal steps.

As glaucoma progresses, arcuate defects enlarge and peripheral visual fields become increasingly restricted.

Very advanced disease may eventually produce severe tunnel vision and irreversible blindness.

Treatment of Chronic Open-Angle Glaucoma

The objective is to lower intraocular pressure sufficiently to slow or prevent further optic nerve damage.

Treatment does not usually restore optic nerve fibres that have already been lost.

22. Prostaglandin Analogues

Prostaglandin analogues, such as latanoprost, are major first-line medications for primary open-angle glaucoma.

They lower intraocular pressure primarily by increasing aqueous humour outflow, particularly through the uveoscleral pathway.

They are effective and can usually be administered once daily.

23. Topical β-Blockers

Timolol and other topical β-blockers lower IOP by reducing aqueous humour production.

They remain useful treatments but may be unsuitable for some patients because of systemic cardiovascular and respiratory effects.

24. Carbonic Anhydrase Inhibitors

Topical carbonic anhydrase inhibitors such as dorzolamide reduce aqueous humour formation.

They may be used alone or in combination with other pressure-lowering medications.

25. Other Topical Treatments

Other medications include α₂-adrenergic agonists, which can reduce aqueous production and influence aqueous outflow.

Combination preparations are frequently used when a single drug does not adequately control intraocular pressure.

26. Pilocarpine

Pilocarpine can increase conventional aqueous outflow by causing ciliary muscle contraction and altering the trabecular drainage pathway.

Although historically important, it is used much less commonly as routine long-term treatment for primary open-angle glaucoma because modern agents are generally better tolerated.

Laser and Surgical Treatment

27. Laser Trabeculoplasty

Laser trabeculoplasty, particularly selective laser trabeculoplasty (SLT), improves aqueous drainage through the trabecular meshwork.

It is now an important treatment for open-angle glaucoma and may be used as initial therapy or when medication does not provide adequate control, depending on local practice and patient factors.

28. Glaucoma Surgery

When medication and/or laser treatment fail to achieve the required pressure reduction, glaucoma surgery may be necessary.

Procedures such as trabeculectomy create an alternative pathway for aqueous drainage.

Various drainage implants and minimally invasive glaucoma procedures are also available for selected patients.

29. Iridectomy and Open-Angle Glaucoma

The original notes list iridectomy as a treatment for chronic open-angle glaucoma.

This requires correction.

Peripheral iridotomy/iridectomy is principally a treatment for angle-closure mechanisms, particularly pupillary block. It is not routine treatment for primary open-angle glaucoma, where the angle is already open.

30. Acute Angle-Closure Glaucoma – Note Form

Onset: sudden.

Eye involvement: usually unilateral during an acute attack.

Pain: severe painful red eye.

Vision: rapidly reduced or blurred; coloured halos may occur.

Cornea: cloudy or hazy because of corneal oedema.

Pupil: characteristically mid-dilated and poorly reactive.

IOP: markedly elevated.

Mechanism: peripheral iris obstructs the trabecular drainage angle.

Trigger: may occur when the pupil becomes mid-dilated, such as in dim light.

Systemic symptoms: headache, nausea, and vomiting may occur.

Initial treatment: rapid pressure reduction with agents such as systemic acetazolamide and topical pressure-lowering medication.

Pilocarpine: produces miosis and can help reopen the drainage angle after pressure begins to fall.

Definitive treatment: laser peripheral iridotomy.

Fellow eye: often requires prophylactic assessment and treatment because it may have the same anatomical predisposition.

Clinical importance: ophthalmic emergency because permanent visual loss can occur rapidly.

31. Primary Open-Angle Glaucoma – Note Form

Onset: chronic and insidious.

Pain: usually absent.

Symptoms: usually asymptomatic early.

Anterior chamber angle: remains open.

IOP: often elevated but can be within the statistically normal range.

Optic disc: progressive glaucomatous cupping.

Visual field: nasal step, paracentral defects and arcuate scotomas; advanced disease can produce severe peripheral field loss.

Latanoprost: increases aqueous outflow and is an important first-line treatment.

β-blockers: reduce aqueous humour production.

Dorzolamide: carbonic anhydrase inhibitor that reduces aqueous production.

Pilocarpine: historically used but much less common in modern routine treatment.

Laser: selective laser trabeculoplasty can improve trabecular aqueous outflow.

Surgery: trabeculectomy or other glaucoma procedures may be required when adequate pressure control cannot otherwise be achieved.

Iridectomy: not routine treatment for primary open-angle glaucoma.

Key Clinical Pattern

Remember acute angle-closure glaucoma as:

Painful + red + reduced vision + hazy cornea + mid-dilated pupil + very high IOP.

It is an ophthalmic emergency requiring immediate pressure reduction followed by definitive laser peripheral iridotomy.

Remember primary open-angle glaucoma as:

Painless + chronic + initially asymptomatic + progressive optic-disc cupping + characteristic visual-field loss.

The goal of treatment is to lower intraocular pressure and prevent further irreversible optic nerve damage, using therapies such as prostaglandin analogues, other topical pressure-lowering drugs, selective laser trabeculoplasty, and surgery when required.