Glaucoma

Glaucoma is a group of progressive optic neuropathies with structural damage to the optic nerve head and corresponding progressive visual field loss. It is most commonly, though not invariably, associated with elevated intraocular pressure. It is a leading cause of irreversible blindness worldwide.

Primary open angle glaucoma is the commonest subtype. It causes gradual, painless visual field loss. Loss is peripheral, with relative preservation of central vision until late, so patients frequently notice nothing until disease is relatively advanced.

This contrasts clearly with acute angle closure glaucoma, which is acute, painful and immediately symptomatic. It is an ophthalmological emergency requiring immediate recognition and treatment.

Classification and pathophysiology

• Primary open angle glaucoma, the commonest subtype, is progressive optic nerve damage generally associated with elevated intraocular pressure. Reduced outflow facility through the trabecular meshwork raises the pressure despite an anatomically normal, open anterior chamber angle. The mechanism of reduced outflow is incompletely understood, and the disease progresses over years to decades.
• Primary angle closure glaucoma results from anatomical crowding or obstruction of the anterior chamber angle, impeding aqueous humour outflow.
• Acute angle closure is sudden, complete obstruction. It produces a rapid, marked rise in intraocular pressure and an acute, painful presentation. It is an emergency because rapid, irreversible optic nerve damage and visual loss follow if it is not promptly treated.
• Normal tension glaucoma is glaucomatous optic neuropathy despite intraocular pressure within the conventionally normal range. It shows that glaucoma is fundamentally a disease of the optic nerve rather than simply of raised pressure. Intraocular pressure is the principal, though not the sole, modifiable risk factor across the spectrum.
• Secondary glaucoma arises from other ocular conditions, including uveitis, trauma, and conditions producing pigment dispersion or pseudoexfoliative material in the anterior chamber angle. A specific mechanism raises intraocular pressure or directly damages the optic nerve.

• Primary open angle glaucoma is characteristically asymptomatic in its early and frequently intermediate stages, because peripheral field loss spares central vision for a prolonged period.
• It is therefore frequently first identified through routine, opportunistic ophthalmic screening rather than patient-reported symptoms. Regular eye examination matters, particularly with risk factors (advancing age, family history, ethnic background, and elevated intraocular pressure found incidentally). Early detection precedes functionally significant field loss.
• Acute angle closure glaucoma presents dramatically with severe, unilateral eye pain, marked blurring of vision, haloes around lights, and nausea and vomiting reflecting the severity of the pain.
• On examination there is a red eye with a fixed, mid-dilated pupil, a hazy, oedematous cornea, and a markedly firm globe on gentle palpation. This classic presentation is an ophthalmological emergency requiring immediate recognition and treatment.
• Advanced, uncontrolled glaucoma of any subtype produces significant visual field loss, beginning peripherally. In the most advanced, poorly controlled cases it progresses to severe tunnel vision and, if left untreated, complete blindness. This end stage is devastating but largely preventable.
• Risk factors to explore in risk assessment include advancing age and family history.
• Ethnic background matters: open angle glaucoma risk is particularly elevated in individuals of African ancestry, and angle closure glaucoma risk in those of East Asian ancestry, reflecting differing anatomical and physiological risk factor prevalence.
• Myopia is associated with elevated open angle glaucoma risk. Hyperopia is associated with elevated angle closure risk, given the anatomical features of the hyperopic eye.
• Medications matter: topical or systemic corticosteroids, and certain medications with anticholinergic or sympathomimetic properties, can precipitate acute angle closure in an anatomically predisposed individual.

• Full ophthalmic examination is the essential diagnostic approach. It incorporates intraocular pressure measurement (tonometry) and assessment of the optic nerve head for the characteristic glaucomatous cupping, which reflects progressive loss of neuroretinal rim tissue.
• Formal visual field assessment (perimetry) establishes baseline severity and monitors progression over time.
• Gonioscopy assesses the anterior chamber angle and directly distinguishes open from closed or narrow angle anatomy. This distinction is essential because management differs fundamentally.
• Optical coherence tomography gives detailed, quantitative assessment of the retinal nerve fibre layer thickness around the optic nerve. It is an increasingly important adjunct for diagnosis and for sensitive detection of subtle progression, complementing visual field assessment.
• Regular, periodic ophthalmic screening, particularly for individuals with risk factors, supports early detection of primary open angle glaucoma given its asymptomatic early course. Treatment can then start before functionally significant field loss develops.
• Acute angle closure glaucoma is diagnosed clinically from the dramatic presentation, with confirmatory tonometry showing markedly elevated intraocular pressure. Start treatment immediately, without delay for formal investigation.

• Primary open angle glaucoma management centres on intraocular pressure reduction. Topical prostaglandin analogue eye drops (including latanoprost) are standard first-line treatment, with favourable efficacy and convenient once daily dosing.
• Topical beta blocker, alpha agonist, and carbonic anhydrase inhibitor eye drops are further options, used as monotherapy or in combination according to response and tolerability.
• Laser trabeculoplasty enhances aqueous outflow through the trabecular meshwork. It is effective either as an alternative to initial topical treatment or as an adjunct where medical treatment alone gives inadequate pressure control.
• Surgery is considered for glaucoma not adequately controlled with medical and laser treatment, or for more advanced, aggressive disease needing greater pressure reduction than less invasive approaches reliably achieve.
• Options are trabeculectomy or, increasingly, minimally invasive glaucoma surgery. The latter generally has lower complication rates but sometimes somewhat lower efficacy than traditional trabeculectomy.
• Acute angle closure glaucoma requires immediate emergency treatment to reduce the markedly elevated intraocular pressure rapidly. Treatment typically combines intravenous acetazolamide (a carbonic anhydrase inhibitor reducing aqueous humour production) with topical agents: a beta blocker, an alpha agonist, and pilocarpine. Pilocarpine constricts the pupil and mechanically pulls the peripheral iris away from the obstructed angle.
• Where medical treatment alone fails to reduce pressure adequately, consider anterior chamber paracentesis.
• Once the acute attack is controlled, definitive treatment is laser peripheral iridotomy. This creates a small opening in the peripheral iris to relieve the pupillary block and prevent recurrence.
• Prophylactic laser peripheral iridotomy of the fellow eye is also generally recommended, because the shared anatomical predisposition carries a substantial risk of a similar acute event.
• Regular, lifelong ophthalmic follow up incorporates periodic intraocular pressure measurement, optic nerve assessment, and formal visual field testing. This monitors progression and guides treatment adjustment in this common, chronic and, if inadequately treated, potentially blinding condition.
• Visual field loss and optic nerve damage already sustained are irreversible. The goal of treatment is therefore to prevent further progression through adequate, sustained intraocular pressure control, not to restore vision already lost.