"Glaucoma" — Practice

Question 1

According to the ISNT rule, the normal neuroretinal rim is thickest

Accepted Answer

D

Question 2

Which antiglaucoma drug is contraindicated in infants?

Accepted Answer

B

Question 3

A patient in acute angle closure has a pressure of 62 mmHg. Why is topical pilocarpine ineffective at this point?

Accepted Answer

B

Question 4

Which finding suggests pigment dispersion glaucoma?

Accepted Answer

A

Question 5

What did the LiGHT trial demonstrate at six years about selective laser trabeculoplasty as first-line treatment?

Accepted Answer

B

Question 6

Why does angle closure occur at mid-dilation rather than when the pupil is fully dilated or fully constricted, and why is the fellow eye treated?

Accepted Answer

Because mid-dilation is the position in which two independent factors are simultaneously at their worst.

The first is pupillary block. Aqueous flows from the posterior to the anterior chamber through the narrow space between the posterior iris surface and the anterior lens surface. Resistance to that flow depends on how closely the two are apposed, and apposition is greatest at mid-dilation. Full constriction pulls the iris taut against the lens over a smaller area, and full dilation lifts the pupil margin away from the lens.

The second is peripheral iris crowding. As the pupil dilates the peripheral iris becomes thicker and more slack, and it bunches into the angle. This effect increases progressively with dilation.

Mid-dilation is therefore where maximum resistance to forward flow coincides with a peripheral iris already crowding the angle. Pressure accumulates behind the iris, bows the periphery forward, and it contacts the trabecular meshwork.

This explains the classic precipitants: dim illumination such as a cinema, emotional stress with sympathetic tone, and pharmacological dilation, whether from mydriatic drops or systemic anticholinergics.

The fellow eye is treated because angle closure is a disease of anatomy, and the two eyes share it. A short axial length, a shallow chamber and a thickened lens are bilateral features, so an eye that has had one attack identifies a fellow eye at high risk. Prophylactic laser iridotomy is quick, safe and prevents an event that can blind.

Question 7

Why do glaucomatous field defects respect the horizontal midline, and why does the patient not notice them?

Accepted Answer

Because of the anatomy of the retinal nerve fibre layer and the way the brain handles the visual field.

Axons from the nasal retina travel in a direct radial course to the optic disc. Axons from the temporal retina cannot cross the macula, because doing so would place nerve fibres over the fovea and degrade central vision. They therefore arch above and below it in the arcuate bundles.

Those superior and inferior bundles meet at the temporal horizontal raphe, and no fibre crosses it. Damage confined to one arcuate bundle therefore produces a field defect confined to one half of the field, with a sharp edge along the horizontal meridian. The nasal step is exactly that edge made visible where the superior and inferior bundles abut.

This is diagnostically useful, because respect for the horizontal midline localises the lesion to the retina or nerve fibre layer, whereas respect for the vertical midline localises it to the chiasm or behind.

The patient does not notice for three reasons. Central acuity is preserved until very late, because the papillomacular bundle is affected last, so they continue to read the chart. The two eyes overlap over most of the field, so a defect in one is covered by the other. And the visual system fills in missing regions rather than presenting them as black areas, so there is no perceptual gap to notice.

The consequence is that patients present when disease is advanced, and a substantial proportion of axons are already lost and cannot be recovered.

Question 8

A 68-year-old with proliferative diabetic retinopathy has a pressure of 48 mmHg, new vessels on the iris, and a closed angle. Why will pressure-lowering treatment alone fail?

Accepted Answer

Because the pressure is a downstream consequence of retinal ischaemia, and the mechanism closing the angle is actively progressing.

Ischaemic retina releases vascular endothelial growth factor. In proliferative diabetic retinopathy the concentration in the vitreous is high, and the factor diffuses forward into the anterior segment, where it induces new vessel growth on the iris surface, which is rubeosis iridis, and across the angle.

Those vessels are accompanied by a fibrovascular membrane. Initially the membrane covers an anatomically open angle and obstructs outflow while gonioscopy still shows angle structures, which is the stage at which the condition is most treatable. The membrane then contracts, dragging the peripheral iris onto the trabecular meshwork and producing progressive synechial closure, which is irreversible.

Aqueous suppressants lower pressure while the drainage pathway is being permanently destroyed, so any benefit is temporary and the eye is often lost.

Effective treatment removes the stimulus. Panretinal photocoagulation ablates ischaemic retina and reduces vascular endothelial growth factor production, though it takes weeks to act. Intravitreal anti-VEGF injection acts within days and is used to buy time, causing rapid regression of the iris vessels, but its effect is temporary if the ischaemia is not treated.

Prostaglandin analogues are usually avoided because of the inflammatory component, and definitive pressure surgery, usually a tube shunt, is undertaken once the eye is quiet.

Question 9

Why is population screening for glaucoma not recommended, and what is done instead?

Accepted Answer

Because glaucoma fails several of the classical criteria that make a disease suitable for screening, even though it meets others convincingly.

It meets the first criteria well. It is an important health problem, with around 11.2 million affected Indians aged 40 and over. It has a long asymptomatic latent phase. And effective treatment exists that alters outcome.

Where it fails is the test. There is no single measurement that is both sensitive and specific. Tonometry, the cheapest and most scalable option, misses roughly half of cases because a large proportion of glaucoma occurs at statistically normal pressures, and it also generates many false positives from ocular hypertensives who will never convert. Perimetry is time-consuming, requires patient cooperation and has a learning curve. Optic disc assessment is reasonably accurate but requires a trained examiner and dilation, which does not scale to a population.

Cost and consequence matter too. A positive screen commits the patient to lifelong follow-up and often lifelong medication, so false positives are not harmless.

What is done instead is opportunistic case finding: examining the optic discs of everyone who attends an eye clinic for any reason, particularly those presenting for cataract or refraction, which captures a large proportion of the at-risk population without a separate programme.

Targeted screening of first-degree relatives is the second strategy, and it is efficient because their risk is several times that of the general population, making the pre-test probability high enough for imperfect tests to be useful.

Practice — "Glaucoma"

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