Retina — Practice

Question 1

Which defines severe non-proliferative diabetic retinopathy?

Accepted Answer

B

Question 2

Which is absolutely contraindicated in suspected retinoblastoma?

Accepted Answer

C

Question 3

A 65-year-old has sudden painless complete visual loss with a pale retina and a cherry red spot. Where should the patient be managed?

Accepted Answer

B

Question 4

Which retinal detachment requires the most urgent surgery?

Accepted Answer

A

Question 5

An infant born at 35 weeks weighing 2,100 g had prolonged oxygen and sepsis. Does Indian guidance require ROP screening?

Accepted Answer

B

Question 6

Explain why a cherry red spot appears in central retinal artery occlusion, and why the same appearance occurs in some storage diseases.

Accepted Answer

Because the fovea is anatomically different from the rest of the retina, and the appearance depends on that difference rather than on any process at the fovea itself.

The retina has two circulations. The central retinal artery supplies the inner retina, meaning the ganglion cell layer, nerve fibre layer and inner nuclear layer. The choroid supplies the outer retina, meaning the photoreceptors and pigment epithelium, across Bruch membrane.

When the central retinal artery occludes, the inner retina infarcts. Ischaemic neurons swell and their cytoplasm becomes opaque, so the retina turns white and no longer transmits the colour of the underlying choroid.

The fovea has no inner retina. It is a pit in which the ganglion cells and inner layers are displaced radially aside so that light reaches the cones directly, which is what gives the fovea its acuity. There is therefore nothing there to infarct and turn white.

The choroidal circulation beneath the fovea is entirely unaffected, so its red colour continues to show through, surrounded by white opaque retina. The spot is not abnormal; the surroundings are.

The same logic explains the cherry red spot in lysosomal storage diseases such as Tay-Sachs and Niemann-Pick. There the ganglion cells are distended with stored material rather than infarcted, and the effect on transparency is identical. The fovea again lacks those cells and remains clear, so the choroid shows through.

Any process that makes the inner retina opaque while sparing the choroid will produce the sign.

Question 7

Why might panretinal photocoagulation be preferred over anti-VEGF for proliferative diabetic retinopathy in an Indian district hospital, despite trial evidence of anti-VEGF efficacy?

Accepted Answer

Because the two treatments differ fundamentally in what happens when the patient stops attending.

Panretinal photocoagulation works by destroying ischaemic peripheral retina. That retina is the source of vascular endothelial growth factor, so removing it removes the stimulus for new vessel growth permanently. The treatment is delivered once, in a small number of sessions, and its effect persists whether or not the patient returns.

Anti-VEGF injection works by neutralising the growth factor already being produced. The ischaemic retina remains, and continues to produce it. The effect of each injection lasts weeks, so treatment must be repeated indefinitely.

Trials comparing the two in proliferative disease found anti-VEGF non-inferior for visual outcomes, and it avoids the peripheral field loss and night vision impairment that photocoagulation causes. On that evidence alone it looks preferable.

The trials, however, were conducted with intensive protocol-driven follow-up. In a setting where patients travel long distances, pay out of pocket, or default after symptoms improve, a patient lost to follow-up after anti-VEGF has an untreated proliferative retinopathy that will progress to vitreous haemorrhage and tractional detachment.

The same patient lost after photocoagulation carries a completed treatment.

This is a general principle rather than a diabetic one: where a durable one-off intervention and a maintenance intervention have similar efficacy under ideal follow-up, the durable one wins wherever follow-up is uncertain. It is also why guidelines developed in high-income health systems cannot be transplanted without considering delivery.

Question 8

Explain the genetics of retinoblastoma and why bilateral disease changes the clinical implications entirely.

Accepted Answer

Retinoblastoma arises from inactivation of both copies of the RB1 tumour suppressor gene on chromosome 13, and Knudson's two-hit hypothesis was constructed from exactly this observation.

In sporadic disease, both hits occur somatically in a single retinal cell. Two independent mutations in one cell is an improbable event, so the tumour is usually unifocal, unilateral, and presents somewhat later.

In heritable disease, the first hit is present in the germline and therefore in every cell of the body. Only one further somatic mutation is needed in any retinal cell for a tumour to form, and there are millions of retinal cells over the vulnerable period. Tumours are therefore frequently multifocal and bilateral, and present earlier.

Bilateral or multifocal disease is thus strong evidence of a germline mutation even without a family history, since most such mutations arise de novo.

The implications extend well beyond the eye. Every cell in the body carries one inactivated copy of a tumour suppressor, so the child has a substantially raised lifelong risk of second malignancies, most characteristically osteosarcoma, and that risk is increased further by radiotherapy, which influences treatment choice.

Trilateral retinoblastoma refers to an associated intracranial primitive neuroectodermal tumour, usually in the pineal gland, which is why neuroimaging is part of staging rather than an optional extra.

Genetic counselling is required for the family, since offspring of an affected individual with a germline mutation have a high transmission risk, and siblings need examination.

None of this follows from a unilateral unifocal tumour in an older child, which is why establishing laterality and focality at the first examination under anaesthesia matters so much.

Question 9

A patient with advanced HIV has painless progressive visual loss with a haemorrhagic necrotising retinitis spreading along the vessels. What is the diagnosis, and why is antiretroviral therapy as important as the antiviral?

Accepted Answer

Cytomegalovirus retinitis, the commonest ocular opportunistic infection in advanced HIV, occurring characteristically at a CD4 count below 50.

The appearance is distinctive: full-thickness retinal necrosis with associated haemorrhage spreading along the vascular arcades, described as a pizza or cottage cheese and ketchup fundus. It is painless, has minimal anterior segment inflammation, and progresses relentlessly, which is why patients present late.

Antiviral treatment with ganciclovir, valganciclovir or foscarnet suppresses viral replication and halts the advancing border of the retinitis. It does not eradicate the virus, which persists latently.

The reason immune reconstitution matters is that the antiviral is suppressive rather than curative. In a patient whose CD4 count remains below 50, retinitis reactivates whenever antiviral levels fall, and lifelong maintenance therapy is required with all its toxicity. Restoring CD4 counts above roughly 100 allows the patient's own immune system to contain the virus, and maintenance can eventually be stopped.

There is a complication to anticipate. As immunity recovers, the restored immune response can produce an inflammatory reaction at sites of existing infection, called immune recovery uveitis, which causes vitritis, cystoid macular oedema and epiretinal membrane. This can itself reduce vision and requires anti-inflammatory treatment rather than more antiviral.

The differential is acute retinal necrosis, caused by varicella zoster or herpes simplex in immunocompetent patients, which differs by being painful, more rapidly progressive, peripheral in onset, and associated with occlusive arteritis.

Practice — Retina

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