"Cornea & External Eye Disease" — Practice

Question 1

Which feature most reliably indicates allergic conjunctivitis?

Accepted Answer

C

Question 2

A farmer struck in the eye by a paddy stalk has an ulcer with a dry raised edge, feathery margins and satellite lesions. Treatment of choice?

Accepted Answer

B

Question 3

A newborn has profuse purulent discharge with marked lid oedema on day 3. Management?

Accepted Answer

B

Question 4

A patient with a dendritic ulcer is given topical steroid and returns with a large geographic ulcer. What happened?

Accepted Answer

B

Question 5

Which corneal dystrophy is autosomal recessive with hazy intervening stroma?

Accepted Answer

C

Question 6

Why are alkali burns worse than acid burns, and why does the extent of limbal blanching predict outcome?

Accepted Answer

Alkali and acid differ in how they interact with tissue, and the difference determines depth of injury.

Alkali saponifies the lipids of cell membranes, dissolving them, and the hydroxyl ion then penetrates progressively through the stroma and into the anterior chamber, where it can damage the trabecular meshwork, iris and lens. Penetration continues for as long as the chemical remains, so the injury deepens over time.

Acid coagulates surface proteins on contact, and that coagulum acts as a physical barrier limiting further penetration, so acid injuries tend to be more superficial. Strong acids such as hydrofluoric acid are exceptions because they behave differently.

This is why immediate copious irrigation is the whole of the emergency treatment, continued until the pH of the fornix normalises. Taking a history first costs tissue.

Limbal blanching predicts outcome because the limbus houses the stem cells that renew the corneal epithelium. Perilimbal vessels are the visible marker of that zone, and blanching indicates ischaemia of the region containing the stem cells.

If enough limbus is destroyed, the cornea has no source of its own epithelium. Conjunctival epithelium migrates across instead, bringing blood vessels and goblet cells, and the result is a vascularised, opaque and unstable surface that no conventional graft can survive on.

The extent of blanching therefore predicts not the immediate appearance but whether the eye can ever be optically rehabilitated.

Question 7

Explain how trachoma causes blindness and why the SAFE strategy has the components it does.

Accepted Answer

Trachoma blinds mechanically rather than infectively, and decades after the infection that started it.

Chlamydia trachomatis serotypes A to C cause repeated episodes of follicular conjunctivitis in childhood, spread by fingers, shared cloths and eye-seeking flies in conditions of crowding and limited water. Each episode is trivial in itself.

Repeated inflammation scars the tarsal conjunctiva, and the classical sign is the Arlt line, a horizontal scar across the upper tarsus. Herbert pits mark the limbus where follicles have resolved.

Scar tissue contracts over years, and the contracting tarsal plate rotates the lid margin inward. The lashes then turn onto the globe, and every blink abrades the cornea. Chronic abrasion in a dry, dusty environment leads to ulceration, secondary infection and finally opacification.

The SAFE components map onto this sequence at different points. Surgery corrects the trichiasis, which is the only intervention that helps someone already at the end stage. Antibiotics, given as mass azithromycin distribution, reduce the community reservoir of active infection. Facial cleanliness reduces transmission, because ocular and nasal discharge on a child's face attracts the flies that carry the organism. Environmental improvement, principally water access and latrines, addresses the conditions in which flies breed and washing is impossible.

Only the first two are medical, and the last two are what actually interrupt transmission, which is why trachoma control succeeded where a purely clinical approach had failed for a century.

In October 2024 WHO validated India as having eliminated trachoma as a public health problem, the third country in the South-East Asia Region.

Question 8

Why has lamellar keratoplasty largely replaced penetrating keratoplasty, and what determines whether a graft will be rejected?

Accepted Answer

Because replacing only the failed layer solves the problem while avoiding most of the cost of replacing everything.

A penetrating graft creates a full-thickness wound around the entire circumference of the cornea. That wound never regains the strength of intact tissue, so the eye remains vulnerable to rupture indefinitely, sutures induce large amounts of astigmatism, and visual rehabilitation takes many months.

It also transplants the donor endothelium, which is the principal target of immune rejection.

Deep anterior lamellar keratoplasty replaces the diseased stroma while retaining the patient's own endothelium, which removes the main rejection target altogether and is therefore appropriate for keratoconus and stromal scarring where the endothelium is healthy.

The endothelial keratoplasties do the reverse for Fuchs dystrophy and pseudophakic bullous keratopathy, replacing only the endothelium through a small incision. Recovery takes weeks rather than months and the globe remains structurally intact.

Rejection is recognised by the Khodadoust line, keratic precipitates advancing across the graft endothelium, with graft oedema and anterior chamber activity, and is treated urgently with intensive steroids.

What determines rejection risk is vascularisation of the host bed. The cornea's immune privilege derives from being avascular and lacking lymphatics, which prevents both the delivery of effector cells and the trafficking of antigen to lymph nodes. Once vessels grow in, from previous infection, chemical injury or chronic inflammation, that privilege is lost and rejection rates rise sharply.

Question 9

A contact lens wearer has had a painful red eye for three weeks, treated as herpetic without improvement. Pain is severe and out of proportion to the signs, and a ring infiltrate is now visible. What is the diagnosis and why is this presentation so dangerous?

Accepted Answer

Acanthamoeba keratitis, and the danger lies almost entirely in the delay.

The organism is a free-living amoeba found in tap water, swimming pools and soil, and it reaches the cornea through contact lens wear, particularly when lenses are rinsed in tap water or worn while swimming.

The cardinal feature is pain grossly disproportionate to the clinical signs, which occurs because the amoeba has a marked tropism for corneal nerves, producing a radial perineuritis early in the disease. A ring infiltrate appears later and is characteristic but not early.

The reason cases are lost is the early course. In the first weeks the epithelial changes can look dendritiform, so the diagnosis made is herpes simplex, and topical steroid frequently follows. Steroid suppresses the host response to an organism that is already difficult to eradicate, and the encysted form is highly resistant.

By the time the ring infiltrate is obvious the stroma is extensively involved, treatment must continue for months with biguanides and diamidines, and the outcome may still be a scarred eye requiring keratoplasty on an inflamed bed.

The practical rule is therefore that disproportionate pain in a contact lens wearer is Acanthamoeba until proved otherwise, and confocal microscopy or culture on non-nutrient agar with an Escherichia coli overlay should be sought rather than assumed unnecessary.

Practice — "Cornea & External Eye Disease"

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