Viva Hot Seat: 100 Ophthalmology Viva and OSCE Stations

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Viva Hot Seat: 100 Ophthalmology Viva and OSCE Stations

Last updated: November 2026

Sit in the examiner's hot seat. 100 stations across every subspecialty, each opening with a short clinical scenario the way a viva or OSCE examiner would, followed by the rapid-fire questions that usually follow (700 in all). Answer each one aloud, then tap to reveal a model answer and mark whether you got it. Your score is saved on this device.

Station 1: Senile cataract Lens

Examiner: A 68-year-old with gradual painless blurring of vision for two years. On the slit lamp you see a grey-white lens opacity with an iris shadow.

What type and stage of cataract is this?
An immature senile cataract: the presence of an iris shadow means clear cortex remains between the pupil margin and the opacity. Name the morphology: nuclear, cortical or posterior subcapsular.
How do you grade it?
LOCS III (Lens Opacities Classification System III) for nuclear opalescence and colour, cortical and posterior subcapsular cataract; or a simple clinical nuclear grade 1–4/5.
What pre-operative work-up do you do?
Visual acuity with pinhole, IOP, pupil reaction and RAPD, slit lamp (pseudoexfoliation, corneal guttata, phacodonesis), dilated fundus (or B-scan if no view), biometry (axial length and keratometry), and systemic review (diabetes, BP, anticoagulants, tamsulosin).
Which IOL formula would you choose?
Modern formulas (Barrett Universal II, Kane) for all eyes. If limited to older formulas: Hoffer Q for short eyes (< 22 mm), SRK/T for long eyes (> 26 mm), Holladay 1 or SRK/T for average eyes.
Why does a nuclear cataract cause second sight?
The sclerosing nucleus raises the refractive index of the lens, causing a myopic shift, so a presbyopic patient may read again without glasses.
What is the commonest intraoperative complication and how do you manage it?
Posterior capsule rupture. Stop, keep the chamber formed with viscoelastic, avoid dropping the nucleus, perform anterior vitrectomy if vitreous presents, and place the IOL in the sulcus (optic capture if possible) or defer.
A day-3 post-op patient has pain, worse vision and hypopyon. What do you do?
Suspect acute endophthalmitis: same-day vitreous tap and intravitreal vancomycin 1 mg and ceftazidime 2.25 mg; consider vitrectomy if vision is light perception only (EVS).

Station 2: Congenital cataract Lens

Examiner: A 6-week-old baby with a white pupil in the right eye noticed in photographs. Red reflex is absent on the right.

What is your first priority?
Urgent assessment because of the risk of dense stimulus deprivation amblyopia; also exclude retinoblastoma with a dilated fundus examination or B-scan.
When should a dense unilateral cataract be operated?
Ideally by 6 weeks of age; dense bilateral cataracts by 8 to 10 weeks, operating the second eye within a week or two.
Which investigations do you do?
Family history and examination of parents; TORCH serology, urine for reducing substances (galactosaemia), calcium and glucose, and a paediatric review for syndromes in bilateral cases.
What surgery do you perform?
Lens aspiration with primary posterior capsulotomy and anterior vitrectomy, because the posterior capsule opacifies rapidly in children.
What did the Infant Aphakia Treatment Study show?
In unilateral cataract operated at 1 to 6 months, an IOL gave no better vision than contact lens aphakia correction at age 5 and caused more reoperations, so many surgeons leave infants under 6 months aphakic.
What is the main long-term complication?
Glaucoma (aphakic or pseudophakic) in up to a quarter of eyes, especially with surgery in the first month, so lifelong IOP monitoring is needed.
Why is amblyopia treatment essential after surgery?
Surgery only clears the media; vision depends on immediate optical correction and patching of the better eye for years.

Read more: Congenital cataract, Leukocoria

Station 3: Cataract with pseudoexfoliation Lens

Examiner: A 72-year-old listed for cataract surgery. Dilated examination shows grey flaky material on the anterior capsule in a target pattern and the pupil dilates only to 5 mm.

What is pseudoexfoliation syndrome?
An age-related systemic disorder of extracellular matrix in which fibrillar material is deposited in the anterior segment and elsewhere; linked to LOXL1 variants.
Why is cataract surgery higher risk?
Poor pupil dilation, weak zonules (phacodonesis, zonular dialysis), shallow chamber, and a higher risk of posterior capsule rupture and dropped nucleus.
How do you manage a small pupil?
Intracameral mydriatics, viscomydriasis, iris hooks or a Malyugin ring.
How do you support weak zonules?
Gentle capsulorhexis of adequate size, hydrodissection, chop techniques, capsular tension ring, or capsular tension segments for larger dialyses.
What late complication should you warn about?
Late in-the-bag IOL dislocation years later, and pseudoexfoliation glaucoma, which needs regular IOP checks.
Which signs on gonioscopy are typical?
Heavy patchy trabecular pigmentation and a Sampaolesi line anterior to Schwalbe line.
Why is the capsulorhexis size important here?
A small rhexis causes capsule contraction (phimosis) which further stresses weak zonules; aim for about 5 to 5.5 mm.

Station 4: Ectopia lentis Lens

Examiner: A tall 14-year-old with long fingers and high myopia. The lens is displaced superotemporally and the zonules are visible in the pupil.

What is the likely diagnosis?
Marfan syndrome (fibrillin-1 mutation), in which the lens typically subluxates superotemporally.
Which other causes of ectopia lentis do you know?
Homocystinuria (inferonasal, with thromboembolic risk), Weill-Marchesani (microspherophakia), sulfite oxidase deficiency, trauma, pseudoexfoliation and high myopia.
Why does homocystinuria matter for anaesthesia?
There is a high risk of thromboembolism under general anaesthesia; hydrate well and check homocysteine before surgery.
What systemic referral is essential in Marfan syndrome?
Cardiology for aortic root dilatation and mitral valve prolapse; the Ghent criteria combine lens dislocation, aortic dilatation and family history.
How do you manage a subluxated lens?
Best correction through the phakic or aphakic part of the pupil first; lensectomy with scleral-fixated, iris-fixated or anterior chamber IOL when vision cannot be corrected or amblyopia threatens.
What causes pupil block glaucoma here?
Anterior dislocation of the lens, especially a spherophakic lens, which can be relieved by dilating, laying supine or laser iridotomy.
What retinal risk should you check?
Retinal detachment, which is more common in Marfan syndrome and after lens surgery.

Read more: Lens hub, Diagnostic criteria

Station 5: Posterior capsule opacification Lens

Examiner: A 60-year-old had uncomplicated cataract surgery two years ago and now reports gradual glare and blurring. Retroillumination shows Elschnig pearls.

What is posterior capsule opacification?
Proliferation and migration of residual lens epithelial cells onto the posterior capsule, forming pearls or fibrosis.
Which IOL features reduce PCO?
A sharp square posterior optic edge, a capsulorhexis that overlaps the optic edge, and thorough cortical clean-up; hydrophobic acrylic lenses have lower rates.
How do you perform Nd:YAG capsulotomy?
A cruciate or circular opening of about 3 to 4 mm with the lowest effective energy, focused slightly behind the capsule, avoiding the IOL.
What are the complications of YAG capsulotomy?
IOP spike, IOL pitting, cystoid macular oedema, retinal detachment (especially in high myopes) and IOL dislocation.
What else can cause poor vision after cataract surgery?
CME, refractive surprise, dry eye, epiretinal membrane, IOL decentration, endophthalmitis and pre-existing macular disease.
Why is PCO more common in children?
Lens epithelial cells are very active, so primary posterior capsulotomy with anterior vitrectomy is routine in young children.
What is capsular block syndrome?
Viscoelastic or fluid trapped behind the IOL in a sealed bag, causing a myopic shift and milky fluid; treated by YAG at the bag edge or capsulotomy.

Station 6: Cystoid macular oedema after cataract surgery Lens

Examiner: A diabetic patient sees well on day one after phaco but returns at six weeks with blurring. OCT shows cystic spaces in the macula.

What is this condition called?
Pseudophakic cystoid macular oedema (Irvine-Gass syndrome), peaking around 4 to 6 weeks after surgery.
What is the mechanism?
Surgical inflammation releases prostaglandins, which break the blood-retinal barrier at the perifoveal capillaries.
Which patients are at higher risk?
Diabetics, uveitis, epiretinal membrane, previous RVO, complicated surgery with vitreous loss or iris trauma, and prostaglandin analogue use.
What does FFA show?
Petaloid hyperfluorescence at the macula from leaking perifoveal capillaries, often with optic disc leakage.
How do you treat it?
Topical NSAID (for example nepafenac or ketorolac) plus topical steroid; then periocular or intravitreal steroid for resistant cases.
Can it be prevented?
Yes, prophylactic topical NSAID in high-risk patients reduces CME (ESCRS PREMED study supported NSAID plus steroid; sub-Tenon triamcinolone helped diabetics).
How do you tell it from diabetic macular oedema?
Pseudophakic CME has petaloid leakage and disc leakage and appears after surgery; DME has microaneurysms and exudates and may predate surgery.

Station 7: Refractive surprise after cataract surgery Lens

Examiner: A patient aiming for emmetropia is -2.50 D one month after uneventful phaco in a 23.5 mm eye.

What are the common causes?
Errors in axial length or keratometry, wrong IOL power selected or inserted, wrong formula or constant, and previous refractive surgery not accounted for.
What do you check first?
Confirm the refraction, then review biometry records, the IOL label and power used, and repeat biometry and topography.
Which formulas perform best?
Barrett Universal II and Kane across axial lengths; Hoffer Q older choice for short eyes; formula choice matters most at the extremes.
How much does a 1 mm axial length error cause?
About 2.5 to 3 dioptres of refractive error in an average eye.
How do you manage it?
Spectacles or contact lenses, IOL exchange (best early), piggyback sulcus IOL, or corneal laser refractive surgery once stable.
How do you handle an eye with previous LASIK?
Use history-free methods such as Barrett True-K or Haigis-L, or the ASCRS calculator, because standard keratometry overestimates corneal power after myopic LASIK.
How do you prevent wrong-lens events?
WHO-style surgical checklist, confirm patient, eye, IOL model and power aloud before insertion.

Station 8: Toric IOLs and astigmatism Lens

Examiner: A cataract patient has 2.5 D of regular with-the-rule corneal astigmatism and wants good distance vision without glasses.

What options do you have to correct astigmatism at cataract surgery?
Toric IOL, limbal relaxing incisions, on-axis incision, and later laser vision correction.
Why must posterior corneal astigmatism be considered?
The posterior cornea usually adds against-the-rule astigmatism, so anterior keratometry alone overcorrects WTR and undercorrects ATR astigmatism. Barrett toric accounts for it.
How do you mark the axis?
Preoperative reference marks at 0 and 180 degrees with the patient sitting (to avoid cyclotorsion), or image-guided systems.
How much effect does rotation have?
Each degree of misalignment loses about 3.3% of the cylinder correction; 30 degrees off gives no benefit.
When does a toric IOL rotate and how do you fix it?
Usually in the first days to weeks, more in long eyes with large bags; reposition after 1 to 3 weeks once the capsule has started to contract.
Which patients are poor candidates?
Irregular astigmatism (keratoconus, scars), zonular weakness and unstable keratometry.
What astigmatism do you aim to leave?
A small amount of with-the-rule residual is better tolerated than against-the-rule in older patients, because ATR increases with age.

Read more: Toric IOL pearls, LRI nomograms

Station 9: Microbial keratitis Cornea

Examiner: A 40-year-old farmer with a painful red eye for 6 days after injury with vegetable matter. There is a dry, greyish infiltrate with feathery margins, satellite lesions and a hypopyon.

What is the likely organism?
Fungal keratitis (filamentous fungi such as Fusarium or Aspergillus): vegetative trauma, dry raised infiltrate, feathery margins, satellite lesions and endothelial plaque.
How do you investigate?
Corneal scraping: Gram stain, KOH mount and calcofluor white for fungi; culture on blood agar, chocolate agar and Sabouraud dextrose agar (non-nutrient agar with E. coli overlay if Acanthamoeba is suspected). Consider confocal microscopy.
What is your treatment?
Natamycin 5% hourly (MUTT I: better than voriconazole for filamentous fungi, especially Fusarium), with oral or intrastromal voriconazole for deep or non-responding ulcers. Avoid steroids.
How would you treat a bacterial ulcer?
Fortified cefazolin 5% plus tobramycin about 1.4% hourly, or a fourth-generation fluoroquinolone monotherapy for small peripheral ulcers.
When may steroids be added in bacterial keratitis?
SCUT: adjunctive steroids gave no overall benefit, but may help deep or central ulcers with poor vision once the organism is controlled; never in fungal or Acanthamoeba keratitis.
What are the indications for therapeutic keratoplasty?
Impending or actual perforation not manageable with glue, and progressive infection despite maximal medical treatment, particularly approaching the limbus.
What are the features of Acanthamoeba keratitis?
Contact lens wearer, pain out of proportion to signs, radial perineuritis, ring infiltrate, and slow response to standard treatment. Treat with biguanides (PHMB or chlorhexidine) with or without propamidine.

Station 10: Herpes simplex keratitis Cornea

Examiner: A 35-year-old with a red, watery, photophobic eye. Fluorescein shows a branching epithelial ulcer with terminal bulbs; corneal sensation is reduced.

What is the diagnosis?
HSV epithelial keratitis (dendritic ulcer). Terminal bulbs, stain of the ulcer bed with fluorescein and the edges with rose bengal, and reduced corneal sensation are typical.
How do you treat it?
Topical antiviral: ganciclovir 0.15% gel five times a day or acyclovir 3% ointment five times a day until healed, or oral acyclovir 400 mg five times a day. Gentle debridement can help. No topical steroid for epithelial disease.
How is herpetic keratitis classified?
By layer: epithelial (dendritic, geographic), stromal (necrotising and immune/interstitial), endotheliitis (disciform, diffuse, linear) and neurotrophic keratopathy.
How do you treat disciform keratitis?
Topical steroid (for example prednisolone acetate 1% tapered slowly) under antiviral cover, usually oral acyclovir 400 mg twice daily.
What did HEDS show about prophylaxis?
Oral acyclovir 400 mg twice daily for a year halved recurrences of ocular HSV, and mattered most for people with previous stromal keratitis.
Name some causes of pseudodendrites.
Herpes zoster, healing epithelial defects, Acanthamoeba, contact lens wear, tyrosinaemia type II and topical drug toxicity.
Why should you avoid steroids alone in a dendritic ulcer?
Steroids enhance viral replication and can enlarge a dendrite into a geographic ulcer and promote stromal melting.

Station 11: Fungal keratitis Cornea

Examiner: A farmer with a two-week history of a painful eye after an injury with vegetable matter. There is a dry-looking grey infiltrate with feathery margins and satellite lesions.

What is the likely diagnosis and which organisms?
Filamentous fungal keratitis, most often Fusarium or Aspergillus in India. Candida (yeast) is more common in compromised eyes.
Which investigations do you send?
Corneal scraping for KOH mount and Gram stain, culture on Sabouraud dextrose agar and blood agar; confocal microscopy if available; corneal biopsy if scrapes are negative and the ulcer is deep.
What did MUTT I show?
Natamycin 5% gave better visual outcomes and fewer perforations than voriconazole 1% for filamentous fungal keratitis, especially Fusarium.
What is your first-line treatment?
Natamycin 5% hourly, tapered over weeks, plus cycloplegic; add oral or intrastromal/intracameral voriconazole for deep or progressing ulcers. Avoid steroids.
When do you consider therapeutic keratoplasty?
For impending or actual perforation, or a worsening ulcer despite maximal medical treatment; excise with a clear margin around the infiltrate.
What is Pythium keratitis and why does it matter?
An oomycete that mimics fungal keratitis but responds poorly to antifungals; antibacterial combinations (linezolid, azithromycin) and early surgery are used.
Why does a hypopyon in fungal keratitis not always clear with antibiotics?
Fungi can penetrate an intact Descemet membrane, so the hypopyon may contain organisms (unlike sterile bacterial hypopyon).

Station 12: Acanthamoeba keratitis Cornea

Examiner: A soft contact lens wearer who rinses lenses in tap water has severe pain out of proportion to signs. You see a ring infiltrate and radial perineural infiltrates.

What is the diagnosis?
Acanthamoeba keratitis. Pain out of proportion, radial keratoneuritis and a ring infiltrate in a contact lens wearer are classic.
What is the main risk factor?
Contact lens wear with exposure to water (swimming, showering, tap-water rinsing). Trauma with soil or water in non-wearers.
How do you confirm it?
Corneal scrape for culture on non-nutrient agar with an E. coli overlay, calcofluor white or Giemsa stain, PCR, and in vivo confocal microscopy showing double-walled cysts.
How do you treat it?
Biguanide (PHMB 0.02% or chlorhexidine 0.02%) with or without a diamidine (propamidine), hourly initially, for months. Polihexanide 0.08% monotherapy is now approved in Europe.
Why is it hard to eradicate?
Cysts are highly resistant and can lie dormant in the stroma, so treatment continues long after symptoms improve.
Is early misdiagnosis common?
Yes. It is often treated first as HSV keratitis because of the epithelial pseudodendrites and stromal infiltrate.
How do you counsel lens wearers to prevent it?
Never let water touch lenses or cases, do not sleep or swim in lenses, rub and rinse with fresh solution and replace the case regularly.

Station 13: Keratoconus Cornea

Examiner: A 17-year-old with allergic eye disease and rapidly changing astigmatism. Retinoscopy shows a scissoring reflex.

What signs of keratoconus do you know?
Scissoring reflex, oil-droplet red reflex, Munson sign, Rizzuti sign, Vogt striae, Fleischer ring, apical thinning and scarring, and acute hydrops.
How do you diagnose it early?
Corneal tomography (for example Pentacam): posterior elevation, pachymetry progression and the Belin-Ambrosio display are more sensitive than anterior curvature alone.
How do you define progression?
Change over time in at least two of: steepening of the anterior surface, steepening of the posterior surface, or thinning (ABCD progression display).
What is corneal collagen cross-linking?
Riboflavin with UV-A light creates covalent cross-links in stromal collagen to halt progression. The Dresden protocol needs a cornea of at least 400 microns after epithelium removal.
How do you correct vision?
Spectacles in mild cases, then rigid gas-permeable, hybrid or scleral lenses; intracorneal ring segments; deep anterior lamellar keratoplasty for advanced scarring.
What is acute hydrops and how do you treat it?
A break in Descemet membrane causing sudden stromal oedema. Treat with hypertonic saline, cycloplegia and sometimes intracameral gas (C3F8 or air) to speed resolution.
Which conditions are associated?
Atopy and eye rubbing, Down syndrome, Leber congenital amaurosis, connective tissue disorders and floppy eyelid syndrome.

Station 14: Fuchs endothelial dystrophy Cornea

Examiner: A 65-year-old woman reports blurred vision that is worst on waking and clears during the day. Specular reflection shows guttata.

What is the diagnosis?
Fuchs endothelial corneal dystrophy: central guttata with endothelial cell loss leading to stromal and later epithelial oedema.
Why is vision worse in the morning?
With the eyes closed there is no tear evaporation, so the cornea swells overnight and thins during the day.
What is the genetics?
Usually late-onset, female predominant; the commonest association is a CTG trinucleotide repeat expansion in TCF4.
How do you assess severity?
Slit lamp grading of guttata confluence, pachymetry, specular microscopy and Scheimpflug tomography signs of subclinical oedema.
What is the surgical treatment of choice?
Endothelial keratoplasty, preferably DMEK (better visual recovery and lower rejection) or DSAEK. Descemet stripping only (DSO) with ROCK inhibitor is an option for central guttata with a healthy periphery.
How does it affect cataract surgery?
Risk of post-operative corneal decompensation; protect the endothelium with dispersive viscoelastic and low phaco energy, and consider a triple procedure if the cornea is already thick.
What medical treatment helps early disease?
Hypertonic saline 5% drops and ointment, and a hairdryer at arm's length in the morning to evaporate tears.

Station 15: Corneal graft rejection Cornea

Examiner: A patient 8 months after penetrating keratoplasty notices redness and blurring. You see keratic precipitates in a line on the graft endothelium.

What is the diagnosis?
Endothelial graft rejection: a Khodadoust line of keratic precipitates advancing across the graft with stromal oedema behind it.
What other types of rejection do you know?
Epithelial rejection (a raised epithelial line), subepithelial infiltrates (Krachmer spots) and stromal rejection.
How do you treat it?
Intensive topical steroid (prednisolone acetate 1% hourly), with or without a periocular or systemic steroid pulse for severe or high-risk cases.
Which factors increase rejection risk?
Vascularised host cornea, previous graft failure, large or eccentric grafts, young age, active inflammation, loose sutures and anterior synechiae.
How do lamellar grafts compare?
DALK avoids endothelial rejection completely; DMEK has the lowest rejection rate of endothelial grafts.
What is primary graft failure?
A graft that is oedematous from the first day and never clears, caused by poor donor endothelium or surgical trauma, not rejection.
What should every keratoplasty patient know?
The RSVP warning signs: redness, sensitivity to light, vision loss and pain, and to attend the same day.

Read more: Keratoplasty types, Cornea hub

Station 16: Dry eye disease Cornea

Examiner: A 50-year-old office worker with burning, grittiness and fluctuating vision that worsens through the day at the computer.

How is dry eye defined (TFOS DEWS)?
A multifactorial disease of the ocular surface characterised by loss of tear film homeostasis, with symptoms; tear instability, hyperosmolarity, inflammation and neurosensory abnormalities play roles.
What are the two main subtypes?
Evaporative (mostly meibomian gland dysfunction) and aqueous deficient (Sjögren and non-Sjögren); most patients have both.
Which tests do you do?
Symptom score (OSDI or DEQ-5), tear break-up time, fluorescein and lissamine green staining, Schirmer test, meibomian gland expression; osmolarity and meibography if available.
How do you treat it step by step?
Education, screen breaks and lid hygiene with warm compresses; preservative-free lubricants; then anti-inflammatories (cyclosporine, lifitegrast, short steroid course), punctal plugs; then serum drops, scleral lenses and procedures.
What features suggest Sjögren syndrome?
Dry mouth, arthralgia, parotid swelling, positive anti-Ro/La antibodies, low Schirmer values; there is a lymphoma risk, so refer to rheumatology.
What treatments target meibomian gland dysfunction?
Warm compresses, lid massage, oral doxycycline or azithromycin, intense pulsed light and thermal pulsation devices.
Which drugs can cause dry eye?
Antihistamines, antidepressants, isotretinoin, beta-blockers, diuretics, and preserved glaucoma drops.

Read more: TFOS DEWS III, Dry eye treatment

Station 17: Vernal keratoconjunctivitis Cornea

Examiner: A 10-year-old boy with intense itching, ropy discharge and photophobia every spring. Lifting the upper lid shows cobblestone papillae.

What is the diagnosis?
Vernal keratoconjunctivitis (palpebral type), a chronic allergic disease of young boys in warm climates.
What limbal signs may be present?
Gelatinous limbal papillae with Horner-Trantas dots (collections of eosinophils).
What is a shield ulcer?
A sterile, oval epithelial defect in the upper cornea with plaque, caused by mechanical trauma from papillae and eosinophil toxins.
How do you treat VKC?
Mast cell stabiliser or dual-action drops (olopatadine), topical cyclosporine 0.1% or tacrolimus for persistent disease, short pulses of topical steroid for flares, and cold compresses.
How do you treat a shield ulcer?
Steroid and cyclosporine to control inflammation, debridement of the plaque, a bandage contact lens or amniotic membrane if it does not heal.
What long-term complications must you watch for?
Steroid-induced glaucoma and cataract, keratoconus from eye rubbing, limbal stem cell deficiency and amblyopia from shield ulcer scarring.
How is atopic keratoconjunctivitis different?
AKC affects adults with eczema, is perennial, involves the lower tarsus more and causes more scarring, keratoconus and herpetic infection.

Station 18: Pterygium Cornea

Examiner: A 45-year-old outdoor worker with a fleshy triangular growth from the nasal conjunctiva encroaching 3 mm onto the cornea.

What is a pterygium and what causes it?
A wing-shaped fibrovascular growth of conjunctiva onto the cornea, linked to UV exposure and limbal stem cell damage.
What are the parts of a pterygium?
Cap (the leading avascular edge), head (on the cornea), neck and body (over the sclera). Stocker line is iron deposition in front of the head.
When do you operate?
Progression towards the visual axis, induced astigmatism, cosmetic concern, restricted movement or diagnostic doubt.
Which technique has the lowest recurrence?
Excision with conjunctival limbal autograft, secured with fibrin glue or sutures. Bare sclera excision alone has recurrence rates up to 80%.
What adjuncts reduce recurrence?
Mitomycin C (intraoperative 0.02%), amniotic membrane, and anti-VEGF has been tried; avoid beta irradiation now because of scleral necrosis.
How does pterygium affect cataract surgery planning?
It flattens the cornea in its meridian and causes with-the-rule astigmatism, so remove it first and wait for keratometry to stabilise before biometry.
Which lesions can mimic a pterygium?
Pseudopterygium (after a burn or ulcer, can be probed underneath), OSSN, pinguecula and limbal dermoid.

Station 19: Stevens-Johnson syndrome Cornea

Examiner: A 25-year-old who developed skin blisters and mucosal ulcers after starting carbamazepine is referred with red, sticky eyes.

What is SJS/TEN?
A severe mucocutaneous drug reaction with epidermal necrosis: SJS under 10% body surface area, TEN over 30%, overlap in between.
Which drugs are common triggers?
Carbamazepine, phenytoin, lamotrigine, allopurinol, sulfonamides, NSAIDs (oxicams) and nevirapine. HLA-B*15:02 predicts carbamazepine SJS in South and East Asians.
What do you do in the acute stage?
Daily examination, aggressive lubrication, topical steroid and antibiotic, glass-rod sweeping of the fornices, and early amniotic membrane transplantation over the lid margins and ocular surface.
Why is early amniotic membrane important?
It reduces late lid margin keratinisation, symblepharon and corneal blindness when applied within the first week.
What are the chronic complications?
Lid margin keratinisation, trichiasis, symblepharon, dry eye, limbal stem cell deficiency, corneal vascularisation and keratinisation.
How do you rehabilitate chronic disease?
Mucous membrane grafts for lid margin keratinisation, scleral lenses (PROSE), limbal stem cell transplantation and, as a last resort, keratoprosthesis (Boston type 1 or 2).
How do you differentiate it from mucous membrane pemphigoid?
SJS is acute and drug triggered with a single episode; pemphigoid is chronic and progressive in older people with linear basement membrane deposits on biopsy.

Station 20: Glaucomatous optic disc Glaucoma

Examiner: You are shown a fundus photo of a disc with a vertical cup-to-disc ratio of 0.8 and thinning of the inferior rim.

What are the signs of glaucomatous cupping?
Raised or asymmetric cup-to-disc ratio (asymmetry > 0.2), focal rim thinning or notching, violation of the ISNT rule, disc haemorrhage, bayonetting and baring of circumlinear vessels, laminar dot sign, peripapillary atrophy (beta zone) and RNFL defects.
What is the ISNT rule?
In a normal disc the neuroretinal rim is thickest Inferiorly, then Superiorly, Nasally and thinnest Temporally. Glaucoma usually thins the inferior and superior rims first.
Describe the progression of visual field defects.
Paracentral scotoma or nasal step, then arcuate (Bjerrum) scotoma, double arcuate (ring) scotoma, leaving a central island and temporal crescent in end stage.
What risk factors for conversion did OHTS identify?
Older age, higher IOP, thinner central corneal thickness, larger vertical cup-to-disc ratio and higher pattern standard deviation.
How do you set a target IOP?
Usually a 20–30% reduction from baseline, lower for advanced damage, younger age, faster progression or normal-tension glaucoma, and reviewed with structural and field progression.
What is first-line treatment today?
A prostaglandin analogue drop, or selective laser trabeculoplasty (SLT) as first-line, supported by the LiGHT trial.
What does a disc haemorrhage signify?
A strong marker of progression, especially in normal-tension glaucoma. It usually resolves in weeks and recurs at the site of rim loss.

Station 21: Acute angle closure Glaucoma

Examiner: A 60-year-old woman presents with a painful red right eye, haloes, headache and vomiting since the evening. The pupil is mid-dilated and the cornea hazy.

What is the diagnosis and how do you confirm it?
Acute primary angle closure. Confirm with raised IOP (often > 40 mmHg) and a closed angle on gonioscopy (after clearing corneal oedema with glycerine if needed); check the fellow eye angle.
What is the mechanism?
Pupil block: relative resistance to aqueous flow at the pupil makes the peripheral iris bow forward and close the angle. Plateau iris and lens-induced (phacomorphic) mechanisms also occur.
What is your immediate medical treatment?
Systemic acetazolamide 500 mg (IV or oral) and, if needed, IV mannitol; topical beta-blocker, alpha-agonist and steroid; then pilocarpine 1–2% once the IOP has started to fall and the iris sphincter is no longer ischaemic. Lie the patient supine.
What is the definitive treatment?
Laser peripheral iridotomy in both eyes (the fellow eye has a high risk of attack). If the attack does not break or the cornea is too hazy, surgical iridectomy or lens extraction.
What did the EAGLE trial show?
Clear lens extraction gave better IOP control, fewer medications and better quality of life than laser iridotomy in primary angle closure and angle-closure glaucoma with IOP of 30 mmHg or more.
Which drugs can precipitate angle closure?
Dilating drops, anticholinergics (antihistamines, tricyclics, antispasmodics), adrenergic agonists, and topiramate (which causes bilateral angle closure by ciliary body swelling, not pupil block).
How do you differentiate it from neovascular glaucoma?
Neovascular glaucoma shows new vessels on the iris and angle, with a history of diabetes or vein occlusion; the angle is closed by fibrovascular membrane, not by iris bowing.

Station 22: Normal-tension glaucoma Glaucoma

Examiner: A 58-year-old with migraine and cold hands has glaucomatous cupping and an arcuate field defect, but IOP never exceeds 18 mmHg.

How do you define normal-tension glaucoma?
Glaucomatous optic neuropathy with IOP consistently within the normal range (21 mmHg or less) and open angles.
What must you exclude?
Diurnal IOP spikes, thin corneas, previous steroid use, burnt-out pigmentary or steroid glaucoma, compressive lesions, previous ischaemic events and B12 deficiency.
When do you order neuroimaging?
Age under 50, rapid progression, pallor out of proportion to cupping, field defects respecting the vertical midline, or reduced central acuity or colour vision.
Which vascular risk factors are associated?
Migraine, Raynaud phenomenon, nocturnal hypotension, sleep apnoea and disc haemorrhages.
What did the Collaborative NTG Study show?
Lowering IOP by 30% slowed field progression, but about half of untreated patients did not progress over five years.
How do you treat it?
Aim for a 30% reduction with prostaglandin analogue or SLT; avoid aggressive antihypertensives at night; trabeculectomy if progression continues.
What is the significance of disc haemorrhages here?
They are more frequent in NTG and predict progression.

Station 23: Pseudoexfoliation glaucoma Glaucoma

Examiner: A 70-year-old with an IOP of 34 mmHg in one eye and 18 in the other. There is flaky material on the lens and pupil margin.

Why is IOP raised?
Pseudoexfoliation material and pigment block the trabecular meshwork.
How does it differ from POAG?
Often unilateral or asymmetric, higher IOP with larger diurnal swings, faster progression and poorer response to drops.
What gonioscopic signs are typical?
Heavy irregular trabecular pigmentation and a Sampaolesi line.
Which treatment options work well?
Prostaglandin analogues first; SLT or ALT works particularly well; trabeculectomy or tube for progression; cataract surgery can lower IOP.
What did the Early Manifest Glaucoma Trial find about pseudoexfoliation?
Pseudoexfoliation was a strong risk factor for progression.
Which genes are linked?
LOXL1 variants, which are common in the general population, so testing is not useful clinically.
What systemic associations have been reported?
Cardiovascular and cerebrovascular disease, hearing loss and abdominal aortic aneurysm, though causation is not proven.

Station 24: Pigment dispersion syndrome Glaucoma

Examiner: A 28-year-old myopic man notices blurred vision and haloes after playing football. Slit lamp shows a vertical spindle of pigment on the endothelium.

What is the diagnosis?
Pigment dispersion syndrome, which may progress to pigmentary glaucoma.
What is the classic triad?
Krukenberg spindle, mid-peripheral spoke-like iris transillumination defects, and dense homogeneous trabecular pigmentation.
What is the mechanism?
Reverse pupil block: a posteriorly bowed concave iris rubs on the zonules and releases pigment.
Why are symptoms triggered by exercise?
Exercise and pupil dilation release a shower of pigment that acutely raises IOP.
How do you treat pigmentary glaucoma?
Prostaglandin analogues and other drops, SLT (use lower energy as the pigmented meshwork absorbs more), and surgery if needed.
Is laser iridotomy helpful?
It flattens the iris, but trials have not shown that it prevents progression to glaucoma, so it is not routinely advised.
Why might IOP improve with age?
Lens growth and physiological miosis reduce iridozonular contact, so pigment release slows (burnt-out phase).

Station 25: Neovascular glaucoma Glaucoma

Examiner: A man with an ischaemic CRVO three months ago now has a painful red eye, IOP 48 mmHg, and new vessels on the iris.

Why does NVG develop after CRVO?
Retinal ischaemia releases VEGF, which drives new vessels on the iris and angle; a fibrovascular membrane then closes the angle.
What is the 100-day glaucoma?
NVG classically appears around three months after ischaemic CRVO.
Which other causes do you know?
Proliferative diabetic retinopathy, ocular ischaemic syndrome (carotid stenosis), long-standing RD and tumours.
How do you treat it?
Intravitreal anti-VEGF to regress vessels quickly, full panretinal photocoagulation for the ischaemia, IOP-lowering drops and acetazolamide, cycloplegic and steroid.
Which surgery do you choose if IOP remains high?
A glaucoma drainage device (Ahmed or Baerveldt), or cyclophotocoagulation in an eye with poor visual potential. Trabeculectomy has a high failure rate.
Which drops should you avoid?
Pilocarpine and prostaglandins may worsen inflammation; miotics are avoided.
Why must you gonioscope at-risk patients?
Angle new vessels can appear before iris new vessels, giving a chance to treat before the angle closes.

Station 26: Primary congenital glaucoma Glaucoma

Examiner: A 4-month-old with watering, photophobia, blepharospasm and large hazy corneas.

What is the classic triad?
Epiphora, photophobia and blepharospasm, with buphthalmos and corneal clouding.
What are Haab striae?
Horizontal or curvilinear breaks in Descemet membrane caused by corneal stretching (unlike vertical birth-trauma striae).
Which gene is most often involved?
CYP1B1, inherited autosomal recessively, common in consanguineous families.
How do you examine the child?
Examination under anaesthesia: IOP (lowered by most anaesthetics except ketamine), corneal diameter, axial length, gonioscopy and optic disc cupping.
What is the treatment?
Surgery: goniotomy (clear cornea) or trabeculotomy, or combined trabeculotomy-trabeculectomy, which is often preferred in India; drops are only a temporary measure.
What corneal diameter is abnormal?
More than 11 mm in a newborn or more than 12 mm in the first year should raise suspicion.
Why is long-term follow-up essential?
Amblyopia, myopia and anisometropia are common, and IOP can rise again years later.

Station 27: Trabeculectomy and the bleb Glaucoma

Examiner: Three weeks after trabeculectomy you see a flat bleb and IOP of 4 mmHg, with a shallow anterior chamber.

What is the principle of trabeculectomy?
A guarded partial-thickness scleral flap creates a fistula from the anterior chamber to a sub-conjunctival bleb.
What are the causes of low IOP with a flat bleb?
A wound leak (check with Seidel test), ciliary body shutdown, or choroidal detachment; overfiltration gives a low IOP with a high bleb.
How do you manage a bleb leak?
Pressure patch, bandage contact lens, aqueous suppressants, autologous blood or glue; surgical revision for persistent leaks.
What antifibrotics are used and why?
Mitomycin C or 5-fluorouracil reduce scarring and failure; MMC increases thin, avascular blebs and late leaks.
What is blebitis?
Infection of the bleb with a milky bleb and preserved vitreous; treat urgently with intensive topical antibiotics. Spread to the vitreous is bleb-related endophthalmitis and needs a tap and inject.
How do you grade blebs?
The Indiana or Moorfields bleb grading systems, describing height, extent, vascularity and leakage.
What causes high IOP and a flat bleb with a deep chamber?
Internal ostium block or flap fibrosis; options include massage, laser suture lysis, needling with 5-FU or MMC.

Station 28: Steroid-induced glaucoma Glaucoma

Examiner: A 12-year-old with vernal keratoconjunctivitis has used over-the-counter dexamethasone drops for months. IOP is 38 mmHg with cupping.

What is the mechanism?
Steroids increase extracellular matrix deposition and reduce outflow through the trabecular meshwork.
Who are steroid responders?
About one-third of people show a moderate rise and 5% a high rise; risk is higher in POAG, first-degree relatives, high myopia, diabetes and children.
Which routes raise IOP most?
Intravitreal and periocular steroids and topical drops more than systemic; dexamethasone and prednisolone more than fluorometholone or loteprednol.
When does IOP usually rise?
Within 2 to 6 weeks of starting treatment, but it can be earlier or later.
How do you manage it?
Stop or reduce the steroid or switch to a weaker one, steroid-sparing therapy (cyclosporine or tacrolimus in VKC), IOP-lowering drops, SLT, and surgery if needed. A depot steroid may need removal.
Why is it common in India?
Steroid eye drops are easily available over the counter and are used for any red eye.
What advice protects patients?
Never use steroid drops without an eye doctor, and check IOP regularly during treatment.

Read more: Eye steroids and regimens, VKC

Station 29: Aqueous misdirection Glaucoma

Examiner: The day after trabeculectomy for angle closure, the anterior chamber is uniformly flat and IOP is 40 mmHg despite a patent iridotomy.

What is the diagnosis?
Aqueous misdirection (malignant glaucoma): aqueous flows backwards into the vitreous, pushing the lens-iris diaphragm forward.
How do you differentiate it from pupil block and choroidal haemorrhage?
Pupil block has iris bombé with a deeper central chamber and resolves with a patent iridotomy; suprachoroidal haemorrhage shows dark choroidal elevations on fundus or B-scan.
Who is at risk?
Eyes with angle closure, small hyperopic eyes and nanophthalmos, especially after filtering or cataract surgery.
What is the medical treatment?
Intensive cycloplegia (atropine), aqueous suppressants, hyperosmotics, and avoiding miotics, which worsen it.
What laser treatment helps in a pseudophakic eye?
Nd:YAG disruption of the anterior hyaloid and posterior capsule to let aqueous pass forward.
What is the definitive surgery?
Pars plana vitrectomy with hyaloido-zonulo-iridectomy so the vitreous cavity communicates with the anterior chamber.
Why is the fellow eye at risk?
It shares the same anatomy, so plan prophylactic iridotomy and caution in its surgery.

Station 30: Diabetic retinopathy Retina

Examiner: A 52-year-old with type 2 diabetes for 12 years. The fundus shows haemorrhages in four quadrants, venous beading in two, and new vessels at the disc.

Classify this retinopathy.
Proliferative diabetic retinopathy (new vessels at the disc). The NPDR features alone would make it very severe NPDR (two or more criteria of the 4-2-1 rule).
What is the 4-2-1 rule?
Severe NPDR: haemorrhages in all 4 quadrants, or venous beading in 2 or more quadrants, or IRMA in 1 or more quadrant. Two or more of these make very severe NPDR.
What are high-risk characteristics (DRS)?
NVD ≥ one-quarter to one-third disc area; any NVD with vitreous or preretinal haemorrhage; or NVE ≥ half disc area with haemorrhage.
How do you treat PDR?
Panretinal photocoagulation, or anti-VEGF injections as an alternative (DRCR Protocol S showed ranibizumab was non-inferior at 2 years), particularly with coexisting DME. Vitrectomy for non-clearing haemorrhage or tractional detachment involving the macula.
What was clinically significant macular oedema (ETDRS)?
Retinal thickening within 500 µm of the foveal centre; hard exudates within 500 µm with adjacent thickening; or thickening of one disc area or more, any part of which is within one disc diameter of the centre. Today we classify DME on OCT as centre-involving or not.
What is first-line treatment for centre-involving DME with vision loss?
Intravitreal anti-VEGF. Protocol T: with vision 20/50 or worse, aflibercept gave better vision than bevacizumab at 1 year.
When should screening start?
Type 2: at diagnosis. Type 1: within 5 years of diagnosis (usually from puberty). Pregnancy: early in each trimester for women with pre-existing diabetes.

Station 31: Rhegmatogenous retinal detachment Retina

Examiner: A 55-year-old myope reports flashes, a shower of floaters and a curtain coming up from below in the left eye for two days.

What sign do you look for in the anterior vitreous?
Shafer's sign (tobacco dust): pigment cells in the anterior vitreous, highly suggestive of a retinal break.
Where would you look for the break (Lincoff rules)?
A superior temporal or nasal detachment: the break is within 1.5 clock hours of its highest border in 98%. A total or superior detachment crossing 12 o'clock: break at 12 or within a triangle 1.5 clock hours either side. An inferior detachment: the higher side shows which side of the disc the break is on. Inferior bullae arise from a superior break.
How do you tell rhegmatogenous from tractional and exudative detachment?
Rhegmatogenous: convex, corrugated, mobile, with a break and tobacco dust. Tractional: concave, immobile, with fibrovascular bands. Exudative: smooth, shifting fluid that moves with posture, no break.
What are the surgical options?
Pneumatic retinopexy (single superior break in the upper two-thirds; PIVOT trial), scleral buckle (young phakic patients, dialysis, no PVD), or pars plana vitrectomy (pseudophakic eyes, posterior or multiple breaks, giant tears, vitreous haemorrhage, PVR).
Why does macular status matter?
Macula-on detachments need urgent surgery to save central vision; for macula-off, visual outcome depends on how long the macula has been detached.
What is PVR and how is it graded?
Proliferative vitreoretinopathy: membranes forming on and under the retina, the main cause of surgical failure. Grade A (haze, pigment clumps), B (rolled edges, wrinkling), C (full-thickness fixed folds), with posterior or anterior location.
Which tamponade agents do you know?
Air, SF6 (lasts about 2 weeks), C3F8 (about 8 weeks) and silicone oil (removed later). Patients must not fly or have nitrous oxide anaesthesia with gas in the eye.

Station 32: Central retinal vein occlusion Retina

Examiner: A 66-year-old hypertensive with sudden painless blurring in one eye. The fundus shows haemorrhages in all four quadrants, dilated tortuous veins and disc swelling.

How do you classify CRVO?
Non-ischaemic (perfused) and ischaemic. Ischaemic features include poor acuity (often worse than 6/60), RAPD, extensive cotton-wool spots, more than 10 disc areas of non-perfusion on FFA and reduced ERG b-wave.
What systemic work-up do you do?
Blood pressure, glucose and HbA1c, lipids, full blood count and ESR. In younger patients add a thrombophilia and hyperviscosity screen.
Which ocular risk factor must you check?
Raised IOP and glaucoma, in both eyes.
How do you treat macular oedema?
Intravitreal anti-VEGF (ranibizumab, aflibercept, bevacizumab, faricimab), with dexamethasone implant as second line or in pseudophakic patients.
When do you do panretinal photocoagulation?
When neovascularisation of the iris, angle or retina appears; not prophylactically, but with close monthly follow-up in ischaemic eyes for the first months.
What did the CVOS show?
Prophylactic PRP did not prevent NVI reliably; treat promptly when new vessels appear. Grid laser did not improve vision in CRVO macular oedema.
What is the prognosis?
Initial acuity is the best predictor; about one-third of non-ischaemic CRVOs convert to ischaemic.

Station 33: Branch retinal vein occlusion Retina

Examiner: A 60-year-old with blurred vision has a wedge of flame haemorrhages in the superotemporal quadrant arising at an arteriovenous crossing.

Why does BRVO occur at AV crossings?
The artery and vein share an adventitial sheath, so a thickened sclerotic artery compresses the vein and causes turbulence and thrombosis.
Which quadrant is most commonly affected?
Superotemporal, because it has the most AV crossings.
What are the main causes of visual loss?
Macular oedema, macular ischaemia and vitreous haemorrhage from neovascularisation.
What did the BVOS show?
Grid laser improved vision in macular oedema persisting for 3 months with vision 6/12 or worse, and scatter laser reduced vitreous haemorrhage once new vessels developed.
What is first-line treatment for macular oedema now?
Intravitreal anti-VEGF, which gives better visual results than grid laser (BRAVO trial).
When do you laser the ischaemic area?
Sectoral scatter laser when retinal or disc new vessels develop.
Which systemic diseases do you check?
Hypertension, diabetes, hyperlipidaemia and smoking.

Station 34: Central retinal artery occlusion Retina

Examiner: A 70-year-old woke with sudden painless loss of vision to counting fingers. There is a cherry-red spot and a pale retina.

Why is there a cherry-red spot?
The inner retina becomes opaque and white from ischaemia, while the thin foveola lets the normal choroid show through.
Why may some vision be preserved?
A cilioretinal artery, present in about 15 to 30% of people, can supply the papillomacular bundle.
What is the most urgent systemic question?
Is this giant cell arteritis? Check ESR, CRP and symptoms (jaw claudication, headache, scalp tenderness) immediately in anyone over 50.
Why is CRAO a stroke equivalent?
It is usually embolic from carotid or cardiac disease, and carries a high risk of cerebral stroke in the following weeks; refer immediately to a stroke unit.
What investigations follow?
Carotid Doppler, ECG and echocardiogram, blood pressure, lipids, glucose and brain imaging.
Do conservative treatments work?
Ocular massage, AC paracentesis and IOP lowering have no proven benefit; thrombolysis within 4.5 hours is under trial and offered in some stroke centres.
What late complication can occur?
Neovascularisation of the iris and neovascular glaucoma, usually within weeks.

Station 35: Neovascular AMD Retina

Examiner: A 74-year-old reports distortion of straight lines for two weeks. There is a grey-green subretinal lesion with haemorrhage at the macula.

What is the diagnosis?
Neovascular (wet) age-related macular degeneration with choroidal neovascularisation (macular neovascularisation).
How do you classify macular neovascularisation?
Type 1 (under the RPE, occult), type 2 (above the RPE, classic) and type 3 (retinal angiomatous proliferation); polypoidal choroidal vasculopathy is a variant of type 1.
Which investigations do you do?
OCT (fluid, PED, hyper-reflective material), OCT angiography, and FFA or ICG (ICG for polyps).
What is the treatment?
Intravitreal anti-VEGF: ranibizumab, aflibercept 2 or 8 mg, bevacizumab, brolucizumab or faricimab, given monthly then on treat-and-extend.
What did the AREDS2 trial show?
Supplements (vitamins C and E, zinc, copper, lutein and zeaxanthin) reduced progression to advanced AMD by about 25% in people with intermediate AMD or advanced AMD in one eye.
Why should smokers not take beta-carotene?
It increased lung cancer risk, which is why AREDS2 replaced it with lutein and zeaxanthin.
What is the role of the Amsler grid?
Home monitoring of the fellow eye for new distortion, prompting an urgent review.

Station 36: Geographic atrophy Retina

Examiner: An 80-year-old with slowly worsening reading vision has sharply demarcated areas of RPE loss through which large choroidal vessels are visible.

What is geographic atrophy?
The advanced dry form of AMD: well-defined areas of RPE, photoreceptor and choriocapillaris loss.
How do you image it?
Fundus autofluorescence (dark areas, with hyperautofluorescent margins predicting growth) and OCT (complete RPE and outer retinal atrophy, cRORA).
Why does reading suffer before acuity?
Atrophy often spares the fovea initially and surrounds it, so central acuity is preserved while the reading field is lost.
Which treatments are approved?
Complement inhibitors: pegcetacoplan (C3) and avacincaptad pegol (C5), given intravitreally, slow growth of atrophy by about 20% but do not improve vision.
What risks do these drugs carry?
Conversion to neovascular AMD, intraocular inflammation and, with pegcetacoplan, rare occlusive retinal vasculitis.
Which genes are linked to AMD?
Complement factor H (CFH), ARMS2/HTRA1 and C3.
How do you help these patients now?
Low vision aids, magnification and eccentric viewing training, good lighting, smoking cessation and AREDS2 supplements where indicated.

Station 37: Central serous chorioretinopathy Retina

Examiner: A 38-year-old stressed executive notices a dim central patch and micropsia in one eye. OCT shows subretinal fluid under the fovea.

Which risk factors do you ask about?
Corticosteroids by any route (including skin creams and inhalers), type A personality and stress, pregnancy, Cushing syndrome and phosphodiesterase inhibitors.
What does FFA show?
A focal leak expanding as an ink-blot or, less often, a smoke-stack pattern.
What does ICG show and why does it matter?
Choroidal hyperpermeability; it guides photodynamic therapy and suggests the pachychoroid spectrum.
What is the natural history?
Most acute cases resolve within 3 months; chronic disease causes RPE atrophy and permanent loss.
How do you treat persistent or chronic CSCR?
Half-dose or half-fluence photodynamic therapy with verteporfin, which was better than micropulse laser in the PLACE trial; focal laser for an extrafoveal leak.
Do eplerenone or spironolactone work?
The VICI trial found no benefit of eplerenone over placebo for chronic CSCR.
What complication may need anti-VEGF?
Secondary choroidal neovascularisation (pachychoroid neovasculopathy).

Read more: CSCR treatment, ICG angiography

Station 38: Macular hole Retina

Examiner: A 67-year-old woman notices a central gap in her vision. OCT shows a full-thickness foveal defect of 300 microns with vitreous still attached at its edges.

How do you stage it?
International Vitreomacular Traction Study classification: small (250 microns or less), medium (250 to 400) or large (over 400), with or without vitreomacular traction. Gass stages 1 to 4 are the older system.
What is the Watzke-Allen test?
A thin slit beam across the hole: the patient sees a break in the line in a full-thickness hole.
What is the treatment?
Pars plana vitrectomy with internal limiting membrane peel and gas tamponade (SF6 or C2F6), with face-down or reading positioning in some cases.
Which factors predict closure?
Smaller diameter, shorter duration and a smaller minimum linear diameter; large chronic holes may need an inverted ILM flap.
What is the role of ocriplasmin?
Pharmacological vitreolysis for small holes with VMT; rarely used now because of modest success and side effects.
What happens to the lens after vitrectomy?
Nuclear sclerotic cataract develops in most phakic eyes within two years.
How do you tell a lamellar hole from a full-thickness hole?
A lamellar hole has an irregular foveal contour with intraretinal splitting but intact photoreceptor layer.

Station 39: Retinopathy of prematurity Retina

Examiner: You are asked to screen a baby born at 29 weeks weighing 1100 g, now four weeks old, on supplemental oxygen.

Who should be screened in India?
Babies born under 34 weeks or under 2000 g, and older or heavier babies with an unstable neonatal course (sepsis, oxygen, transfusions).
When should the first examination be?
By day 20 to 30 of life, or 31 weeks postmenstrual age, whichever is later; in India by day 20 to catch aggressive disease.
How do you classify ROP (ICROP3)?
Zone (I to III, with posterior zone II), stage (1 demarcation line to 5 total detachment), extent in clock hours, plus disease, and aggressive ROP (A-ROP).
What is plus disease?
Dilated, tortuous posterior pole vessels in at least two quadrants, indicating active disease that usually needs treatment.
What is type 1 ROP and how do you treat it?
Zone I any stage with plus, zone I stage 3, or zone II stage 2 or 3 with plus (ETROP); treat within 48 to 72 hours with laser to avascular retina or intravitreal anti-VEGF.
Advantages and disadvantages of anti-VEGF?
Good for zone I and A-ROP and less myopia, but needs long follow-up for late reactivation and has uncertain systemic effects.
What long-term problems follow?
Myopia, strabismus, amblyopia, retinal detachment and glaucoma.

Station 40: Diabetic macular oedema Retina

Examiner: A 55-year-old diabetic with 6/18 vision. OCT shows central thickening of 450 microns with cysts and hard exudates near the fovea.

How do you classify DME today?
By OCT: centre-involving or non-centre-involving. The older term clinically significant macular oedema came from ETDRS.
What is first-line treatment for centre-involving DME with reduced vision?
Intravitreal anti-VEGF. Protocol T found aflibercept better than bevacizumab when vision was 6/15 or worse.
When are steroids preferred?
Pseudophakic eyes, poor responders to anti-VEGF, patients who cannot attend frequently, and recent cardiovascular events.
What did Protocol V show?
Eyes with centre-involving DME and good vision (6/7.5 or better) could be observed closely, starting anti-VEGF only if vision dropped.
Which OCT biomarkers predict poor outcome?
Disorganisation of retinal inner layers (DRIL), ellipsoid zone disruption, hyper-reflective foci and subretinal fluid.
What systemic factors matter?
Glycaemic, blood pressure and lipid control; fenofibrate slows retinopathy progression (FIELD, ACCORD-Eye); renal disease and anaemia worsen oedema.
What is the role of focal laser now?
Mainly for non-centre-involving oedema with leaking microaneurysms, or as an adjunct.

Station 41: Post-operative endophthalmitis Retina

Examiner: Three days after cataract surgery, a patient has pain, hand-movement vision, a hypopyon and no red reflex.

What is the diagnosis and the commonest organism?
Acute post-operative endophthalmitis; coagulase-negative staphylococci are commonest.
What do you do immediately?
Same-day vitreous tap (or vitrectomy) for culture, and intravitreal vancomycin 1 mg/0.1 mL and ceftazidime 2.25 mg/0.1 mL (amikacin 0.4 mg if allergic).
What did the EVS show?
Immediate vitrectomy was better than tap and inject only in eyes with light-perception vision; systemic antibiotics added no benefit.
Is the EVS still applied rigidly?
Many surgeons now do early vitrectomy at lower thresholds because modern small-gauge vitrectomy is safer.
What does intracameral antibiotic prophylaxis achieve?
The ESCRS study showed intracameral cefuroxime reduced endophthalmitis about fivefold; moxifloxacin is widely used in India.
What causes chronic post-operative endophthalmitis?
Cutibacterium (Propionibacterium) acnes, with a white plaque in the capsular bag and granulomatous inflammation months later.
How do you prevent it?
Povidone-iodine 5% to the conjunctival sac and 10% to the skin, lid hygiene, sterile draping of lashes, and intracameral antibiotic.

Station 42: Retinitis pigmentosa Retina

Examiner: A 25-year-old with night blindness since childhood and tunnel vision. The fundus shows bone-spicule pigmentation, attenuated arterioles and a waxy pale disc.

What is the classic triad?
Bone-spicule pigmentation, arteriolar attenuation and waxy disc pallor.
Which inheritance patterns occur?
Autosomal dominant (best prognosis), autosomal recessive (commonest) and X-linked (worst prognosis, RPGR).
What does the ERG show?
Reduced or extinguished rod responses early, then cone responses, with delayed implicit times.
Which syndromes are associated?
Usher (deafness), Bardet-Biedl (obesity, polydactyly), Refsum (high phytanic acid), Kearns-Sayre and abetalipoproteinaemia (Bassen-Kornzweig).
Why are Refsum and abetalipoproteinaemia important?
They are treatable: low-phytanic-acid diet in Refsum, and vitamins A and E in abetalipoproteinaemia.
Which treatable complications occur?
Cystoid macular oedema (carbonic anhydrase inhibitors) and posterior subcapsular cataract (surgery).
What gene therapy is available?
Voretigene neparvovec (Luxturna) for biallelic RPE65 mutations.

Station 43: Choroidal melanoma Retina

Examiner: A 60-year-old has a pigmented dome-shaped choroidal lesion 4 mm thick with orange pigment and subretinal fluid.

Which features suggest melanoma rather than a naevus?
TFSOM-UHHD: thickness over 2 mm, subretinal fluid, symptoms, orange pigment, margin near the disc, ultrasound hollowness, absent halo and absent drusen.
What does B-scan show?
A dome or collar-stud (mushroom) mass with low internal reflectivity (acoustic hollowness) and choroidal excavation.
What does a collar-stud shape mean?
The tumour has broken through Bruch membrane.
What did COMS show?
For medium tumours, iodine-125 plaque brachytherapy gave the same survival as enucleation; pre-enucleation radiotherapy did not help large tumours.
Where does it metastasise?
The liver, so lifelong liver imaging and liver function tests are needed.
Which genetic markers predict prognosis?
Monosomy 3 and BAP1 loss predict metastasis; class 1 and 2 gene expression profiling is used.
What new systemic treatment exists?
Tebentafusp improves survival in HLA-A*02:01-positive metastatic uveal melanoma.

Read more: COMS findings, Ocular tumours

Station 44: Acute anterior uveitis Uvea

Examiner: A 30-year-old man with a painful red photophobic eye and low back stiffness in the mornings. There are fine KPs, 2+ cells and a small hypopyon.

What is the likely association?
HLA-B27-associated acute anterior uveitis, here with ankylosing spondylitis (inflammatory back pain). Fibrinous reaction and hypopyon are typical.
Granulomatous vs non-granulomatous: how do you tell?
Granulomatous: large greasy mutton-fat KPs, iris nodules (Koeppe at the pupil margin, Busacca on the iris surface) and chronic course (sarcoid, TB, VKH, syphilis). Non-granulomatous: fine KPs, acute course (HLA-B27).
How do you grade anterior chamber cells (SUN)?
Cells in a 1 mm × 1 mm slit beam: 0 (< 1), 0.5+ (1–5), 1+ (6–15), 2+ (16–25), 3+ (26–50), 4+ (> 50).
How do you treat it?
Frequent topical steroid (prednisolone acetate 1%) with a cycloplegic (homatropine or cyclopentolate, atropine if severe) to relieve ciliary spasm and break or prevent posterior synechiae. Taper steroids slowly.
Which investigations would you order?
For a first, typical unilateral HLA-B27 picture: HLA-B27 and sacroiliac imaging. For recurrent, bilateral, granulomatous or atypical uveitis: syphilis serology, chest X-ray or CT, ACE and lysozyme, Mantoux or IGRA, and others guided by history.
What are the complications?
Posterior synechiae, cataract, secondary glaucoma (inflammatory or steroid-induced), cystoid macular oedema, band keratopathy (chronic, especially in JIA) and hypotony.
Which systemic drug is approved as steroid-sparing for non-infectious uveitis?
Adalimumab (VISUAL I and II; SYCAMORE for JIA uveitis with methotrexate).

Station 45: Vogt-Koyanagi-Harada disease Uvea

Examiner: A 32-year-old woman with headache and tinnitus followed by bilateral blurring. There are multiple serous retinal detachments and disc hyperaemia.

What is VKH?
A bilateral granulomatous panuveitis caused by autoimmunity against melanocytes, more common in pigmented races.
What are the phases?
Prodromal (headache, meningism, tinnitus), acute uveitic (exudative detachments), convalescent (sunset-glow fundus, vitiligo, poliosis) and chronic recurrent.
What must you exclude by history?
Penetrating injury or eye surgery, which would suggest sympathetic ophthalmia.
What does FFA show?
Multiple pinpoint leaks in the acute phase that pool into the detachments (starry sky), with disc leakage.
What do OCT and ICG show?
Subretinal fluid with septae and a thickened choroid on OCT; hypofluorescent dark dots on ICG.
How do you treat it?
Early high-dose systemic steroid (often IV methylprednisolone then oral prednisolone tapered over at least 6 months) with early immunosuppressives to prevent chronic disease.
What are the late complications?
Cataract, glaucoma, choroidal neovascularisation and subretinal fibrosis.

Station 46: Behçet disease Uvea

Examiner: A 28-year-old man with recurrent mouth ulcers and genital ulcers has a hypopyon in one eye and retinal infiltrates with vasculitis.

What are the diagnostic criteria?
ICBD scoring: oral ulcers, genital ulcers, ocular lesions, skin lesions, neurological signs, vascular lesions and a positive pathergy test.
What type of uveitis is typical?
A non-granulomatous panuveitis with an occlusive necrotising retinal vasculitis; the hypopyon shifts with head position and the eye may be quiet.
Which HLA is associated?
HLA-B51, common along the old Silk Road.
How do you treat posterior Behçet?
Steroids plus azathioprine; anti-TNF agents (infliximab or adalimumab) or interferon-alpha for sight-threatening or resistant disease.
Which drug should you avoid?
Cyclosporine in patients with neuro-Behçet, as it can worsen neurological disease.
Why is prognosis guarded?
Recurrent occlusive vasculitis causes retinal ischaemia, optic atrophy and blindness, especially in young men.
What is the pathergy test?
A pustule appearing 24 to 48 hours after a sterile needle prick of the skin.

Read more: Behçet treatment, Uveitis hub

Station 47: Ocular toxoplasmosis Uvea

Examiner: A 22-year-old with floaters has a fluffy white focus of retinitis next to an old pigmented scar, with dense vitritis.

What is the diagnosis?
Recurrent ocular toxoplasmosis: active retinochoroiditis adjacent to an old scar (satellite lesion), with a headlight-in-the-fog appearance.
How is it acquired?
Undercooked meat, cat faeces or contaminated water and vegetables, and congenitally across the placenta.
When do you treat?
Lesions near the macula or disc, near a major vessel, large lesions, severe vitritis, and immunocompromised or pregnant patients.
Which regimens are used?
Trimethoprim-sulfamethoxazole twice daily, or pyrimethamine with sulfadiazine and folinic acid, or intravitreal clindamycin with dexamethasone; oral steroid added after 24 to 48 hours.
Why not give steroids alone?
They allow uncontrolled parasite proliferation and fulminant retinitis.
How do you treat a pregnant woman?
Spiramycin in the first trimester (avoid pyrimethamine, which is teratogenic); coordinate with obstetrics.
How can recurrences be reduced?
Long-term trimethoprim-sulfamethoxazole every 2 or 3 days reduced recurrences in trials.

Station 48: CMV retinitis Uvea

Examiner: A man with advanced HIV (CD4 count 30) has floaters. The fundus shows a granular white retinitis with haemorrhages along the vessels.

What is the typical appearance?
Pizza-pie or cottage-cheese-and-ketchup: white granular necrosis with haemorrhages along vessels; a quieter granular form spreads at the edges.
At what CD4 count does it occur?
Usually under 50 cells per microlitre.
How do you treat it?
Oral valganciclovir 900 mg twice daily for induction, with intravitreal ganciclovir 2 mg for sight-threatening lesions, then maintenance; restart antiretroviral therapy.
What is immune recovery uveitis?
Inflammation, CME and ERM when antiretrovirals restore immunity in eyes with previous CMV retinitis.
When can maintenance be stopped?
When CD4 counts stay above 100 for 3 to 6 months on antiretrovirals and the retinitis is inactive.
What complication causes late visual loss?
Rhegmatogenous retinal detachment through atrophic retina, often needing vitrectomy with silicone oil.
Who else is at risk now?
Transplant and chemotherapy patients, and those on biologics.

Station 49: Sympathetic ophthalmia Uvea

Examiner: Six weeks after an open globe injury to the left eye, the patient develops blurring and photophobia in the uninjured right eye.

What is sympathetic ophthalmia?
A bilateral granulomatous panuveitis after penetrating trauma or surgery to one eye, caused by autoimmunity to uveal antigens.
What are the terms for the two eyes?
The exciting eye (injured) and the sympathising eye (fellow).
What fundus signs occur?
Dalen-Fuchs nodules (yellow-white spots of epithelioid cells between RPE and Bruch membrane) and exudative detachments.
When does it occur?
Usually within 3 months of the injury (80% within a year), but it can appear decades later.
How do you treat it?
High-dose systemic steroid plus early steroid-sparing immunosuppression.
Is enucleation of the exciting eye helpful?
Enucleation within 2 weeks of injury may prevent it, but once SO has started, removing an eye with useful vision is not advised.
Which surgery commonly triggers it today?
Vitreoretinal surgery is now a major cause, along with trauma.

Station 50: JIA-associated uveitis Uvea

Examiner: A 5-year-old girl with oligoarticular arthritis and positive ANA is referred for screening. Her eyes are white but there are cells in the anterior chamber.

Why is this uveitis dangerous?
It is chronic, painless and white, so it is missed until band keratopathy, cataract or glaucoma appear.
Which children are at highest risk?
Oligoarticular JIA, ANA positive, onset under 6 years, and within 4 years of arthritis onset.
How often do you screen?
High-risk children every 3 months, decreasing over time; screening continues for years after arthritis onset.
What is the classic triad of complications?
Band keratopathy, cataract and glaucoma (with posterior synechiae).
How do you treat it?
Topical steroid, then methotrexate as first steroid-sparing drug, then adalimumab (supported by SYCAMORE).
Why is cataract surgery risky in these children?
High risk of inflammation, membranes and hypotony; the eye must be quiet for at least 3 months, often with no IOL in young children.
How is it different from HLA-B27 uveitis in children?
Enthesitis-related arthritis gives acute, painful, red unilateral anterior uveitis.

Station 51: Tubercular uveitis Uvea

Examiner: A 40-year-old from an endemic area has granulomatous anterior uveitis with broad posterior synechiae and serpiginous-like choroiditis.

Which ocular signs suggest TB?
Broad-based posterior synechiae, granulomatous KPs, serpiginous-like choroiditis, choroidal tubercles or tuberculoma, occlusive retinal vasculitis.
Which tests do you use?
Interferon-gamma release assay (QuantiFERON) or tuberculin skin test, chest imaging (CT more sensitive), and PCR of ocular fluid where possible.
How is the diagnosis usually made?
Presumed: a compatible clinical picture with evidence of TB infection and exclusion of other causes; the COTS group gives guidance on when to start ATT.
How do you treat it?
Antitubercular therapy for at least 6 to 9 months with corticosteroids to control inflammation.
What is a paradoxical reaction?
Temporary worsening after starting ATT due to an immune response to released antigens.
Which drug in ATT is toxic to the eye?
Ethambutol causes optic neuropathy (dose-related, check vision and colour at baseline and monthly); rifabutin causes uveitis.
What is Eales disease?
An idiopathic occlusive periphlebitis in young Indian men, associated with TB hypersensitivity.

Station 52: Scleritis Uvea

Examiner: A 55-year-old woman with rheumatoid arthritis has a deep, boring eye pain that wakes her at night and a violaceous red eye.

How do you tell scleritis from episcleritis?
Scleritis is painful and tender with a bluish-red hue; deep vessels do not move or blanch with phenylephrine 10%. Episcleritis is mildly uncomfortable and blanches.
How do you classify scleritis?
Anterior (diffuse, nodular, necrotising with inflammation, scleromalacia perforans) and posterior.
Which systemic diseases do you look for?
Rheumatoid arthritis, granulomatosis with polyangiitis (ANCA), relapsing polychondritis, SLE, IBD and infections such as herpes zoster, TB and syphilis.
How do you treat it?
Oral NSAIDs for diffuse or nodular disease, systemic steroids, then immunosuppressives or rituximab for necrotising or ANCA-associated disease.
Why is necrotising scleritis an emergency?
It signals active systemic vasculitis with high mortality if untreated, and can perforate.
How does posterior scleritis present?
Pain, choroidal folds, exudative detachment and disc swelling; B-scan shows thickened sclera with fluid in Tenon space (T-sign).
What is scleromalacia perforans?
Painless scleral thinning in long-standing rheumatoid arthritis, without inflammation.

Station 53: Optic neuritis vs papilloedema Neuro-ophthalmology

Examiner: A 28-year-old woman has reduced vision in one eye for 4 days with pain on eye movement. The disc looks normal.

What is the diagnosis and the key signs?
Typical (demyelinating) retrobulbar optic neuritis: unilateral subacute vision loss, pain on eye movement, RAPD, reduced colour vision (red desaturation), central or diffuse field loss, normal disc in two-thirds.
What did ONTT show?
IV methylprednisolone followed by oral steroids sped recovery but did not change final vision; oral prednisolone alone at standard dose increased the recurrence rate. MRI white-matter lesions predicted multiple sclerosis (about 50% at 15 years if present).
What are atypical features that suggest NMOSD or MOGAD?
Severe or bilateral loss, marked disc swelling, poor recovery, long-segment or chiasmal involvement on MRI (NMOSD), perineural enhancement (MOGAD), and absence of pain. Test aquaporin-4 and MOG antibodies.
How does papilloedema differ?
Papilloedema is bilateral disc swelling from raised intracranial pressure, with good central vision and colour vision early, enlarged blind spot, headache, transient visual obscurations, and no RAPD unless asymmetric.
How do you grade papilloedema?
Frisén scale 0–5, from a C-shaped halo of nasal swelling (grade 1) to obscuration of the vessels on the disc (grades 4–5).
How do you manage idiopathic intracranial hypertension?
Brain MRI with venography to exclude a venous sinus thrombosis or mass, then lumbar puncture (raised opening pressure, normal CSF). Weight loss and acetazolamide (IIHTT), with optic nerve sheath fenestration or CSF shunting for threatened vision.
What is pseudopapilloedema?
Elevated disc without true swelling: optic disc drusen (detected with B-scan, autofluorescence or OCT), tilted discs, hypermetropic crowded discs and myelinated nerve fibres.

Station 54: Horner syndrome Neuro-ophthalmology

Examiner: A 45-year-old with neck pain after a gym workout has a mild left ptosis and a smaller left pupil, more obvious in dim light.

What are the signs?
Mild ptosis, miosis with dilation lag in the dark, apparent enophthalmos, inverse ptosis of the lower lid, and anhidrosis depending on the level.
How do you confirm it pharmacologically?
Apraclonidine 0.5% reverses the anisocoria (the Horner pupil dilates); cocaine 4 to 10% fails to dilate the Horner pupil.
How do you localise it?
Hydroxyamphetamine dilates a first- or second-order Horner pupil but not a third-order one; clinical clues help more in practice.
What is the urgent concern in this patient?
Carotid artery dissection: painful acute Horner needs same-day CT or MR angiography of the head and neck.
Which causes affect each neuron?
First: brainstem stroke, syringomyelia. Second: Pancoast tumour, neck surgery, neuroblastoma in children. Third: carotid dissection, cavernous sinus lesions, cluster headache.
What is special about congenital Horner?
Iris heterochromia (lighter iris on the affected side); in acquired childhood Horner, exclude neuroblastoma.
Why is the ptosis mild?
Only Müller muscle (sympathetic) is affected; the levator is intact.

Station 55: Third nerve palsy Neuro-ophthalmology

Examiner: A 50-year-old with sudden headache has complete ptosis, an eye that is down and out, and a dilated unreactive pupil.

What is your first concern?
A posterior communicating artery aneurysm compressing the nerve; this needs emergency CT angiography or MRA.
Why is the pupil involved in compression?
Pupillomotor fibres run superficially in the nerve and are affected first by compression; ischaemia damages the core and usually spares the pupil.
What causes a pupil-sparing palsy?
Microvascular ischaemia from diabetes, hypertension or hyperlipidaemia, usually painful and recovering within 3 months; image if under 50 or not resolving.
What is aberrant regeneration?
Misdirected fibres cause lid elevation on adduction or depression (pseudo-von Graefe) and pupil constriction on eye movement; it points to compression or trauma, not ischaemia.
How does a nuclear third nerve palsy present?
Bilateral ptosis (single central caudal nucleus) and contralateral superior rectus weakness.
Name some brainstem syndromes involving the third nerve.
Weber (contralateral hemiparesis), Benedikt (contralateral tremor), Claude (contralateral ataxia).
How do you manage diplopia long term?
Prisms or occlusion first, then strabismus surgery and ptosis surgery once stable for 6 to 12 months.

Station 56: Sixth nerve palsy Neuro-ophthalmology

Examiner: A 30-year-old woman with headaches and horizontal double vision worse at distance cannot abduct the right eye.

Why is the sixth nerve a false localising sign?
Its long intracranial course over the petrous apex makes it vulnerable to raised intracranial pressure from any cause.
What do you check in this patient?
Optic discs for papilloedema, blood pressure and BMI; consider idiopathic intracranial hypertension and urgent imaging.
What is Gradenigo syndrome?
Petrous apicitis from otitis media causing sixth nerve palsy, facial pain (fifth nerve) and ear discharge.
What are other causes?
Microvascular ischaemia, trauma, tumours (clivus chordoma, nasopharyngeal carcinoma), cavernous sinus disease and, in children, post-viral palsy.
How do you tell it from Duane syndrome?
Duane is congenital with globe retraction and palpebral fissure narrowing on adduction, and usually no diplopia.
How do you treat persistent palsy?
Prisms, botulinum toxin to the medial rectus, and later transposition surgery for complete palsy.
Why does a child with acute sixth nerve palsy need imaging?
To exclude pontine glioma and other posterior fossa tumours.

Station 57: Fourth nerve palsy Neuro-ophthalmology

Examiner: A man after a motorcycle accident has vertical double vision, worse on looking down to read, and tilts his head to the left.

How do you confirm the side?
Parks-Bielschowsky three-step test: right hypertropia, worse on left gaze and on right head tilt indicates right superior oblique palsy.
Why is the fourth nerve vulnerable to trauma?
It is long and thin and exits the dorsal midbrain, where both nerves can be damaged together against the tentorium.
How do you tell congenital from acquired?
Old photographs with a head tilt, large vertical fusional amplitudes, and facial asymmetry suggest congenital decompensated palsy.
What is the double Maddox rod test for?
Measuring excyclotorsion; more than 10 degrees suggests bilateral palsy.
Which surgery corrects it?
Inferior oblique weakening for overaction, superior oblique tuck, or contralateral inferior rectus recession depending on the pattern.
Why does reading worsen symptoms?
The superior oblique is the main depressor in adduction, which is needed for reading.
What does a nuclear fourth nerve lesion cause?
A contralateral superior oblique palsy, because the nerve decussates.

Station 58: Idiopathic intracranial hypertension Neuro-ophthalmology

Examiner: An overweight 26-year-old woman with daily headaches, pulse-synchronous tinnitus and transient visual obscurations has bilateral disc swelling.

What are the diagnostic criteria?
Papilloedema, normal neurological exam (except sixth nerve palsy), normal MRI with MR venography, normal CSF composition and raised opening pressure (25 cm H2O or more in adults).
Why is MR venography essential?
To exclude cerebral venous sinus thrombosis, which can mimic IIH.
Which drugs are linked?
Tetracyclines, vitamin A and retinoids, lithium, growth hormone and steroid withdrawal.
What did the IIH Treatment Trial show?
Acetazolamide plus weight loss improved visual fields more than weight loss alone in mild visual loss.
How do you monitor vision?
Visual fields (perimetry), acuity, colour, disc photographs and OCT of the RNFL.
When is surgery needed?
Fulminant or progressive visual loss: optic nerve sheath fenestration, CSF shunting or venous sinus stenting.
What newer treatment is under study?
GLP-1 agonists such as exenatide reduce intracranial pressure and help weight loss.

Station 59: Giant cell arteritis Neuro-ophthalmology

Examiner: A 75-year-old with a new headache, scalp tenderness and jaw pain on chewing has sudden loss of vision. The disc is chalky white and swollen.

What is the diagnosis?
Arteritic anterior ischaemic optic neuropathy from giant cell arteritis.
Which blood tests help?
ESR and CRP (CRP is more sensitive), and platelets (thrombocytosis).
What do you do before the biopsy?
Start high-dose steroid immediately: IV methylprednisolone 1 g daily for 3 days in visual loss, then oral prednisolone. Do not wait for the biopsy.
How long after starting steroids is a biopsy still useful?
Up to about 2 weeks; take at least 1.5 to 2 cm because of skip lesions. Temporal artery ultrasound (halo sign) is an alternative.
Why is the fellow eye at risk?
Without treatment the second eye is affected in days to weeks in a large proportion of patients.
Which steroid-sparing drug is approved?
Tocilizumab (IL-6 inhibitor), shown in the GiACTA trial to reduce steroid dose and relapses.
How does arteritic AION differ from NAION?
Arteritic: older, systemic symptoms, chalky white disc, severe loss, choroidal non-perfusion on FFA. NAION: hyperaemic swelling and a small crowded disc in the other eye.

Station 60: Non-arteritic AION Neuro-ophthalmology

Examiner: A 58-year-old diabetic woke up with an inferior field loss in one eye. The disc is sectorally swollen with flame haemorrhages, and the other disc has no cup.

What is the mechanism?
Hypoperfusion of the short posterior ciliary arteries supplying the optic nerve head, in a small crowded disc (disc at risk).
Why on waking?
Nocturnal hypotension, worsened by evening antihypertensives, is thought to contribute.
Which risk factors do you ask about?
Hypertension, diabetes, sleep apnoea, hyperlipidaemia, and drugs such as PDE-5 inhibitors and semaglutide (association under study).
What is the typical field defect?
Altitudinal, more often inferior.
Is there an effective treatment?
No proven treatment; the Ischaemic Optic Neuropathy Decompression Trial showed optic nerve sheath decompression was harmful. Control vascular risk factors.
What is the prognosis?
Usually stable after a few weeks; about 40% improve slightly; the fellow eye is affected in about 15% over 5 years.
Why must you always exclude GCA?
Arteritic AION threatens both eyes within days and needs steroids immediately.

Station 61: Chiasmal compression Neuro-ophthalmology

Examiner: A 45-year-old man bumps into door frames and has headaches. Confrontation suggests loss of both temporal fields.

What is the field defect and the commonest cause?
Bitemporal hemianopia from a pituitary adenoma compressing the chiasm from below, so the defect usually begins superotemporally.
How do craniopharyngiomas differ?
They compress from above, so the defect often starts inferotemporally; they occur in children and older adults and calcify.
What is band atrophy?
Horizontal (bow-tie) pallor of the optic disc from loss of nasal retinal fibres crossing in the chiasm.
What is pituitary apoplexy?
Sudden haemorrhage or infarction of a pituitary tumour causing headache, visual loss, ophthalmoplegia and hypopituitarism; an emergency needing steroids and often surgery.
Which endocrine tests do you request?
Prolactin, growth hormone and IGF-1, cortisol, TSH and free T4, LH, FSH and sex hormones.
How are prolactinomas treated?
With dopamine agonists (cabergoline), which shrink the tumour; other adenomas usually need trans-sphenoidal surgery.
What does OCT add?
Ganglion cell layer thinning in a binasal pattern, and a thin RNFL predicts poorer visual recovery after surgery.

Station 62: Ocular myasthenia gravis Neuro-ophthalmology

Examiner: A 60-year-old has variable ptosis and double vision that are worse in the evening. The ptosis worsens on sustained upgaze.

What is myasthenia gravis?
An autoimmune disease with antibodies against the acetylcholine receptor (or MuSK, LRP4) at the neuromuscular junction.
Which bedside tests help?
Ice pack test (ptosis improves after 2 minutes of cooling), sustained upgaze fatigue, Cogan lid twitch and the sleep test.
Which investigations confirm it?
Acetylcholine receptor antibodies (often negative in purely ocular disease), single-fibre EMG (most sensitive) and repetitive nerve stimulation.
Which other test is important?
CT of the chest for thymoma, and thyroid function (associated thyroid eye disease).
How do you treat ocular myasthenia?
Pyridostigmine for symptoms, then low-dose steroids or immunosuppressants; the EPITOME trial supported prednisolone.
What proportion becomes generalised?
About half within 2 years; steroids may reduce this risk.
Which drugs can worsen myasthenia?
Aminoglycosides, fluoroquinolones, macrolides, beta-blockers (including timolol drops), magnesium and checkpoint inhibitors.

Station 63: Childhood esotropia Paediatrics and strabismus

Examiner: A 3-year-old whose parents noticed an inturning of the right eye, worse when looking at near objects, for six months.

How do you examine the deviation?
Corneal reflexes (Hirschberg), cover-uncover test (tropia vs phoria), alternate cover test with prisms at distance and near, ocular movements, and assessment of fixation and vision in each eye.
How do you estimate the angle with the Hirschberg test?
Each 1 mm of decentration of the corneal reflex is about 7° (roughly 15 prism dioptres). A reflex at the pupil margin is about 15°, at the mid-iris about 30°, at the limbus about 45°.
What is the most important next step?
Cycloplegic refraction (cyclopentolate 1%, or atropine in very young or dark irides) and fundus examination; correct hypermetropia fully.
What is refractive accommodative esotropia?
An esotropia caused by uncorrected hypermetropia (often +2 to +6 D) with normal AC/A, fully corrected by glasses. A high AC/A type has a larger deviation at near, treated with bifocals.
How do you treat amblyopia?
Correct the refractive error first (refractive adaptation), then patching (2 hours a day as effective as 6 hours for moderate amblyopia in PEDIG studies) or atropine penalisation; binocular treatments are an option.
When is surgery indicated?
For the residual non-accommodative deviation after full glasses correction and amblyopia treatment. Infantile esotropia (onset before 6 months) is usually operated early.
What are the features of infantile esotropia?
Onset before 6 months, large stable angle (often > 30 Δ), cross-fixation, little refractive error, latent nystagmus, dissociated vertical deviation and inferior oblique overaction.

Station 64: Leukocoria and retinoblastoma Paediatrics and strabismus

Examiner: A mother brings her 18-month-old because the left pupil looks white in flash photographs.

Give the differential diagnosis of leukocoria.
Retinoblastoma (must be excluded first), congenital cataract, persistent fetal vasculature, Coats disease, retinopathy of prematurity (stage 5), toxocariasis, retinal detachment and coloboma.
What is the genetics of retinoblastoma?
The RB1 tumour suppressor gene on chromosome 13q14. Knudson's two-hit hypothesis: heritable cases (about 40%) carry one germline mutation and are often bilateral and earlier; non-heritable cases need two somatic hits and are unilateral.
How do you investigate?
Examination under anaesthesia with dilated indirect ophthalmoscopy, B-scan ultrasound (calcification), and MRI of the orbits and brain (avoid CT because of radiation in heritable disease). Never biopsy an eye with suspected retinoblastoma.
What does the international classification grade?
ICRB groups A to E: A small tumours away from the fovea and disc, through to E with neovascular glaucoma, massive haemorrhage or tumour filling the eye (usually enucleation).
What treatment options exist?
Intravenous or intra-arterial chemotherapy, focal treatment (laser, cryotherapy, plaque brachytherapy), intravitreal chemotherapy for seeds, and enucleation for advanced eyes.
What is trilateral retinoblastoma?
Bilateral retinoblastoma with a midline intracranial primitive neuroectodermal tumour, usually pinealoblastoma.
Which second cancers are a risk?
In heritable disease: osteosarcoma (the commonest), soft-tissue sarcomas and melanoma, more so after external beam radiotherapy. Siblings and offspring need screening.

Station 65: Amblyopia Paediatrics and strabismus

Examiner: A 6-year-old fails a school vision test: 6/36 in the right eye and 6/6 in the left. Refraction shows +4.00 D in the right and +0.50 D in the left.

What type of amblyopia is this?
Anisometropic amblyopia, from a constantly blurred image in the more hypermetropic eye.
What are the other types?
Strabismic, stimulus deprivation (cataract, ptosis), meridional (astigmatism), and bilateral ametropic.
What is the first step in treatment?
Full cycloplegic refraction and glasses worn full time; refractive adaptation alone improves many children over 16 weeks (PEDIG).
How much patching is needed?
PEDIG showed 2 hours a day was as effective as 6 hours for moderate amblyopia, and 6 hours as effective as full time for severe.
What alternatives to patching exist?
Atropine 1% penalisation of the better eye (daily or weekends), Bangerter filters and dichoptic digital therapy.
Up to what age can treatment work?
Best under 7, but PEDIG showed improvement in many children aged 7 to 12 and some teenagers who had not been treated before.
What risk follows stopping treatment?
Recurrence in about a quarter within a year, so taper rather than stop suddenly.

Station 66: Intermittent exotropia Paediatrics and strabismus

Examiner: Parents notice their 4-year-old's eye drifting outward when tired or daydreaming, and the child closes one eye in bright sunlight.

What is the diagnosis?
Intermittent exotropia, the commonest form of exotropia in children.
How do you classify it?
Basic, divergence excess (larger at distance) and convergence insufficiency type (larger at near); simulated divergence excess becomes basic after patching or +3.00 D lenses.
How do you assess control?
The Newcastle Control Score (home and clinic control at distance and near) or the office control score.
Why does the child close one eye in sunlight?
Bright light disrupts fusion and causes the deviation, so closing one eye avoids diplopia.
What non-surgical options exist?
Observation, correcting refractive error, overminus lenses and part-time patching.
When do you operate?
Poor or deteriorating control, a deviation that is manifest most of the time, or loss of stereopsis; usually bilateral lateral rectus recession.
What did PEDIG find about observation?
Most children with good control do not deteriorate quickly over 3 years, so observation is reasonable.

Station 67: Duane retraction syndrome Paediatrics and strabismus

Examiner: A 7-year-old girl cannot move her left eye outward, and the eye retracts with narrowing of the lid opening when she looks to the right.

What is the mechanism?
Congenital absence of the sixth nerve nucleus with misdirected innervation of the lateral rectus by the third nerve, causing co-contraction on adduction.
How is it classified (Huber)?
Type 1 limited abduction (commonest), type 2 limited adduction, type 3 limited abduction and adduction.
Why is diplopia uncommon?
It is congenital, and children adopt a face turn to keep binocular vision in primary position.
Which features are typical?
Left eye, female predominance, globe retraction, upshoots or downshoots on adduction.
What associations do you check?
Hearing loss, Goldenhar syndrome, Klippel-Feil anomaly and Okihiro syndrome (radial ray defects).
When is surgery indicated?
A significant face turn, deviation in primary position, or large upshoots; medial rectus recession on the affected side is typical. Never resect the lateral rectus.
How do you tell it from a sixth nerve palsy?
Duane has retraction and fissure narrowing on adduction, little deviation in primary position and no diplopia.

Station 68: Brown syndrome Paediatrics and strabismus

Examiner: A child cannot elevate the right eye when it is turned inward, but elevation in abduction is normal.

What is Brown syndrome?
Restricted movement of the superior oblique tendon through the trochlea, limiting elevation in adduction.
How do you confirm restriction?
Positive forced duction test when the eye is pulled up in adduction.
How do you tell it from inferior oblique palsy?
Brown syndrome has a positive forced duction test, a V pattern and no superior oblique overaction; inferior oblique palsy has an A pattern and positive head tilt findings.
What acquired causes exist?
Inflammation of the trochlea in rheumatoid arthritis, sinusitis, trauma and after superior oblique tuck.
How do you treat acquired inflammatory Brown?
Oral NSAIDs or a steroid injection near the trochlea.
When does congenital Brown need surgery?
Hypotropia in primary position, an abnormal head posture or loss of binocular vision; superior oblique tenotomy with a spacer is typical.
What is the natural history?
Many congenital cases improve spontaneously in childhood.

Station 69: Congenital nasolacrimal duct obstruction Paediatrics and strabismus

Examiner: A 9-month-old has had a watery, sticky right eye since birth; pressure over the lacrimal sac expresses mucus.

Where is the obstruction?
At the valve of Hasner at the lower end of the nasolacrimal duct, which has failed to canalise.
What is the natural history?
Most cases (about 90%) resolve by 12 months of age.
What is the first treatment?
Crigler massage (downward pressure over the sac) and topical antibiotic for infections.
When do you probe?
Usually around 12 months if it persists; PEDIG found probing successful in most children (roughly 80 to 90%) in the first year or two of life.
What do you do if probing fails?
Repeat probing with silicone intubation or balloon dacryoplasty, and DCR in older children with persistent obstruction.
What is a congenital dacryocele?
A bluish swelling below the medial canthus at birth from distension of the sac; it can become infected and obstruct the nose, so early probing is often needed.
Which other cause of watering must you exclude?
Congenital glaucoma: look for photophobia, corneal enlargement and haze.

Station 70: Myopia control in children Paediatrics and strabismus

Examiner: An 8-year-old's myopia has increased from -1.50 D to -3.00 D in one year. Both parents are myopic.

Why does progression matter?
High myopia raises the lifetime risk of myopic maculopathy, retinal detachment, glaucoma and cataract.
What lifestyle advice works?
At least 2 hours outdoors daily, which delays onset of myopia, and limiting near work and screen time.
What does low-dose atropine achieve?
Atropine 0.01 to 0.05% slows progression; LAMP found 0.05% the most effective with tolerable side effects.
Which optical options exist?
Defocus-incorporating spectacle lenses (DIMS, HAL), myopia control soft contact lenses (MiSight) and orthokeratology.
What is repeated low-level red light therapy?
Daily short exposures to red light that slowed myopia in Chinese trials; concerns remain about retinal safety.
How do you monitor progression?
Cycloplegic refraction and axial length every 6 months; axial length is the most reliable measure.
Can treatments be combined?
Yes, for example atropine with orthokeratology or defocus spectacles, which may add benefit.

Station 71: Infantile nystagmus Paediatrics and strabismus

Examiner: A 4-month-old has shaking eyes since about 8 weeks of age. The parents also notice the baby does not seem to fix and follow well.

What is your first diagnostic step?
Look for an underlying visual problem: albinism, congenital cataract, optic nerve hypoplasia, aniridia, retinal dystrophies (Leber congenital amaurosis, achromatopsia).
Which signs of albinism should you look for?
Iris transillumination, foveal hypoplasia, and pale fundus; VEP shows crossed asymmetry.
Which test helps confirm a retinal cause?
Electroretinography.
What features suggest infantile nystagmus syndrome?
Horizontal, conjugate, dampened by convergence, with a null point and sometimes a head turn; it is absent in sleep and oscillopsia is unusual.
Which signs suggest acquired neurological nystagmus?
Onset after 6 months, vertical or asymmetric nystagmus, oscillopsia or other neurological signs; these need urgent imaging.
What is spasmus nutans?
A triad of fine pendular nystagmus, head nodding and torticollis in infancy; it resolves but needs imaging to exclude optic pathway glioma.
How can you help these children?
Correct refractive error, low vision support, and surgery (Anderson-Kestenbaum) for a significant head turn.

Station 72: Ptosis Oculoplasty and orbit

Examiner: A 25-year-old with drooping of the left upper lid since birth. The lid lags on downgaze.

What is the likely type of ptosis?
Congenital (dystrophic) myogenic ptosis: lid lag on downgaze and poor levator function due to a fibrotic levator muscle.
Which measurements do you take?
MRD1 (normal 4–5 mm), palpebral fissure height, levator function (lid excursion from downgaze to upgaze with the brow fixed; normal 12–15 mm), skin crease height, Bell's phenomenon, corneal sensation and jaw-winking.
How does levator function guide surgery?
Good (10 mm or more): levator aponeurosis advancement or Müller muscle resection. Fair (5–9 mm): levator resection. Poor (4 mm or less): frontalis sling.
What is Marcus Gunn jaw-winking?
Synkinesis between the trigeminal (pterygoid) and oculomotor nerves: the ptotic lid elevates on jaw movement.
How do you differentiate the causes of acquired ptosis?
Aponeurotic (elderly, high skin crease, good function), neurogenic (III nerve palsy with down-and-out eye; Horner with miosis and mild ptosis), myasthenic (variable, fatigable, Cogan lid twitch, positive ice-pack test) and mechanical (tumour, oedema).
Why does congenital ptosis need early attention?
A lid covering the visual axis causes deprivation amblyopia, and ptosis can induce astigmatism, so check vision and refraction in every child.
What is pseudoptosis?
Apparent ptosis from hypotropia, enophthalmos, contralateral lid retraction, dermatochalasis or brow ptosis.

Station 73: Thyroid eye disease Oculoplasty and orbit

Examiner: A 42-year-old woman with Graves disease has bilateral prominent eyes, lid retraction and gritty discomfort.

Name the lid signs.
Dalrymple sign (upper lid retraction in primary gaze), von Graefe sign (lid lag on downgaze), Kocher sign (staring look), and Stellwag sign (infrequent blinking).
How do you measure proptosis?
Hertel exophthalmometry: normal values are usually up to about 20 mm, and an asymmetry of more than 2 mm is significant.
How do you assess activity?
Clinical Activity Score (7 points at first visit): spontaneous retrobulbar pain, pain on eye movement, lid redness, conjunctival redness, lid swelling, chemosis, caruncle swelling. 3 or more out of 7 means active disease.
What is sight-threatening thyroid eye disease?
Dysthyroid optic neuropathy (reduced vision, colour desaturation, RAPD, field defect, disc swelling) and severe exposure keratopathy or corneal breakdown.
How do you treat moderate-to-severe active disease?
IV methylprednisolone pulses (EUGOGO: 4.5 g cumulative over 12 weeks), with mycophenolate; alternatives include teprotumumab, tocilizumab and orbital radiotherapy. Stop smoking, control thyroid function, use selenium in mild disease.
How is dysthyroid optic neuropathy managed?
Urgent high-dose IV methylprednisolone; if no response within 1–2 weeks, urgent orbital decompression.
In what order are rehabilitative surgeries done?
Orbital decompression first, then strabismus surgery, then eyelid surgery, once the disease has been inactive for about 6 months.

Station 74: Orbital cellulitis Oculoplasty and orbit

Examiner: A 9-year-old with sinusitis has a red, swollen upper lid, proptosis, painful restricted eye movements and fever.

How do you tell orbital from preseptal cellulitis?
Orbital cellulitis has proptosis, painful or restricted movements, reduced vision, RAPD or colour loss; preseptal cellulitis has lid swelling only.
What is the commonest source?
Ethmoid sinusitis spreading through the thin lamina papyracea.
How do you classify it (Chandler)?
1 preseptal cellulitis, 2 orbital cellulitis, 3 subperiosteal abscess, 4 orbital abscess, 5 cavernous sinus thrombosis.
When do you order a CT scan?
Proptosis, ophthalmoplegia, reduced vision, unclear examination, no improvement in 24 to 48 hours, or suspected abscess.
How do you treat it?
Admission, IV broad-spectrum antibiotics (for example ceftriaxone plus metronidazole, adding vancomycin if MRSA risk), nasal decongestants and ENT review.
When is drainage needed?
Large abscess, worsening vision or optic nerve compromise, no response to antibiotics, and older children or adults with abscess.
What signs suggest cavernous sinus thrombosis?
Bilateral signs, multiple cranial nerve palsies, reduced consciousness and septic features.

Station 75: Basal cell carcinoma of the eyelid Oculoplasty and orbit

Examiner: A 68-year-old farmer has a pearly nodule with rolled edges, telangiectasia and a central ulcer on the lower lid near the medial canthus.

What is the commonest eyelid malignancy?
Basal cell carcinoma, about 90% of eyelid malignancies, most often on the lower lid.
Which subtypes do you know?
Nodular (commonest), morpheaform or sclerosing (ill-defined, aggressive), superficial and pigmented.
Why is a medial canthal BCC worrying?
It can invade the orbit and lacrimal system along tissue planes, and recurs more often.
What is the treatment of choice?
Excision with histological margin control: Mohs micrographic surgery or frozen section control, then reconstruction.
How do BCCs spread?
Locally; metastasis is extremely rare.
What are the options for unresectable or orbital disease?
Hedgehog pathway inhibitors (vismodegib, sonidegib), radiotherapy or exenteration.
How do you reconstruct lid defects?
Direct closure up to about a third (more with a canthotomy), Tenzel flap for moderate defects, Hughes or Cutler-Beard flaps for large ones.

Read more: Eyelid tumours, Oculoplasty hub

Station 76: Sebaceous gland carcinoma Oculoplasty and orbit

Examiner: A 62-year-old woman has had a recurrent chalazion in the upper lid three times in a year, with loss of lashes over it.

What must you suspect?
Sebaceous gland carcinoma, the masquerader of chronic chalazion and unilateral blepharoconjunctivitis.
Why is it relatively common in India?
It forms a much higher proportion of eyelid malignancies in Asian populations than in Western ones.
What clinical signs raise suspicion?
Madarosis, yellowish nodule, upper lid predominance, recurrent chalazion in an older patient and chronic unilateral redness.
How do you confirm it?
Full-thickness biopsy; oil red O staining on fresh tissue shows lipid, and pagetoid spread may need map biopsies of the conjunctiva.
How is it treated?
Wide excision with margin control, map biopsies, cryotherapy or topical mitomycin C for pagetoid spread, and exenteration for orbital invasion.
Where does it spread?
To pre-auricular and submandibular lymph nodes, with a significant risk of distant metastasis.
Which syndrome is associated?
Muir-Torre syndrome, with visceral malignancies such as colorectal cancer.

Read more: Eyelid tumours, Ocular tumours

Station 77: Involutional entropion and ectropion Oculoplasty and orbit

Examiner: A 78-year-old with a red, irritable eye has the lower lid turned inwards, with lashes rubbing the cornea.

What are the causes of involutional entropion?
Horizontal lid laxity, disinsertion of the lower lid retractors and overriding of the preseptal orbicularis.
How do you test lid laxity?
Distraction test (more than 6 mm is lax) and snap-back test.
What temporary measures help?
Taping the lid, Quickert everting sutures or botulinum toxin to the orbicularis.
What is the definitive surgery?
Lateral tarsal strip to tighten the lid plus retractor reinsertion (Jones procedure).
What causes ectropion?
Involutional laxity, cicatricial (skin shortage), paralytic (facial palsy) and mechanical (tumours).
How do you treat cicatricial ectropion?
Release of the scar and a full-thickness skin graft, often with lid tightening.
What causes cicatricial entropion in India?
Trachoma and Stevens-Johnson syndrome, needing tarsal rotation procedures.

Read more: Eyelid malpositions, Trachoma

Station 78: Orbital floor fracture Oculoplasty and orbit

Examiner: A teenager hit by a cricket ball has double vision on looking up, numbness of the cheek and upper lip, and a sunken eye.

What is a blowout fracture?
A fracture of the thin orbital floor (or medial wall) from a sudden rise in orbital pressure, with the rim intact.
Why is the cheek numb?
Injury to the infraorbital nerve running in the floor.
What is a white-eyed blowout fracture?
A trapdoor fracture in children with muscle entrapment, little bruising, severe restriction and vagal symptoms (nausea, bradycardia); it needs surgery within 24 to 48 hours.
Which imaging do you request?
CT orbits with thin coronal sections.
When do you operate?
Entrapment with restriction, enophthalmos over 2 mm, or a fracture involving more than half the floor; usually within 2 weeks.
What advice do you give in the meantime?
No nose blowing (risk of orbital emphysema), oral antibiotics in some protocols, and steroids to reduce swelling.
What must you examine for?
Globe injury: hyphema, commotio retinae, retinal tears and open globe.

Station 79: Adult nasolacrimal duct obstruction Oculoplasty and orbit

Examiner: A 55-year-old woman has had a watery left eye for a year and a swelling at the medial canthus that discharges pus on pressure.

Which tests do you do?
Fluorescein dye disappearance, syringing (regurgitation from the opposite punctum suggests nasolacrimal duct block), and Jones tests.
What does regurgitation through the same punctum mean?
Obstruction of that canaliculus.
How do you treat acute dacryocystitis?
Systemic antibiotics, warm compresses and drainage of an abscess; DCR once the infection settles.
What is a dacryocystorhinostomy?
Creating a bypass from the lacrimal sac into the nasal cavity through the lacrimal bone, by an external or endoscopic approach.
What success rates are expected?
Around 90% for external DCR; endonasal results are similar in experienced hands.
What signs suggest a lacrimal sac tumour?
A firm mass above the medial canthal tendon, bloody tears, or a mass that does not empty on pressure; these need imaging and biopsy.
When is a Lester Jones tube needed?
Proximal canalicular obstruction that cannot be reconstructed (conjunctivo-DCR).

Station 80: Unilateral proptosis Oculoplasty and orbit

Examiner: A 40-year-old has slowly progressive painless proptosis of the right eye pushing it down and in over two years.

What is the commonest cause of proptosis in adults?
Thyroid eye disease, both unilateral and bilateral.
How do you measure proptosis?
Hertel exophthalmometer; a difference of more than 2 mm between the eyes is significant.
What does downward and inward displacement suggest?
A lesion in the superotemporal orbit, such as a lacrimal gland tumour (pleomorphic adenoma).
How do you manage a suspected pleomorphic adenoma?
Complete excision without prior biopsy, because breaching the capsule causes recurrence and malignant change.
Which tumour is commonest in adult orbits?
Cavernous venous malformation (haemangioma), intraconal, causing axial proptosis.
Which causes in children are urgent?
Rhabdomyosarcoma (rapid onset), orbital cellulitis, metastatic neuroblastoma (bilateral bruising) and leukaemia.
What does proptosis that increases with Valsalva suggest?
An orbital venous varix; pulsatile proptosis suggests a carotid-cavernous fistula or a sphenoid wing defect.

Station 81: Open globe injury Trauma

Examiner: A metal worker hammering steel felt something hit his eye. Vision is 6/60, the pupil is peaked, and there is a small corneal wound with a positive Seidel test.

How do you classify the injury (BETT)?
An open globe: penetrating (entry only), perforating (entry and exit), intraocular foreign body, or rupture (blunt). Zone I cornea, zone II up to 5 mm behind the limbus, zone III beyond.
What do you do in the emergency room?
Rigid shield (no pad or pressure), no drops or ointment, nil by mouth, analgesia and antiemetics, tetanus cover and systemic antibiotics (for example oral moxifloxacin).
Which imaging do you request?
CT orbits with thin slices to look for a foreign body; MRI is contraindicated until a metallic body is excluded. Avoid B-scan with an open wound unless done gently.
What is the ocular trauma score?
A score from initial acuity, rupture, endophthalmitis, perforation, retinal detachment and RAPD that predicts final vision.
When should the wound be repaired?
As soon as possible, ideally within 24 hours, to reduce endophthalmitis risk.
Why is a peaked pupil important?
It points towards the wound, where iris is often prolapsed.
Which late risk must you warn about?
Sympathetic ophthalmia in the fellow eye.

Station 82: Traumatic hyphema Trauma

Examiner: A 12-year-old hit by a shuttlecock has blurred vision and a 2 mm level of blood in the anterior chamber.

What is your initial management?
Bed rest with head elevated, a shield, topical steroid and cycloplegic, IOP control, and avoiding antiplatelet drugs and NSAIDs.
What is the main risk in the first days?
Rebleeding, usually at 3 to 5 days, which carries a worse prognosis.
Why must sickle cell status be checked?
Sickled cells block the trabecular meshwork, so IOP rises at lower levels; avoid carbonic anhydrase inhibitors and hyperosmotics, and operate earlier.
What is corneal blood staining?
Haemoglobin entering the stroma, risked by a total hyphema with raised IOP and endothelial damage; it can cause amblyopia in children.
When do you wash out the hyphema?
IOP over 50 mmHg for 5 days or over 35 mmHg for 7 days (lower thresholds with sickle disease), early corneal staining or a total hyphema for 5 days.
Which late complication should be screened for?
Angle recession glaucoma; gonioscopy after a few weeks, and lifelong IOP checks.
Which posterior segment injuries can accompany it?
Commotio retinae, choroidal rupture, retinal dialysis and vitreous haemorrhage.

Read more: Traumatic hyphema, Gonioscopy

Station 83: Intraocular foreign body Trauma

Examiner: A man drilling metal without goggles has a small self-sealing corneal entry wound and a hole in the iris; vision is 6/12.

Which history raises suspicion of an IOFB?
Hammering metal on metal, drilling, grinding or explosions.
How do you locate it?
CT is the investigation of choice; B-scan can help; X-ray if CT is unavailable. MRI is contraindicated for metallic bodies.
What is siderosis bulbi?
Iron toxicity: iris heterochromia (darker), dilated pupil, rust-coloured lens deposits, pigmentary retinopathy and reduced ERG.
What does copper do?
Pure copper causes acute endophthalmitis; copper alloys cause chalcosis with a sunflower cataract and Kayser-Fleischer ring.
Which inert foreign bodies are tolerated?
Glass, plastic, gold, silver, platinum and stone.
How do you remove a posterior IOFB?
Pars plana vitrectomy with forceps or an intraocular magnet, ideally within 24 hours, with intravitreal antibiotics.
What organism is feared after soil-contaminated injury?
Bacillus cereus, which causes fulminant endophthalmitis within hours.

Station 84: Chemical injury Trauma

Examiner: A worker had lime (chuna) splashed into his eyes ten minutes ago. He is in severe pain with a white limbus.

What is your first action?
Immediate copious irrigation with saline or tap water for at least 30 minutes, until the pH is neutral (7 to 7.5), and sweep the fornices to remove particles.
Why are alkalis worse than acids?
Alkalis saponify cell membranes and penetrate deeply; acids coagulate surface proteins, which limits penetration.
How do you grade it?
Roper-Hall (corneal haze and limbal ischaemia in clock hours) or Dua (limbal involvement in clock hours and conjunctival involvement as a percentage).
Why is limbal ischaemia important?
It indicates limbal stem cell loss, which predicts persistent epithelial defects, vascularisation and conjunctivalisation.
What is the medical treatment?
Topical steroid for the first 1 to 2 weeks, antibiotic, cycloplegic, preservative-free lubricants, topical and oral vitamin C, and doxycycline to reduce collagenase.
When is amniotic membrane used?
Early in moderate to severe burns to promote healing and reduce inflammation and symblepharon.
How do you rehabilitate chronic stem cell deficiency?
Limbal stem cell transplantation (CLAU, SLET for unilateral cases) followed by keratoplasty if needed.

Station 85: Retrobulbar haemorrhage Trauma

Examiner: After a fall, an elderly patient on warfarin has a tense proptosed eye, IOP 55 mmHg, a RAPD and hand-movement vision.

What is the diagnosis?
Orbital compartment syndrome from retrobulbar haemorrhage.
What is the immediate treatment?
Lateral canthotomy and inferior cantholysis at the bedside, without waiting for imaging.
Why the urgency?
Raised orbital pressure compresses the optic nerve and its blood supply; irreversible damage can occur within about 90 minutes.
How do you do a lateral canthotomy?
Local anaesthetic, clamp the lateral canthus, cut horizontally to the orbital rim, then cut the inferior crus of the lateral canthal tendon until the lid moves freely.
Which signs show success?
The lower lid becomes lax, IOP drops and vision or the RAPD improves.
Which other measures help?
IV acetazolamide, mannitol and steroid, and reversing anticoagulation.
When else can this occur?
After retrobulbar or peribulbar anaesthesia, orbital or sinus surgery, and in bleeding disorders.

Station 86: Traumatic optic neuropathy Trauma

Examiner: A motorcyclist with a forehead injury above the eyebrow has 6/60 vision in one eye, a RAPD and a normal-looking disc.

Why does the disc look normal?
The injury is usually indirect, in the optic canal, so the disc becomes pale only after 3 to 6 weeks.
What is the mechanism of indirect injury?
Force transmitted from the frontal bone to the optic canal shears the nerve and its vessels.
Which investigation do you request?
CT of the orbits and optic canal to look for fractures, bone fragments and haematoma.
What did the CRASH trial show?
High-dose steroids in head injury increased mortality, so megadose steroids are no longer recommended.
What did the International Optic Nerve Trauma Study find?
No clear benefit for steroids or optic canal decompression over observation.
When is surgery considered?
Bone fragments impinging on the nerve, or an orbital haematoma causing compression.
What is the prognosis?
Poor initial vision (no light perception) predicts a poor outcome; some patients improve spontaneously.

Read more: Ocular trauma hub, Neuroimaging

Station 87: Retinoscopy Optics and refraction

Examiner: You are asked to perform retinoscopy at a working distance of 66 cm. In one meridian you see a with movement.

What does with movement mean?
The far point lies behind the observer: the eye is hypermetropic, emmetropic or myopic by less than the working distance dioptres; add plus lenses.
What does against movement mean?
The far point lies between the observer and the eye (myopia greater than the working distance); add minus lenses.
How do you correct for working distance?
Subtract the dioptric value of the working distance: 1.5 D at 66 cm, 2 D at 50 cm.
What does a scissoring reflex suggest?
Irregular astigmatism, as in keratoconus.
What does cycloplegia add in children?
It relaxes accommodation and reveals latent hypermetropia; cyclopentolate 1% is used, atropine in very young or esotropic children.
How do you find the axis of astigmatism?
Rotate the streak until the reflex aligns with the streak (no break or skew); neutralise each principal meridian separately.
What is dynamic retinoscopy used for?
Assessing accommodation at near, for example the MEM technique.

Station 88: Subjective refraction and the cross-cylinder Optics and refraction

Examiner: After retinoscopy gives -1.00/-1.50 x 180, you refine the cylinder with a Jackson cross-cylinder.

What is a Jackson cross-cylinder?
A lens with equal plus and minus cylinders at right angles (for example +0.25/-0.50), so the spherical equivalent is zero.
How do you refine the axis?
Place the JCC handle along the cylinder axis and flip; rotate the axis towards the preferred minus-cylinder position, in smaller steps, until both views are equal.
How do you refine the power?
Align the JCC axes with the cylinder axis and flip; add minus cylinder if the minus position is preferred, and adjust the sphere by half the change to keep the circle of least confusion on the retina.
Why refine the axis before the power?
An axis error causes a residual cylinder that makes power refinement inaccurate.
What is the duochrome test?
Letters on red and green backgrounds: if red is clearer, add minus; if green is clearer, add plus (RAM-GAP). It relies on chromatic aberration.
What is the fogging technique?
Adding plus to relax accommodation before refining the sphere, especially in younger patients.
How do you finish the refraction?
Binocular balancing (prism dissociation or alternate occlusion) and checking the maximum plus for best acuity.

Station 89: Presbyopia and the near add Optics and refraction

Examiner: A 45-year-old hypermetrope has difficulty reading small print and holds the phone at arm's length.

What is presbyopia?
Age-related loss of accommodation, mainly from reduced lens elasticity; symptoms usually begin in the early forties.
Why do hypermetropes notice it earlier?
They use part of their accommodation for distance, leaving less for near.
How do you determine the near add?
From age, amplitude of accommodation (keep half in reserve) and the patient's working distance; refine with the near cross-cylinder or trial.
What are typical adds?
About +1.00 D at 40 to 45 years, +1.50 to +2.00 D at 50, and +2.50 D at 60 for 40 cm.
Which spectacle options exist?
Single-vision readers, bifocals, progressive addition lenses and office (occupational) lenses.
Which pharmacological option is approved?
Pilocarpine 1.25% drops create a pinhole effect; aceclidine is newer. Watch for retinal detachment risk and poor night vision.
What surgical options are available?
Monovision with LASIK or IOLs, multifocal or EDOF IOLs, and corneal inlays (largely abandoned).

Read more: Presbyopia eye drops, Monovision

Station 90: Anisometropia and aniseikonia Optics and refraction

Examiner: A 50-year-old needs -1.00 D in the right eye and -5.00 D in the left, and complains of strain and double vision with new glasses.

What is anisometropia?
A difference in refractive error between the two eyes, usually significant at 1 D or more for hypermetropia and astigmatism, and more for myopia.
What is aniseikonia?
A difference in image size between the eyes; about 1% magnification difference per dioptre of anisometropia with spectacles. Differences over 5% are often not tolerated.
What is Knapp law?
In axial anisometropia, a lens at the anterior focal point (about 15 mm) gives equal image sizes; in practice contact lenses often work better because most anisometropia also has a refractive component.
What causes vertical diplopia when reading?
Induced vertical prism when looking down through different powers (Prentice rule); slab-off prism or separate readers help.
Why are contact lenses useful?
They reduce aniseikonia and prismatic effects compared with spectacles.
How do you handle it at cataract surgery?
Aim to reduce the difference to under 2 to 3 D, or plan the second eye soon after the first.
Why is it important in children?
It causes anisometropic amblyopia, which needs full correction and patching.

Station 91: Low vision aids Optics and refraction

Examiner: A 70-year-old with advanced dry AMD has 6/60 vision in both eyes and wants to read the newspaper.

How is low vision defined in India?
Under the RPwD Act 2016, low vision is best-corrected acuity of 6/18 or worse, down to 3/60, in the better eye, or a field of 10 to 40 degrees; blindness is acuity worse than 3/60 or a field under 10 degrees.
How do you estimate the magnification needed?
Kestenbaum rule: the reciprocal of the distance acuity gives the add needed to read N5 print (6/60 = 10/1, so about +10 D).
What types of near aids are available?
High-plus spectacles, hand-held and stand magnifiers, electronic video magnifiers and smartphone apps.
What distance aids are available?
Hand-held telescopes and spectacle-mounted telescopes.
What non-optical measures help?
Good lighting, contrast enhancement, large print, typoscopes and eccentric viewing training.
What is the drawback of high-power spectacles?
A very short working distance, which reduces comfort and needs prisms for binocular use.
Which certificates should you discuss?
The disability certificate under the RPwD Act, which gives access to benefits.

Station 92: Contact lenses Optics and refraction

Examiner: A 22-year-old with -6.00 D myopia wants to switch from glasses to contact lenses and also plays sports.

What is the vertex distance correction for -6.00 D?
About -5.50 D at the cornea (spectacles at 12 mm); correction is needed for powers above about 4 D.
How do soft and RGP lenses differ?
Soft lenses are comfortable and easy to adapt; RGP lenses correct corneal astigmatism and irregular corneas better, give sharper vision and allow more oxygen.
What is the LARS rule?
For toric soft lenses: if the marking rotates Left, Add the rotation to the axis; if Right, Subtract.
Which complications should you warn about?
Microbial keratitis (Pseudomonas, Acanthamoeba), giant papillary conjunctivitis, corneal neovascularisation and contact lens-induced red eye.
What is the biggest risk factor for keratitis?
Overnight wear; daily disposable lenses have the lowest risk.
Which lenses suit keratoconus?
RGP, hybrid, piggyback, Rose K and scleral lenses.
What advice keeps lenses safe?
Hand washing, no water contact, no sleeping in lenses, case replacement monthly, and removal if the eye is red or painful.

Station 93: Interpreting a visual field Investigations

Examiner: You are given a Humphrey 24-2 printout with a superior arcuate defect respecting the horizontal midline.

How do you read a field printout systematically?
Patient name, test and date; reliability indices; grey scale; total and pattern deviation plots; global indices (MD, PSD, VFI); GHT.
Which reliability indices matter?
Fixation losses (under 20%), false positives (under 15%) and false negatives.
What does a defect respecting the horizontal midline suggest?
Glaucoma or another retinal nerve fibre layer cause (branch occlusion, AION); vertical midline defects suggest chiasmal or retrochiasmal lesions.
What is the pattern deviation plot?
The total deviation corrected for generalised depression (cataract, small pupil), showing focal defects.
How do you define a glaucomatous field defect (Hodapp-Parrish-Anderson)?
GHT outside normal limits, or a cluster of 3 or more non-edge points at p under 5% with one under 1% on pattern deviation, or PSD at p under 5%, confirmed on repeat.
When do you use a 10-2 test?
Advanced glaucoma, paracentral defects, hydroxychloroquine screening and macular disease.
How do you detect progression?
Guided progression analysis and trend analysis of VFI or MD over at least 5 reliable fields.

Station 94: Reading a macular OCT Investigations

Examiner: You are shown an OCT scan through the fovea with a dome-shaped elevation of the RPE and a small pocket of fluid above it.

Name the layers you see from inside out.
ILM, RNFL, ganglion cell layer, IPL, INL, OPL, ONL, external limiting membrane, ellipsoid zone, interdigitation zone, RPE-Bruch complex and choroid.
What does a dome-shaped RPE elevation represent?
A pigment epithelial detachment: serous, fibrovascular (in neovascular AMD) or drusenoid.
How do you tell intraretinal from subretinal fluid?
Intraretinal fluid forms cysts within the neurosensory retina; subretinal fluid lies between the photoreceptors and the RPE.
What is the double-layer sign?
Separation of the RPE from Bruch membrane by a shallow irregular PED, suggesting type 1 neovascularisation, often non-exudative.
Which feature suggests a good visual prognosis?
An intact ellipsoid zone and external limiting membrane.
What does OCT angiography add?
Shows flow in vessels without dye: neovascular networks, capillary dropout and foveal avascular zone size.
Which artefacts mislead OCT readers?
Segmentation errors, decentration, motion and shadowing from vitreous opacities or haemorrhage.

Station 95: Fundus fluorescein angiography Investigations

Examiner: You are asked to explain an FFA showing areas of hyperfluorescence that increase in size and intensity over time.

What are the phases of an FFA?
Choroidal (pre-arterial, about 10 seconds), arterial, arteriovenous (laminar flow), venous and late (recirculation) phases.
What does increasing hyperfluorescence in size and intensity mean?
Leakage, for example from new vessels, CNV or a CSCR leak.
What are the causes of hyperfluorescence?
Leakage, pooling, staining, window defect (transmission) and autofluorescence.
What causes hypofluorescence?
Blocked fluorescence (blood, pigment) and filling defects (non-perfusion, occlusion).
What side effects of fluorescein should you warn about?
Yellow skin and urine, nausea, vasovagal episodes and rarely anaphylaxis; have resuscitation equipment ready.
When is ICG preferred?
For choroidal disease: polypoidal choroidal vasculopathy, CSCR, choroiditis and tumours, as ICG is protein-bound and fluoresces in infrared.
What does a window defect look like?
Early hyperfluorescence from RPE atrophy that fades with the choroidal flush and does not increase in size.

Station 96: Ocular B-scan ultrasound Investigations

Examiner: A patient with a dense vitreous haemorrhage after a fall has no fundal view. You perform a B-scan.

What are you looking for in vitreous haemorrhage?
Retinal detachment, retinal tears, posterior vitreous detachment, a foreign body or a tumour.
How do you tell RD from PVD on B-scan?
RD is thick, highly reflective (100% spike on A-scan), attached at the disc and ora, and moves less; PVD is thin, mobile, may be attached at the disc and has lower reflectivity.
What does a choroidal detachment look like?
Smooth, thick, dome-shaped elevations that do not attach to the disc and may touch in the middle (kissing choroidals).
How does a choroidal melanoma appear?
A dome or collar-stud mass with low to medium internal reflectivity, acoustic hollowness and choroidal excavation.
What does calcification suggest?
Retinoblastoma in a child, or disc drusen, choroidal osteoma and phthisis.
What is the T-sign?
Fluid in Tenon space around the optic nerve, seen in posterior scleritis.
What are the A-scan uses?
Axial length for biometry and tissue characterisation of masses (standardised echography).

Read more: B-scan patterns, Biometry check

Station 97: Electrophysiology Investigations

Examiner: A 12-year-old with poor night vision and a near-normal fundus is referred for electrophysiology.

Which test assesses the whole retina?
The full-field ERG (ISCEV standard), separating rod and cone function.
What do the a-wave and b-wave represent?
The a-wave comes from photoreceptors; the b-wave from bipolar and Müller cells.
What is an electronegative ERG?
A b-wave smaller than the a-wave, showing inner retinal dysfunction: X-linked retinoschisis, congenital stationary night blindness, CRAO and melanoma-associated retinopathy.
What does the EOG measure?
The standing potential of the RPE; the Arden ratio (light peak to dark trough) is normal above 1.8. It is abnormal in Best disease even with a normal ERG.
What does the VEP assess?
The visual pathway up to the occipital cortex: delayed P100 in demyelination, reduced amplitude in compression.
When is multifocal ERG useful?
Localised macular dysfunction: hydroxychloroquine toxicity, occult macular dystrophy and early cone disease.
Which conditions give an extinguished ERG?
Advanced retinitis pigmentosa, Leber congenital amaurosis, total retinal detachment and ophthalmic artery occlusion.

Station 98: Ocular anaesthesia General and basic sciences

Examiner: Before cataract surgery, a patient on clopidogrel asks which anaesthetic you will use and what the risks are.

Which anaesthetic techniques do you know?
Topical (with or without intracameral lidocaine), sub-Tenon, peribulbar, retrobulbar and general anaesthesia.
Which is safest in anticoagulated patients?
Topical or sub-Tenon anaesthesia, which avoid sharp needles and have the lowest risk of haemorrhage.
What are the complications of retrobulbar block?
Retrobulbar haemorrhage, globe perforation (higher in long myopic eyes and staphyloma), optic nerve injury, brainstem anaesthesia and the oculocardiac reflex.
What is brainstem anaesthesia?
Spread of anaesthetic along the optic nerve sheath to the CSF, causing confusion, apnoea, contralateral amaurosis and cardiovascular collapse within minutes.
What is the oculocardiac reflex?
Bradycardia from traction on the extraocular muscles or pressure on the globe (trigeminal afferent, vagal efferent), common in squint surgery in children; treat by stopping traction and giving atropine.
Which nerve is often spared by a retrobulbar block?
The trochlear nerve, which lies outside the muscle cone, so the superior oblique may still move.
What does the hyaluronidase add?
Faster and wider spread of the anaesthetic through tissues.

Station 99: Ocular side effects of systemic drugs General and basic sciences

Examiner: A patient with rheumatoid arthritis has taken hydroxychloroquine for seven years and is referred for screening.

What is the safe dose of hydroxychloroquine?
No more than 5 mg/kg actual body weight per day (AAO 2016); risk rises with duration, renal disease and tamoxifen use.
When should screening start?
A baseline exam within the first year, then annually after 5 years (earlier in high-risk patients).
Which tests detect early toxicity?
SD-OCT and automated fields (10-2, plus 24-2 or 30-2 in Asian patients because of pericentral toxicity), with fundus autofluorescence and multifocal ERG.
Which drug causes vortex keratopathy?
Amiodarone (also chloroquine, indomethacin and Fabry disease); it rarely affects vision.
Which drugs can cause optic neuropathy?
Ethambutol, isoniazid, linezolid, amiodarone and methanol.
Which drug causes floppy iris syndrome?
Tamsulosin and other alpha-1A blockers, making cataract surgery harder.
Which drug causes bilateral angle closure through ciliary body swelling?
Topiramate; treat by stopping the drug and with cycloplegics and steroids, not iridotomy.

Station 100: Community ophthalmology General and basic sciences

Examiner: In your viva you are asked about the leading causes of blindness in India and the national programme.

What are the leading causes of blindness in India?
Cataract is the leading cause of blindness; uncorrected refractive error is the leading cause of visual impairment. Glaucoma, corneal opacity and diabetic retinopathy follow.
What is the national programme called?
The National Programme for Control of Blindness and Visual Impairment (NPCBVI), started in 1976 as the NPCB.
How does the WHO define blindness?
Presenting acuity worse than 3/60 in the better eye, or a field under 10 degrees around fixation.
What is effective cataract surgical coverage?
A WHO indicator combining access to cataract surgery and good visual outcome, reflecting quality as well as quantity.
What is the SAFE strategy?
For trachoma: Surgery for trichiasis, Antibiotics (azithromycin), Facial cleanliness and Environmental improvement. India was validated as having eliminated trachoma as a public health problem in 2024.
What is VISION 2020?
The WHO and IAPB global initiative (1999 to 2020) to eliminate avoidable blindness, now succeeded by the WHO World Report on Vision and integrated people-centred eye care.
How do you organise a cataract camp safely?
Screening at camps but surgery in fixed base hospitals, standard sterilisation, biometry for all, IOL implantation and follow-up.

These answers are short on purpose: they are what an examiner wants in the first sentence. Expand each one from the linked pages and standard textbooks before your exam. Drug doses and trial results were checked against current sources in November 2026; always confirm doses locally.

📘 Want more exam-ready material? See Most Commons in Ophthalmology on Kindle, or browse all my books.

Written by Dr. Dhaval Patel, MD (Ophthalmology, AIIMS New Delhi)

Consultant, Cataract & Refractive Surgery — among a small number of AIIMS-trained ophthalmologists practicing in Gujarat. Read full credentials & experience or view his 28 publications on ResearchGate.

📚 Also the author of OKAT Decoded and other high-yield ophthalmology exam-prep books used by residents and PG aspirants.

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