Spot the Diagnosis: 226 Ophthalmology Case Quizzes

Acanthamoeba keratitis. Pain out of proportion, a ring infiltrate and radial perineuritis are the clues. Tap water exposure is the classic risk factor. See microbial keratitis.

Keratoconus. Munson sign and Vogt striae. Get a tomography scan and consider corneal cross-linking if it is progressing. See keratoconus and topography tips.

Herpes simplex epithelial (dendritic) keratitis. Terminal bulbs and reduced sensation separate HSV dendrites from the pseudodendrites of zoster or Acanthamoeba. Stop the steroid and start oral or topical antivirals. See dendritic ulcers.

Herpes zoster ophthalmicus (Hutchinson sign). Vesicles on the tip of the nose mean the nasociliary branch is involved, so eye involvement is likely. Start oral antivirals within 72 hours. See herpetic eye disease.

Fungal (filamentous) keratitis. Vegetative trauma, feathery margins and satellite lesions point to Fusarium or Aspergillus. Scrape for KOH and culture; start natamycin 5%. See fortified drops and antifungals and microbial keratitis.

Pseudomonas keratitis. Rapid progression with a ring of stromal haze in a contact lens wearer is Pseudomonas until proven otherwise. Scrape, then start fortified or fluoroquinolone drops hourly. See microbial keratitis.

Vernal keratoconjunctivitis with a shield ulcer. Giant tarsal papillae in a young boy with seasonal itching; the shield ulcer forms from mechanical and toxic damage by the papillae. Treat aggressively with steroids or ciclosporin and remove the plaque. See red eye guide.

Limbal vernal keratoconjunctivitis (Horner–Trantas dots). Trantas dots are collections of eosinophils and epithelial cells at the limbus in VKC. See red eye guide.

Gonococcal ophthalmia neonatorum. Discharge in the first 2–4 days with hyperacute pus suggests gonococcus, which can perforate the cornea. Gram stain, culture and systemic ceftriaxone. See red eye and conjunctivitis.

Chlamydial ophthalmia neonatorum. Onset at 5–14 days points to chlamydia. Treat with oral erythromycin, which also covers the risk of chlamydial pneumonia. See conjunctivitis.

Adenoviral epidemic keratoconjunctivitis with subepithelial infiltrates. Preauricular nodes, a contact history and later nummular subepithelial infiltrates are classic. Strict hygiene; mild steroids only if the infiltrates reduce vision. See conjunctivitis and returning to school or work.

Trachoma (Arlt line, Herbert pits, trichiasis). Herbert pits are scarred limbal follicles, unique to trachoma. The WHO SAFE strategy covers surgery, antibiotics, face washing and environment. See red eye and conjunctivitis.

Rosacea keratitis (blepharokeratoconjunctivitis). Meibomian disease plus marginal vascularised infiltrates; treat lids and give oral doxycycline (azithromycin in children). See dry eye and blepharitis treatment.

Phlyctenular keratoconjunctivitis. A hypersensitivity reaction to staphylococcal or tubercular antigens; in endemic areas check for TB. Topical steroids settle it quickly. See red eye guide.

Peripheral ulcerative keratitis. PUK in a patient with systemic vasculitis is a sign of active, potentially life-threatening disease and needs systemic immunosuppression, not just drops. See cornea hub.

Mooren ulcer. A diagnosis of exclusion: idiopathic, painful peripheral ulcerative keratitis with an undermined leading edge. See cornea hub.

Band keratopathy. Calcium in Bowman layer with 'Swiss cheese' holes where nerves pass. Causes: chronic uveitis (JIA), hypercalcaemia, renal failure, silicone oil. Remove with EDTA chelation. See lines and rings in the eye.

Vortex keratopathy (cornea verticillata). Usually harmless; also seen with chloroquine and in Fabry disease. Amiodarone can also rarely cause optic neuropathy, which matters more. See ocular side effects of drugs.

Kayser–Fleischer ring (Wilson disease). Copper deposits in peripheral Descemet membrane. Look also for a sunflower cataract. See lines and rings.

Ocular surface squamous neoplasia. OSSN is more common with HIV, UV exposure and in older people. Excise with the no-touch technique plus cryotherapy, or treat with topical chemotherapy. See ocular tumours.

Recurrent corneal erosion syndrome. Classic morning pain after previous trauma or basement membrane dystrophy. Lubricating ointment at night; stromal puncture or PTK if it keeps recurring. See corneal dystrophies made easy.

Sjögren syndrome (aqueous-deficient dry eye). Check anti-Ro and anti-La antibodies and refer to rheumatology; Sjögren carries a raised lymphoma risk. See dry eye (TFOS DEWS III).

Ocular mucous membrane pemphigoid. Progressive cicatrising conjunctivitis with symblepharon; biopsy for linear basement membrane immunofluorescence. Needs systemic immunosuppression. See cornea hub.

Stevens–Johnson syndrome / toxic epidermal necrolysis. Acute ocular care (lubrication, steroid, amniotic membrane) prevents lifelong cicatricial complications. Stop the offending drug. See drug reactions in the eye.

Post-LASIK corneal ectasia. Risk factors include a thin residual stromal bed, high percentage tissue altered and undetected keratoconus. Corneal cross-linking can halt progression. See refractive surgery for residents and keratoconus.

Pterygium. The Stocker line marks the advancing head. Operate if it threatens the visual axis, causes astigmatism or is cosmetically troubling; excision with a conjunctival autograft has the lowest recurrence. See pterygium surgery.

Fuchs endothelial corneal dystrophy. Morning blur from overnight stromal oedema is classic. Endothelial keratoplasty (DMEK) is the treatment of choice when vision fails; plan cataract surgery with endothelial protection. See Fuchs dystrophy.

Endothelial graft rejection (Khodadoust line). Treat urgently with intensive topical steroids (hourly), sometimes with periocular or systemic steroids. Rejection is the commonest cause of graft failure after PK. See keratoplasty.

Lattice corneal dystrophy (TGFBI, amyloid). Lattice is amyloid (stains with Congo red); granular is hyaline (Masson trichrome) with discrete crumb-like opacities; macular is recessive with glycosaminoglycans (Alcian blue) and diffuse haze. Mnemonic: Marilyn Monroe Always Gets Her Men in LA City. See corneal dystrophies.

Molluscum contagiosum with toxic follicular conjunctivitis. Viral particles shed from the lid lesion cause the conjunctivitis. Remove the lesion (curettage, cryotherapy or incision); in widespread lesions in adults, consider HIV. See conjunctivitis.

Demodex blepharitis. Cylindrical dandruff (collarettes) is pathognomonic. Treat with lid hygiene, tea tree oil products, or lotilaner 0.25% drops where available; also treat associated rosacea and meibomian gland dysfunction. See ocular microbiology.

Urrets-Zavalia syndrome. A fixed dilated pupil with iris atrophy after keratoplasty, linked to raised IOP, air or gas in the chamber and mydriatics; avoid long-acting dilating drops and leave no large air bubble against the iris. See keratoplasty.

Acute post-operative endophthalmitis. Pain plus reduced vision plus hypopyon after surgery needs an urgent tap and intravitreal antibiotics. See emergencies on call.

Marfan syndrome with ectopia lentis. Superotemporal subluxation with intact zonules is typical. Check the heart (aortic root) and refer to cardiology. See lens hub.

Homocystinuria. Inferonasal subluxation with broken zonules and a thrombosis risk, which matters for general anaesthesia. Check plasma homocysteine. See lens hub.

Weill–Marchesani syndrome (microspherophakia). Small spherical lenses cause pupil block; miotics paradoxically make it worse. Treat with a peripheral iridotomy or lens removal. See lens hub.

Snowflake (true diabetic) cataract. Rapid bilateral subcapsular snowflake opacities in young people with high blood sugar, from sorbitol accumulation. See lens hub.

Sunflower cataract (Wilson disease or a copper foreign body). Copper deposits under the anterior capsule; look for a Kayser–Fleischer ring. A copper intraocular foreign body (chalcosis) gives the same picture. See lines and rings.

Nuclear sclerotic cataract (second sight / index myopia). Increasing refractive index of the hardening nucleus produces a myopic shift. See cataract surgery FAQ.

Posterior subcapsular cataract. Steroids, diabetes, radiation and uveitis cause PSC; it affects near vision and glare badly because it sits near the nodal point. See cataract surgery FAQ.

Phacolytic glaucoma. Lens proteins leaking through an intact capsule block the trabecular meshwork. The angle is open, so the treatment is cataract extraction. See glaucoma hub.

Phacomorphic glaucoma. A swollen lens pushes the iris forward and closes the angle. The asymmetry of chamber depth tells you the lens is the cause. Lower IOP, then remove the lens. See angle closure.

True exfoliation of the lens capsule. Infrared exposure splits the capsule (glassblower's cataract). Not to be confused with pseudoexfoliation, which is a deposit. See pseudoexfoliation.

Pseudoexfoliation syndrome. Weak zonules and a small pupil raise the risk of complications during cataract surgery. It also causes a secondary open-angle glaucoma. See pseudoexfoliation and cataract surgery in PXF.

Pseudophakic cystoid macular oedema (Irvine–Gass). Peaks at 4–6 weeks. Treat with topical NSAID plus steroid; diabetics and uveitis patients are at higher risk. See cataract surgery FAQ.

Toxic anterior segment syndrome (TASS). Onset within 12–48 hours, limbus-to-limbus oedema and no vitritis distinguish TASS from infection. Cause: contaminated solutions or instruments. Treat with intensive topical steroid. See endophthalmitis guide.

Chronic (delayed) endophthalmitis from Cutibacterium acnes. A capsular plaque with recurrent inflammation; the organism hides in the capsular bag. Treatment may need IOL and capsule removal. See endophthalmitis guide.

Uveitis-glaucoma-hyphaema (UGH) syndrome. The IOL chafes the iris and ciliary body. Transillumination shows iris defects; ultrasound biomicroscopy shows the haptic position. Treat inflammation and IOP; IOL exchange or repositioning is often needed. See IOL dislocation and PCO and sulcus IOL.

Pigment dispersion syndrome. Krukenberg spindle, radial mid-peripheral transillumination defects and exercise-induced pigment release are classic. See pigment dispersion.

Acute primary angle-closure. Lower the IOP (acetazolamide, topical drops, mannitol if needed), then laser iridotomy to both eyes. See angle closure.

Primary open-angle glaucoma. Usually silent; matched disc and field damage confirms it. Set a target IOP and start treatment. See glaucoma hub and target IOP.

Normal-tension glaucoma. Exclude compressive lesions if the picture is atypical. Lowering IOP by 30% still slows progression (CNTGS). See normal-tension glaucoma.

Neovascular glaucoma. The '90-day glaucoma' after ischaemic CRVO. Anti-VEGF injection, PRP and IOP control, often surgery. See glaucoma hub.

Iridocorneal endothelial (ICE) syndrome. Unilateral, in middle-aged women; abnormal endothelium migrates over the angle and iris. Variants: Chandler, essential iris atrophy, Cogan–Reese. See glaucoma hub.

Posner–Schlossman syndrome (glaucomatocyclitic crisis). Often linked to CMV in the anterior chamber. Treat with topical steroid and IOP-lowering drugs; consider aqueous PCR. See uveitis.

Primary congenital glaucoma (Haab striae). The triad of epiphora, photophobia and blepharospasm with buphthalmos. Surgery (goniotomy or trabeculotomy) is the main treatment. See congenital glaucoma.

Overfiltration with a shallow chamber. Low IOP with a big bleb means too much flow. Check for a wound leak with Seidel testing; consider choroidal detachment. See bleb grading and hypotony.

Aqueous misdirection (malignant glaucoma). Aqueous flows backwards into the vitreous, pushing the lens–iris diaphragm forward. Atropine, aqueous suppressants, and YAG hyaloidotomy or vitrectomy. See bleb complications.

Angle-recession glaucoma. Torn ciliary muscle after blunt trauma; risk is greater when more than 180° is recessed. Monitor for life. See ocular trauma.

Sturge–Weber syndrome. Raised episcleral venous pressure and angle anomalies cause glaucoma. Choroidal haemangioma gives a 'tomato ketchup' fundus. See glaucoma hub.

Carotid–cavernous fistula. Arterialised episcleral veins, chemosis, proptosis, raised episcleral venous pressure and a bruit. High-flow fistulas follow trauma. See neuro-ophthalmology hub.

Plateau iris configuration. Anteriorly placed ciliary processes push the peripheral iris into the angle. Ultrasound biomicroscopy confirms; treat with laser iridoplasty or lens extraction. See angle closure.

Steroid-induced ocular hypertension. Typical onset 2–6 weeks; dexamethasone and prednisolone are the worst culprits. Stop or switch to a weaker steroid; treat the IOP. See steroid regimens.

Glaucoma with a disc (Drance) haemorrhage. A disc haemorrhage is a strong sign of progression, especially in normal-tension glaucoma. See disc haemorrhage in glaucoma.

Drug-induced bilateral angle closure (ciliochoroidal effusion). Topiramate and sulfa drugs cause ciliary body swelling. Iridotomy does not help; stop the drug, use cycloplegics and aqueous suppressants. See drug reactions in the eye.

Axenfeld–Rieger syndrome. Posterior embryotoxon with iris strands, a neural crest disorder. Look for dental and umbilical anomalies; about half develop glaucoma. See eye embryology made easy.

Retained viscoelastic causing an IOP spike. Common in the first 24 hours. Release some aqueous through the paracentesis and give aqueous suppressants. See cataract surgery FAQ.

Prostaglandin analogue side effects. Hypertrichosis, iris pigmentation and periorbital fat atrophy (prostaglandin-associated periorbitopathy). Iris darkening is permanent. See glaucoma medications chart.

Silicone oil emulsification with secondary glaucoma. Emulsified oil droplets block the trabecular meshwork ("inverse hypopyon" superiorly). Remove the oil when the retina is stable; inferior iridectomy prevents pupil block with oil in aphakia. See secondary glaucomas and PVR.

Retinal tear / rhegmatogenous retinal detachment. Pigment in the anterior vitreous ("tobacco dust", Shafer sign) strongly suggests a retinal break. Do a full indented peripheral examination.

Central retinal artery occlusion. The cherry-red spot appears because the fovea has no inner retina to whiten, so the choroid shows through. Segmented blood columns are "box-carring". Refer urgently through the stroke pathway.

Central serous chorioretinopathy. Stress and corticosteroid exposure (from any route) are the key risk factors. On angiography, look for an "ink-blot" or "smokestack" leak. See CSCR.

Vitreous haemorrhage from proliferative diabetic retinopathy. Perform B-scan ultrasound to exclude a retinal detachment underneath, and treat the fellow eye's PDR.

Neovascular (wet) age-related macular degeneration. Treat promptly with intravitreal anti-VEGF; delay costs vision. See AMD and treat-and-extend.

Polypoidal choroidal vasculopathy. Polyps on ICG are diagnostic. Treat with anti-VEGF, with or without photodynamic therapy (EVEREST II). See ICG angiography and AMD.

Central retinal vein occlusion. 'Blood and thunder' fundus. Check for hypertension, diabetes, glaucoma and hyperviscosity; watch for neovascularisation, especially in the ischaemic form. See retina hub.

Branch retinal vein occlusion. Most occur superotemporally at an AV crossing. Macular oedema responds to anti-VEGF; laser for neovascularisation. See retina hub.

HIV retinopathy. The commonest ocular finding in HIV, a microvasculopathy. Test for HIV and check CD4; screen for CMV retinitis if the CD4 count is low. See uveitis work-up.

Sickle cell (proliferative) retinopathy. Sea-fan neovascularisation, commonest in HbSC disease. Peripheral laser if it bleeds or is extensive. See retina hub.

Angioid streaks (pseudoxanthoma elasticum). Breaks in a calcified Bruch membrane. Causes: PXE, Paget disease, sickle cell, Ehlers–Danlos. Watch for CNV; avoid contact sports. See retina hub.

X-linked retinoschisis. Foveal schisis in a boy with a negative ERG (RS1 gene). Carbonic anhydrase inhibitors may reduce the schisis. See electrophysiology made easy.

Stargardt disease. ABCA4 mutation; the 'dark choroid' is lipofuscin blocking choroidal fluorescence. Avoid vitamin A supplements; use UV protection. See genes and eye diseases.

Best vitelliform macular dystrophy. Abnormal EOG with a normal ERG is the signature (BEST1). See electrophysiology made easy.

Retinitis pigmentosa. The classic triad. ERG shows rod loss first. Look for CME and cataract, both treatable. See genes and electrophysiology made easy.

Gyrate atrophy. Ornithine aminotransferase deficiency; treat with a low-arginine diet and vitamin B6 in responsive patients. See genes and eye diseases.

Choroideremia. X-linked (CHM gene); female carriers show patchy pigment changes. A target for gene therapy trials. See genes and eye diseases.

Multiple evanescent white dot syndrome (MEWDS). Young myopic women more often; self-limiting. OCT shows ellipsoid zone disruption. See uvea hub.

Acute posterior multifocal placoid pigment epitheliopathy (APMPPE). Usually recovers well. Rarely linked to cerebral vasculitis: ask about headache. See uvea hub.

Perioperative posterior ischaemic optic neuropathy. Blood loss, hypotension and prone positioning. Poor prognosis; prevention is key. See ischaemic optic neuropathy.

Valsalva retinopathy. Sub-ILM or subhyaloid haemorrhage from ruptured perifoveal capillaries. Most clear; Nd:YAG membranotomy can drain a large one. See Valsalva, Terson and Purtscher.

Terson syndrome. Intraocular haemorrhage with intracranial bleeding; it marks a worse prognosis. Vitrectomy if it does not clear. See Terson syndrome.

Purtscher retinopathy. Complement-mediated microembolism after chest compression, also in acute pancreatitis (Purtscher-like). See Purtscher retinopathy.

Full-thickness macular hole. Vitrectomy with ILM peel and gas closes over 90%. Small holes with traction may close with vitreolysis. See macular hole staging.

Epiretinal membrane. Common after age 50 or after retinal surgery and vein occlusion. Vitrectomy and membrane peel if vision is affected. See OCT macula reference.

Myopic choroidal neovascularisation. Usually type 2, responds to few anti-VEGF injections. Also look for lacquer cracks and Fuchs spots. See myopia.

Exudative (serous) retinal detachment. Shifting fluid and smooth surface. Causes: VKH, posterior scleritis, tumours, CSCR, toxaemia. Treat the cause, not with a buckle. See retinal detachment guide.

Coats disease. Mostly young boys, unilateral. Can look like retinoblastoma (leukocoria); treat with laser or cryotherapy to the abnormal vessels. See leukocoria.

Eales disease. Idiopathic peripheral occlusive vasculitis in young men, often with TB hypersensitivity. Laser to ischaemic retina. See Eales disease.

Hydroxychloroquine retinopathy. Screen yearly after 5 years (earlier with risk factors). Keep dose ≤5 mg/kg real body weight per day. Asian patients may show pericentral damage first. See drug toxicity in the eye.

Severe NPDR with centre-involving diabetic macular oedema. The 4-2-1 rule defines severe NPDR. Treat centre-involving DME with anti-VEGF; with good vision, close observation is an option (Protocol V). Control glucose, BP and lipids. See diabetic retinopathy.

Macular telangiectasia type 2 (MacTel). Bilateral, more common in diabetics; FFA shows late temporal leakage without CME on OCT. Revakinagene taroretcel (Encelto) was approved in the US in 2025; treat any secondary CNV with anti-VEGF. See OCT macula reference and intravitreal implants.

Solar retinopathy. Photochemical damage to the foveal photoreceptors. Vision often improves over months but can leave a permanent scotoma. Prevention: certified eclipse glasses or pinhole projection. See OCT macula reference.

Cone (cone-rod) dystrophy. Cones fail first, so photophobia and colour loss come early. Exclude hydroxychloroquine toxicity in any bull's-eye maculopathy. Tinted lenses and low vision aids help; genetic testing guides counselling. See inherited retinal dystrophies.

Vogt-Koyanagi-Harada disease. Bilateral granulomatous panuveitis with serous detachments plus meningeal, auditory and integumentary signs. See VKH.

JIA-associated chronic anterior uveitis. Silent and dangerous: screen every 3 months in high-risk children. Methotrexate and adalimumab are often needed. See uveitis made easy.

Sarcoidosis. Mutton-fat KPs, iris nodules, periphlebitis and snowballs. Chest X-ray or CT for hilar nodes; ACE and lysozyme support it. See uveitis work-up.

Behçet disease. Occlusive retinal vasculitis is the sight-threatening part; treat with azathioprine, interferon or infliximab. See Behçet disease.

Birdshot chorioretinopathy. One of the strongest HLA associations known. Needs long-term immunosuppression. See uveitis made easy.

Sympathetic ophthalmia. Bilateral granulomatous panuveitis after injury or surgery to one eye; Dalen–Fuchs nodules. Needs systemic immunosuppression. See ocular trauma.

Fuchs uveitis syndrome. Often linked to rubella. Avoid long steroid courses; cataract surgery goes well. Glaucoma can develop. See uveitis made easy.

CMV retinitis. 'Pizza pie' retinitis in immunosuppression. Intravitreal and systemic ganciclovir or valganciclovir. See uveitis work-up.

Acute retinal necrosis. VZV or HSV; same-day antivirals (IV acyclovir or oral valaciclovir with intravitreal ganciclovir). High risk of retinal detachment. See uveitis work-up.

Ocular syphilis (acute syphilitic posterior placoid chorioretinitis). 'The great imitator'. Test syphilis serology in every uveitis patient; treat as neurosyphilis with IV penicillin. See uveitis work-up.

Tubercular serpiginous-like choroiditis. Unlike classic serpiginous, it is multifocal and may start away from the disc. Needs antitubercular therapy plus steroids. See uveitis work-up.

Primary vitreoretinal lymphoma. A masquerade syndrome; vitreous biopsy (IL-10 : IL-6 > 1) and brain MRI. CNS lymphoma often follows. See masquerade syndromes.

Scleritis. Pain that disturbs sleep and non-blanching deep vessels separate scleritis from episcleritis. Screen for rheumatoid arthritis and vasculitis (ANCA). See red eye guide.

Episcleritis. Benign and often self-limiting; lubricants or a short course of topical NSAID or mild steroid. See red eye guide.

Pars planitis (idiopathic intermediate uveitis). Snowbanks and snowballs; CME is the main cause of vision loss. Check MRI if neurological symptoms (MS link in adults). See uveitis made easy.

Ocular cysticercosis. Common in India; the scolex is the white dot. Remove the cyst surgically; treat neurocysticercosis if present. See uvea hub.

Ocular toxocariasis. Unilateral, in children; can mimic retinoblastoma. ELISA for Toxocara antibodies supports it. See leukocoria.

Inflammatory bowel disease-associated uveitis. Crohn disease and ulcerative colitis cause anterior uveitis, episcleritis and scleritis; HLA-B27 overlap is common. See uveitis made easy.

Ocular toxoplasmosis (reactivation). The "headlight in the fog" appearance beside an old scar is classic. Treat lesions near the disc or macula, or with heavy vitritis: pyrimethamine with sulfadiazine and folinic acid, or trimethoprim-sulfamethoxazole, with oral steroids after 24–48 hours. See ocular toxoplasmosis.

Idiopathic intracranial hypertension. Pulsatile tinnitus and transient visual obscurations are classic. Exclude venous sinus thrombosis and a mass with MRI and MR venography before lumbar puncture. See papilloedema.

Horner syndrome from carotid artery dissection. A painful acute Horner needs urgent CT or MR angiography of the neck. See pupil examination.

Arteritic anterior ischaemic optic neuropathy (giant cell arteritis). Start high-dose steroids immediately to protect the fellow eye. See GCA.

Retrobulbar optic neuritis. "The patient sees nothing and the doctor sees nothing." Arrange an MRI of the brain and orbits. See optic neuritis.

Left internuclear ophthalmoplegia. The INO is named after the side of the adduction failure (the medial longitudinal fasciculus lesion). In older patients think of stroke; in young patients, multiple sclerosis. See INO.

Non-arteritic anterior ischaemic optic neuropathy (NAION). The 'disc at risk' in the fellow eye is the clue. Check ESR and CRP to exclude giant cell arteritis; control vascular risk factors. See optic neuritis vs NAION vs AAION.

Leber hereditary optic neuropathy. Maternal inheritance (mitochondrial DNA 11778 most common). Idebenone may help; advise against smoking and alcohol. See genes and eye diseases.

Ocular myasthenia gravis. Fatigable, variable ptosis and diplopia with normal pupils. Check acetylcholine receptor antibodies; watch for generalised disease and thymoma. See myasthenia gravis and the eye.

Pupil-sparing (ischaemic) third nerve palsy. Microvascular ischaemia spares the superficial pupil fibres. Still image if atypical, and expect recovery by 3 months. See ocular motility made easy.

Third nerve palsy from a posterior communicating artery aneurysm. Painful, pupil-involving III palsy is a neurosurgical emergency: same-day CT or MR angiography. See ocular motility made easy and cranial nerve palsies.

Right fourth nerve palsy. Trauma is the commonest acquired cause. Head tilt is away from the affected side; the three-step test confirms. See ocular motility made easy.

Gradenigo syndrome (petrous apicitis). Otitis media, sixth nerve palsy and trigeminal pain. Urgent imaging and IV antibiotics. See cranial nerve palsies.

Raised intracranial pressure (false localising sixth nerve palsies). The long course of the sixth nerve over the petrous apex makes it vulnerable to stretching. Urgent imaging. See papilloedema.

Dorsal midbrain (Parinaud) syndrome from a pineal tumour. Look for a pinealoma in young men; hydrocephalus in children. See pupils made easy.

Chronic progressive external ophthalmoplegia. Mitochondrial; symmetric loss means no diplopia. Kearns–Sayre adds pigmentary retinopathy and heart block before age 20: check an ECG. See neuro-ophthalmology hub.

Optic nerve sheath meningioma. The triad of visual loss, optic atrophy and optociliary shunt vessels. MRI shows 'tram-track' calcification. See ocular tumours.

Optic pathway glioma in neurofibromatosis type 1. NF1 children need yearly eye checks until about age 8. Lisch nodules on the iris support the diagnosis. See ocular tumours.

Pituitary macroadenoma. Compression from below hits the inferior crossing fibres first. MRI and endocrine tests. See visual pathway made easy.

Pituitary apoplexy. Haemorrhage or infarction of the tumour; give IV hydrocortisone (adrenal crisis risk) and arrange urgent neurosurgical review. See neuro-ophthalmology hub.

Right occipital infarct (posterior cerebral artery). Macular sparing because of dual blood supply to the occipital pole. Check driving eligibility. See visual pathway made easy.

Anton syndrome (cortical blindness with denial). Bilateral occipital damage with confabulation. Normal pupils and fundi help separate it from anterior pathway disease. See visual pathway made easy.

Cerebral venous sinus thrombosis. It mimics idiopathic intracranial hypertension; always do MR venography. Anticoagulate. See papilloedema.

Optic disc pit maculopathy. Fluid passes through the pit into the retina. Observe if vision is good; vitrectomy with gas, sometimes with ILM peeling or juxtapapillary laser, for persistent detachment. See congenital disc anomalies.

Myelinated retinal nerve fibres (Straatsma syndrome when with high myopia and amblyopia). Usually harmless; the triad with axial myopia and amblyopia needs full correction and patching. Do not confuse with cotton wool spots or papilloedema. See congenital disc anomalies.

Optic disc drusen (pseudopapilloedema). EDI-OCT and autofluorescence confirm drusen and avoid unnecessary lumbar puncture. Follow the fields: slowly progressive defects are common in adults. See papilloedema vs pseudopapilloedema.

Foster Kennedy syndrome (olfactory groove or sphenoid wing meningioma). The tumour compresses one optic nerve (atrophy) and raises intracranial pressure (papilloedema in the other eye). Urgent MRI. Pseudo-Foster Kennedy is sequential NAION. See neuroimaging.

Adie tonic pupil. Denervation supersensitivity of the iris sphincter after ciliary ganglion damage. With reduced tendon reflexes, it is Holmes-Adie syndrome. Benign; reading glasses help the accommodative problem. See pupil made easy.

Argyll Robertson pupils. Light-near dissociation with small pupils is classic for neurosyphilis: check treponemal serology and CSF. Diabetes can give a similar picture. See pupil made easy.

Retinoblastoma. Leukocoria with intralesional calcification on ultrasound (or CT) is retinoblastoma until proven otherwise. See retinoblastoma genetics.

Retinopathy of prematurity, zone II stage 3 with plus disease. Type 1 ROP: treat within 48–72 hours with laser or anti-VEGF. See retinopathy of prematurity.

Fully accommodative esotropia. Full cycloplegic correction is the treatment; no surgery needed. See strabismus hub and glasses in children.

Infantile esotropia. Onset before 6 months, large angle, cross-fixation; often needs early surgery. Look for dissociated vertical deviation later. See strabismus hub.

Duane retraction syndrome type 1. Congenital absence of the sixth nerve nucleus with aberrant innervation of the lateral rectus by the third nerve. Usually left eye, more girls. See strabismus reference.

Brown syndrome. Restriction of the superior oblique tendon sheath; often improves. Differentiate from inferior oblique palsy by the positive forced duction. See strabismus reference.

Anisometropic amblyopia. Full glasses first (refractive adaptation for up to 18 weeks), then patching or atropine penalisation if needed. See amblyopia treatment updates.

Congenital nasolacrimal duct obstruction. Blocked valve of Hasner. Most clear by age 1 with massage; probing if not. See nasolacrimal duct obstruction.

Unilateral congenital cataract. Surgery by 6 weeks of age for unilateral cases, then aggressive optical correction and patching. See congenital cataract.

Congenital rubella syndrome. Cataract, microphthalmia, salt-and-pepper retinopathy, deafness and heart defects (PDA). See congenital cataract.

Aniridia with WAGR syndrome (Wilms tumour). PAX6 deletion with WT1 deletion on 11p13. Sporadic aniridia needs abdominal ultrasound screening. See genes and eye diseases.

Oculocutaneous albinism. Foveal hypoplasia and excessive decussation at the chiasm (asymmetric VEP). Sun protection and low-vision support. See paediatric ophthalmology hub.

Spasmus nutans. Usually resolves by age 3–4, but an MRI is needed to exclude a chiasmal glioma. See nystagmus.

Intermittent exotropia. The most common exotropia in children. Observe, minus lenses or part-time patching; surgery if control worsens. See strabismus hub.

Primary congenital glaucoma. Normal infant corneal diameter is about 10 mm; above 12 mm in the first year is abnormal. Surgery is needed. See congenital glaucoma.

Periocular infantile haemangioma. Grows for months then involutes. Treat with oral propranolol if it threatens vision (occluding the pupil or causing astigmatism). See oculoplasty hub.

Orbital rhabdomyosarcoma. The commonest primary orbital malignancy in children: urgent imaging and biopsy. See ocular tumours.

Hydrocephalus with dorsal midbrain compression. Upgaze palsy and lid retraction in infants; urgent neurosurgical referral. See paediatric ophthalmology hub.

Abusive head trauma (shaken baby). Multilayered haemorrhages to the ora with retinoschisis are highly specific. Document, photograph and involve child protection. See paediatric ophthalmology hub.

Convergence insufficiency. Office-based vergence therapy works best (CITT). See strabismus hub.

Limbal dermoid with Goldenhar syndrome (oculo-auriculo-vertebral spectrum). Limbal dermoids can cause astigmatism and amblyopia: correct the refraction and treat amblyopia; excise (often with a lamellar graft) for cosmesis or vision. Check the spine and ears. See paediatric ophthalmology.

Morning glory disc anomaly. Arrange MRI with MR angiography: associations include basal encephalocele and moyamoya disease. Serous retinal detachment can develop later; treat amblyopia. See congenital disc anomalies.

Thyroid eye disease. The commonest cause of proptosis in adults. Check thyroid function and TSH-receptor antibodies; stop smoking; selenium for mild disease. See thyroid eye disease.

Dysthyroid optic neuropathy. Sight-threatening: IV methylprednisolone, then orbital decompression if no response within 1–2 weeks. See thyroid eye disease.

Orbital cellulitis. Proptosis and painful restricted movements mean the infection is behind the septum. Admit, IV antibiotics, CT for subperiosteal abscess. See orbital cellulitis.

Rhino-orbital-cerebral mucormycosis. Emergency: IV liposomal amphotericin B, urgent surgical debridement and control of diabetes. See orbital cellulitis.

Pleomorphic adenoma of the lacrimal gland. Remove intact with its capsule; incisional biopsy risks recurrence and malignant change. See ocular tumours.

Orbital cavernous venous malformation (cavernous haemangioma). The commonest benign orbital mass in adults. Removal if it compresses the optic nerve or causes symptoms. See ocular tumours.

Ocular adnexal lymphoma. 'Salmon patch' conjunctival lesions; biopsy and systemic staging. Low-grade MALT lymphoma responds to radiotherapy. See ocular tumours.

Basal cell carcinoma. The commonest eyelid malignancy, mostly on the lower lid. Excision with frozen-section or Mohs control of margins. See ocular tumours.

Sebaceous gland carcinoma. The masquerader of the lid: biopsy any recurrent chalazion in the elderly. Can spread through pagetoid change. See ocular tumours.

Involutional entropion. Horizontal laxity, disinserted retractors and overriding orbicularis. Surgery: lateral tarsal strip with everting sutures. See oculoplasty hub.

Paralytic ectropion. Also check for lagophthalmos and exposure keratopathy. Lubricate, consider a gold weight or tarsorrhaphy. See oculoplasty hub.

Congenital (dystrophic) ptosis. A poorly developed levator muscle. If it covers the pupil, operate early to prevent amblyopia; often needs a frontalis sling. See blepharoptosis.

Marcus Gunn jaw-winking syndrome. Aberrant innervation of the levator by the motor branch of the trigeminal nerve (pterygoid). See blepharoptosis.

Involutional (aponeurotic) ptosis. Levator aponeurosis stretches or disinserts. Advancement of the aponeurosis is the usual repair. See blepharoptosis.

Canaliculitis (Actinomyces). Pouting punctum with concretions. Curettage of the canaliculus; topical antibiotics alone fail. See oculoplasty hub.

Acute dacryocystitis. Systemic antibiotics; DCR later. Avoid probing during the acute stage. See nasolacrimal obstruction.

Benign essential blepharospasm. Botulinum toxin injections every 3–4 months are the mainstay. See oculoplasty hub.

Floppy eyelid syndrome. Lids evert during sleep against the pillow. Treat the sleep apnoea and tighten the lids. See oculoplasty hub.

Xanthelasma palpebrarum. Check fasting lipids: about half of patients have dyslipidaemia and it is linked with cardiovascular risk. Removal (excision, laser, trichloroacetic acid) is cosmetic; recurrence is common. See eyelid tumours.

Severe alkali chemical injury. A white eye after alkali is a bad sign (limbal ischaemia). Irrigate immediately until pH 7, then intensive steroids, vitamin C and doxycycline. See chemical injury.

Trapdoor orbital floor fracture with muscle entrapment. 'White-eyed blowout' in a child is a surgical emergency (oculocardiac reflex, muscle ischaemia). Repair within 24–48 hours. See orbital fracture.

Orbital compartment syndrome (retrobulbar haemorrhage). Lateral canthotomy and cantholysis within minutes; do not wait for imaging. See resident procedures.

Retained intraocular foreign body. 'Hammer and chisel' history needs a CT (not MRI) to look for an IOFB. Iron can cause siderosis later. See open globe injuries.

Siderosis bulbi. Iron toxicity from a retained foreign body; ERG shows declining b-wave. Remove the foreign body. See ocular siderosis.

Traumatic hyphaema in sickle trait. Sickled cells block the meshwork, and acetazolamide can worsen sickling. Monitor closely and consider early washout. See hyphaema.

Open globe injury (corneoscleral laceration with iris prolapse). Shield the eye, keep nil by mouth, give IV antibiotics and tetanus cover, and repair urgently. Do not press on the eye. See open globe injuries.

Ultraviolet (arc eye) keratitis. Starts 6–12 hours after exposure. Cycloplegic, lubricating ointment, oral analgesia; heals in 24–48 hours. See ocular trauma.

Traumatic optic neuropathy. Indirect injury to the intracanalicular nerve. High-dose steroids are no longer recommended (CRASH trial). See ocular trauma.

Commotio retinae (Berlin oedema). Photoreceptor outer segment disruption; resolves in most, but pigment changes or macular hole can follow. See ocular trauma.

Bleb-related infection (blebitis progressing to endophthalmitis). Thin, cystic, leaking blebs (especially after mitomycin) and contact lens wear are risk factors. Blebitis alone needs intensive topical antibiotics; with hypopyon or vitritis, tap and inject. See bleb complications and endophthalmitis guide.

Occult posterior scleral rupture. Low IOP, a deep chamber and bloody chemosis after blunt trauma suggest a hidden rupture, usually behind the rectus insertions. Explore in theatre; avoid any pressure on the globe. See open globe injuries.

Small choroidal melanoma. Risk factors for growth: 'To Find Small Ocular Melanoma Using Helpful Hints Daily' (thickness >2 mm, fluid, symptoms, orange pigment, margin near disc, ultrasound hollowness, absence of halo and drusen). See ocular tumours.

Choroidal metastases. The commonest intraocular malignancy in adults; breast in women, lung in men. Systemic workup and oncology review. See ocular tumours.

Circumscribed choroidal haemangioma. Orange colour and high reflectivity separate it from melanoma (low reflectivity). Treat symptomatic fluid with PDT. See ocular tumours.

Retinal haemangioblastoma (von Hippel–Lindau disease). VHL gene on chromosome 3; screen for cerebellar haemangioblastoma, renal cell carcinoma and phaeochromocytoma. See genes and eye diseases.

Retinal astrocytic hamartoma (tuberous sclerosis). Adenoma sebaceum, epilepsy and learning difficulty; ash-leaf skin patches under Wood's lamp. See genes and eye diseases.

Malignant (grade 4) hypertensive retinopathy. A hypertensive emergency: admit for controlled BP lowering. Look later for Elschnig spots and Siegrist streaks. See retina hub.

Pre-eclampsia with serous retinal detachment. Choroidal ischaemia causes exudative detachments, which resolve after delivery. Manage blood pressure urgently with obstetrics. See eye drugs in pregnancy.

Leukaemic retinopathy (Roth spots). White-centred haemorrhages are seen in leukaemia, anaemia and bacterial endocarditis. Also check for optic nerve infiltration, which is an emergency. See retina hub.

Infective endocarditis (Roth spots). Blood cultures and echocardiogram; look also for endogenous endophthalmitis. See retina hub.

Endogenous Candida endophthalmitis. Common in line sepsis, TPN and immunosuppression. Systemic antifungals (fluconazole or voriconazole); intravitreal or vitrectomy if the vitreous is involved. See endophthalmitis guide.

Amaurosis fugax (transient monocular vision loss). A TIA of the eye: urgent stroke workup with carotid Doppler, ECG and lipids. Rule out GCA in the elderly. See retinal artery occlusion.

Hollenhorst plaque (cholesterol embolus). Signals carotid atheroma: refer for carotid imaging and stroke prevention. See retinal artery occlusion.

Ocular ischaemic syndrome. Severe carotid stenosis (usually >90%). Unlike CRVO, the veins are dilated but not tortuous. Arrange carotid imaging. See retina hub.

Myotonic dystrophy. Polychromatic 'Christmas tree' cataract, ptosis, low IOP and frontal balding. Autosomal dominant CTG repeat (DMPK). See lens hub.

Congenital hypertrophy of the RPE in familial adenomatous polyposis (Gardner syndrome). Multiple, bilateral, pisciform CHRPE lesions suggest FAP: refer for colonoscopy. See genes and eye diseases.

Solitary congenital hypertrophy of the RPE (CHRPE). Benign; photograph and monitor. Unlike FAP lesions, it is single and large. See ocular tumours.

Phosphodiesterase-6 inhibition (cyanopsia). PDE5 inhibitors also partly inhibit retinal PDE6. Harmless and temporary; rarely linked to NAION. See drug reactions in the eye.

Ethambutol toxic optic neuropathy. Dose-related; stop ethambutol and check colour vision regularly. Recovery may be incomplete. See drug reactions in the eye.

Methanol poisoning. Formic acid damages the optic nerve. Fomepizole or ethanol, bicarbonate for acidosis and urgent haemodialysis. See neuro-ophthalmology hub.

Osteogenesis imperfecta. Thin sclera lets the choroid show through. Type I collagen defect (COL1A1, COL1A2); the thin cornea and sclera rupture easily with trauma. See genes and eye diseases.

Choroidal naevus (low risk). Drusen and no TFSOM-DIM risk factors suggest a benign naevus. Photograph at baseline, review at 6 months, then yearly. See choroidal naevus vs melanoma.

Iris melanoma. Growth, feeder vessels, ectropion uveae and secondary glaucoma suggest melanoma rather than an iris naevus. Ultrasound biomicroscopy shows the extent; treat by excision or plaque or proton beam radiotherapy. See ocular tumours.

Primary acquired melanosis with atypia progressing to conjunctival melanoma. Unilateral acquired pigmentation in a fair-skinned adult is PAM; a nodule or rapid spread suggests melanoma. Treat with no-touch excision, cryotherapy and topical mitomycin C; map the margins with biopsies. See ocular tumours.