GC121 Acute Visual Loss
Acute visual loss is the sudden decrease or complete loss of vision in one or both eyes, resulting from ocular, neurological, or vascular emergencies such as retinal artery occlusion, retinal detachment, optic neuritis, or vitreous hemorrhage.
Acute Visual Loss — Comprehensive Exam-Ready Notes
This lecture (GC 121, Dr. Andrew Kuk) is a core ophthalmology session that teaches you to systematically approach a patient who suddenly cannot see. The overarching philosophy is deceptively simple: think front-to-back (cornea → anterior chamber → lens → vitreous → retina → optic disc → brain), and categorize causes by transient vs. persistent, painful vs. painless, and anatomical location. [1]
Why this lecture matters for exams: Past papers consistently test you on being able to (1) generate a differential diagnosis for acute visual loss, (2) identify key clinical features that distinguish causes, (3) know which causes are emergencies requiring immediate ophthalmology referral, and (4) understand the systemic associations (cardiovascular, autoimmune, neurological). Questions have appeared as MCQs, SAQs, and mini-cases in 2020–2025 papers. [7][8][9][10][11]
Learning Objectives (inferred from slides and PBL):
- Formulate a systematic differential diagnosis for acute visual loss.
- Take a focused history and perform a targeted examination.
- Recognize the "must-not-miss" emergencies: acute angle closure glaucoma (AACG), central retinal artery occlusion (CRAO), giant cell arteritis (GCA)/arteritic anterior ischaemic optic neuropathy (AAION), retinal detachment, endophthalmitis.
- Understand initial investigations and when to refer urgently.
The lecture repeatedly emphasizes: organize your thinking anatomically from anterior to posterior. This is the single most important framework for both clinical practice and exams. [1]
Why front-to-back works: Light enters the eye through the cornea and must pass through every structure to reach the retina and optic nerve. A problem at any point along this path can cause visual loss. By mentally walking from front to back, you won't miss anything.
The Three Classification Axes
| Axis | Categories | Clinical Utility |
|---|---|---|
| Duration | Transient vs. Persistent | Transient → think vascular (TIA, vasospasm), mechanical (subluxation). Persistent → structural pathology |
| Pain | Painful vs. Painless | Painful → more anterior (cornea, AC, lens). Painless → more posterior (vitreous, retina). Key exceptions: optic neuritis and AAION are posterior but painful |
| Anatomy | Cornea → AC → Lens → Vitreous → Retina → Optic Disc → Brain | The comprehensive "catch-all" approach |
High-Yield Hint
Painful = more anterior; Painless = more posterior is the lecture's key mnemonic hint. But always remember the exceptions: optic neuritis (pain on eye movement) and AAION/GCA (headache, jaw claudication) are posterior but painful. [1]
Clinical Approach
The lecture specifies these exact history points — they are directly examinable: [1]
| History Category | Key Questions | Why It Matters |
|---|---|---|
| Presenting complaint | Onset (sudden vs. gradual), duration, unilateral vs. bilateral, pain, trauma, foreign body exposure, contact lens use | Narrows the differential immediately |
| Past Ophthalmic Hx | Previous eye surgeries/lasers, previous similar episodes | Post-surgical patients → endophthalmitis risk; recurrent episodes → uveitis, migraine |
| Past Medical Hx | Cardiovascular (HTN, hyperlipidaemia, DM), Neurological (CVA, TIA, demyelinating/autoimmune disease), Haematological (bleeding tendencies) | Systemic risk factors guide the differential: CVS → vascular occlusions/amaurosis; Neuro → optic neuritis (MS); Haem → vitreous haemorrhage |
Additional history points to ask (from PBL and supporting context):
- Preceding activities: reading in dim light, using cold medications with antihistamines → AACG [1]
- Coryzal illness → viral keratitis (HSV) [1]
- Dirty water exposure → Acanthamoeba keratitis [1]
- Floaters/flashes → retinal detachment or posterior vitreous detachment [1]
- Distortion of straight lines (metamorphopsia) → macular pathology (AMD, macular oedema) [3]
- "Curtain coming down" → retinal detachment or amaurosis fugax
- Jaw claudication, scalp tenderness, temporal headache in elderly → GCA [5]
Examination: front to back! [1]
| Step | What to Assess | Relevant Findings |
|---|---|---|
| Visual Acuity (VA) | Snellen chart (with correction/pinhole), each eye separately | The single most important measurement. If VA < 6/9, suspect refractive error → correct with pinhole first [6] |
| IOP | Tonometry | ↑IOP → AACG (can be > 40 mmHg); also check in RVO/NVG |
| Anterior segment (slit lamp) | Cornea: epithelial defect (fluorescein staining), oedema, infiltrate, foreign body. AC: cells, flare, fibrin, hypopyon, hyphaema, AC depth. Iris: synechiae, rubeosis. Lens: clarity, position | Slit lamp is the workhorse of ophthalmic examination |
| Posterior segment (dilated fundal exam) | Vitreous: haemorrhage, cells. Retina: haemorrhages, cotton-wool spots, exudates, pallor ("cherry red spot"), detachment, neovascularization. Optic disc: swelling, pallor, cupping | Dilated exam is essential — you cannot adequately assess the retina and disc without dilation |
| Pupils | RAPD (relative afferent pupillary defect) via swinging flashlight test | RAPD indicates asymmetric optic nerve or extensive retinal disease on the affected side |
The lecture lists these specific investigations: [1]
Anterior segment imaging:
- Specular microscopy (endothelial cell count)
- OCT (anterior segment)
- Keratometry
- Slit lamp photography
Posterior segment imaging:
- Ultrasound B-scan — crucial when you can't see the fundus (e.g., dense vitreous haemorrhage, dense cataract) → rules out retinal detachment, intraocular foreign body, tumour
- OCT macula — gold standard for macular oedema, subretinal fluid, AMD changes
- Fluorescein fundus angiography (FFA) — maps retinal vascular pathology (leakage, ischaemia, neovascularization)
Systemic workup:
- Brain and orbit CT/MRI — optic neuritis (MRI with gadolinium to look for demyelination), compressive lesions, stroke
- Bloods — ESR/CRP (GCA), FBC, glucose, HbA1c, lipids, clotting profile, protein C/S, antiphospholipid antibodies, autoimmune panel
- ERG/EOG — electroretinogram/electro-oculogram for retinal function assessment (specialized)
Transient causes (also front to back): [1]
| # | Cause | Mechanism | Key Features |
|---|---|---|---|
| 1 | Glare | Excessive light scattering (e.g., from posterior capsule opacification, early cataract) | Usually positional/situational |
| 2 | Corneal surface disruption | Tear film instability transiently disrupts optical surface | Dry eye, recurrent erosion syndrome |
| 3 | Lens subluxation | Partial dislocation → lens edge enters visual axis intermittently | Marfan's, homocystinuria, trauma |
| 4 | Amaurosis fugax (TIA) | Transient retinal ischaemia from emboli (carotid, cardiac) or GCA | Painless, "curtain down" monocular visual loss lasting seconds to minutes. Demands urgent cardiovascular workup |
| 5 | Migraine (vasospasm) | Cortical spreading depression → visual aura; retinal vasospasm | Positive phenomena (scintillating scotoma), usually < 60 min, often followed by headache |
Amaurosis Fugax = Ophthalmic Emergency
Causes of Persistent Acute Visual Loss (Front to Back)
Corneal causes: epithelial defect, foreign body, oedema (from inflammation/high IOP), keratitis [1]
All of these are painful because the cornea is the most densely innervated structure in the body (via ophthalmic division of CN V). That's why corneal pathology causes intense pain, tearing, photophobia, and blepharospasm.
Anterior chamber causes: hyphaema, uveitis ± hypopyon, acute angle closure glaucoma [1]
- Hyphaema: Blood in the anterior chamber. Traumatic (most common) vs. spontaneous (bleeding disorders, rubeosis iridis). Can obstruct aqueous outflow → secondary glaucoma.
- Uveitis: Inflammation of the uveal tract (iris, ciliary body, choroid). Anterior uveitis = iritis/iridocyclitis.
- AACG: True ophthalmic emergency (see deep dive below).
Lens causes: post-traumatic cataract/foreign body, dislocation [1]
Lens dislocation can be traumatic or spontaneous (Marfan syndrome — supero-temporal displacement; homocystinuria — infero-nasal displacement). A fully dislocated lens can fall into the vitreous or anterior chamber, causing acute visual loss and potentially AACG.
Vitreous causes: haemorrhage, vitritis [1]
- Vitreous haemorrhage is painless — there are no pain fibres in the vitreous.
- Vitritis = inflammatory cells in vitreous, usually from posterior uveitis or endophthalmitis.
Retinal causes: vascular occlusions (CRVO/BRVO and CRAO/BRAO), haemorrhage or oedema at macula, detachment [1]
Optic disc causes: swelling = optic neuritis vs. AAION (GCA) vs. NAION (ischaemia) vs. papilloedema; avulsion [1]
This is where the lecture highlights the critical distinction between three causes of optic disc swelling:
| Feature | Optic Neuritis | AAION (GCA) | NAION | Papilloedema |
|---|---|---|---|---|
| Age | Young (20-45) | Elderly ( > 50, avg 70) | Middle-aged/elderly | Any |
| Pain | Pain on eye movement | Headache, jaw claudication, scalp tenderness | Usually painless | Headache (↑ICP) |
| Laterality | Unilateral | Unilateral (but can affect other eye within days-weeks) | Unilateral | Bilateral |
| VA loss | Moderate-severe | Severe (may be devastating) | Moderate | Mild initially (transient obscurations) |
| Visual field | Central scotoma | Altitudinal defect | Altitudinal defect | Enlarged blind spot |
| Disc appearance | Swollen (may be normal in retrobulbar neuritis) | Pale, chalky-white swelling with haemorrhages | Hyperaemic disc oedema with haemorrhages | Bilateral swelling, hyperaemia |
| RAPD | Present | Present | Present | Usually absent (bilateral) |
| Key investigation | MRI brain/orbits (demyelination) | ESR/CRP (very high ESR, often > 100), temporal artery biopsy | CV risk factor assessment | Neuroimaging (CT/MRI) for ↑ICP cause |
| Systemic association | MS (50% develop MS within 15y) | GCA / PMR | HTN, DM, hyperlipidaemia | Space-occupying lesion, IIH, meningitis |
| Urgency | Semi-urgent | EMERGENCY — start steroids before biopsy | Urgent CV workup | Urgent neuroimaging |
AAION/GCA: The Must-Not-Miss Diagnosis
If you suspect GCA (elderly patient with new headache, jaw claudication, scalp tenderness, raised ESR/CRP, and acute visual loss), start high-dose systemic corticosteroids IMMEDIATELY — even before temporal artery biopsy. [1][5] The goal is to prevent permanent bilateral blindness. Treatment started on clinical suspicion alone is the standard of care. GCA responds dramatically to steroids (symptoms resolve within 48-72h). [5]
Deep Dives on Important Causes
History: coryzal illness (viral), trauma (unusual organisms like fungal), contact lens user (bacterial, amoeba), dirty water exposure (amoeba) [1]
Management: recognise early, initiate topical treatment early, refer to ophthalmology for cornea scraping and adjustment of Rx [1]
Why early recognition matters: Corneal infection can progress rapidly to corneal perforation and endophthalmitis. Every hour of delay worsens the prognosis.
| Organism | Risk Factor | Key Feature |
|---|---|---|
| Bacterial (Pseudomonas, Staph) | Contact lens wear (especially overnight wear, poor hygiene) | Rapid progression, purulent discharge, corneal infiltrate |
| Viral (HSV) | Coryzal illness, previous cold sores | Dendritic ulcer on fluorescein staining (pathognomonic) |
| Fungal | Trauma with vegetable matter (e.g., gardening injury) | Indolent course, feathery-edged infiltrate, satellite lesions |
| Acanthamoeba | Contact lens + dirty water (swimming, shower) | Severe pain out of proportion to findings, ring-shaped infiltrate, perineural infiltrates |
Preceding event: reading in dim light; cold Rx (antihistamines used as decongestant lead to mild pupil dilation + unknown narrow angle = AACG) [1]
Acute symptoms: blurring, eye pain, headache, nausea [1]
Acute signs: injected (redness), mid-dilated pupils, shallow AC, corneal oedema, decreased VA, raised IOP [1]
Management: recognise early and consult ophthalmology! Constrict pupil — break the cycle with pilocarpine. Lower IOP: ALL topical agents and systemic agents. Ophthalmology: laser ALPI/PI, surgical PI, early cataract OT [1]
Mechanism from first principles:
- In a predisposed eye (short axial length = hyperopia, shallow anterior chamber, thick lens), the iris lies close to the lens.
- When the pupil dilates (dim lighting, sympathomimetics, anticholinergics), the peripheral iris bunches up and blocks the trabecular meshwork (the drainage angle).
- Aqueous humour cannot drain → IOP rises rapidly (can exceed 60 mmHg) → corneal oedema (cloudy vision, halos around lights), severe pain, vagal symptoms (nausea, vomiting, bradycardia).
- Pilocarpine (a muscarinic agonist) constricts the pupil, pulling the iris root away from the angle and breaking the acute attack.
- IOP-lowering agents: topical beta-blockers (timolol), alpha-agonists (brimonidine/apraclonidine), carbonic anhydrase inhibitors (dorzolamide topical, acetazolamide IV/oral), IV mannitol (osmotic agent).
- Definitive treatment: laser peripheral iridotomy (PI) creates a bypass hole in the peripheral iris, allowing aqueous to flow directly from the posterior to anterior chamber, preventing future attacks. Must do the fellow eye prophylactically because it is anatomically similar.
Drug-Induced AACG
Antihistamines (used as decongestants in cold remedies) can precipitate AACG in patients with undiagnosed narrow angles. [1] This is a common exam question stem. Other culprits: anticholinergics (atropine, ipratropium), sympathomimetics (phenylephrine eye drops), TCAs, SSRIs, topiramate (via a different mechanism — ciliary body swelling).
The AOS PBL also presents a classic AACG case: 65-year-old woman with hyperopia +3D, severe left eye pain, decreased vision ("count fingers"), frontal headache, and nausea. [2] This is the textbook demographic: elderly, hyperopic, female.
Causes: Idiopathic (50%), HLA-B27 related (20%) — ankylosing spondylitis, Reiter's disease, IBD, psoriasis; Viral (10%) — HSV, HZV, CMV; Iatrogenic — surgical complications, trauma, implants (IOL), corneal transplant rejection [1]
Ophthalmic signs: AC cells, fibrin, flare, hypopyon, PAS, posterior synechiae, iris bombé, keratitic precipitates, corneal oedema [1]
Management: refer to ophthalmology for pupil dilation (check no posterior extension), steroids [1]
Key terminology explained:
- Cells and flare: Inflammatory cells and protein leakage in the aqueous humour, seen as particles floating in the slit lamp beam (cells) and haziness of the beam (flare) — like dust particles in a shaft of sunlight.
- Hypopyon: A layered collection of white cells in the inferior anterior chamber — gravity-dependent. Seen in severe anterior uveitis, endophthalmitis, and Behcet's disease.
- Posterior synechiae (PS): Adhesions between the posterior iris and the anterior lens capsule. If circumferential (360°) → iris bombé (iris bows forward because aqueous is trapped behind it → secondary angle closure).
- Keratitic precipitates (KPs): Inflammatory cell deposits on the corneal endothelium. Fine KPs suggest non-granulomatous uveitis; "mutton-fat" KPs (large, greasy) suggest granulomatous uveitis (sarcoidosis, TB, syphilis).
Why dilate the pupil? Cycloplegics (e.g., atropine, cyclopentolate) serve three purposes: (1) prevent/break posterior synechiae by keeping the pupil mobile, (2) reduce ciliary muscle spasm → pain relief, (3) stabilize the blood-aqueous barrier.
Past paper relevance: The 2020 MCQ asked: "Which of the following is NOT associated with anterior uveitis? A. JIA, B. Osteoarthritis, C. Psoriatic arthritis, D. Behcet disease" — Answer: B (Osteoarthritis). OA is a non-inflammatory degenerative joint disease and has no association with uveitis. [7]
RVO risk factors: HTN, DM, smoking, obesity, hypercoagulation disorders (Protein C and S deficiency, antiphospholipid syndrome), glaucoma [1]
RVO systemic associations: hyperlipidaemia, SLE, sarcoidosis, TB, syphilis, multiple myeloma, cryoglobulinaemia, leukaemia, lymphoma, sickle cell disease [1]
RAO risk factors: HTN, hyperlipidaemia, hyperviscosity syndromes. Retinal blood supplied by retinal artery as it branches out from the optic disc. Classifications: BRAO, CRAO (more common) — retinal artery emboli [1]
| Feature | CRVO | CRAO |
|---|---|---|
| Mechanism | Thrombosis at lamina cribrosa where CRV and CRA share a common adventitial sheath; or compression from arteriolopathy | Embolic occlusion (carotid plaque, cardiac source) or thrombosis, or GCA |
| Fundoscopy | "Stormy sunset" / "blood and thunder" — widespread flame-shaped haemorrhages, dilated tortuous veins, cotton-wool spots, disc oedema, macular oedema | "Pale retina with cherry-red spot" — the fovea appears red because the thin retina there allows underlying choroidal blood to show through, while the surrounding ischaemic retina turns pale/opaque |
| VA | Variable (mild in non-ischaemic, severe in ischaemic) | Severely reduced (often counting fingers or worse) |
| RAPD | Present in ischaemic CRVO | Present |
| Onset | Painless, sudden | Painless, sudden |
| Complications | Macular oedema (main cause of visual loss), neovascularization → vitreous haemorrhage, neovascular glaucoma | Neovascularization (less common), optic atrophy |
| Treatment | Anti-VEGF intravitreal injections for macular oedema; PRP for neovascularization | Ophthalmic emergency — limited treatment window. Ocular massage, anterior chamber paracentesis to lower IOP, carbogen inhalation. Rule out GCA. Intra-arterial thrombolysis rarely used. |
| Systemic workup | CV risk factors, hypercoagulability screen | Carotid duplex, cardiac echo, ESR/CRP (GCA), CV risk factors |
CRAO is a Stroke Equivalent
CRAO should be treated with the same urgency as an acute ischemic stroke. The retinal artery is an end artery — there is no collateral circulation. Irreversible retinal damage occurs within 90-120 minutes of complete occlusion. Every minute counts. [1]
Causes: trauma, neovascularization from proliferative diabetic retinopathy / vascular occlusions, posterior vitreous detachment / retinal tear, bleeding tendencies [1]
Clinical presentation: Sudden painless visual loss with floaters, "cobwebs," or a "red haze." Vision may be worse in the morning because blood settles onto the macula during sleep. [4]
Why this matters: You cannot see the fundus through a dense vitreous haemorrhage → B-scan ultrasound is essential to rule out underlying retinal detachment or tumour. [1][4]
Dry AMD Mx: education, stop smoking, intake macular carotenoids (spinach, cabbage, broccoli), vitamins: AREDS2 supplement (Vit C, E, alpha-carotene/lutein/zeaxanthin, and zinc), regular Amsler grid monitoring [1]
Wet AMD Mx: refer to ophthalmology for anti-VEGF injections / laser [1]
Mechanism: Age-related macular degeneration involves progressive degeneration of the retinal pigment epithelium (RPE) and photoreceptors at the macula.
- Dry AMD (90%): Drusen deposits (lipid/protein accumulation between RPE and Bruch's membrane) → geographic atrophy. Slow, progressive central visual loss.
- Wet AMD (10%): Choroidal neovascularization (CNV) breaks through Bruch's membrane → leakage, haemorrhage, exudation under the retina → rapid, severe central visual loss. This is the type that presents as "acute" visual loss.
Amsler grid: A grid of horizontal and vertical lines used for self-monitoring. Patients with macular disease see distortion (metamorphopsia) or scotomas in the grid. The 2024 PBL case describes a patient with distortion for several days before acute deterioration → classic wet AMD presentation. [3]
Risk factors: high myopia ( > -6D), family history, eye rubbing (eczema), systemic disease (Marfan's), trauma [1]
Presentation: persistent floaters/flashes, progressively worsening visual field defect [1]
Management: recognise early and refer to ophthalmology — laser / cryopexy / surgery [1]
Mechanism: The neurosensory retina separates from the underlying RPE. Three types:
- Rhegmatogenous (most common): a full-thickness retinal break allows vitreous fluid to enter the subretinal space. Often preceded by posterior vitreous detachment (PVD) → vitreous traction → retinal tear.
- Tractional: fibrovascular membranes (from PDR, RVO) contract and pull the retina off.
- Exudative/serous: fluid accumulates without a break (tumours, inflammation, severe hypertension).
Key clinical pearl: Flashes (photopsia) = vitreous traction on the retina. New floaters + flashes = retinal tear until proven otherwise. If the patient describes a "shadow" or "curtain" progressing across their visual field, the retina is already detaching.
Already covered in the comparison table above. The lecture emphasizes the differential of disc swelling: optic neuritis vs. AAION (GCA) vs. NAION vs. papilloedema. [1]
Not included in original list as not quite "acute" but is most destructive [1]
Categorized into exogenous and endogenous [1]
History: recent ocular surgery, trauma, immunosuppressed/immunocompromised [1]
Recognise early! Low threshold of suspicion and consult ophthalmology: B-scan, CT abdomen, U/S liver, systemic antibiotics, vitreous tap and inject antibiotics, vitrectomy [1]
| Type | Mechanism | Common Organisms | Timing |
|---|---|---|---|
| Exogenous | External inoculation (post-cataract surgery, intravitreal injection, trauma, corneal ulcer perforation) | Coag-negative Staph (post-op), Staph aureus (trauma), Streptococcus, Pseudomonas | Usually within days to weeks of surgery/trauma |
| Endogenous | Haematogenous seeding from distant infection | Candida, Klebsiella (especially in East Asia), E. coli | Look for systemic source: liver abscess (hence the CT abdomen/U/S liver), endocarditis, IV drug use, immunosuppression |
Endophthalmitis After Cataract Surgery
Any patient presenting with increasing pain, redness, and decreasing vision after recent intraocular surgery should be considered to have endophthalmitis until proven otherwise. The lecture stresses a low threshold of suspicion because delayed treatment leads to permanent blindness. [1]
| Painless (more posterior) | Painful (more anterior + exceptions) |
|---|---|
| Glare | Corneal epithelial defect |
| Corneal surface disruption | Foreign body |
| Hyphaema (bleeding disorder — non-traumatic) | Corneal oedema |
| Lens subluxation/dislocation (non-traumatic) | Keratitis |
| Vitreous haemorrhage | Hyphaema (traumatic) |
| Vitritis | Uveitis |
| Retinal vascular occlusions | AACG |
| Macular haemorrhage/oedema | Post-traumatic cataract/foreign body |
| Retinal detachment | Traumatic subluxation/dislocation |
| Amaurosis fugax (TIA) | Optic neuritis (pain on eye movement) |
| Migraine (vasospasm) | AAION / GCA (headache, jaw claudication) |
| Papilloedema (headache from ↑ICP) | |
| Avulsion (trauma) |
Table reconstructed from lecture slides 16-17 [1]
Main questions to ask: Onset, Pain, Transient [1]
Think of obvious reasons which the patient will likely be aware of: Trauma, Contact lens, Recent eye surgery [1]
Hints:
- Painful = more anterior
- Painless = more posterior
- Transient = systemic vascular issues
- Persistent = everything else → go anatomical front to back [1]
Integration with Related Material
Ischaemic Optic Neuropathy (ION): Acute, painless visual loss in adults from microvascular infarction of the optic nerve. Anterior ION (AION) — more common, usually unilateral, optic disc swollen, altitudinal VF defects, impaired flow from posterior ciliary arteries. Two variants: arteritic (GCA — emergency) and non-arteritic (NAION — commonest cause of acute optic disc swelling in those > 50). Posterior ION (PION) — less common, usually bilateral, optic disc normal, variable VF defects, systemic hypotension (e.g., cardiac bypass surgery, prolonged spinal surgery). [12]
Glaucoma definition: a form of optic neuropathy, characterized by visual field loss, usually associated with raised intraocular pressure. Classification: acute vs. chronic, open angle vs. closed angle, primary vs. secondary, high IOP vs. normal/low IOP. [13]
Proliferative diabetic retinopathy is a major cause of vitreous haemorrhage (neovascularization bleeds into vitreous). Rubeotic glaucoma occurs when new vessels form on the iris → obstruct drainage angle → AACG. This connects back to the lecture's discussion of vitreous haemorrhage causes. [14]
GCA: commonest form of primary vasculitis. Demographics: F:M = 2:1, rarely < 50y, average onset 70y. ESR characteristically very high (reaching 100 mm/h). Treatment: urgent high-dose prednisolone 1-2mg/kg/day → slowly tapered over 1-2 years. [5]
A visual acuity of 6/12 means that a normal patient can read the letter at 12 meters while the patient can read the same letter at 6 meters. Pinhole corrects refractive errors (myopia, hyperopia, astigmatism) but does NOT correct presbyopia (presbyopia is a loss of accommodation, not a simple refractive error). Answer B is correct; C is incorrect because astigmatism CAN be corrected by pinhole. [9]
Likely Exam Questions
Q1. A 65-year-old man with poorly controlled HTN, hyperlipidaemia, and angina presents with sudden painless loss of vision in the right eye. VA is 6/60 OD, 6/9 OS. There is a right RAPD. Fundoscopy shows a pale retina with a cherry-red spot at the fovea. What is the most likely diagnosis?
- Answer: Central retinal artery occlusion (CRAO) — classic triad: painless sudden severe visual loss + RAPD + pale retina with cherry-red spot in a patient with cardiovascular risk factors.
Q2. A 70-year-old woman presents with acute left eye visual loss, left temporal headache, and jaw claudication. ESR is 95 mm/h. What is the MOST IMPORTANT next step?
- Answer: Start high-dose systemic corticosteroids immediately — even before temporal artery biopsy. Biopsy should still be done (within 2 weeks, as histological changes persist despite steroids for this period), but treatment must not be delayed.
Q3. Which of the following is NOT associated with anterior uveitis? (A) Ankylosing spondylitis, (B) Osteoarthritis, (C) Psoriatic arthritis, (D) Behcet disease
- Answer: B (Osteoarthritis) — OA is degenerative, not inflammatory, and has no association with uveitis. [7]
Q4. A 45-year-old woman on cold medication (containing antihistamines) presents with sudden severe left eye pain, headache, nausea, and blurred vision. VA is "count fingers" in the left eye. Examination shows a mid-dilated non-reactive left pupil, injected conjunctiva, shallow anterior chamber, and corneal oedema. IOP is 58 mmHg. (a) What is the diagnosis? (1 mark) (b) Explain the mechanism of how the cold medication precipitated this condition. (2 marks) (c) Outline the immediate management. (3 marks)
Markscheme:
- (a) Acute angle closure glaucoma
- (b) Antihistamines have anticholinergic effects → pupil dilation → peripheral iris bunches up against trabecular meshwork in a predisposed eye with narrow angle → aqueous outflow blocked → IOP rises acutely
- (c) Topical pilocarpine to constrict pupil and break the cycle; Topical IOP-lowering agents (beta-blocker, alpha-agonist, CAI); Systemic IOP-lowering (IV acetazolamide, IV mannitol if needed); Urgent ophthalmology referral for definitive treatment (laser PI). Anti-emetic for nausea.
Q5. List 6 causes of acute visual loss, organized anatomically from front to back. (6 marks)
- Markscheme: One mark each for any six: corneal keratitis, AACG, uveitis with hypopyon, vitreous haemorrhage, CRAO/CRVO, retinal detachment, macular haemorrhage (wet AMD), optic neuritis, AAION. (Must be organized front to back for full marks.)
| Year | Question | Topic | Key Point |
|---|---|---|---|
| 2020 Q11 | Bending of straight lines in central VF in retired life-guard | Wet AMD (metamorphopsia) | UV exposure is a risk factor for AMD; Amsler grid abnormality |
| 2020 Q12 | NOT associated with anterior uveitis | OA is NOT associated | Know the HLA-B27 associations |
| 2021 Q13 | Bilateral blurred vision on hydroxychloroquine | Bull's eye maculopathy | Chloroquine/HCQ toxicity — retinal screening recommended |
| 2022 Q84 | VA interpretation with pinhole | 6/12 definition, pinhole corrects refractive errors | Know the Snellen fraction meaning |
| 2023 Q15 | Sudden blurred left eye with DM/HTN/stroke hx | Left RAPD; vitreous haemorrhage as DDx | RAPD on side of lesion; vitreous haemorrhage in diabetic |
| 2024 Q83 | Painless red eye on DOACs | Subconjunctival haemorrhage | Not all red eyes = visual loss; know benign causes |
| 2025 Q11 | DM with dot-blot haemorrhages all 4Q + hard exudates at macula | Diabetic macular oedema | DMO can occur at ANY stage of DR; hard exudates near macula = clue |
Common Mistakes Students Make
- Confusing RAPD side: The RAPD is on the AFFECTED eye (the eye with the optic nerve or extensive retinal pathology). The 2023 Q15 tests this — left eye visual loss = left RAPD. [8]
- Forgetting that optic neuritis disc may look NORMAL: In retrobulbar neuritis (the most common form), the inflammation is behind the globe — "the patient sees nothing and the doctor sees nothing." The disc looks normal initially.
- Assuming all disc swelling = papilloedema: Papilloedema specifically means disc swelling from raised intracranial pressure and is bilateral. Optic neuritis and ION cause disc swelling too but are different entities.
- Not asking about cold medications / antihistamines in AACG history — this is a classic trigger highlighted in the lecture. [1]
- Mixing up CRVO and CRAO fundoscopy: CRVO = "blood and thunder" (haemorrhages everywhere). CRAO = pale retina with cherry-red spot. They are opposite appearances!
- Forgetting the fellow eye in AACG: Always do prophylactic laser PI in the fellow eye — it has the same narrow-angle anatomy.
High Yield Summary
Approach: Onset → Pain → Transient → Front-to-Back anatomy. Painful = anterior; Painless = posterior; Transient = vascular/systemic.
Must-not-miss emergencies:
- AACG: Painful, red eye, mid-dilated pupil, raised IOP → pilocarpine + IOP-lowering agents + urgent ophth referral for laser PI
- CRAO: Painless, cherry-red spot, RAPD → stroke-equivalent workup, consider GCA
- GCA/AAION: Elderly + headache + jaw claudication + high ESR → start steroids IMMEDIATELY
- Retinal detachment: Flashes + floaters + progressive field loss → urgent ophth for surgery
- Endophthalmitis: Post-op eye with increasing pain/redness/↓VA → vitreous tap + inject antibiotics ± vitrectomy
Exam favourites: AACG mechanism and triggers, uveitis associations (HLA-B27), CRAO vs CRVO fundoscopy, RAPD localization, AMD management (dry vs wet), VA/pinhole interpretation, drug-induced eye disease (antihistamines→AACG, HCQ→bull's eye maculopathy).
Active Recall - Acute Visual Loss
[1] Lecture slides: GC 121. Acute Visual Loss.pdf (all pages) [2] AOS material: AOS - Ophthalmology.pdf (PBL Scenario 2, p.6) [3] Medicine lecture: 2024 General Clerkship - Acute Visual Loss_Student Copy.pdf (Patient 3, pp.6-7) [4] Senior notes: Ryan Ho Opthalmology.pdf (pp.39, 54) [5] Senior notes: Ryan Ho Rheumatology.pdf (p.95 — GCA/PMR) [6] Senior notes: Ryan Ho Fundamentals.pdf (p.89 — VA assessment) [7] Past papers: 2020 Fourth Summative Assessment MCQ paper.pdf (Q11, Q12) [8] Past papers: 2023 Fourth Summative MCQ.pdf (Q15) [9] Past papers: 2022 Fourth Summative MCQ.pdf (Q84) [10] Past papers: 2024 Fourth Summative MCQ.pdf (Q83) [11] Past papers: 2025 Fourth Summative MCQ.pdf (Q11) [12] Lecture slides: GC 124. Neuro Ophthalmology.pdf (p.48 — Ischaemic Optic Neuropathy) [13] Lecture slides: GC 122. Chronic Visual Loss.pdf (pp.17, 44) [14] Senior notes: Ryan Ho Endocrine.pdf (p.96 — Diabetic retinopathy classification and complications)
GC119 Vaginal Discharge Obstetric And Gynaecological Infections
Vaginal discharge resulting from obstetric and gynaecological infections encompasses abnormal genital tract secretions caused by pathogens such as Candida, bacterial vaginosis organisms, Trichomonas, Chlamydia, or Neisseria gonorrhoeae during pregnancy or in the gynaecological setting, requiring prompt identification and treatment to prevent complications.
GC122 Chronic Visual Loss
Chronic visual loss is a gradual, progressive decline in visual acuity or visual field occurring over weeks to months, commonly caused by conditions such as cataracts, glaucoma, age-related macular degeneration, or diabetic retinopathy.