The lecture specifies these exact history points — they are directly examinable: ^[1]

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]

• The slit-lamp photographs illustrate why the anterior segment is examined as an optical cross-section: localize corneal epithelium/stroma, anterior-chamber cells or blood/pus, iris and lens rather than calling every red eye “conjunctivitis.”
• Hyphaema vs hypopyon: both form a horizontal fluid level. Hyphaema is a dark-red blood layer; hypopyon is a pale white-yellow leukocyte layer. Either can obscure the pupil and accompany raised IOP or severe intraocular pathology.
• Lens displacement: a visible lens equator with an aphakic crescent is the key sign of subluxation; the traumatic slide also shows a rosette cataract and an intraocular foreign body.
• Fundus view: a clear red reflex permits retinal detail. Hazy red media suggests vitreous haemorrhage; a grey, corrugated, elevated sheet is detached retina; a normal-looking disc does not exclude retrobulbar optic neuritis.

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 cannot see the fundus (e.g., dense vitreous haemorrhage or cataract) to look for retinal detachment or a mass. Do not press on a suspected open globe; CT orbits is preferred for suspected intraocular foreign body, with urgent ophthalmic/trauma input ^[23]
• 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)

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.

Visual anchors from the slide: an epithelial defect fluoresces bright green; corneal oedema produces diffuse haze and may show Descemet folds in the slit beam; microbial keratitis appears as a focal white stromal infiltrate with an overlying epithelial defect, sometimes with a hypopyon ^[1].

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).

The photographs make the bedside distinction concrete: red fluid level = hyphaema; white-yellow fluid level = hypopyon. Hypopyon is a sign of severe inflammation/infection, not a diagnosis by itself.

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.

The slide’s rosette-shaped lens opacity is characteristic of traumatic cataract; the separate image shows an intraocular foreign body, and the displaced lens image shows the lens edge/aphakic crescent rather than a uniformly round pupil ^[1].

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.
• In the fundus photograph, vitreous blood creates a diffuse orange-red haze that obscures vessels and retinal detail; dense haemorrhage may eliminate the fundus view entirely.

Retinal causes: vascular occlusions (CRVO/BRVO and CRAO/BRAO), haemorrhage or oedema at macula, detachment ^[1]

Fundus pattern recognition: CRVO is the diffuse “blood-and-thunder” retina; CRAO is pale with a cherry-red fovea; submacular haemorrhage is a dark-red collection centred beneath/around the fovea; lipid exudates around a thickened macula support oedema; rhegmatogenous detachment is grey, elevated and corrugated, often with a causative break ^[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:

History: coryzal illness (viral), trauma (unusual organisms like fungal), contact lens user (bacterial, amoeba), dirty water exposure (amoeba) ^[1]

The slide says “initiate topical treatment early,” but the safe interpretation is: stop contact-lens wear, arrange same-day ophthalmology, obtain corneal scrapings when indicated and start organism-appropriate intensive topical antimicrobial therapy under the local pathway. Do not start an unspecified drop or topical corticosteroid empirically ^[20].

Why early recognition matters: Corneal infection can progress rapidly to corneal perforation and endophthalmitis. Every hour of delay worsens the prognosis.

The upper photograph shows a dense central white stromal infiltrate with surrounding corneal haze and a hypopyon; the lower photograph shows a branching fluorescein-positive dendritic epithelial lesion. Topical corticosteroids can worsen HSV epithelial, fungal, Acanthamoeba and Nocardia keratitis. In bacterial disease, a specialist may consider steroid only after effective antibiotics and a demonstrated response/identified organism ^[20].

Preceding event: reading in dim light; a cold remedy containing an anticholinergic antihistamine or sympathomimetic can dilate the pupil and precipitate pupillary-block angle closure in a predisposed narrow-angle eye ^[1][16]

Acute symptoms: blurring, eye pain, headache, nausea ^[1]

Acute signs: injected (redness), mid-dilated pupils, shallow AC, corneal oedema, decreased VA, raised IOP ^[1]

The slide’s “pilocarpine + ALL agents” phrase is an unsafe shortcut. This is an immediate ophthalmic emergency: confirm the mechanism, check contraindications, give analgesia/antiemetic support, rapidly lower IOP with protocol-selected topical and systemic therapy, then perform definitive laser treatment ^[16].

Mechanism from first principles:

1. In a predisposed eye (short axial length = hyperopia, shallow anterior chamber, thick lens), the iris lies close to the lens.
2. When the pupil dilates (dim lighting, sympathomimetics, anticholinergics), the peripheral iris bunches up and blocks the trabecular meshwork (the drainage angle).
3. 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).
4. Initial therapy rapidly suppresses aqueous production (for example, protocol-selected topical timolol/dorzolamide and apraclonidine, plus systemic acetazolamide when appropriate). Consider hyperosmotic therapy if pressure remains very high; renal, cardiac, pulmonary and drug-allergy contraindications matter ^[16].
5. Pilocarpine is not the first move at very high pressure because an ischaemic iris may not respond. The Royal College pathway defers it when IOP is > 40 mmHg, then uses it after pressure begins to fall in a confirmed pupillary-block/plateau-iris mechanism ^[16].
6. 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. The fellow eye is normally treated prophylactically, often in the same session, unless contraindicated ^[16].

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.

Lecture-era proportions: Idiopathic (50%), HLA-B27 related (20%) — axial spondyloarthritis/ankylosing spondylitis, reactive arthritis (historically “Reiter 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: same-day ophthalmic assessment. Cycloplegic and corticosteroid treatment depends on localization and cause; exclude infectious keratitis, endophthalmitis and herpetic disease before giving steroid, and do not initiate steroid blindly from a red-eye photograph.

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.

What the photograph adds: the irregular, scalloped pupil is pulled toward points of posterior synechiae. This is a structural clue to previous/current anterior uveitis, not merely “anisocoria.”

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]

Causes: trauma, neovascularization from proliferative diabetic retinopathy / vascular occlusions, posterior vitreous detachment / retinal tear, bleeding tendencies ^[1]

Clinical presentation: Sudden painless floaters, “cobwebs,” red haze or variable visual loss; severity depends on haemorrhage density and whether the visual axis is obscured ^[4].

Why this matters: You cannot see the fundus through a dense vitreous haemorrhage, so B-scan ultrasound is used to assess for an underlying retinal tear/detachment or mass after an open globe has been excluded ^[1][4].

What the images show: the fundus becomes diffusely hazy/orange with vessels disappearing behind blood. The accompanying anterior-segment photograph shows fine abnormal iris vessels (rubeosis iridis), a clue to severe retinal ischaemia/neovascular disease rather than the haemorrhage itself. An acute vitreous haemorrhage may conceal a retinal tear/detachment and warrants urgent retinal assessment; B-scan is used only after excluding an open globe.

The slide’s dry-AMD supplement list is inaccurate: AREDS2 contains vitamin C, vitamin E, zinc, copper, lutein and zeaxanthin — not alpha- or beta-carotene. It benefits people with intermediate AMD or late AMD in one eye, not people without AMD or with early AMD ^[19].

Wet AMD: prompt retinal referral for intravitreal anti-VEGF, the usual first-line treatment. Photodynamic therapy is now much less common and used selectively, often with anti-VEGF; nonspecific “laser” is not an interchangeable first-line option ^[19].

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]

Fundus images: a sharply dark submacular haemorrhage and a larger haemorrhagic/exudative macular lesion suggest active neovascular AMD; circinate yellow hard exudates surrounding the macula indicate chronic vascular leakage/oedema and are not, by themselves, diagnostic of AMD ^[1].

Slide risk-factor list: high myopia (> -6D), family history, eye rubbing/eczema, Marfan syndrome and trauma ^[1]. Also ask about previous retinal tear/detachment and prior intraocular/cataract surgery ^[21].

Presentation: persistent floaters/flashes, progressively worsening visual field defect ^[1]

Management: same-day emergency eye assessment. Laser/cryopexy can seal selected retinal tears; established detachment generally requires retinal surgery. Do not reassure or offer a routine clinic slot when new flashes/floaters are accompanied by a curtain or field loss ^[21].

Mechanism: The neurosensory retina separates from the underlying RPE. Three types:

1. 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.
2. Tractional: fibrovascular membranes (from PDR, RVO) contract and pull the retina off.
3. 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.

What the photograph shows: a bullous grey retina is lifted into the vitreous, with rippling/corrugation and a visible superior retinal break. The attached retina beyond the detachment retains its normal orange-red appearance ^[1].

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]

What the comparison images show: a normal disc has sharp margins and visible vessels crossing the rim; true oedema blurs/elevates the margin and can obscure small vessels. Optic neuritis may still have a normal disc when inflammation is retrobulbar. Papilloedema describes disc oedema from raised intracranial pressure (usually bilateral), not every swollen disc. A chalky-pale swollen disc with profound loss in an older patient should trigger immediate GCA treatment ^[17].

The slide graphic’s “IV corticosteroids” should not be read as automatic treatment for every optic neuritis. In typical demyelinating optic neuritis, high-dose steroid can accelerate recovery but does not improve final visual outcome; the need and route depend on MRI features and whether MS, MOGAD, NMOSD, infection or another atypical cause is suspected ^[17].

The slide says endophthalmitis is “not quite acute”; clinically, acute postoperative endophthalmitis is a rapidly destructive emergency, commonly presenting within the first 2 weeks after an intraocular procedure ^[22].

Categorized into exogenous and endogenous ^[1]

History: recent ocular surgery, trauma, immunosuppressed/immunocompromised ^[1]

Recognise early and contact the vitreoretinal service immediately. When infection is suspected, intraocular sampling and empiric intravitreal antibiotics should not be delayed; vitrectomy is selected according to severity and context ^[22].

Management differs by route. For presumed acute postoperative bacterial endophthalmitis, vitreous/aqueous sampling plus intravitreal broad-spectrum antibiotics is the core emergency treatment; routine systemic antibiotics did not improve outcome in the classic post-cataract trial. In endogenous endophthalmitis, systemic antimicrobial therapy and source control are central in addition to intravitreal therapy. CT abdomen/liver ultrasound is therefore source-directed (not mandatory for every postoperative case), with particular attention to Klebsiella liver abscess in the Hong Kong/East Asian context ^[22].

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 occurs almost exclusively after age 50 and can cause sudden irreversible visual loss. ESR/CRP/platelets support the diagnosis but no single marker confirms or excludes it. Start high-dose glucocorticoid immediately when ocular ischaemia is suspected, then obtain urgent specialist confirmation and an individualized steroid-sparing/taper plan; do not delay treatment for biopsy ^[5][17].

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]