• Etymology: "Glaucoma" from Greek glaukos = bluish-green (describing the appearance of the cornea)
• Pathophysiology: In a predisposed eye (shallow anterior chamber, thick lens), the iris can be pushed forward (pupillary block mechanism), physically blocking the trabecular meshwork at the drainage angle. Aqueous humour cannot drain → intraocular pressure (IOP) rises rapidly (often > 40–60 mmHg, normal 10–21 mmHg) → corneal oedema (explains hazy vision and halos around lights), ischaemic damage to the optic nerve, and retinal ischaemia ^[1][3]
• Why halos? Corneal oedema causes light to scatter and diffract, producing rainbow-coloured halos around point light sources
• Why mid-dilated fixed pupil? The high IOP causes iris sphincter ischaemia → the pupil cannot constrict. Sympathetic tone causes partial dilation. The pupil is therefore "mid-dilated" (4–6 mm) and non-reactive

AACG is particularly relevant in Hong Kong due to higher prevalence in East Asian populations. ^[1][3]

• Severe corneal infection (bacterial, viral e.g., HSV) or corneal ulceration can cause acute visual loss through corneal opacification
• Contact lens wear is a major risk factor for microbial keratitis
• Pathophysiology: infection → inflammatory infiltrate → corneal opacity → blocked light transmission

• Aetiology: proliferative diabetic retinopathy (most common), posterior vitreous detachment (PVD) ± retinal tear, ocular trauma, coagulopathy ^[6]
• Pathophysiology: Blood enters the vitreous cavity from ruptured normal vessels (trauma, PVD tearing a vessel) or from pathological neovascularization (PDR). Blood in the vitreous blocks light from reaching the retina → sudden painless visual loss
• Clinical pearl: "worse in the morning" because blood settles on the macula overnight when supine ^[6]
• Patients may describe "red hues," floaters, shadows, or "cobwebs"

• Inflammation of the uveal tract (iris, ciliary body, choroid)
• Anterior uveitis → inflammatory cells and protein ("flare") in the anterior chamber → reduces media clarity
• Causes include HLA-B27–associated diseases (ankylosing spondylitis), sarcoidosis, Behçet's disease, infections
• Usually presents with painful red eye, photophobia, and blurred vision rather than profound visual loss

• Etymology: "Central" = main trunk; "retinal" = retinal vasculature; "artery" = arterial supply; "occlusion" = blockage
• Aetiology: usually embolic in origin ^[5]
  • Carotid artery atherosclerosis: most common (cholesterol emboli = Hollenhorst plaques)
  • Cardiogenic embolism: more important in younger patients (AF, valvular disease, endocarditis)
  • Small artery disease (DM, HTN)
  • Vasculitis, e.g., GCA — must be excluded in any elderly patient with CRAO ^[4][5]
• Pathophysiology: Embolus lodges at the narrowest point of the CRA (at the lamina cribrosa where the artery enters the eye). Inner retinal layers are deprived of blood supply → retinal ganglion cell death begins within minutes. The retina has no ischaemic tolerance — irreversible damage occurs within 90–100 minutes (similar to brain tissue)
• Fundoscopy: ischaemic retinal whitening + oedema, cherry-red spot over macula, attenuated arteries, ± visible embolus (Hollenhorst plaque) ^[5]
• RAPD is ALWAYS present regardless of macular sparing ^[5]

• Embolus lodges in a branch of the CRA → ischaemia of a sector of retina → sudden monocular loss of a specific visual field ^[5]
• Fundoscopy: sectoral retinal whitening, partial cherry-red spot, embolus more commonly seen than in CRAO (~2/3) ^[5]
• Less than half have impaired visual acuity (because the macula may be spared)

• Pathophysiology: Thrombotic occlusion of the central retinal vein (at the lamina cribrosa, where the vein and artery share a common adventitial sheath — atherosclerotic thickening of the artery can compress the vein). Venous congestion → increased hydrostatic pressure → haemorrhages, oedema, and ischaemia
• Fundoscopy of CRVO: "blood and thunder" or "pizza pie" fundus — widespread flame-shaped haemorrhages in all four quadrants, dilated tortuous veins, cotton wool spots, disc oedema, macular oedema
• BRVO: similar but confined to the territory of the affected branch vein
• Risk factors: HTN (strongest), DM, hyperlipidaemia, glaucoma, hyperviscosity (e.g., polycythaemia vera, leukaemia)
• Classification:
  • Non-ischaemic (mild/moderate): Better prognosis, fewer haemorrhages
  • Ischaemic (severe): Poorer prognosis, extensive haemorrhages, ↑risk of neovascularization → neovascular glaucoma ("90-day glaucoma")

• Types:
  • Rhegmatogenous (most common): "rhegma" = Greek for break/tear. A retinal tear allows liquefied vitreous to track under the neurosensory retina, separating it from the RPE
  • Tractional: Fibrovascular proliferation (e.g., in PDR) pulls the retina off the RPE
  • Exudative/serous: Fluid accumulates under the retina without a tear (e.g., in severe HTN, tumours, inflammatory conditions)
• Pathophysiology of rhegmatogenous RD: Age-related vitreous liquefaction and syneresis → posterior vitreous detachment (PVD) → if the vitreous is adherent to the retina at certain points, traction during PVD creates a retinal tear → liquid vitreous enters through the tear → neurosensory retina detaches from RPE → photoreceptors lose their metabolic support from the RPE and choroidal circulation → progressive visual loss
• Warning symptoms (prodrome of PVD ± retinal tear):
  • Floaters: "cobwebs," translucent strands and specks ^[9]
  • Flashes (photopsia): "flickering light" — caused by mechanical traction on the retina stimulating the photoreceptors ^[9]

The significance of flashing lights (photopsia) in a patient with new floaters is that it indicates vitreous traction on the retina — this is a warning sign for retinal tear and impending retinal detachment. These patients need urgent dilated fundoscopy. ^[9]

• Progressive visual field loss: Patients classically describe a "curtain" or "shadow" coming across the vision — this corresponds to the area of detached retina
• If macula detaches ("macula-off"): Central vision is lost, and even with successful reattachment surgery, visual recovery is poorer

• Includes central serous chorioretinopathy (CSCR), acute wet age-related macular degeneration (AMD)
• Wet AMD: Choroidal neovascularization → subretinal/sub-RPE fluid/blood → sudden central visual distortion (metamorphopsia) or scotoma
• CSCR: Focal RPE dysfunction → serous detachment of the neurosensory retina at the macula → central blurring, often in young-middle aged stressed males or corticosteroid users

• Etymology: "Optic" = relating to vision/optic nerve; "neuritis" = inflammation of a nerve
• Inflammatory demyelination of the optic nerve
• Causes: ^[7]
  • Multiple sclerosis (MS): Most common association in Caucasian populations; ON is the presenting feature in ~1/3 of MS patients
  • Neuromyelitis optica spectrum disorder (NMOSD): "neuro" = nerve, "myelitis" = spinal cord inflammation, "optica" = optic nerve involvement. Anti-aquaporin-4 (AQP4) antibodies. More common in Asian populations and tends to be more severe/bilateral
  • MOG-IgG disease: Anti-myelin oligodendrocyte glycoprotein antibodies
  • Infectious: syphilis, TB, viral
  • Post-infectious / post-vaccination
• Pathophysiology: Immune-mediated demyelination of the optic nerve → impaired signal conduction → visual loss. Inflammation causes pain (the optic nerve sheath is innervated by meningeal branches of the trigeminal nerve, and the inflamed nerve swells within its sheath)
• Why pain on eye movement? The extraocular muscles (especially medial and superior rectus) insert close to the optic nerve sheath. Movement tugs on the inflamed nerve
• Clinical features:
  • Subacute unilateral visual loss (develops over hours to days, reaches nadir over 1–2 weeks)
  • Pain: retro-orbital, worsened by eye movement
  • ↓Visual acuity, ↓colour vision (dyschromatopsia — tested with Ishihara plates), RAPD positive
  • Fundoscopy: may show optic disc oedema (papillitis, ~1/3) or may be normal (retrobulbar neuritis — "the patient sees nothing and the doctor sees nothing", ~2/3)
  • Optic atrophy on fundoscopy in chronic/recurrent cases ^[7]

• Pituitary tumour → compression of optic chiasm → bitemporal hemianopia ^[8]
• Other causes: meningioma, orbital tumour, thyroid eye disease (apical crowding → compressive optic neuropathy in Graves' orbitopathy) ^[11]
• Graves' ophthalmopathy: oversized recti + orbital fat → apical crowding → compressive optic neuropathy; symptoms include slowly progressive ↓vision (especially colour vision, contrast sensitivity); signs include optic disc oedema/pallor, RAPD+, central scotoma with inferior arcuate defects ^[11]
• Pituitary apoplexy (acute haemorrhage/infarction of a pituitary adenoma) can cause acute visual loss — this is a neurosurgical emergency

• Bilateral optic disc swelling due to raised ICP
• Pathophysiology: ↑ICP → impaired axoplasmic flow in the optic nerve → disc swelling
• Visual acuity is typically preserved initially (unlike optic neuritis or AION), but there is enlargement of the blind spot and transient visual obscurations (seconds-long episodes of greying/blacking out of vision, often with postural change)
• If chronic/untreated → progressive visual field loss and eventual optic atrophy

• Posterior cerebral artery (PCA) infarction → contralateral homonymous hemianopia
• Bilateral PCA infarction → cortical blindness (pupils normal, patient may deny blindness — Anton's syndrome)
• Patients with homonymous hemianopia may describe "can't see on one side" and may bump into objects on the affected side

• Acute haemorrhage or infarction of a pituitary adenoma → sudden expansion → compression of optic chiasm and surrounding structures
• Acute bitemporal hemianopia, headache, ophthalmoplegia (CN III, IV, VI run through the cavernous sinus adjacent to the pituitary), altered consciousness ^[8]

• Amaurosis fugax ("fugax" = Latin for fleeting): painless transient monocular visual loss, typically lasting seconds to minutes ^[2][4]
  • Causes: retinal artery insufficiency (embolic, e.g., carotid atherosclerosis), GCA, vasospasm (migraine)
  • This is a warning sign for impending CRAO or stroke and demands urgent investigation
• Migraine aura: Scintillating scotomas, zigzag lines (fortification spectra), typically bilateral and lasting 15–30 minutes, followed by headache. Visual phenomena are positive (see things that aren't there) rather than negative (loss of vision)
• Papilloedema-related transient visual obscurations: Brief (seconds), bilateral, related to posture

• Tested with Snellen chart, one eye at a time, with spectacles on ^[2]
• VA expressed as d/D (d = distance at which patient reads, D = distance at which a normal person can read the same line) ^[2]
• If VA < 6/9 → suspect refractive error → correct with pinhole (pinhole eliminates refractive error by reducing the aperture; if VA improves, the problem is refractive, not pathological) ^[2]
• If VA < 6/120 (can't read first row): ^[2]
  • Can the patient count fingers (CF)?
  • If no, can they detect hand movements (HM)?
  • If no, can they detect light perception (LP)?
  • If no → no light perception (NLP) — worst possible VA

• RAPD (relative afferent pupillary defect) — tested with swinging flashlight test ^[1][2]
• Present in: CRAO, optic neuritis, AION, extensive retinal detachment, any significant unilateral optic nerve pathology
• Absent in: Media opacity alone (cataract, vitreous haemorrhage), purely macular disease, refractive error, retrochiasmal lesions (because both eyes' afferent signals have mixed by then)
• Fixed mid-dilated pupil: AACG (iris sphincter ischaemia from ↑IOP)

A normal pupil examination (no RAPD) in a patient with significantly reduced VA in one eye should make you consider: media opacity, macular disease, refractive error, or functional (non-organic) visual loss. A positive RAPD with good VA means look for a large peripheral retinal or optic nerve lesion that hasn't yet affected central acuity. ^[1][2]

This is arguably the single most important examination in acute visual loss.

• Normal: 10–21 mmHg
• AACG: IOP often > 40–60 mmHg → rock-hard globe on palpation (can compare with palpation of the normal eye through closed eyelids as a rough screen)
• CRVO: ↑IOP is both a risk factor and a complication (neovascular glaucoma)

• Test for cranial nerve palsies (CN III, IV, VI → ophthalmoplegia), motor/sensory deficits (stroke), and signs of ↑ICP (papilloedema, altered consciousness)

• Already discussed in detail. Key point: always test with spectacles on, one eye at a time. If VA < 6/9, use pinhole to correct for refractive error. ^[2]
• If VA < 6/120: test counting fingers (CF) → hand movements (HM) → light perception (LP) → no light perception (NLP) ^[2]

• The most useful bedside test in acute visual loss ^[1]
• Performed in a dim room, asking the patient to fixate on a distant target
• Swing a bright light from one eye to the other, holding for ~3 seconds on each eye
• Positive RAPD: the affected pupil dilates when the light swings to it (because the brain perceives the light as "dimmer" compared to what it just received from the normal eye)
• RAPD present in: CRAO, CRVO (extensive/ischaemic), optic neuritis, AION, compressive optic neuropathy, extensive retinal detachment
• RAPD absent in: media opacity (cataract, vitreous haemorrhage), macular disease, refractive error, retrochiasmal lesions ^[2][6][8]

• Patient sits 1m away, covers one eye, fixates on examiner's nose
• Examiner wiggles fingers in each quadrant — patient reports when they see movement
• Why this works: Each quadrant of the visual field maps to a specific part of the visual pathway. A defect in one quadrant localizes the lesion.
• More formal testing: Amsler grid (a grid of horizontal and vertical lines with a central fixation dot) — detects central scotoma and metamorphopsia (distortion of lines), highly sensitive for macular pathology ^[1]

The GC PBL Patient 3 describes central scotoma with metamorphopsia detected on Amsler grid → classic for wet AMD. ^[1]

• Goldmann applanation tonometry (gold standard, done at slit lamp)
• Non-contact tonometry (air-puff) — screening
• Rough bedside estimate: palpate globe through closed eyelids (compare both sides) — in AACG the affected eye feels "rock hard"
• Normal: 10–21 mmHg
• AACG: typically > 40–60 mmHg

• Examines cornea, anterior chamber, lens, and anterior vitreous in magnified detail
• Key findings:

The single most important investigation in acute visual loss — it is both a bedside test and a diagnostic investigation.

Essential in any elderly patient ( > 50y) with acute visual loss to exclude GCA. ^[9][19][20]

For GCA: check ESR and CRP urgently in any patient > 50y with acute visual loss ± headache ± jaw claudication ± scalp tenderness. Do NOT wait for results before starting steroids if clinical suspicion is high. ^[9][19]

These are critical in retinal vascular occlusions (CRAO, CRVO) because they share risk factors with stroke and systemic vascular disease.

• What it is: Non-invasive, cross-sectional imaging of the retina using near-infrared light (analogous to ultrasound but using light instead of sound). Provides micron-resolution images of retinal layers.
• Why it matters in acute visual loss:

Diabetic macular oedema can only be diagnosed by slit-lamp retinal biomicroscopy (measurement of retinal thickness) or indirect ophthalmoscopy — fundoscopy may be normal or only show mild NPDR ^[17]. In modern practice, OCT has largely replaced clinical biomicroscopy for this purpose.

• What it is: IV fluorescein dye is injected; sequential photographs of the retina are taken as the dye transits through the retinal and choroidal vasculature
• Why it matters:

• When to use: When the fundus cannot be visualized (e.g., dense vitreous haemorrhage, dense cataract)
• Key findings:

Ocular USG is especially important when vitreous haemorrhage obscures the fundus — it can identify associated PVD, retinal tears/detachment, tumours, and IOFB ^[5]

MRI is superior to CT for detecting early ischaemic stroke, optic nerve lesions, and posterior fossa pathology. However, CT is faster and more available, and is the first-line imaging in suspected acute stroke to exclude haemorrhage. ^[24][25]

• Gold standard for confirming GCA ^[9][19][20]
• Findings: panarteritis with mixed infiltrates (lymphocytes, plasma cells, macrophages), fragmentation of internal elastic lamina, necrosis of media ± giant cells (not necessary for diagnosis) ^[20]
• Must be ordered urgently ( < 24–48 hours) — delay risks permanent visual impairment ^[20]
• False negatives occur due to skip lesions (patchy, non-contiguous inflammation) — a negative biopsy does not exclude GCA if clinical suspicion is high ^[19]
• Biopsy should ideally be ≥1 cm in length and performed on the clinically affected side ^[19]

• Non-invasive alternative/adjunct to biopsy ^[19]
• Key finding: "halo sign" — hypoechoic circumferential wall thickening around the temporal artery representing perivascular oedema/inflammation
• Can also assess other H&N and lower limb vessels for large vessel involvement

• Definitive test for confirming angle closure in AACG
• Uses a special contact lens with mirrors to visualize the drainage angle
• Usually performed after acute IOP has been lowered (the oedematous cornea can make visualization difficult during the acute attack)

The granulomatous inflammation of the posterior ciliary arteries is an active, ongoing process. The fellow eye can become involved within days. High-dose steroids suppress the inflammatory cascade — the sooner you start, the sooner you halt the arteritis.

• Osteoporosis prophylaxis: Calcium, vitamin D, ± bisphosphonate (because patients will be on steroids for 1-2 years)
• PPI: Gastroprotection during high-dose steroid therapy
• Monitor: ESR, CRP, blood glucose (steroid-induced hyperglycaemia) at each visit

The IOP in AACG is typically > 40-60 mmHg (normal 10-21). At these pressures, the retinal ganglion cells and optic nerve are being progressively damaged by ischaemia (the perfusion pressure to the optic nerve = mean arterial pressure minus IOP; when IOP is extremely high, perfusion drops dangerously). The corneal endothelium is also overwhelmed, causing oedema and pain. Every minute counts.

Phase 1: Acute IOP Lowering (Medical)

The goal is to lower IOP rapidly using multiple agents working via different mechanisms:

Why multiple agents? Each works by a different mechanism — combining them gives additive IOP reduction. Think of it like draining a bathtub: you can turn off the tap (↓production with timolol, apraclonidine, acetazolamide), open the drain (↑outflow with pilocarpine), and remove water from the tub (osmotic agent).

Phase 2: Definitive Treatment — Laser Peripheral Iridotomy (PI)

• Laser PI creates a small hole in the peripheral iris → allows aqueous to flow directly from posterior chamber to anterior chamber → bypasses the pupillary block → angle opens → IOP normalizes
• Performed once the acute attack has been broken and the cornea is clear enough for the laser to pass through
• Fellow eye: prophylactic laser PI — because the fellow eye has the same anatomical predisposition and is at high risk of an attack ^[1]

Contraindications / Cautions:

• Timolol: asthma, COPD, bradycardia, heart block (β-blocker effects are systemic even from topical drops — absorbed via nasolacrimal duct into systemic circulation)
• Pilocarpine: not effective at very high IOP (iris sphincter ischaemia); causes miosis → can worsen vision
• Acetazolamide: sulfa allergy, severe renal/hepatic impairment, hypokalaemia (it's a carbonic anhydrase inhibitor → causes metabolic acidosis and K⁺ wasting)
• Mannitol: heart failure (volume overload risk), renal failure (cannot excrete)

The retina has no ischaemic tolerance — irreversible ganglion cell death begins within 90-100 minutes (similar to brain in stroke). By the time most patients present, the window for salvage has often passed. However, some interventions may help if initiated early.

The most important management in CRAO is actually the systemic vascular workup — because CRAO is a stroke equivalent, the patient is at high risk of stroke. Manage like a TIA/stroke: carotid Doppler, ECG (AF), echocardiography, antiplatelet therapy (aspirin), statin, BP control, glucose control. ^[6]

Contraindications for thrombolysis: Same as for ischaemic stroke — previous haemorrhagic stroke, active bleeding, aortic dissection, recent intracranial surgery, severe uncontrolled HTN ^[26]

This is the most important "complication" to understand: a patient with CRAO carries the same vascular risk as a stroke patient. ^[1][6]