Ophthalmology: Retinal Visual Loss

• Approach: Sudden Visual Loss | Gradual Visual Loss
• Vascular causes: Amaurosis Fugax | Retinal Artery Occlusion | Retinal Vein Occlusion | Giant Cell Arteritis and the Eye | Non-arteritic Ischaemic Optic Neuropathy
• Retina and macula: Retinal Detachment | Vitreous Haemorrhage | Dry AMD | Wet AMD | Diabetic Retinopathy | Diabetic Eye Screening and Treatment | Hypertensive Retinopathy | Other Macular Problems | Inherited Retinal Disease
• Optic nerve: Optic Neuritis | Papilloedema | Optic Atrophy and Toxic Optic Neuropathy
• Revision: Drug Reference Table | Spot the Diagnosis | Exam-style Scenarios | Key Points | Guidelines and Further Reading

👁️ The retina and optic nerve — painless loss of vision usually comes from here. Some causes are true emergencies: retinal artery occlusion is a stroke of the eye, giant cell arteritis can blind both eyes within days, and a retinal detachment needs surgery before the macula comes off. Others — AMD and diabetic retinopathy — are the main causes of sight loss in the UK, and much of that loss is now preventable with screening and anti-VEGF injections.
Your four questions for every patient: Sudden or gradual — and transient or persistent? One eye or both? Could this be GCA (age over 50, headache, jaw claudication)? What do the red reflex, pupils (RAPD) and fundus show?

Sudden Visual Loss

💡 Clinical Pearl: In anyone over 50 with sudden visual loss, check ESR and CRP and ask about GCA symptoms — the second eye can be lost within days.

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Gradual Visual Loss

• Refractive error — improves with pinhole.
• Cataract — glare, dull red reflex.
• Dry AMD — gradual central loss, difficulty reading and recognising faces.
• Glaucoma — silent peripheral field loss.
• Diabetic maculopathy.
• Compressive optic neuropathy — pituitary tumour (bitemporal field loss), meningioma, thyroid eye disease.
• Toxic or nutritional optic neuropathy — ethambutol, B12 deficiency, alcohol and tobacco.
• Inherited retinal disease — night blindness, tunnel vision.
• Drugs — hydroxychloroquine maculopathy.
• Bilateral, gradual, with normal eyes — consider cortical causes (posterior cortical atrophy, a variant of Alzheimer's disease).

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Amaurosis Fugax

• What it is: Transient monocular visual loss from a temporary blockage of the retinal circulation — the eye's version of a TIA.
• Features:
  • Sudden, painless loss of vision in one eye, often like a curtain coming down.
  • Lasts seconds to minutes (usually under 15), then full recovery.
  • Emboli (bright cholesterol plaques — Hollenhorst plaques) may be seen in retinal arteries.
• Causes:
  • Carotid artery stenosis (embolism).
  • Cardiac emboli (atrial fibrillation, valve disease).
  • Giant cell arteritis (over 50).
  • Vasospasm (younger people); hyperviscosity; antiphospholipid syndrome.
• Management — as for TIA (NICE NG128):
  • Aspirin 300 mg immediately (unless contraindicated or GCA suspected — check ESR/CRP).
  • Refer for specialist assessment within 24 hours (TIA clinic).
  • Carotid Doppler, ECG, BP, lipids, glucose.
  • Carotid endarterectomy for symptomatic stenosis of 50–99% (NASCET).
  • Secondary prevention — antiplatelet, statin, BP control.
  • No driving for 1 month (Group 1).

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Retinal Artery Occlusion

• Central retinal artery occlusion (CRAO) — a stroke of the eye.
• Features:
  • Sudden, profound, painless loss of vision in one eye (often counting fingers or worse).
  • RAPD.
  • Pale, swollen retina with a cherry-red spot at the macula (the thin fovea shows the intact choroid underneath).
  • Narrow arteries; sometimes a visible embolus.
• Branch retinal artery occlusion — loss of part of the field; pale wedge of retina.
• Causes:
  • Emboli — carotid disease, AF, valve disease.
  • Giant cell arteritis (5–10% — always check ESR and CRP).
  • Thrombophilia, vasculitis, sickle cell (young people).
• Management:
  • Treat as an acute stroke — immediate referral to the stroke team (and ophthalmology). Some centres consider IV thrombolysis within 4.5 hours (evidence still emerging).
  • Exclude GCA — ESR, CRP; start steroids if suspected.
  • Older measures (ocular massage, lowering eye pressure) have no proven benefit.
  • Stroke work-up — brain imaging (MRI often shows silent strokes), carotid imaging, ECG and heart monitoring, echo.
  • Secondary prevention — antiplatelet, statin, BP control.
  • Watch for neovascular glaucoma in the following weeks.
• Prognosis: Vision rarely recovers much; prevention of stroke is the main goal.

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Retinal Vein Occlusion

• Who: Older people with hypertension, diabetes, high cholesterol, smoking, glaucoma. In young people — thrombophilia, hyperviscosity (myeloma, polycythaemia), vasculitis, oral contraceptives.
• Features:
  • Painless blurred vision in one eye (sudden or over days).
  • Central (CRVO) — haemorrhages in all four quadrants ("stormy sunset" or "blood and thunder"), swollen tortuous veins, disc swelling, cotton wool spots.
  • Branch (BRVO) — haemorrhages in one sector, often where an artery crosses a vein.
  • Ischaemic CRVO may have an RAPD.
• Tests: BP, FBC, ESR, glucose and HbA1c, lipids, U&E, thyroid; protein electrophoresis; thrombophilia screen only in young or unusual cases.
• Management:
  • Urgent ophthalmology (within days).
  • Treat risk factors — BP, diabetes, lipids, eye pressure.
  • Macular oedema — intravitreal anti-VEGF injections (ranibizumab, aflibercept, faricimab) or a dexamethasone implant.
  • Neovascularisation — laser photocoagulation (pan-retinal) to prevent vitreous haemorrhage and neovascular glaucoma ("90-day glaucoma" after ischaemic CRVO).
  • Routine anticoagulation or antiplatelets are not recommended for RVO itself.

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Giant Cell Arteritis and the Eye

• Why it matters: GCA can cause permanent blindness in one eye, and then the other within days, through arteritic anterior ischaemic optic neuropathy (AAION) or retinal artery occlusion.
• Warning symptoms:
  • Age over 50; new headache; scalp tenderness; jaw claudication.
  • Polymyalgia symptoms; weight loss, fever.
  • Visual symptoms — transient visual loss, double vision.
• Eye signs (AAION):
  • Sudden severe painless loss of vision; RAPD.
  • Pale ("chalky white"), swollen optic disc.
• Management:
  • Start steroids immediately — don't wait for a biopsy.
    • With visual symptoms — IV methylprednisolone (e.g. 500 mg–1 g daily for 3 days) or oral prednisolone 60–100 mg, per local pathway.
    • Without visual symptoms — prednisolone 40–60 mg daily.
  • ESR and CRP; temporal artery ultrasound or biopsy within 1–2 weeks of starting steroids.
  • Same-day ophthalmology and rheumatology.
  • Tocilizumab for relapsing or refractory disease.
• See the Neurological Emergencies chapter.

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Non-arteritic Ischaemic Optic Neuropathy

• What it is: A small "stroke" of the front of the optic nerve, not due to arteritis. The commonest acute optic neuropathy over 50.
• Risk factors:
  • Small, crowded optic disc ("disc at risk").
  • Hypertension, diabetes, high cholesterol, smoking.
  • Obstructive sleep apnoea.
  • Night-time low BP (taking BP drugs at bedtime).
  • Drugs — PDE-5 inhibitors (sildenafil), amiodarone; reported very rarely with semaglutide.
• Features:
  • Painless visual loss, often noticed on waking.
  • Altitudinal field defect (upper or lower half).
  • RAPD; swollen (sometimes sectoral) disc with haemorrhages.
  • Normal ESR and CRP, no GCA symptoms.
• Management:
  • Exclude GCA first.
  • No proven treatment; treat vascular risk factors; screen for sleep apnoea.
  • About 15–20% develop it in the other eye within 5 years.

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Retinal Detachment

• What it is: The retina separates from the layer underneath. The commonest type follows a retinal tear (from posterior vitreous detachment), letting fluid get under the retina.
• Risk factors:
  • Myopia (short sight).
  • Previous cataract surgery.
  • Eye trauma.
  • Previous detachment (either eye); family history.
  • Diabetic retinopathy (tractional detachment).
  • Marfan and Stickler syndromes.
• Features:
  • Flashes (photopsia) and new floaters.
  • A shadow or curtain spreading from the edge of the vision.
  • Central vision lost once the macula detaches.
  • Painless.
  • Grey, billowing retina on fundoscopy; may be hard to see without dilation.
• Management:
  • Same-day ophthalmology — especially if the macula is still attached ("macula-on"), as surgery can save central vision.
  • Retinal tear without detachment — laser or cryotherapy to seal it.
  • Detachment surgery — vitrectomy with a gas or oil bubble, scleral buckle, or pneumatic retinopexy.
  • After gas: no flying and avoid nitrous oxide anaesthesia until the gas has gone (it expands); head positioning as advised.

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Vitreous Haemorrhage

• Features: Sudden shower of floaters, "smoke" or cobwebs, or sudden loss of vision; painless; poor red reflex; retina hard to see.
• Causes:
  • Proliferative diabetic retinopathy (the commonest).
  • Retinal tear from posterior vitreous detachment.
  • Retinal vein occlusion with new vessels.
  • Trauma; wet AMD; sickle cell retinopathy.
  • Terson syndrome (with subarachnoid haemorrhage).
• Management:
  • Urgent ophthalmology (same day if no known cause — to exclude a tear or detachment).
  • B-scan ultrasound if the retina can't be seen.
  • Treat the cause (laser for new vessels); vitrectomy if it doesn't clear.
  • Anticoagulants are usually continued (specialist advice).

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Dry AMD

• Age-related macular degeneration — the leading cause of sight loss in the UK. Dry (atrophic) AMD makes up about 85–90%.
• Risk factors:
  • Age (over 50, rising sharply).
  • Smoking (the main modifiable one).
  • Family history; genetics (complement factor H).
  • White ancestry; women.
  • Obesity, cardiovascular disease.
• Features:
  • Gradual loss of central vision over years — difficulty reading and recognising faces.
  • Needs more light; colours fade.
  • Peripheral vision is kept (people don't go fully blind).
  • Drusen (yellow deposits) and pigment changes at the macula; geographic atrophy in late disease.
• Management (NICE NG82):
  • Stop smoking.
  • Diet rich in leafy greens and oily fish.
  • AREDS2-type supplements (vitamins C and E, zinc, lutein, zeaxanthin) may slow progression in intermediate AMD (avoid beta-carotene in smokers — lung cancer).
  • Low vision aids; sight impairment registration; support for Charles Bonnet syndrome.
  • Complement inhibitors for geographic atrophy (e.g. pegcetacoplan) are licensed elsewhere but not available on the NHS.
  • Amsler grid at home — check each eye regularly; report new distortion urgently (conversion to wet AMD).

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Wet AMD

• What it is: Abnormal new blood vessels grow under the macula (choroidal neovascularisation), leak fluid and bleed. Driven by VEGF. Without treatment, central vision can be lost within months.
• Features:
  • Rapid (days to weeks) distortion — straight lines look wavy or bent (metamorphopsia).
  • Central blur or a dark patch.
  • Haemorrhage or fluid at the macula; OCT shows fluid under or within the retina.
• Management:
  • Urgent referral to a macular (rapid-access) clinic — treatment should start as soon as possible.
  • Diagnosis — OCT; fluorescein angiography.
  • Intravitreal anti-VEGF injections:
    • Aflibercept, ranibizumab (including biosimilars), faricimab (also blocks angiopoietin-2), and others.
    • Given into the eye under local anaesthetic, initially monthly, then at extended intervals ("treat and extend") — often for years.
    • Risks — endophthalmitis (rare), raised pressure, retinal tear.
  • Early treatment stabilises or improves vision in most patients.

⚠️ Safety Pearl: Sudden distortion of straight lines in an older person is wet AMD until proven otherwise — refer urgently. Every week of delay costs vision.

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Diabetic Retinopathy

• What it is: Damage to the small retinal blood vessels from high glucose — leakage (exudates, oedema), blockage (ischaemia) and new vessel growth.
• Risk factors: Duration of diabetes; poor glucose control; hypertension; high lipids; pregnancy; kidney disease; smoking.
• UK screening grades:

• Diabetic macular oedema — the commonest cause of vision loss in diabetes; fluid swelling at the macula, best seen on OCT.
• Early worsening — a rapid fall in HbA1c (e.g. starting insulin, GLP-1 agonists, bariatric surgery, pregnancy) can transiently worsen retinopathy. Make sure screening is up to date in people with existing retinopathy.
• Other diabetic eye problems — earlier cataract, neovascular glaucoma, cranial nerve palsies (pupil-sparing third nerve palsy), fluctuating vision with glucose swings, NAION.

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Diabetic Eye Screening and Treatment

• NHS Diabetic Eye Screening Programme:
  • Everyone with diabetes from age 12.
  • Retinal photographs after dilating drops (no driving afterwards).
  • Yearly; since 2023–24, people at lowest risk (no retinopathy at their last two screens) are invited every 2 years.
  • Pregnancy — screening at first antenatal visit and in each trimester (more often if retinopathy).
  • Screening doesn't replace an optometrist's eye test.
• Prevent progression:
  • Glucose control (individualised HbA1c target).
  • BP control. Lipids; stop smoking.
• Treatment (ophthalmology):
  • Proliferative retinopathy — pan-retinal photocoagulation (PRP) laser: destroys peripheral ischaemic retina to reduce VEGF and make new vessels regress. Side effects: reduced peripheral and night vision (may affect driving fields). Anti-VEGF is an alternative or add-on.
  • Diabetic macular oedema — intravitreal anti-VEGF (aflibercept, ranibizumab, faricimab) first line; dexamethasone or fluocinolone implants; focal laser.
  • Vitrectomy — non-clearing vitreous haemorrhage, tractional retinal detachment.

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Hypertensive Retinopathy

• Grade 3–4 changes with very high BP (e.g. 180/120 or more) indicate a hypertensive emergency (accelerated or malignant hypertension) — same-day admission (NICE NG136). Look for AKI, heart failure, encephalopathy, and TMA.
• Lower BP in a controlled way (not too fast — risk of optic nerve and brain ischaemia).
• Look for secondary causes (renal artery stenosis, phaeochromocytoma, Conn's).
• See the Hypertension chapter.

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Other Macular Problems

• Central serous chorioretinopathy:
  • Young to middle-aged men, often stressed; linked to steroids (any route, including inhaled, nasal and skin creams).
  • Blurred or dim central vision, distortion; fluid under the macula on OCT.
  • Usually settles within 3–6 months; stop steroids if possible.
• Macular hole — older women; central blur and distortion; a full-thickness hole on OCT. Vitrectomy with gas (face-down positioning).
• Epiretinal membrane — thin scar tissue over the macula ("cellophane"); distortion; surgery if troublesome.
• Cystoid macular oedema — after cataract surgery, uveitis, diabetes, vein occlusion; prostaglandin drops can contribute.
• Hydroxychloroquine maculopathy — "bull's-eye" maculopathy (late) — see the Neuro-ophthalmology, Systemic and Paediatric chapter for screening.
• Myopic maculopathy — high myopia; may develop new vessels (anti-VEGF).

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Inherited Retinal Disease

• Retinitis pigmentosa — the commonest group:
  • Night blindness first (rods affected), often in childhood or teens.
  • Gradual tunnel vision; central vision lost late.
  • Bone-spicule pigmentation in the peripheral retina, pale waxy disc, thin vessels.
  • Inheritance — autosomal dominant, recessive or X-linked.
  • Syndromes — Usher syndrome (with deafness), Bardet–Biedl (obesity, polydactyly, kidney disease), Refsum disease, Kearns–Sayre syndrome.
• Stargardt disease — inherited macular dystrophy in children and young adults.
• Treatment:
  • Genetic diagnosis and counselling (NHS Genomic Medicine Service).
  • Gene therapy — voretigene neparvovec for RPE65 gene variants (NICE-recommended).
  • Low vision support; driving advice (fields).
• Inherited retinal disease is one of the leading causes of sight impairment in working-age adults in the UK.

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Optic Neuritis

• Who: Young adults (20–45), women more than men.
• Features:
  • Reduced vision over hours to days, usually one eye.
  • Pain on eye movement (most).
  • Reduced colour vision (red desaturation), RAPD, central scotoma.
  • Disc normal (retrobulbar) or swollen.
  • Uhthoff phenomenon later (worse vision with heat or exercise).
• Causes: Multiple sclerosis (often the first presentation), MOG antibody disease, NMOSD (aquaporin-4 — severe, bilateral), sarcoidosis, infection.
• Management:
  • MRI brain and orbits; antibodies (AQP4, MOG) if atypical.
  • High-dose steroids speed recovery but don't change the final outcome in typical MS-related optic neuritis; urgent for atypical cases (NMOSD, MOG).
  • Most recover well over weeks to months.
• Atypical features (refer urgently): no pain, severe loss, both eyes, no recovery after 3 weeks, very swollen disc with haemorrhages, age over 50.
• See the MS and Neuroinflammatory chapter.

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Papilloedema

• What it is: Bilateral optic disc swelling from raised intracranial pressure. (Disc swelling from other causes is called "optic disc swelling", not papilloedema.)
• Features:
  • Headache (worse lying down, coughing, morning), nausea, vomiting.
  • Transient visual obscurations — seconds of greying out, especially on standing.
  • Pulsatile tinnitus; double vision (sixth nerve palsy).
  • Vision is usually normal early; enlarged blind spot; later field loss.
  • Disc signs — blurred margins, elevated disc, loss of venous pulsation, haemorrhages.
• Causes:
  • Space-occupying lesion (tumour, abscess).
  • Idiopathic intracranial hypertension (IIH).
  • Cerebral venous sinus thrombosis.
  • Hydrocephalus; meningitis; malignant hypertension (grade 4 retinopathy).
  • Drugs — tetracyclines, retinoids, high-dose vitamin A, lithium, steroid withdrawal.
• Management:
  • Urgent same-day brain imaging — CT or MRI with venography.
  • Then LP with opening pressure if imaging shows no mass.
  • IIH (mainly young women with obesity): weight loss (including GLP-1 agonists), acetazolamide, headache management; urgent surgery (CSF shunt, venous stenting, optic nerve sheath fenestration) if vision is failing.
• Pseudopapilloedema — raised-looking discs without raised pressure (optic disc drusen, crowded discs in hypermetropia); OCT and ultrasound help.
• See the Headache chapter.

⚠️ Safety Pearl: In papilloedema, good visual acuity is not reassuring — vision can be lost suddenly and permanently. Fields need monitoring, and failing fields need urgent treatment.

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Optic Atrophy and Toxic Optic Neuropathy

• Optic atrophy — a pale disc from loss of optic nerve fibres; the end result of many conditions.
• Causes:
  • Previous optic neuritis (MS).
  • Ischaemia (GCA, NAION).
  • Glaucoma (cupped, not just pale).
  • Compression — pituitary tumour, meningioma, aneurysm, thyroid eye disease.
  • Long-standing papilloedema.
  • Trauma.
  • Toxic and nutritional — see below.
  • Inherited — Leber hereditary optic neuropathy (LHON): young men, painless sequential loss in one eye then the other, mitochondrial DNA (passed down the maternal line); idebenone.
  • Syphilis.
• Toxic and nutritional optic neuropathy — gradual, bilateral, symmetrical central vision loss and poor colour vision:
  • Ethambutol (TB) — check acuity and colour vision before and during treatment; stop if vision changes.
  • Methanol poisoning — acute, severe, with acidosis.
  • Vitamin B12 and folate deficiency; thiamine.
  • Alcohol and tobacco (often with poor nutrition).
  • Amiodarone, linezolid (long courses), isoniazid.
  • Copper deficiency (after bariatric surgery, zinc excess).
• Visual field patterns — see the Neurological Localisation chapter.

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Drug Reference Table

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Spot the Diagnosis

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Exam-style Scenarios

1. A 72-year-old man has sudden painless loss of vision in his right eye 2 hours ago. Vision is hand movements; there is a right RAPD and a cherry-red spot. He has AF and is not anticoagulated.
Answer: Central retinal artery occlusion.

• Treat as an acute stroke — immediate stroke team and ophthalmology referral (thrombolysis may be considered within 4.5 hours).
• Urgent ESR and CRP to exclude GCA.
• Stroke work-up; anticoagulation for AF after specialist assessment; statin, BP control.

2. A 78-year-old woman has a week of headache, scalp tenderness and jaw pain on chewing. This morning she lost vision in her left eye. CRP is 110.
Answer: Giant cell arteritis with arteritic AION.

• Start high-dose steroids immediately (IV methylprednisolone per local pathway).
• Same-day ophthalmology and rheumatology; temporal artery ultrasound or biopsy.
• Bone protection and gastroprotection; consider tocilizumab.

3. An 81-year-old notices that lines on her bathroom tiles look wavy in her right eye over the last 10 days.
Answer: Suspected wet AMD.

• Urgent referral to the rapid-access macular clinic (OCT).
• Intravitreal anti-VEGF injections if confirmed.
• Stop smoking; Amsler grid monitoring of the other eye.

4. A 45-year-old with type 2 diabetes has new vessels on the disc at screening. HbA1c 98 mmol/mol, BP 158/96.
Answer: Proliferative diabetic retinopathy (R3).

• Urgent ophthalmology referral for pan-retinal photocoagulation (or anti-VEGF).
• Improve glucose control gradually; treat BP and lipids.
• Tell the DVLA if laser treatment affects both eyes (field check).

5. A 58-year-old short-sighted man had cataract surgery a year ago. He now has flashes and floaters, and today a shadow over the lower half of his vision. Acuity is 6/9.
Answer: Retinal detachment, probably macula-on.

• Same-day ophthalmology — urgent surgery to save central vision.
• Avoid strenuous activity while awaiting review.

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Key Points

• Sudden visual loss over 50: always consider GCA — ESR, CRP, and steroids immediately if suspected.
• Amaurosis fugax is a TIA: aspirin and specialist review within 24 hours.
• CRAO is a stroke of the eye: cherry-red spot, RAPD — stroke pathway and work-up.
• CRVO: haemorrhages in all quadrants; treat risk factors; anti-VEGF for macular oedema; watch for neovascular glaucoma.
• NAION: altitudinal field loss on waking with a swollen disc and normal inflammatory markers.
• Flashes, floaters and a curtain = retinal detachment — same-day referral, especially if macula-on.
• Dry AMD: gradual; stop smoking, supplements in intermediate disease, low vision support.
• Wet AMD: sudden distortion — urgent anti-VEGF injections.
• Diabetic screening from age 12, yearly (2-yearly if lowest risk); new vessels need urgent PRP laser.
• Grade 4 hypertensive retinopathy (disc swelling) with severe hypertension is an emergency.
• Papilloedema needs same-day imaging with venography, then LP; good acuity is not reassuring.
• Toxic optic neuropathy: bilateral central loss and poor colour vision — ethambutol, methanol, B12 deficiency.

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Guidelines and Further Reading

• NICE NG82: Age-related macular degeneration
• NICE NG128: Stroke and TIA in over 16s — diagnosis and initial management
• NHS Diabetic Eye Screening Programme — grading and extended intervals for people at lowest risk
• The Royal College of Ophthalmologists: guidelines on retinal vein occlusion, diabetic retinopathy and AMD
• BSR guideline on the diagnosis and management of giant cell arteritis
• NICE NG136: Hypertension in adults
• BNF — for current doses

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