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Vision Loss — Recognition, Immediate First Aid & Referral in Primary Care 9-step diagnostic pathway · Ophthalmic emergencies to chronic disease · UK GP / RCGP SCA
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⚡ Snapshot. The whole pathway on one page: act now, triage, classify, treat today and safety-net. The Steps tab holds the detail.

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1
Safety

Red Flags — Ophthalmic and neurological emergencies

Acute vision loss is an emergency until proven otherwise. GP role: recognise; give immediate first aid where appropriate; arrange the correct urgent referral via the local (local) eye-emergency, TIA or stroke pathway; communicate relevant history and medication; manage systemic risk factors after specialist diagnosis. Reserve 999 for neurological deficits, instability or unsafe transfer.

Sudden painless monocular loss Sudden persistent monocular loss (e.g. CRAO) is an ophthalmic and vascular emergency → Immediate eye-emergency/stroke pathway; 999 if ongoing neurological symptoms, acutely unwell, or local arrangements require ambulance transfer. Do not delay transfer for primary-care investigations.
Sudden painless binocular loss Especially with diplopia, dysarthria, ataxia, weakness, altered consciousness or severe headache → immediate stroke assessment 999. Other causes include bilateral ocular disease, toxic/metabolic causes, cortical blindness, severe hypotension and functional visual loss.
Painful red eye + vision loss + halos Painful red eye with reduced vision, haloes, headache, nausea/vomiting or an abnormal pupil (e.g. acute angle closure) → Immediate ophthalmology. Do not delay transfer for routine testing; no GP glaucoma drops unless directed by ophthalmology.
Temporal headache + jaw claudication + age >50 Giant cell arteritis → Same-day: give the local emergency GCA steroid regimen immediately (usually prednisolone 60 mg with visual symptoms) + same-day ophthalmology/rheumatology.
Vision loss + neurological symptoms Facial droop or limb weakness (anterior circulation), or posterior circulation features — acute vertigo with ataxia, diplopia, dysarthria, dysphagia, limb or truncal ataxia, nystagmus, crossed signs or occipital field loss → stroke or TIA / SOL → 999
Curtain / shadow across visual field Moving curtain or shadow in vision → retinal detachment → same-day eye casualty / local urgent eye service
Amaurosis fugax Transient monocular blindness (seconds to minutes, fully resolving) → suspected TIA → refer immediately; specialist assessment within 24 h (NICE NG128 — do not use ABCD2 to downgrade urgency). Persistent deficit → acute stroke pathway
Chemical eye injury Alkali or acid splash → start copious irrigation immediately (before history, VA or examination) and continue until ocular surface pH is neutral, rechecking after irrigation → urgent eye emergency; 999 if systemic toxicity, severe bilateral exposure or unable to irrigate safely. Do not patch.
Contact-lens wearer with painful red eye Pain, photophobia, corneal opacity or reduced vision → keratitis/corneal ulcer → same-day ophthalmology. Do not prescribe topical steroid; avoid patching.
Vision loss is one of the highest-stakes presentations in general practice. CRAO is treated as an ocular equivalent of acute ischaemic stroke for urgent vascular assessment, but there is no universally established ophthalmic treatment window or GP-administered reperfusion treatment — ocular massage, paracentesis, hyperbaric oxygen and thrombolysis have variable evidence and are specialist-led. NICE thrombolysis windows apply to selected cerebral ischaemic stroke within organised stroke services. Giant cell arteritis is the most preventable cause of permanent blindness in adults over 50 — starting high-dose corticosteroids immediately, before biopsy results, is correct management. Any delay risks permanent, sometimes bilateral, blindness. Retinal detachment involving the macula ("macula-off") carries a much worse visual prognosis, so same-day assessment matters. Amaurosis fugax is a TIA — early stroke risk is highest in the first days, so specialist assessment within 24 h (NICE NG128).
2
Diagnose

History — Characterise onset, pattern, and associated features

The history alone localises the lesion anatomically in the majority of cases. Apply the onset–laterality–type–pain framework systematically.

Onset speed
Sudden (seconds–minutes) → vascular (CRAO, CRVO, GCA, vitreous haemorrhage). Hours–days → inflammatory/infective. Weeks–months → chronic (AMD, glaucoma, cataract, DR)
Laterality
Unilateral → ocular or optic nerve pathology. Bilateral simultaneous → neurological (occipital cortex, bilateral optic nerves). Bilateral sequential → GCA, MS, systemic
Type of visual loss
Central scotoma → macular disease (AMD, CRAO central). Peripheral loss → glaucoma, retinitis pigmentosa. Curtain/shadow → retinal detachment. Hemianopia → stroke, pituitary tumour
Pain
Painful loss → acute angle-closure glaucoma (severe), anterior uveitis (moderate), optic neuritis (ache on eye movement), orbital cellulitis, scleritis. Painless → most posterior causes.
Floaters and flashes
New floaters + photopsia (flashes) → posterior vitreous detachment (PVD) or retinal tear. Dense sudden floaters + vision loss → vitreous haemorrhage. "Floater shower" → urgent same-day review
Systemic associations
Temporal headache + scalp tenderness + jaw claudication → GCA. Neurological symptoms → stroke / MS. Rash + uveitis → sarcoid, HLA-B27 conditions (ankylosing spondylitis, Reiter's)
Medical history
Diabetes (diabetic retinopathy); hypertension (CRVO, CRAO, hypertensive retinopathy); AF (embolic CRAO); MS (optic neuritis); sickle cell (proliferative retinopathy)
Medications
Hydroxychloroquine (retinal toxicity — annual monitoring after 5 years, or after 1 year if high risk); ethambutol (optic neuritis); amiodarone (corneal microdeposits); vigabatrin (visual field constriction)
The onset–laterality–type–pain framework localises the lesion before any examination. Sudden painless monocular loss = vascular occlusion until proven otherwise — act immediately. Central vision loss (inability to read, recognise faces) points to macular pathology. Peripheral vision loss (bumping into things, tunnel vision) points to glaucoma or retinitis pigmentosa — often asymptomatic until late. The distinction between a homonymous hemianopia (neurological, post-chiasmal) and monocular field defect (ocular, pre-chiasmal) is critical and requires careful testing of each eye separately. Always ask about metamorphopsia (straight lines appearing wavy) — this is the hallmark of macular disease and AMD conversion from dry to wet.
3
Diagnose

Classification — Acute vs chronic and anatomical localisation

Acute (<24 hrs) — Emergency
CRAO; CRVO; retinal detachment; acute angle-closure glaucoma; giant cell arteritis; optic neuritis (acute); vitreous haemorrhage; trauma; chemical injury; keratitis/corneal ulcer
Subacute (days–weeks)
Optic neuritis (MS, MOG-associated disease, NMOSD, infective/inflammatory; compressive or ischaemic optic neuropathy are differentials — typically pain on eye movement + central scotoma); anterior uveitis; orbital cellulitis; infective endophthalmitis; central serous chorioretinopathy
Chronic (weeks–months)
Age-related macular degeneration (AMD — dry or wet); chronic open-angle glaucoma; diabetic retinopathy; cataract; refractive error; hydroxychloroquine maculopathy
Ocular anatomy
Cornea (keratitis, ulcer); lens (cataract); vitreous (haemorrhage, PVD); retina (AMD, DR, detachment, CRAO/CRVO); optic nerve (neuritis, GCA, glaucoma, papilloedema)
Neurological pathway
Optic chiasm (pituitary tumour → bitemporal hemianopia); optic tract/radiation (stroke → homonymous hemianopia); occipital cortex (posterior stroke → homonymous hemianopia with macular sparing)
Systemic causes
Hypertensive retinopathy; diabetic retinopathy; GCA; sarcoidosis; syphilis; HIV-related; severe anaemia; raised ICP (papilloedema → chronic bilateral blurring)
Anatomical localisation drives both urgency and referral destination. Anterior segment pathology (cornea, iris, lens) → urgent ophthalmology. Posterior segment (retina, choroid) → emergency ophthalmology for acute causes. Optic nerve (GCA, optic neuritis, glaucoma) → depends on cause: GCA = same day start steroids; optic neuritis = urgent neurology/ophthalmology; glaucoma = urgent outpatient. Neurological pathway (chiasm to cortex) → neurology, often with urgent MRI. Bitemporal hemianopia is pituitary adenoma until proven otherwise — urgent MRI pituitary. The RCGP SCA frequently presents visual field patterns that require anatomical localisation.
4
Diagnose

Examination — Focused ophthalmological and neurological assessment

Visual acuity (VA)
Snellen chart at 6m or Snellen card at 3m. Each eye separately. With habitual correction if available. Document method and result (6/6, 6/9 etc.); if unable to read the chart, record counting fingers, hand movements or perception of light. Clinically important — document whenever possible.
Visual fields
Confrontation testing. Cover each eye in turn. Central scotoma (AMD, optic neuritis); peripheral constriction (glaucoma); hemianopia (compare examiner's field). Finger counting in quadrants. Confrontation is a screening test and may miss subtle defects; a new homonymous hemianopia or persistent field defect needs urgent neurological/ophthalmic assessment.
Pupils — RAPD test
Swinging light test: RAPD (relative afferent pupillary defect) supports significant asymmetric optic nerve or retinal disease (e.g. GCA, CRAO, optic neuritis) but is not specific; bilateral symmetrical disease may show no RAPD. Both pupils dilate when light swings to affected eye.
Colour vision
Ishihara plates if available — red colour desaturation on affected side → optic nerve disease. Optic neuritis: red looks washed out / dull on affected eye.
External eye
Red eye (anterior uveitis, acute glaucoma, scleritis, conjunctivitis); proptosis (orbital cellulitis, thyroid eye disease); ptosis; nystagmus
Fundoscopy
Optic disc: swelling — papilloedema (bilateral, raised ICP), optic neuritis, anterior ischaemic optic neuropathy (GCA — often pale swollen disc), malignant hypertension, or pseudopapilloedema; pallor (optic atrophy, CRAO); cupping — C/D ratio alone is not diagnostic of glaucoma (asymmetry, rim thinning/notching, fields and IOP considered together). Retina: haemorrhages, exudates (e.g. widespread retinal haemorrhages in CRVO). A normal direct ophthalmoscopy does not exclude retinal pathology.
Temporal arteries
In all patients >50 with new vision loss: palpate temporal arteries bilaterally — tenderness, thickening, beading, absent pulsation → GCA until proven otherwise; a normal pulse or non-tender artery does not exclude GCA
Neurological examination
Cranial nerves III, IV, VI (diplopia, ptosis, eye movements); facial sensation (V); visual field defects vs central scotoma; BP measurement (hypertensive emergency retinopathy)
The RAPD (swinging light test) is the single most important GP examination finding for vision loss — it detects unilateral optic nerve or severe retinal dysfunction with high sensitivity and costs nothing. A positive RAPD with acute vision loss in a patient over 50 is GCA or CRAO until proven otherwise. Fundoscopy can change management in acute vision loss — a pale disc with cherry-red spot = CRAO; a swollen disc needs urgent specialist assessment. Documenting VA formally is clinically important — "vision seems reduced" is inadequate in a referral letter. Suspected true papilloedema (bilateral disc swelling with headache, vomiting, reduced consciousness, focal neurology or transient visual obscurations) requires same-day emergency neurological assessment and imaging.
5
Diagnose

Investigations — Targeted and cause-appropriate

Suspected GCA — urgent
CRP + ESR or plasma viscosity + FBC; U&E/LFTs if appropriate, before or shortly after treatment. A normal ESR or CRP does not exclude GCA. Do not wait for results before starting steroids. Temporal artery ultrasound and/or biopsy via the local fast-track GCA service — do not delay corticosteroids while awaiting either.
Vascular causes (CRAO/CRVO/amaurosis)
BP both arms; ECG (AF → embolic source); FBC; HbA1c; cholesterol; urgent vascular imaging and cardiac assessment through the local TIA/stroke pathway (timing per NICE and local hyperacute stroke arrangements). RVO: BP, diabetes assessment, lipids, FBC, renal function where appropriate, other tests by history and age — no routine thrombophilia testing; RVO is not itself an indication for anticoagulation (RCOphth).
Diabetic retinopathy
HbA1c; BP; eGFR + ACR; lipids. NHS Diabetic Eye Screening Programme (DESP): annual, or every 2 years for people with no retinopathy on their two most recent screens (England, since October 2023) — GP to ensure enrolment and act on the screening report via the local pathway. Not every screen-detected abnormality needs ophthalmology referral; DESP grading differs from hospital eye-service monitoring (NICE NG242). New visual symptoms → urgent assessment.
Optic neuritis
MRI brain + orbits is specialist-requested — urgent neurology/ophthalmology referral. Differentials: MS, MOG-associated disease, NMOSD, compressive or ischaemic optic neuropathy, infection, inflammatory disease. Do not request MRI independently without specialist input. VEPs (visual evoked potentials) — specialist-led.
Glaucoma investigations
IOP (tonometry); OCT retinal nerve fibre layer; Humphrey visual field testing; gonioscopy — all ophthalmology-led. Referral should be based on primary-eye-care testing, not C/D ratio alone: optic nerve-head damage, reproducible glaucomatous visual-field defect, or IOP ≥24 mmHg on Goldmann-type applanation (repeat unless urgent) — not non-contact tonometry alone (NICE NG81). Do not start glaucoma drops in primary care.
AMD investigations
Self-monitoring for new distortion, blurred/grey patches, reduced central vision or objects appearing smaller (Amsler grid may be offered where useful); OCT macula (ophthalmology); no blood tests required for AMD diagnosis. Suspected wet AMD → urgent macula service, normally within 1 working day (not an emergency — NICE NG82).
Do NOT routinely
CT head for isolated monocular pathology without neurological features; fluorescein angiography (specialist-only); carotid duplex outside TIA pathway; PET-CT in primary care; thrombophilia screen for isolated RVO; GP-requested MRI for optic neuritis
ESR and CRP must not delay steroids in suspected GCA — the principle of "treat first, investigate second" applies here unambiguously. Temporal artery biopsy remains positive for up to 2 weeks after starting steroids, so treatment does not invalidate biopsy. ESR or CRP can be normal in GCA — do not use a normal ESR to exclude GCA if clinical suspicion is present. For CRAO and amaurosis fugax, the TIA pathway provides rapid carotid imaging (to detect ipsilateral carotid stenosis requiring endarterectomy), cardiac monitoring (24h ECG for AF), and antiplatelet therapy. Hydroxychloroquine: annual retinal monitoring generally begins after 5 years of use, or after 1 year if high-risk features (dose >5 mg/kg/day based on actual body weight, eGFR <60, tamoxifen or chloroquine), using OCT and fundus autofluorescence with fields and/or mfERG as indicated (RCOphth) — the prescriber ensures the monitoring referral is made.
6
Refer

Referral Criteria — The most time-critical referrals in general practice

999 / Immediate
Visual loss with facial droop, dysarthria, weakness, ataxia, reduced consciousness or severe headache; sudden binocular loss with neurological features; penetrating eye injury or severe ocular trauma; chemical injury with systemic toxicity, severe bilateral exposure or inability to irrigate safely; instability or unsafe transfer
Same-day Ophth A&E
Sudden persistent monocular loss (e.g. CRAO — via local eye-emergency/stroke pathway); acute angle closure (painful red eye + reduced vision + haloes + nausea/abnormal pupil); retinal detachment symptoms (curtain/shadow, new field defect); shower of floaters, flashes or vitreous haemorrhage (urgent retinal assessment even if examination normal — PVD cannot be distinguished from a tear without dilated examination); GCA with visual symptoms; painful photophobic red eye with reduced vision; contact-lens keratitis; fever/proptosis/ophthalmoplegia (orbital cellulitis); suspected optic neuritis. Use the local urgent eye-care service where it provides same-day assessment.
Same-day — TIA pathway
Transient monocular visual loss presumed vascular = suspected TIA → refer immediately for specialist assessment within 24 hours (NICE NG128); do not use ABCD2 to downgrade urgency
Same-day — GCA protocol
Age >50 + vision loss + headache / jaw claudication / tender temporal artery → Give the local emergency GCA regimen now (usually prednisolone 60 mg OD with visual symptoms) + same-day ophthalmology/rheumatology. Do not await ESR result. Without visual symptoms: usually 40–60 mg + urgent fast-track GCA service.
Urgent Ophthalmology (24–48h)
Suspected acute anterior uveitis — same-day ophthalmology, not next-day (painful photophobic red eye, consensual photophobia, irregular pupil); central retinal vein occlusion (no acute vascular intervention but urgent); unexplained optic-disc swelling without features of raised ICP
Suspected cancer: Ophthalmology
Suspected ocular melanoma on ophthalmoscopy (NICE NG12 (updated April 2026)); absent red reflex in a child → consider urgent referral for ophthalmological assessment for retinoblastoma, appointment within 2 weeks (NICE NG12); absent red reflex with a new-onset squint → refer immediately (NICE NG127). Unexplained optic-disc swelling → urgent specialist assessment (same-day if papilloedema suspected — see Neurology); unexplained progressive visual loss → urgent ophthalmology
Routine Ophthalmology
Cataract affecting function or quality of life (glare, contrast loss, reading or driving difficulty), considering patient preference and benefit–risk (NICE NG77: no fixed visual acuity threshold); glaucoma or ocular hypertension meeting NICE NG81 referral criteria; dry AMD without new symptoms; suspected wet AMD is NOT routine — NICE NG82: urgent referral to a macula service, normally within 1 working day; hydroxychloroquine monitoring
Neurology / Neurosurgery
Bitemporal hemianopia (urgent MRI pituitary — pituitary adenoma); suspected true papilloedema, especially with headache, vomiting, reduced consciousness, focal neurology or transient visual obscurations → same-day emergency neurological assessment and imaging (modality and lumbar puncture sequence are specialist decisions; no LP until mass lesion and contraindications excluded); new homonymous hemianopia; optic neuritis with MS features
The referral urgency in vision loss is uniquely consequence-laden — a routine referral for a same-day condition can result in permanent blindness within hours. The suspected cancer pathway applies only to suspected intraocular malignancy (uveal melanoma). Everything else with acute vision loss is same-day or emergency. Cataract extraction has one of the lowest QALY costs in all of surgery — do not delay routine referral when VA is functionally impaired. The GP's most critical role in wet AMD is timely recognition and rapid referral — delay in initiating anti-VEGF directly correlates with worse visual outcome. Suspected true papilloedema requires same-day emergency neurological assessment and imaging, not an optometrist referral.
7
Treat

Treatment — Immediate GP-initiated interventions and primary care management

Most definitive treatment is specialist-led. GP role: 1) recognise; 2) immediate first aid where appropriate; 3) arrange the correct urgent referral; 4) communicate relevant history and medication; 5) manage systemic risk factors after specialist diagnosis. Specialist treatments below are for awareness only — not GP prescribing instructions.

Giant Cell Arteritis — vision affected
Prednisolone Start NOW
Visual loss, diplopia or other ischaemic visual symptoms: give the local emergency GCA regimen immediately (usually 60 mg OD) and arrange same-day ophthalmology/rheumatology — IV methylprednisolone may be considered by the hospital team. No visual symptoms: usually 40–60 mg OD depending on presentation and local protocol (BSR 2020). Gastroprotection and bone protection according to fracture risk and steroid duration. Taper over about 18–24 months, rheumatology-led.
Amaurosis fugax (suspected TIA)
Aspirin 300 mg Stat
Give 300 mg only if TIA is considered likely and there is no contraindication or significant bleeding risk, per the local stroke pathway; refer for specialist assessment within 24 h. Persistent CRAO: activate the local stroke/eye-emergency pathway — antiplatelet and lipid-lowering treatment follow stroke/TIA assessment and local protocol; anticoagulation for AF is specialist-led after confirmation. Retinal vein occlusion does not routinely need antiplatelet or anticoagulant treatment.
Chemical eye injury
Immediate irrigation
Start copious irrigation immediately (saline/Hartmann's, or tap water if not immediately available) — before history, VA or detailed examination; do not delay to obtain topical anaesthetic. Remove contact lenses and particulate matter; evert lids. Brush off powdered chemicals first if water activates them. Continue until ocular surface pH is neutral or near-neutral in both eyes, rechecking after irrigation (severe alkali injuries may need much longer); continue during transfer if pH remains abnormal. Do not patch. Consult TOXBASE for unusual chemicals. Arrange urgent ophthalmological assessment.
Diabetic retinopathy (prevention)
Optimise systemic disease
HbA1c target individualised by diabetes type, treatment, frailty, comorbidity, hypoglycaemia risk and preference (NICE NG28/NG17); a rapid substantial fall in HbA1c can temporarily worsen retinopathy — inform the eye team if intensive glucose-lowering is started with significant retinopathy or macular oedema (NICE NG242); BP to NICE NG136 targets (NICE NG17 for type 1 diabetes); atorvastatin 20 mg OD for primary prevention (NICE NG238); ACEi (ramipril) if microalbuminuria; smoking cessation.
Wet AMDAnti-VEGF intravitreal injection (ranibizumab, aflibercept, bevacizumab) — ophthalmology-led. GP role: urgent referral to a macula service, normally within 1 working day (not 999/emergency); treatment generally starts within 14 days where indicated. Regimen (e.g. treat-and-extend) is ophthalmology-led; response varies.
Open-angle glaucomaGlaucoma eye drops (e.g. timolol, latanoprost) — specialist-initiated only; not for GP initiation, including in suspected acute angle closure unless directed by ophthalmology. GP role: watch for systemic beta-blocker effects (bradycardia, bronchospasm in asthmatics, fatigue, depression). Do not prescribe topical timolol in asthma.
Optic neuritis (MS)Specialist-led treatment (e.g. IV methylprednisolone) — hospital/neurology decision, not a GP regimen. Refer urgently to ophthalmology/neurology; MRI is specialist-requested. Not all optic neuritis is MS.
Anterior uveitisSpecialist-directed topical treatment only — ophthalmology-initiated after slit-lamp assessment. GP: do not delay referral; do not prescribe topical steroids without slit lamp examination.

Next steps: see Giant cell arteritis · Stroke and TIA · Glaucoma · Macular degeneration

Prednisolone for GCA must be started by the GP — this is the most time-critical prescribing decision in ophthalmic primary care. Untreated, the other eye can lose vision within days of the first. Starting steroids before biopsy is confirmed by the BSR GCA guideline (2020) as the correct approach. Anti-VEGF treatment can preserve vision in wet AMD, although response varies — the GP's role is rapid recognition and referral, not watching and waiting. Never prescribe topical corticosteroid eyedrops in primary care without ophthalmological assessment — they can worsen undiagnosed herpetic keratitis (dendrite ulcer) and can permanently damage vision.
8
Lifestyle

Prevention and Secondary Prevention — Modifiable risk factors for sight loss

Smoking cessation Smoking is the strongest modifiable risk factor for AMD and increases CRAO/CRVO risk via atherosclerosis. Refer to NHS Stop Smoking Service. Cessation is part of cardiovascular and AMD risk management.
Blood pressure control Treat to NICE NG136 clinic targets (below 140/90 mmHg under 80; below 150/90 mmHg aged 80 and over). Hypertension is the primary modifiable risk factor for CRVO, hypertensive retinopathy, and disc haemorrhages in glaucoma. Manage as part of overall cardiovascular risk.
Glycaemic control Glycaemic control against an individualised HbA1c target reduces retinopathy risk (DCCT / UKPDS). A rapid, substantial HbA1c fall can temporarily worsen retinopathy — inform the eye team if intensive treatment is started with significant retinopathy or macular oedema (NICE NG242).
AMD self-monitoring Advise people with AMD to monitor for new distortion, blurred/grey patches, reduced central vision or objects appearing smaller, and to contact their eye-care professional promptly if these occur. An Amsler grid may be offered where useful. Suspected wet AMD → macula service, normally within 1 working day.
AREDS2 supplements Not for all AMD — benefit depends on disease stage and the fellow eye. Formulations vary (particularly zinc dose); beta-carotene-containing formulations carry smoking-related cautions. Use a product appropriate to the ophthalmologist's advice.
NHS Diabetic Eye Screening Retinal photography for everyone with diabetes aged 12 and over: annual, or every 2 years after two consecutive screens with no retinopathy (England, since October 2023); more often if retinopathy is found. GP responsibility: ensure all diabetic patients are enrolled and attending. Non-attenders require active follow-up — missed screening is a missed opportunity to treat pre-proliferative changes before vision is affected.
Eye protection Safety eyewear for DIY, grinding, and industrial work. UV-protective sunglasses — reduces lifetime UV exposure linked to cataract and AMD. Particularly important post-cataract surgery (no UV protection from intraocular lens).
Regular optician review2-yearly eye tests for all adults (annual if diabetic, glaucoma suspect, or over 70). NHS-funded for those over 60, diabetics, glaucoma suspects. Optometrists detect early glaucoma, AMD, and DR before symptoms develop.
Smoking is the most important modifiable risk factor for AMD — a fact many patients are unaware of. Framing AMD risk as a smoking-related disease resonates more powerfully than generic health messages. AREDS2-type supplementation may benefit selected people with intermediate or advanced AMD as advised by ophthalmology; it is not for all AMD. The NHS Diabetic Eye Screening Programme is one of the most successful public health initiatives in the UK — it identifies and treats sight-threatening diabetic retinopathy before symptoms develop. GP practices should have recall systems ensuring all diabetic patients attend their screening (annual, or every 2 years if low risk). Non-attendance is a significant clinical governance concern.
9
Safety

Follow-Up, Monitoring & Safety-Netting

GCA on steroids
Follow the local GCA fast-track/rheumatology protocol for tapering and relapse management. Primary care: monitor symptoms, visual function, relapse features, blood pressure, glucose, infection risk and steroid toxicity; ensure osteoporosis prevention according to fracture risk and steroid duration.
Post-CRAO / amaurosis
Stroke/TIA service follow-up; vascular imaging and cardiac assessment via the local TIA/stroke pathway; antiplatelet/anticoagulation as directed by the stroke team; cardiovascular risk factor optimisation in primary care; eye follow-up specialist-led
Retinal vein occlusion
Eye follow-up is specialist-led (depends on ischaemia, macular oedema, anti-VEGF treatment and neovascularisation risk). Primary care: systemic cardiovascular risk management; no routine antiplatelet, anticoagulation or thrombophilia testing.
AMD — dry
Hospital ophthalmology review not necessarily required — community optometry and self-monitoring may be appropriate. Supplements only as advised by ophthalmology; lifestyle advice. Educate: new distortion or reduced central vision → prompt eye-care assessment and referral via the macula pathway.
AMD — wet (anti-VEGF)
Ophthalmology-led (regimen such as treat-and-extend set by the macula service). GP: monitor for systemic anti-VEGF effects (hypertension, rarely thromboembolic events); ensure attendance.
Diabetic retinopathy
NHS DESP screening (distinct from hospital eye-service monitoring of established retinopathy). HbA1c and BP reviewed per the individualised diabetes plan. Act on the DESP report and local pathway; treatment (laser, anti-VEGF or observation) depends on the lesion, VA, macular oedema, pregnancy status, OCT and ophthalmology assessment (NICE NG242).
Hydroxychloroquine
Annual retinal monitoring generally begins after 5 years of use, or after 1 year if high-risk features: dose >5 mg/kg/day based on actual body weight, eGFR <60 mL/min/1.73 m², tamoxifen or chloroquine (OCT and fundus autofluorescence; fields and/or mfERG as indicated — RCOphth). Prescriber: ensure the monitoring referral is made, record actual-body-weight dose, review renal function and tamoxifen. Do not stop solely on an uncertain or "possible" result — act on definite toxicity in conjunction with the specialist.
Immediate / 999
Any sudden new persistent visual loss → immediate same-day assessment via the local urgent eye-care or stroke pathway; call 999 if associated with stroke symptoms, severe systemic illness, inability to transfer safely or suspected acute stroke. New neurological deficit or severe headache with vision change → 999. Fever + proptosis + vision loss (orbital cellulitis) → same-day emergency assessment.
Same-day eye service / A&E
New floaters + flashes (even if VA normal — retinal tear); new visual field defect, curtain or shadow; vision that goes dark and then recovers (possible TIA — specialist assessment within 24 h); painful red eye with reduced vision or haloes, or a contact-lens wearer with a painful red eye; aged over 50 with new headache, scalp tenderness or jaw pain on chewing (possible GCA — steroid and same-day assessment); new distortion or reduced central vision in known AMD (prompt — macula pathway); vision loss on GCA steroid taper (relapse)
Referral failsafe
Confirm urgent referrals have been received and attended. Record local eye-emergency, TIA and stroke contact routes.
Driving (DVLA) and support
Advise not to drive while new visual symptoms are present or until acuity and fields have been assessed. A car (Group 1) driver must read a number plate at 20 metres, with acuity of at least 6/12 with both eyes open (glasses allowed), and meet the field standard. The patient must stop driving and tell DVLA if they cannot meet the standard, have a visual field defect, or have a notifiable condition such as AMD or glaucoma affecting both eyes; Group 2 (bus and lorry) standards are stricter. Document the advice. Where sight loss is permanent: low-vision services and certification of visual impairment (CVI).
GCA steroid monitoring is a complex long-term primary care responsibility — relapses are common during taper and require prompt steroid dose increase. Bone protection should be addressed according to fracture risk and steroid duration, following the local GCA pathway. Self-monitoring advice (with an Amsler grid where useful) helps identify wet AMD early: "contact your eye-care professional promptly if straight lines look wavy or your central vision changes".
Educational use only. Recognition, immediate first aid and referral guide; local eye-emergency, TIA and stroke pathways take precedence. Pathway based on: NICE NG128 Stroke and TIA, NICE NG82 AMD, NICE NG81 Glaucoma, NICE QS180 Serious eye disorders, NICE NG242 Diabetic retinopathy, RCOphth Emergency eye care (2024), Angle closure glaucoma (2022), Retinal vein occlusion (2022) and hydroxychloroquine monitoring guidance, EULAR imaging in large vessel vasculitis (2023 update), NICE TA518, BSR GCA Guideline 2020, RCOphth Hydroxychloroquine and Chloroquine Retinopathy: Recommendations on Monitoring (2020), NHS Diabetic Eye Screening Programme, NICE NG81 (Glaucoma 2017), International consensus diagnostic criteria for optic neuritis (Petzold et al., Lancet Neurology 2022, international), NICE NG77 (Cataracts 2017). Always adapt to individual patient context and local pathways.