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Vision Loss β€” Acute and Chronic Assessment in Primary Care 9-step diagnostic pathway Β· Ophthalmic emergencies to chronic disease Β· UK GP / RCGP SCA
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The full reasoning pathway β€” sudden vision loss is an emergency: separate painless vascular/retinal causes from painful causes, act within the treatment window (CRAO & GCA), then manage gradual loss and safety-net.StartDecisionInvestigateActionReferStop / Admit
PresentationVision loss
Sudden vs gradual, painful vs painless, monocular vs binocular, transient vs persistent; flashes/floaters/curtain; GCA symptoms. Examine visual acuity, fields, fundus, pupils (RAPD).
Step 1 Β· Safety β€” sight- & life-threateningSudden loss or GCA?
  • CRAO ("stroke of the eye") β€” sudden painless monocular loss, RAPD, pale retina/cherry-red spot
  • Giant cell arteritis β€” vision loss + headache/jaw claudication/scalp tenderness, ↑ESR/CRP (can blind both eyes within days)
  • Retinal detachment β€” flashes, floaters, a "curtain"; vitreous haemorrhage; wet AMD
  • Amaurosis fugax (transient) β†’ TIA Β· acute angle-closure glaucoma (painful)
YES β€” emergency
Stop Β· escalateEmergency ophthalmology
Sudden loss β†’ same-day emergency eye unit. Suspected GCA β†’ high-dose prednisolone immediately + urgent ESR/CRP + ophthalmology/rheumatology. Amaurosis fugax β†’ TIA pathway (aspirin 300 mg).
NO β€” characterise
Step 2 Β· AssessBy pattern
Acuity, fields, fundoscopy, RAPD localise the lesion; vascular-risk assessment; ESR/CRP if any GCA suspicion.
Step 3 Β· which pattern?
Painless sudden
Vascular / retinal
CRAO, CRVO, retinal detachment (flashes/floaters/curtain), vitreous haemorrhage (diabetic), wet AMD (distortion + central loss).
Painful sudden
Inflammatory
Optic neuritis (pain on eye movement, ↓colour vision, RAPD β€” ?MS), acute angle-closure glaucoma, anterior uveitis.
Gradual
Chronic
Cataract, dry AMD, open-angle glaucoma, diabetic retinopathy, refractive error β†’ optometry/ophthalmology.
Step 7 Β· act on the cause
Step 7 Β· Action β€” within the windowTime-critical for several
  • GCA: start high-dose steroids immediately on clinical suspicion β€” do not wait for ESR/temporal artery biopsy; protects the other eye.
  • CRAO: emergency referral (ocular massage/measures have limited evidence) + treat as a vascular event (secondary prevention, exclude GCA).
  • Retinal detachment / vitreous haemorrhage / wet AMD: emergency/urgent ophthalmology (laser/surgery; anti-VEGF for wet AMD).
  • Optic neuritis: ophthalmology/neurology (MRI, ?MS); cataract/refractive/dry AMD: routine optometry/ophthalmology.
Step 6 Β· escalation thresholds
Step 6 Β· ReferEscalation thresholds
  • Emergency same-day any sudden vision loss, suspected GCA (after starting steroid), retinal detachment, acute glaucoma.
  • TIA pathway amaurosis fugax (transient monocular loss).
  • Ophthalmology / optometry gradual loss (cataract, AMD, glaucoma, diabetic retinopathy).
Step 8 Β· risk reduction & support
Step 8 Β· Risk reduction & supportProtect the remaining vision
Cardiovascular-risk control (BP, lipids, diabetes, stop smoking) for retinal vascular disease and AMD Β· diabetic retinopathy screening Β· attend optician for glaucoma/refractive monitoring Β· low-vision services, registration (CVI), and driving (DVLA) advice where vision is affected Β· AREDS supplements for appropriate AMD.
Step 9 Β· safety-net & DVLA
Step 9 Β· Safety-net, follow-up & drivingWhen to come back
Emergency for any sudden loss, new curtain/flashes/floaters, or vision loss with headache/jaw claudication (GCA). DVLA: advise on visual-standard requirements and notification where vision is affected. Ensure GCA bloods/biopsy and ophthalmology follow-up happen; monitor and treat the underlying vascular risk.
⚠️ Sudden vision loss is time-critical: central retinal artery occlusion is a stroke of the eye, and GCA can blind both eyes within days β€” refer emergently and start steroids immediately if GCA is suspected, before the ESR result.
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Safety

Red Flags β€” Ophthalmic and neurological emergencies

Acute vision loss is an emergency until proven otherwise. Time-to-treatment determines visual outcome. Act immediately β€” assess then act, not the other way around.

Sudden painless monocular loss Central retinal artery occlusion (CRAO) β†’ 999 β€” stroke equivalent. Treatment window 4–6 hrs.
Sudden painless binocular loss Bilateral simultaneous loss β†’ posterior circulation stroke (basilar artery) β†’ 999
Painful red eye + vision loss + halos Acute angle-closure glaucoma β†’ 999 A&E. IOP up to 60–80 mmHg; permanent damage within hours.
Temporal headache + jaw claudication + age >50 Giant cell arteritis β†’ Same-day: start prednisolone 60 mg IMMEDIATELY + same-day ophthalmology.
Vision loss + neurological symptoms Diplopia, dysarthria, facial droop, limb weakness β†’ posterior stroke / SOL β†’ 999
Curtain / shadow across visual field Moving curtain or shadow in vision β†’ retinal detachment β†’ same-day ophthalmology A&E
Amaurosis fugax Transient monocular blindness (seconds to minutes, fully resolving) β†’ TIA β†’ same-day TIA pathway (NICE NG128)
Chemical eye injury Alkali or acid splash β†’ irrigate immediately Γ— 30 min BEFORE transfer β†’ 999 / A&E. Do not patch.
Vision loss is one of the highest-stakes presentations in general practice. CRAO is the ocular equivalent of ischaemic stroke β€” emergent intervention within 4–6 hours (IOP-lowering, ocular massage, vascular interventions at specialist centres) may restore vision. Giant cell arteritis is the most preventable cause of permanent blindness in adults over 50 β€” starting high-dose corticosteroids immediately, before biopsy results, is correct management. Delay of even 24 hours risks bilateral permanent blindness. Retinal detachment involving the macula ("macula-off") carries a much worse visual prognosis β€” 90% surgical success if treated within 24 hours, dropping significantly beyond 72 hours. Amaurosis fugax is a TIA β€” 10% stroke risk in the next 48 hours without treatment.
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Diagnose

History β€” 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) β†’ vascular (CRAO, CRVO, GCA, vitreous haemorrhage). Hours–days β†’ inflammatory/infective. Weeks–months β†’ chronic (AMD, glaucoma, cataract, DR)
Laterality
Unilateral β†’ ocular or optic nerve pathology. Bilateral simultaneous β†’ neurological (occipital cortex, bilateral optic nerves). Bilateral sequential β†’ GCA, MS, systemic
Type of visual loss
Central scotoma β†’ macular disease (AMD, CRAO central). Peripheral loss β†’ glaucoma, retinitis pigmentosa. Curtain/shadow β†’ retinal detachment. Hemianopia β†’ stroke, pituitary tumour
Pain
Painful loss β†’ acute angle-closure glaucoma (severe), anterior uveitis (moderate), optic neuritis (ache on eye movement), orbital cellulitis, scleritis. Painless β†’ most posterior causes.
Floaters and flashes
New floaters + photopsia (flashes) β†’ posterior vitreous detachment (PVD) or retinal tear. Dense sudden floaters + vision loss β†’ vitreous haemorrhage. "Floater shower" β†’ urgent same-day review
Systemic associations
Temporal headache + scalp tenderness + jaw claudication β†’ GCA. Neurological symptoms β†’ stroke / MS. Rash + uveitis β†’ 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 (macular toxicity β€” requires annual ophthalmology monitoring); 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 β€” 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 β€” 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) β€” this is the hallmark of macular disease and AMD conversion from dry to wet.
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Diagnose

Classification β€” Acute vs chronic and anatomical localisation

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

Examination β€” Focused ophthalmological and neurological assessment

Visual acuity (VA)
Snellen chart at 6m or Snellen card at 3m. Each eye separately. With correction if available. Document as 6/6, 6/9 etc. Baseline for all referral letters β€” medicolegally essential.
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.
Pupils β€” RAPD test
Swinging light test: RAPD (relative afferent pupillary defect) present β†’ unilateral optic nerve disease (GCA, CRAO, optic neuritis). Both pupils dilate when light swings to affected eye.
Colour vision
Ishihara plates if available β€” red colour desaturation on affected side β†’ 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 β†’ raised ICP; GCA β€” pale swollen disc); pallor (optic atrophy, CRAO); cupping (glaucoma C/D ratio >0.6). Retina: haemorrhages, exudates, "stormy sunset" (CRVO).
Temporal arteries
In all patients >50 with new vision loss: palpate temporal arteries bilaterally β€” tenderness, thickening, beading, absent pulsation β†’ GCA until proven otherwise
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 β€” 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 changes management in up to 25% of patients with acute vision loss β€” a pale disc with cherry-red spot = CRAO; a blurred disc = papilloedema (neurosurgical emergency). Documenting VA formally using Snellen is a medicolegal minimum β€” "vision seems reduced" is inadequate in a referral letter or if a complaint arises. Papilloedema (bilateral blurred disc margins, absent venous pulsation, haemorrhages) indicates raised ICP and requires same-day neurosurgery referral.
5
Diagnose

Investigations β€” Targeted and cause-appropriate

Suspected GCA β€” urgent
ESR (usually >50, often >100) + CRP + FBC (normochromic normocytic anaemia common). Do not wait for results before starting steroids. Temporal artery biopsy arranged by ophthalmology/rheumatology within 1–2 weeks.
Vascular causes (CRAO/CRVO/amaurosis)
BP both arms; ECG (AF β†’ embolic source); FBC; HbA1c; cholesterol; carotid duplex (via TIA pathway); thrombophilia screen if young + CRVO
Diabetic retinopathy
HbA1c; BP; eGFR + ACR; lipids. Annual NHS Diabetic Eye Screening Programme (DESP) β€” GP to ensure enrolment. Ophthalmology if symptomatic or screen-detected changes.
Optic neuritis
MRI brain + orbits with gadolinium β€” urgent neurology/ophthalmology referral. Do not request MRI independently without specialist input. VEPs (visual evoked potentials) β€” specialist-led.
Glaucoma investigations
IOP (tonometry); OCT retinal nerve fibre layer; Humphrey visual field testing; gonioscopy β€” all ophthalmology-led. GP role: identify and refer suspects (cupped disc, family history, IOP concern).
AMD investigations
Amsler grid (simple home monitoring β€” provide to all AMD patients); OCT macula (ophthalmology); no blood tests required for AMD diagnosis. Refer for anti-VEGF if wet AMD suspected.
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
ESR and CRP must not delay steroids in suspected GCA β€” 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 is normal in approximately 10% of GCA β€” 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 requires annual ophthalmological screening from year 5 of use (RCOphth 2018 guideline) β€” this is a GP prescribing responsibility to ensure monitoring is in place.
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Refer

Referral Criteria β€” The most time-critical referrals in general practice

999 / Immediate
Sudden painless vision loss (CRAO β€” stroke equivalent); bilateral acute loss (posterior stroke); chemical eye injury; penetrating eye injury; vision loss + neurological deficit
Same-day Ophth A&E
Acute angle-closure glaucoma (red eye + fixed mid-dilated pupil + halos + nausea); retinal detachment (curtain/shadow defect); vitreous haemorrhage (dense sudden floaters + VA loss); GCA with vision affected
Same-day β€” TIA pathway
Amaurosis fugax (any transient monocular visual loss, now fully resolved) β†’ TIA clinic or SDEC within 24 hours per NICE NG128
Same-day β€” GCA protocol
Age >50 + vision loss + headache / jaw claudication / tender temporal artery β†’ Start prednisolone 60 mg OD NOW + same-day ophthalmology. Do not await ESR result.
Urgent Ophthalmology (24–48h)
Anterior uveitis (red eye + photophobia + reduced VA + keratic precipitates); optic neuritis; central retinal vein occlusion (no acute vascular intervention but urgent); orbital cellulitis
2WW Ophthalmology
Suspected intraocular tumour (uveal melanoma β€” pigmented choroidal lesion); unexplained optic disc swelling; unexplained progressive unexplained visual loss in any age
Routine Ophthalmology
Symptomatic cataract (VA <6/18 affecting function or driving); chronic open-angle glaucoma (suspect or known, poorly controlled); wet AMD (anti-VEGF initiation); hydroxychloroquine monitoring
Neurology / Neurosurgery
Bitemporal hemianopia (urgent MRI pituitary β€” pituitary adenoma); papilloedema (CT head same day β€” raised ICP, space-occupying lesion); optic neuritis with MS features
The referral urgency in vision loss is uniquely consequence-laden β€” a routine referral for a same-day condition can result in permanent blindness within hours. The 2WW 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 β€” 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 β€” delay in initiating anti-VEGF directly correlates with worse visual outcome. Bilateral papilloedema on fundoscopy is a neurosurgical emergency requiring same-day CT head, not an optometrist referral.
7
Treat

Treatment β€” Immediate GP-initiated interventions and primary care management

Most definitive treatment is specialist-led. The GP's role is immediate life-saving/sight-saving initiation and optimal systemic disease management.

Giant Cell Arteritis β€” vision affected
Prednisolone Start NOW
60 mg OD if vision is affected (or 500 mg IV methylprednisolone if already lost vision β€” hospital admission). 40 mg OD if no vision loss yet. Add PPI (omeprazole 20 mg OD), calcium + vitamin D, bisphosphonate (alendronate 70 mg weekly). Slow taper over 1–2 years under rheumatology/ophthalmology.
Amaurosis fugax / CRAO
Aspirin 300 mg Stat
300 mg loading dose immediately. Then 75 mg OD. Activate TIA pathway. Clopidogrel if aspirin-intolerant. Statin (atorvastatin 80 mg OD). Anticoagulate if AF confirmed (DOAC).
Chemical eye injury
Immediate irrigation
Irrigate immediately with tap water or saline β‰₯30 minutes before transfer. Check pH (litmus paper) β€” aim for neutral 7.0. Alkali burns penetrate deeper than acid. Transfer to A&E after irrigation.
Diabetic retinopathy (prevention)
Optimise systemic disease
HbA1c <48 mmol/mol (7%); BP <130/80 mmHg; atorvastatin 20–40 mg OD; ACEi (ramipril) if microalbuminuria; smoking cessation. Reduces progression to sight-threatening DR by ~50%.
Wet AMDAnti-VEGF intravitreal injection (ranibizumab, aflibercept, bevacizumab) β€” ophthalmology-led. GP role: rapid referral, no delay. Treatment typically monthly for 3 doses then PRN. Preserves or improves vision in >90% if treated promptly.
Open-angle glaucomaTimolol 0.25% BD eyedrops (or latanoprost 0.005% nocte) β€” ophthalmology-initiated. GP role: watch for systemic beta-blocker effects (bradycardia, bronchospasm in asthmatics, fatigue, depression). Do not prescribe topical timolol in asthma.
Optic neuritis (MS)IV methylprednisolone 1g Γ— 3 days β€” hospital/neurology-initiated. Speeds recovery but does not improve final visual acuity. Refer urgently for MRI brain + ophthalmology opinion.
Anterior uveitisTopical prednisolone acetate 1% hourly + cyclopentolate 1% TDS (mydriasis to prevent posterior synechiae) β€” ophthalmology-initiated. GP: do not delay referral; do not prescribe topical steroids without slit lamp examination.
Prednisolone for GCA must be started by the GP β€” this is the most time-critical prescribing decision in ophthalmic primary care. The contralateral eye loses vision in 30% of untreated GCA cases within days of the first affected eye. Starting steroids before biopsy is confirmed in NICE NG80 (GCA guideline 2023) as the correct approach. Anti-VEGF treatment has transformed wet AMD outcomes from inevitable progressive blindness to vision preservation or improvement in the majority β€” the GP's role is rapid recognition and referral, not watching and waiting. Never prescribe topical corticosteroid eyedrops in primary care without ophthalmological assessment β€” they can worsen undiagnosed herpetic keratitis (dendrite ulcer) and can permanently damage vision.
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Lifestyle

Prevention and Secondary Prevention β€” Modifiable risk factors for sight loss

Smoking cessation Smoking doubles the risk of AMD (strongest modifiable risk factor) and increases CRAO/CRVO risk via atherosclerosis. Refer to NHS Stop Smoking Service. Cessation reduces AMD progression risk by 40%.
Blood pressure control Target <130/80 mmHg. Hypertension is the primary modifiable risk factor for CRVO, hypertensive retinopathy, and disc haemorrhages in glaucoma. Each 10 mmHg reduction β†’ 13% lower risk of retinopathy.
Glycaemic control HbA1c <48 mmol/mol (7%) reduces diabetic retinopathy progression by 50% (DCCT / UKPDS). Each 1% HbA1c reduction = 37% reduction in microvascular complications. The single most modifiable DR risk factor.
Amsler grid monitoring Provide Amsler grid to all AMD patients for daily self-monitoring. Any new distortion, waviness, or scotoma β†’ same-day ophthalmology (wet AMD conversion requires urgent anti-VEGF).
AREDS2 supplements For intermediate or advanced AMD in one eye: lutein 10 mg + zeaxanthin 2 mg + vitamin C 500 mg + vitamin E 400 IU + zinc 80 mg. Reduces progression to advanced AMD by 25% (AREDS2 trial).
NHS Diabetic Eye Screening Annual retinal photography for all patients with diabetes. GP responsibility: ensure all diabetic patients are enrolled and attending. Non-attenders require active follow-up β€” 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 β€” 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 β€” a fact many patients are unaware of. Framing AMD risk as a smoking-related disease resonates more powerfully than generic health messages. AREDS2 supplementation has robust RCT evidence (NNT approximately 8 to prevent progression to advanced AMD over 5 years) and is cost-effective β€” it should be routinely discussed with AMD patients. The NHS Diabetic Eye Screening Programme is one of the most successful public health initiatives in the UK β€” it identifies and treats sight-threatening diabetic retinopathy before symptoms develop. GP practices should have recall systems ensuring all diabetic patients attend annual screening. Non-attendance is a significant clinical governance concern.
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Safety

Follow-Up, Monitoring & Safety-Netting

GCA on steroids
Weekly: ESR/CRP while tapering. Monthly: BP, glucose, weight (steroid side effects). 3-monthly: DEXA after 3 months (osteoporosis prevention). Rheumatology-led taper over 1–2 years. Relapse = increase prednisolone dose.
Post-CRAO / amaurosis
TIA clinic follow-up; 48-hour carotid duplex; ongoing antiplatelet / anticoagulation; cardiovascular risk factor optimisation; annual ophthalmology review
AMD β€” dry
Annual ophthalmology review; Amsler grid daily; AREDS2 supplements; lifestyle advice. Educate: any new distortion β†’ same-day ophthalmology (wet conversion).
AMD β€” wet (anti-VEGF)
Ophthalmology-led: monthly injections initial 3 months then PRN. GP: monitor for systemic anti-VEGF effects (hypertension, rarely thromboembolic events); ensure attendance.
Diabetic retinopathy
Annual NHS DESP. HbA1c and BP at every GP appointment. Ophthalmology if screen detects R2 (pre-proliferative) or R3 (proliferative) changes β€” laser or anti-VEGF.
Hydroxychloroquine
Annual ophthalmological review from year 5 of use (RCOphth 2018). GP to flag on repeat prescription. Discontinue if maculopathy detected.
999 now
Any sudden new vision loss (even if previous episodes of vision loss); new neurological deficit; severe headache with vision change; fever + proptosis + vision loss (orbital cellulitis)
Same-day GP / A&E
New floaters + flashes (even if VA normal β€” retinal tear); new visual field defect; Amsler grid distortion in known AMD; vision loss on GCA steroid taper (relapse)
GCA steroid monitoring is a complex long-term primary care responsibility β€” relapses occur in up to 50% of patients during taper and require prompt steroid dose increase. The GP must ensure bone protection is in place from day 1 of steroid therapy (calcium, vitamin D, bisphosphonate) β€” long-term high-dose steroids cause osteoporosis in the majority without prophylaxis. Patient-held Amsler grids for AMD are one of the most cost-effective safety-netting tools in ophthalmic primary care β€” providing the card and explaining its use at every appointment takes 30 seconds and can save vision. The instruction "come back same day if lines look wavy" is the safety net that identifies wet AMD conversion before irreversible foveal damage occurs.
Educational use only. Pathway based on: NICE NG80 (GCA 2023), NICE NG128 (Stroke/TIA 2022), NICE NG82 (AMD 2018), RCOphth Hydroxychloroquine Guidelines (2018), NICE Diabetic Eye Screening (2016), NICE NG3 (Glaucoma 2017), RCOphth Clinical Guidelines for Optic Neuritis (2022), NICE CKS Acute Vision Loss (2024). Always adapt to individual patient context and local pathways.