πŸ‘οΈ Blurry Vision

RCGP SCA Algorithm β€” UK Primary Care

NICE NG81RCOphth guidelinesCKS Visual problems10-min consult
πŸ‘οΈ
Blurry / Reduced Vision β€” New or Worsening Covers acute visual loss, gradual visual deterioration, diplopia, refractive error, and ocular emergencies
Progress 0 / 9
The full reasoning pathway β€” separate sudden blurring (often sight- or life-threatening) from gradual blurring, and screen for the neurological and vascular causes. Treat the cause and safety-net.StartDecisionInvestigateActionReferStop / Admit
PresentationBlurred vision
Sudden vs gradual, mono vs binocular, transient vs persistent, associated pain/neurology/headache. Examine acuity, fields, fundus, pupils.
Step 1 Β· Safety β€” sudden loss / neuro emergencySudden loss or neurological emergency?
Sudden persistent blur/loss (retinal/optic/vascular) Β· transient (amaurosis = TIA) Β· with headache + neurology (stroke) Β· GCA features Β· acute red painful eye.
YES
Stop Β· EscalateEmergency
Sudden visual loss β†’ emergency ophthalmology. Stroke/TIA features β†’ stroke pathway. GCA β†’ steroids.
NO
AssessClarify what β€œblurred” means
Improves with blinking β†’ dry eye (commonest). Distinguish from scotoma, diplopia, floaters/flashes and distortion. Monocular diplopia (persists with one eye shut) β†’ ocular (cataract); binocular β†’ ocular malalignment (acute β†’ cranial nerve palsy / intracranial lesion). A fixed dilated pupil with a 3rd-nerve palsy is a surgical emergency (aneurysm).
Step 3 Β· common causes
Refractive / cataract
Commonest gradual
Refractive error, cataract; optometry; reassure.
Vascular / retinal
Investigate
Diabetic retinopathy, retinal vein/artery occlusion, AMD; ophthalmology.
Neurological
Do not miss
Optic neuritis, raised ICP (papilloedema), stroke, MS.
Step 6 Β· ReferEscalation
Emergency sudden visual loss / stroke / GCA. Ophthalmology retinal/optic disease; optometry gradual refractive/cataract.
Step 8 Β· treat cause & risk reduction
Step 8 Β· Treat the cause & risk reductionBy diagnosis
Refractive/cataract: optometry, glasses, cataract referral. Diabetic/hypertensive retinopathy: optimise glycaemic control and BP, ensure retinal screening. Vascular risk (stroke/TIA, GCA): smoking cessation, BP/lipid/antiplatelet management. Counsel on DVLA visual standards and not driving if vision is impaired below standard.
Step 9 Β· review & safety-net
Step 9 Β· Review & safety-netRecheck & urgent return advice
Review that referred causes are progressing and chronic disease (diabetes/glaucoma) is monitored. 999 / same-day eye unit for sudden visual loss, transient binocular blur (TIA β€” aspirin + TIA pathway), curtain/shadow or flashes-floaters (retinal detachment), painful red eye with haloes (acute glaucoma), or GCA features aged 50+ (start steroids). Safety-net any new sudden change as an emergency.
⚠️ Sudden blurring is the emergency: transient binocular blur can be a TIA, and sudden monocular loss can be vascular or GCA β€” both need urgent action, unlike gradual refractive change.
1
Safety

Red Flags β€” Ocular Emergencies Not to Miss

Acute visual loss is an ophthalmological emergency until proven otherwise. Speed matters β€” some causes have treatment windows of hours.

Sudden painless monocular visual loss Curtain/shadow coming down, complete loss β†’ 999 Central retinal artery occlusion β€” treatment window 4–6 hours. Also CRVO, retinal detachment
Painful red eye + reduced vision + haloes Mid-dilated fixed pupil, rock-hard eye, vomiting β†’ 999 Acute angle closure glaucoma β€” IOP can reach 60–80 mmHg, irreversible optic nerve damage
Visual loss + headache + scalp tenderness >50y Jaw claudication, temporal artery tenderness β†’ Same-day Giant cell arteritis β€” start prednisolone 60 mg immediately, do not wait for ESR
Binocular visual loss + headache + vomiting Papilloedema, disc swelling β†’ 999 Raised intracranial pressure β€” SOL, pseudotumour cerebri
Floaters + flashing lights + curtain defect New onset, especially myopic patient β†’ Same-day Retinal tear/detachment β€” urgent ophthalmology within 24h (macular-sparing)
Visual loss + facial weakness/slurred speech Sudden onset, other stroke features β†’ 999 Posterior circulation stroke. FAST. Thrombolysis window
Chemical or penetrating eye injury Alkali (cement, bleach) far worse than acid β†’ 999 Irrigate immediately with water/saline for 20 min before transport
Acute visual loss in diabetic patient Sudden vitreous haemorrhage, tractional RD β†’ Same-day Urgent ophthalmology. Proliferative diabetic retinopathy complication

Central retinal artery occlusion is the ocular equivalent of a stroke β€” recanalization therapies (ocular massage, anterior chamber paracentesis, thrombolysis) have a treatment window of 4–6 hours after which retinal ischaemia becomes irreversible. Giant cell arteritis is the most common missed ocular emergency in primary care β€” starting prednisolone immediately (before biopsy) is correct because biopsy results remain positive for 2–4 weeks after starting steroids. Delaying by even 24 hours risks bilateral blindness.

2
Diagnose

Characterise the Visual Problem

Onset & duration
Sudden (<24h): vascular, retinal detachment, acute glaucoma. Subacute (days–weeks): optic neuritis, uveitis. Gradual (months–years): cataract, AMD, glaucoma, refractive error
Monocular vs binocular
Monocular: eye or pre-chiasmal problem (retina, optic nerve, cornea). Binocular: post-chiasmal (brain β€” occipital cortex, visual pathways). Critical distinction
Painful vs painless
Painful: acute angle closure glaucoma, uveitis, corneal disease, optic neuritis (pain on eye movement). Painless: retinal vascular, AMD, cataract, ARMD
Type of blurring
Central: AMD, macular disease. Peripheral/field defect: glaucoma (arcuate), stroke (hemianopia). Floaters/flashing: vitreous/retinal. Halos/starbursts: cataract, refractive error
Diplopia
Monocular (persists with other eye covered): corneal or lens. Binocular (resolves with cover): cranial nerve palsy (III, IV, VI), thyroid eye disease, myasthenia. New-onset binocular diplopia = urgent referral
Medical history
Diabetes (diabetic retinopathy), hypertension (hypertensive retinopathy, CRVO), AF (embolic CRAO), MS (optic neuritis), autoimmune (uveitis), corticosteroids (cataract, glaucoma)
Drug history
Hydroxychloroquine (macular toxicity β€” annual monitoring), amiodarone (corneal deposits), ethambutol (optic neuritis), sildenafil (visual disturbance), tamoxifen (maculopathy)

The monocular vs binocular distinction is the most important early differentiator β€” covering each eye individually in consultation takes 10 seconds and separates ocular pathology from neurological pathology. New binocular diplopia in an elderly patient with hypertension strongly suggests microvascular cranial nerve palsy (III, IV, VI) β€” usually self-limiting but must exclude posterior communicating artery aneurysm (third nerve palsy with ptosis and dilated pupil = aneurysm until proven otherwise). Hydroxychloroquine maculopathy is preventable β€” annual eye checks should be confirmed at every review.

3
Diagnose

Classify the Likely Diagnosis

Refractive error
Gradual bilateral blur (both near and far), improves with squinting, no pain, no other symptoms. Refer optometrist. Most common cause overall
Cataract
Gradual, worse in bright light, halo around lights, monocular diplopia, worse distance vision. Confirmed by ophthalmology. Surgical management
Age-related macular degeneration
Central vision loss (reading, faces), distorted straight lines (metamorphopsia), Amsler grid abnormal. Wet AMD: sudden central loss. Check NICE NG82 pathway
Glaucoma
Peripheral field loss (arcuate scotoma), may be painless and asymptomatic until advanced. IOP may be normal (normal tension glaucoma). Optic disc cupping on fundoscopy
Diabetic retinopathy
Background, pre-proliferative, proliferative stages. National Diabetic Eye Screening Programme β€” annual screening in all DM patients. Vitreous haemorrhage = acute loss
Optic neuritis
Subacute monocular visual loss, pain on eye movement, reduced colour vision (especially red desaturation), RAPD present. Age 20–45, associated with MS in 50%
Dry eye / corneal
Fluctuating blur (improves with blinking/lubricants), gritty sensation, worse in dry/air-conditioned environments. Extremely common β€” check before extensive investigation

Dry eye disease is the most common cause of "blurry vision" in primary care β€” it accounts for 20% of all ophthalmology outpatient referrals and most do not need specialist review. A simple test: ask if vision improves after blinking β€” yes = dry eye/surface disease. AMD affects 600,000 people in the UK and is the leading cause of blindness in over-50s. Wet AMD requires urgent referral for intravitreal anti-VEGF (ranibizumab/aflibercept) β€” treatment within 2 weeks significantly improves visual outcome.

4
Diagnose

Targeted Examination β€” What GPs Can Assess

Visual acuity
Snellen chart at 6 m (or near card). Record best corrected VA (with glasses). 6/6 normal. 6/60 or worse = significant impairment. Pinhole test: improves with pinhole = refractive error
Pupil reactions
Direct + consensual. RAPD (afferent pupillary defect = relative APD using swinging torch test) β†’ optic nerve or retinal pathology (optic neuritis, CRVO, CRAO)
Visual fields
Confrontation fields: compare to examiner's. Bitemporal hemianopia (pituitary lesion), homonymous hemianopia (stroke/space-occupying lesion)
Extraocular movements
Check all 6 directions. Pain on movement β†’ optic neuritis. Limitation β†’ cranial nerve palsy (III = down-out, IV = vertical diplopia stairs, VI = lateral gaze failure)
External eye
Red eye (conjunctiva, cornea, ciliary injection). Proptosis (thyroid eye disease). Lid abnormalities. Corneal haziness (acute glaucoma)
Fundoscopy
Disc (papilloedema, cupping, pallor). Vessels (AV nipping, silver wiring). Macula (drusen = AMD, haemorrhage). Cotton wool spots, flame haemorrhages, neovascularisation
IOP (if tonometer available)
Normal 10–21 mmHg. >30 mmHg = urgent referral. Acute angle closure = IOP typically 40–70 mmHg. Most GPs do not have tonometry β€” refer if suspected

The pinhole test is the most underused tool in primary care β€” it can distinguish refractive error (improves with pinhole) from pathological visual loss (does not improve) in 30 seconds. RAPD is the key sign for optic nerve disease β€” it indicates asymmetric afferent input and is present in optic neuritis, CRVO, and CRAO. A complete third nerve palsy with a dilated pupil (surgical third nerve) must be differentiated from a pupil-sparing microvascular third nerve palsy β€” dilated pupil = aneurysm, emergency CT angiography required.

5
Diagnose

Investigations β€” When to Test What

Suspected GCA
ESR (typically >50, often >100), CRP (elevated), FBC (normochromic anaemia, thrombocytosis). Do NOT wait for results β€” start prednisolone if clinical suspicion high
Vascular visual loss
FBC, ESR/CRP, clotting, lipids, HbA1c, BP, ECG (AF as embolic source), carotid Doppler if TIA-equivalent
Optic neuritis
Refer neurology β€” MRI brain and orbits (gadolinium) to assess MS lesion burden. Do not initiate steroids in primary care (reduces attack duration but not long-term outcome)
Diabetic review
HbA1c, BP, lipids, urine ACR. Confirm National Diabetic Eye Screening appointment up to date (annual). Refer if screen abnormal
Thyroid eye disease
TFTs (TSH, T4, T3), TRAb antibodies (thyroid receptor antibodies). CT/MRI orbits (extraocular muscle enlargement). Refer endocrinology + ophthalmology
Amsler grid
Simple self-monitoring tool for AMD β€” central grid distortion = macular pathology. Provide to all over-50s with gradual central visual loss to self-monitor between appointments
When NOT to investigate
Do NOT order CT head for gradual bilateral blur improving with pinhole β€” this is refractive error, refer optometrist. Do NOT delay prednisolone for ESR in suspected GCA

GCA bloods should be sent simultaneously with starting prednisolone β€” never delay treatment waiting for results. ESR can be normal in 10–20% of GCA, so CRP is essential alongside. In CRAO, 25% have an identifiable cardiac embolic source β€” AF is the most common; ECG and echocardiogram are part of the secondary prevention workup. Optic neuritis MRI demonstrates white matter lesions in 50% of patients at first episode β€” the MRI result determines the 10-year MS conversion risk and guides disease-modifying therapy decisions.

6
Refer

Referral β€” Urgency Stratification

999
Acute angle closure glaucoma, CRAO (4–6h window), chemical eye injury, visual loss + stroke features, eclampsia-related visual loss, orbital cellulitis
Same-day ophthalmology
Suspected retinal detachment (curtain/floaters), vitreous haemorrhage, suspected endophthalmitis (post-procedure), acute uveitis with hypopyon, suspected GCA (start prednisolone + refer)
Urgent <1 week ophthalmology
Wet AMD (sudden central vision loss), new optic disc swelling (papilloedema), central or branch retinal vein occlusion, new proptosis, third nerve palsy with dilated pupil (CT angiography first)
2WW
Painless progressive monocular visual loss with no clear cause β€” exclude intraocular malignancy (uveal melanoma). Unexplained optic atrophy. New afferent pupillary defect
Routine ophthalmology
Suspected cataract (functional impairment), chronic glaucoma (raised IOP found by optometrist β€” refer their letter), stable diabetic retinopathy above background, stable dry AMD
Optometrist (not hospital)
Gradual bilateral blur (refractive error first), mild dry eye, stable mild cataracts, routine glaucoma monitoring (shared care). Saves hospital capacity
Neurology
Optic neuritis (MRI + MS assessment), suspected pituitary lesion (bitemporal hemianopia), myasthenia gravis (fatigable ptosis + diplopia)

The RCOphth pathway for wet AMD requires treatment within 2 weeks β€” each week of delay loses approximately 1–2 lines of vision permanently. Anti-VEGF (ranibizumab, aflibercept) preserves or improves vision in 90% of wet AMD patients when treated promptly. Optometrist-led triage pathways (primary eyecare acute referral services, PEARS) are available in most NHS areas and can see urgent eye problems within 24–48 hours, freeing A&E and ophthalmology capacity for genuine emergencies.

7
Treat

Immediate & Primary Care Treatment

GCA (suspected)
Prednisolone 60 mg OD Start immediately
Do not wait for ESR/CRP. Visual loss already present: 500 mg–1g IV methylprednisolone (admit). Bone protection: alendronate + calcium/VitD. Taper guided by symptoms + CRP
Dry eye
Hypromellose 0.3% drops First-line
4–6Γ— daily, or Carbomer gel (Viscotears) for night-time. Preservative-free if using >4Γ— daily. Omega-3 supplements evidence-based adjunct
Vascular CV risk reduction
Anti-platelet + statin Secondary prevention
Aspirin 75 mg OD (CRAO/BRVO with AF β†’ anticoagulate). Atorvastatin 80 mg. BP control <130/80. Stop smoking. Refer for carotid assessment if CRAO
Acute angle closure (pre-hospital)
999 + position upright Emergency
Lying supine worsens attack. If acetazolamide 500 mg IV available (A&E): use. Pilocarpine 2% topical (if available in surgery). Definitive: laser iridotomy
AcuteIdentify ophthalmic emergency β€” CRAO/acute glaucoma/GCA: 999/same-day. Chemical injury: irrigate immediately. Time is vision
Primary careCardiovascular risk factor control β€” BP, HbA1c, lipids, smoking cessation. Protects against diabetic retinopathy, vascular occlusions, GCA flares
ChronicMonitoring and specialist-initiated treatment β€” anti-VEGF (wet AMD), laser photocoagulation (retinopathy), trabeculectomy (glaucoma) β€” all specialist. GP ensures systemic risk factors controlled

In GCA, the risk of visual loss in the fellow eye without treatment is 30–50% within days β€” starting high-dose prednisolone before biopsy is the correct management. For diabetic macular oedema (the commonest cause of visual loss in working-age adults), HbA1c control is the most important intervention β€” each 1% HbA1c reduction reduces diabetic retinopathy progression by 25%. Intravitreal anti-VEGF for wet AMD costs ~Β£800/injection (6–12 per year) but preserves independence and prevents residential care β€” highly cost-effective NICE approval.

8
Lifestyle

Eye Health & Protective Interventions

Smoking cessation Smoking doubles AMD risk and triples cataract risk. Single most modifiable risk factor for ocular disease. Refer to stop-smoking service. Also increases CRAO/CRVO risk via thrombogenesis.
Glycaemic control (DM) HbA1c <53 mmol/mol (7%) reduces progression of diabetic retinopathy by 25–76% (UKPDS). Every GP consultation with a diabetic patient is an opportunity to optimise HbA1c.
Blood pressure control SBP <130 mmHg reduces retinal vascular events, hypertensive retinopathy, and optic nerve damage. Target more aggressively in diabetic eye disease.
UV protection UV sunglasses and hat reduce cataract risk. UV-B most harmful. Polarised lenses more comfortable. Particularly important post-cataract surgery (lens no longer filters UV).
Diet β€” carotenoids Lutein + zeaxanthin (leafy greens: kale, spinach) reduce AMD progression by 25% (AREDS2 trial). AREDS2 supplement recommended for intermediate AMD by RCOphth.
Screen breaks / 20-20-20 rule Every 20 min, look at something 20 feet away for 20 seconds. Reduces digital eye strain and accommodative spasm. Reduces dry eye from reduced blink rate.
Diabetic eye screening adherence Annual NDESP screening uptake is only 78% β€” at every DM consultation, confirm screening appointment is booked. Unscreened patients are the highest risk for preventable blindness.
Home monitoring (AMD) Amsler grid for AMD patients β€” check weekly. Attend same day if new distortion or central scotoma. Wet AMD can develop from dry AMD rapidly β€” self-monitoring saves vision.

The AREDS2 trial (Age-Related Eye Disease Study 2) demonstrated that supplementation with lutein 10 mg + zeaxanthin 2 mg reduces AMD progression to advanced disease by 18–25% over 5 years. Diabetic eye screening is the most cost-effective preventive intervention in diabetes β€” each case of blindness prevented saves Β£70,000 in social care costs. The 22% of diabetic patients who do not attend screening have 3Γ— higher rates of preventable visual impairment.

9
Safety

Follow-Up, Monitoring & Safety-Netting

GCA β€” steroid taper
Prednisolone: reduce by 10 mg/2 weeks to 20 mg, then 2.5 mg/4 weeks to 10 mg, then 1 mg/4–8 weeks. Monitor CRP at each reduction. Relapse = increase by 5–10 mg. Duration typically 1–2 years
GCA β€” monitoring
BP (steroid-induced hypertension), weight, glucose (steroid-induced DM), bone density (DEXA), osteoporosis prevention (alendronate 70 mg weekly). Annual ophthalmology review
Post-retinal detachment repair
Ophthalmology follow-up. Driving restrictions (6 weeks standard). Advice on other eye β€” 10% bilateral retinal detachment. Myopes: annual dilated fundoscopy
AMD monitoring
Wet AMD: ophthalmology manages anti-VEGF frequency. Dry AMD: annual review + Amsler grid monitoring. AREDS2 supplement recommendation at intermediate stage
Diabetic retinopathy
Annual NDESP. HbA1c/BP/lipids at every GP review. Refer if screen shows above background changes. Pregnancy: diabetic eye review in 1st trimester and at 28 weeks
Safety-net 999
Any sudden visual loss in one or both eyes, acute painful red eye with cloudy vision, visual loss with headache/vomiting/confusion, any sudden onset binocular visual field loss
Safety-net same-day
New floaters + flashes, sudden central blur in known AMD patient (same-day AMD service), any new RAPD, unexplained progressive visual loss over days
Low vision registration
VA 3/60–6/60: partially sighted. VA <3/60: severely sight impaired (blind). GP can initiate CVI (Certificate of Visual Impairment) via ophthalmologist. Access to benefits, RNIB, rehabilitation

GCA steroid tapers are typically 18–24 months and require careful monitoring β€” relapse rate is 50% if steroids are stopped too quickly. Tocilizumab (IL-6 inhibitor) is now NICE-approved for relapsing/refractory GCA (TA518), allowing faster steroid taper and reducing cumulative steroid-related harm. AMD same-day emergency services (Macular Society) exist in most NHS regions β€” patients should have the service number. Pregnancy dramatically worsens diabetic retinopathy β€” women planning pregnancy should have pre-conception ophthalmology review and tightened glycaemic control.

Educational use only. Based on: NICE NG81 (AMD 2018), NICE NG81, RCOphth Clinical Guidelines, BSR GCA guidelines, National Diabetic Eye Screening Programme, AREDS2 trial data, CKS Visual problems. Always adapt to individual patient context.