Transient visual loss

Transient visual loss is loss or disturbance of vision that resolves completely within 24 hours, usually within minutes. It may be monocular (retinal or optic nerve origin) or binocular (cortical origin).

Clinical relevance. Transient monocular visual loss (amaurosis fugax) is a transient ischaemic attack of the retina. The risk of stroke is highest in the first days, with carotid stenosis of 50 to 99 percent the main target. Giant cell arteritis causing transient loss threatens permanent blindness in days.

Classification.

• Monocular: embolic or haemodynamic (carotid, ophthalmic artery, cardiac), giant cell arteritis, vasospasm (migraine), optic disc oedema (transient visual obscurations), glaucoma (intermittent angle closure), ocular surface (dry eye, corneal), and Uhthoff phenomenon.
• Binocular: occipital ischaemia (vertebrobasilar), migraine aura, occipital seizure, hypotension and orthostasis, papilloedema, hypoglycaemia and functional.

Key distinctions. A curtain descending or ascending over seconds with resolution in 1 to 5 minutes indicates retinal embolism. Positive visual phenomena (zigzag lines, scintillation) spreading over 5 to 20 minutes with headache indicate migraine aura. Brief greyouts lasting seconds on standing or bending indicate papilloedema or orthostasis.

History. Which eye (ask the patient to cover each eye after an episode), onset speed, shape (curtain, grey out, central blur, positive phenomena, flashing lights), duration, frequency, trigger (standing, bright light, exercise, hot bath, eye movement, neck position).

Associated headache, nausea, flashes, floaters, double vision, weakness, numbness, speech disturbance, jaw claudication, scalp tenderness, fever, weight loss.

Previous episodes, vascular risk factors, atrial fibrillation, valvular disease, migraine history, medication (vasodilators, phosphodiesterase inhibitors), and eye disease.

Examination. Visual acuity, pupils, fields, fundus (emboli: Hollenhorst plaques; disc swelling; haemorrhages; retinal pallor; vein dilatation), intraocular pressure and anterior chamber depth, blood pressure in both arms and lying and standing, pulse rhythm, carotid and ophthalmic bruits, cardiac murmurs, temporal arteries, and a neurological examination.

Red flags

• Monocular loss lasting seconds to minutes with vascular risk factors (transient ischaemic attack)
• Age over 50 with headache, jaw claudication, scalp tenderness, fever or weight loss
• Neurological symptoms with the episode, or double vision, vertigo or bilateral loss (vertebrobasilar)
• Transient loss followed by permanent loss
• Papilloedema, daily headache with visual obscurations
• Recent neck trauma or pain (carotid dissection)
• Cardiac murmur, fever, or intravenous drug use (endocarditis)
• Positive phenomena with a first aura after age 40, or aura with weakness

Special groups. Pregnancy: pre-eclampsia, venous sinus thrombosis and reversible vasoconstriction. Children: migraine, seizures. Older adults: embolic disease and giant cell arteritis. Region specific: sickle cell disease, HIV and rheumatic heart disease.

Monocular ischaemic and vascular

• Carotid artery atherosclerotic stenosis with embolism, carotid dissection, ophthalmic artery stenosis, ocular ischaemic syndrome
• Cardiac embolism: atrial fibrillation, valve disease, endocarditis, myxoma, patent foramen ovale
• Giant cell arteritis, other vasculitis, antiphospholipid syndrome, hypercoagulable states, hyperviscosity, sickle cell disease, polycythaemia
• Retinal migraine and vasospasm
• Impending central retinal vein occlusion, hypotension with severe carotid disease

Monocular non-vascular

• Papilloedema (transient visual obscurations), optic disc drusen
• Intermittent angle closure glaucoma
• Uhthoff phenomenon (optic neuritis recovering, multiple sclerosis), optic nerve compression with eye position change
• Dry eye, corneal irregularity, tear film instability, lid and lens factors
• Vitreous floaters, posterior vitreous detachment, intermittent vitreous haemorrhage

Binocular

• Vertebrobasilar ischaemia and occipital transient ischaemic attack
• Migraine with aura (visual aura)
• Occipital seizure, posterior reversible encephalopathy syndrome, cerebral venous sinus thrombosis, reversible cerebral vasoconstriction syndrome
• Orthostatic hypotension, arrhythmia, syncope, severe anaemia, hypoglycaemia
• Idiopathic intracranial hypertension, hydrocephalus
• Pituitary lesions, functional and psychogenic causes

Reasoning. Treat transient monocular loss in a patient over 50 as an urgent vascular event until proven otherwise. Examine the eye, the heart and the carotids, and exclude giant cell arteritis the same day.

First line. Vital signs, blood pressure in both arms, lying and standing, 12 lead ECG, capillary glucose, visual acuity, fields and fundus, and temporal artery examination.

Blood tests. Full blood count, ESR, C reactive protein, platelet count, glucose and HbA1c, lipids, urea, creatinine, electrolytes, clotting screen, troponin when indicated, blood cultures with a murmur or fever, thrombophilia and antiphospholipid antibodies in younger patients, and haemoglobin electrophoresis.

Imaging and cardiac tests.

• Carotid duplex ultrasound, CT or MR angiography of head and neck within 24 hours for suspected transient ischaemic attack; MRI brain with diffusion weighted imaging for silent infarction.
• Echocardiography (transthoracic, then transoesophageal or bubble study as indicated) and prolonged ambulatory cardiac rhythm monitoring (up to 14 days, or an implantable loop recorder) to find atrial fibrillation.
• Temporal artery ultrasound or biopsy for suspected giant cell arteritis.
• Fundus photography, optical coherence tomography and fluorescein angiography for retinal disease; automated perimetry and gonioscopy when glaucoma is suspected.
• MRI brain with venography, lumbar puncture with opening pressure (over 25 cmH2O in adults is abnormal) after imaging for suspected idiopathic intracranial hypertension.
• EEG when occipital seizures are suspected.
• Tilt table testing for suspected orthostatic or vasovagal causes.

Limitations. Examination between episodes is often normal. Atrial fibrillation may be paroxysmal and need prolonged monitoring. ESR and C reactive protein can be normal in giant cell arteritis.

Transient monocular loss from suspected embolism (transient ischaemic attack of the retina). Specialist assessment within 24 hours.

• Aspirin 300 mg orally immediately.
• For a high risk event (ABCD2 score of 4 or more, or high risk imaging, with no contraindication), give clopidogrel 75 mg and aspirin 75 mg daily for 21 days. Load with clopidogrel 300 mg when starting dual therapy.
• Then continue single antiplatelet therapy: clopidogrel 75 mg daily preferred, or aspirin 75 mg daily with a proton pump inhibitor in selected patients.
• Atorvastatin 80 mg orally at night, with a subsequent target LDL cholesterol under 1.8 mmol/L.
• Blood pressure control with a long term target under 130/80 mmHg, glucose control, smoking cessation, weight and exercise.
• Symptomatic carotid stenosis of 50 to 99 percent (measured by the NASCET method; benefit is greatest at 70 to 99 percent): carotid endarterectomy within 2 weeks of the event, or stenting in selected patients.
• Atrial fibrillation: anticoagulation with apixaban 5 mg orally twice daily, or another direct oral anticoagulant. Reduce apixaban to 2.5 mg twice daily if two of age 80 or more, weight 60 kg or less, creatinine 133 micromol/L or more. Assess timing and bleeding risk.
• Endocarditis, cardiac source or patent foramen ovale: cardiology and infectious disease care (patent foramen ovale closure considered in young patients with cryptogenic events).

Giant cell arteritis. Prednisolone 40 to 60 mg orally each morning started before biopsy, with aspirin 75 mg daily, a proton pump inhibitor and bone protection. If visual symptoms persist or recur, give methylprednisolone 500 mg to 1 g IV daily for 3 days. Same day specialist review.

Carotid dissection. Emergency stroke care; antithrombotic therapy (aspirin 300 mg orally daily, or anticoagulation) by stroke specialist decision, and imaging of vessels.

Retinal migraine and migraine aura. Exclude vascular causes first. Acute treatment: sumatriptan 50 to 100 mg orally at onset (not during aura alone; contraindicated in ischaemic heart disease, stroke, uncontrolled hypertension and with ergots or monoamine oxidase inhibitors), or ibuprofen 400 to 600 mg or aspirin 900 mg.

Prevention for frequent episodes:

• Propranolol 40 mg orally twice daily increased to a usual 80 to 160 mg daily (maximum 240 mg daily).
• Or amitriptyline 10 mg at night increased by 10 mg weekly to 25 to 75 mg.
• Or topiramate 25 mg at night increased by 25 mg weekly to 50 mg twice daily (halve when creatinine clearance is under 70 mL/min; teratogenic).

Avoid combined oral contraceptives when aura is present (stroke risk).

Papilloedema and idiopathic intracranial hypertension. Weight loss of 5 to 10 percent. Acetazolamide 500 mg orally twice daily increased by 500 mg each week to a maximum of 4 g daily as tolerated (halve when creatinine clearance is 10 to 50 mL/min, avoid under 10 mL/min). Serial visual fields.

Urgent neurosurgical or ophthalmic intervention (optic nerve sheath fenestration or shunting) for threatened vision. Treat any underlying tumour or venous thrombosis.

Intermittent angle closure. Laser peripheral iridotomy by ophthalmology.

Orthostatic hypotension and arrhythmia. Treat the cause. Use fluids 2 to 3 L daily and salt 6 to 9 g daily when no heart failure, renal disease or supine hypertension.

Midodrine 2.5 mg orally three times daily increased weekly to a maximum of 10 mg three times daily (last dose 4 hours before bed), or fludrocortisone 0.05 to 0.1 mg daily increased weekly to a maximum of 0.3 mg daily. Pacing or ablation by cardiology.

Occipital seizures. Levetiracetam 500 mg orally twice daily increased every 2 weeks to a usual 1 to 1.5 g twice daily (maximum 3 g daily).

Or lamotrigine 25 mg daily for 2 weeks then 50 mg daily for 2 weeks, increased by 50 to 100 mg every 1 to 2 weeks to a usual 100 to 200 mg daily.

Uhthoff phenomenon and demyelination. Neurology assessment and MRI; avoid overheating.

Dry eye and ocular surface causes. Lubricants (hypromellose 0.3 percent or sodium hyaluronate 0.1 to 0.2 percent, 1 drop 4 to 6 times daily), lid hygiene and blink training.

Functional visual loss. Explanation after serious causes are excluded.

Driving and safety. Advise not to drive after transient ischaemic attack or visual loss until assessed (local rules vary), and avoid hazardous activities until reviewed.

Monitoring. Repeat blood pressure, glucose and lipids; cardiac monitoring results; carotid imaging; visual acuity and fields; inflammatory markers and steroid effects in giant cell arteritis.

Referral and escalation. Same day for suspected giant cell arteritis or recurrent episodes. Stroke prevention clinic within 24 hours for transient ischaemic attack. Ophthalmology for fundal findings, glaucoma or papilloedema. Vascular surgery for carotid stenosis. Cardiology for embolic cardiac sources. Neurology for migraine, seizures and demyelination.

Admission criteria. Crescendo episodes, high risk transient ischaemic attack with carotid stenosis awaiting urgent surgery, giant cell arteritis with visual loss, suspected endocarditis, hypertensive emergency, or neurological signs.

Discharge and safety netting. Return urgently for permanent visual loss, weakness, speech change, facial droop, double vision, severe headache, jaw pain, or more frequent episodes. Advise on risk factor control and adherence to antiplatelet and statin therapy.