Synopsis
Use the time course and anatomical pattern of visual loss to recognise retinal, optic-nerve and cerebral emergencies, including episodes that have already resolved.
- Establish the exact onset or last-known-well time, duration, recovery and whether symptoms remain present.
- Clarify whether the whole of one eye or the same side of the visual scene was affected; patients may mistake a homonymous deficit for monocular loss.
- Ask about darkness or missing vision as well as positive phenomena such as flashing or spreading zigzags, but avoid treating either category as diagnostic alone.
Key red flags
Abrupt monocular blackout remains urgent after recovery; suspected TIA requires immediate referral for specialist assessment within twenty-four hours of symptom onset, without using ABCD2 to defer review.
Investigation priorities
Establish current deficits and localise the affected visual pathway.
Management branches
A new visual deficit remains present or accompanies an acute neurological syndrome.
- Record onset or last-known-well time and the current deficit, and check glucose and neurological findings where relevant.
- Contact emergency ophthalmology and the stroke service according to the suspected localisation without waiting for a complete outpatient-style eye examination.
Key medicines
Aspirin for a resolved suspected TIAStart 300 mg orally once daily immediately when a clinician suspects TIA, unless contraindicated, and continue pending urgent specialist assessment and an agreed secondary prevention plan.
Glucocorticoids for GCA with ischaemic visual symptomsUnder urgent specialist direction, BSR permits methylprednisolone 500 mg–1 g intravenously once daily for up to three consecutive days, followed by oral prednisolone. If intravenous therapy is not immediately possible, start oral treatment without delay; prednisolone 60–100 mg orally once daily may be used for up to three days, then continue the specialist-directed regimen and eventual taper.