Synopsis
Identify acute ischaemic stroke rapidly, localise the neurological syndrome, and obtain the brain and vascular imaging needed for safe reperfusion decisions without avoidable delay.
- Stroke should be suspected when a focal neurological deficit begins suddenly, even when FAST is negative, symptoms are mild, the patient is young or posterior circulation features dominate.
- Record the exact last-known-well time, not merely the discovery time; wake-up and unknown-onset strokes may still be eligible for advanced-imaging-selected reperfusion.
- Stabilise airway, breathing and circulation, check capillary glucose, temperature, oxygen saturation and seizure activity, but run these actions in parallel with emergency stroke-team activation.
- Urgent non-contrast CT excludes haemorrhage and major structural mimics but can look normal in early ischaemia; a normal scan never rules out acute ischaemic stroke.
- Add CT angiography promptly when thrombectomy could be relevant, and use perfusion CT or MRI-based selection according to the treatment window and the local comprehensive stroke pathway.
- Assess a structured deficit score such as NIHSS while remembering that it can underweight disabling aphasia, hand weakness, gait ataxia and posterior circulation signs.
- Do not routinely lower moderately raised blood pressure before reperfusion assessment; extreme pressure, thrombolysis thresholds and other hypertensive emergencies require protocol-led treatment.
- Keep the patient nil by mouth until a trained swallow screen, avoid unnecessary transfer delay, and repeat examination and imaging if neurological deterioration occurs.
Key red flags
Falling consciousness, vomiting, new pupillary asymmetry or progressive hemiplegia may indicate large infarction, haemorrhagic transformation, seizure or raised intracranial pressure and needs immediate reassessment.
Sudden headache with meningism, anticoagulant use or marked hypertension requires urgent exclusion of intracranial haemorrhage even when focal deficit suggests ischaemia.
Fluctuating brainstem signs, quadriparesis or reduced consciousness can reflect basilar occlusion and should trigger immediate comprehensive-stroke-centre discussion.
Hypoxia, hypotension, severe hypoglycaemia or hyperglycaemic crisis threatens brain and systemic survival and must be corrected alongside imaging, not before calling the stroke team.
A seizure at onset does not exclude stroke; persistent focal deficit or an occlusion on angiography still requires specialist reperfusion consideration.
Investigation priorities
Find immediate mimics and correct physiological variables that worsen cerebral injury.
Management branches
A new sudden focal neurological deficit is present or has only partly improved.
- Activate the acute stroke team, record last-known-well and discovery time, establish premorbid function and obtain a concise witness history.
- Assess airway, breathing, circulation, capillary glucose, oxygen saturation, temperature and seizure activity while securing intravenous access without delaying transfer.
- Document the focal examination and NIHSS, anticoagulant name and last dose, recent procedures, bleeding history and current blood pressure.
- Transfer directly to emergency brain and arterial imaging through the fastest local pathway and keep the patient nil by mouth pending swallow screening.