Stroke Emergency — Recognition, Treatment & Time-Critical Action Guide — Symptoms, Causes & Treatment | MyMedicPlus

A stroke is a sudden-onset neurological deficit caused by disruption of cerebral blood supply — either by arterial occlusion (ischaemic stroke, 87% of cases) causing brain infarction, or by vessel rupture causing haemorrhage (haemorrhagic stroke, 13%). Stroke is the second leading cause of death and the leading cause of adult disability worldwide, affecting 15 million people per year. Every minute of untreated ischaemic stroke, approximately 1.9 million neurons die — emphasising that stroke is the most extreme medical time emergency. A Transient Ischaemic Attack (TIA or 'mini-stroke') causes identical symptoms but resolves within 24 hours. TIA carries a 10% risk of completed stroke within 48 hours and is a neurological emergency requiring same-day specialist assessment. The FAST acronym (Face drooping, Arm weakness, Speech difficulty, Time to call emergency services) is the internationally recognised public awareness tool — early presentation enables thrombolytic therapy (alteplase within 4.5 hours) and mechanical thrombectomy (within 24 hours) that can restore neurological function.

Ischaemic stroke causes: large artery atherosclerosis (carotid or vertebral artery stenosis/occlusion — 25%), cardioembolism (atrial fibrillation — most common cause of embolic stroke — increases stroke risk 5-fold; other cardiac sources: patent foramen ovale, prosthetic valves, endocarditis — 30%), small vessel disease/lacunar infarction (hypertension-related perforating artery disease — 20%), cryptogenic (undetermined — 25%), and other causes (vasculitis, dissection, hypercoagulable states). Haemorrhagic stroke: intracerebral haemorrhage (ICH) — caused by hypertension (most common), cerebral amyloid angiopathy, anticoagulant use, AVM; subarachnoid haemorrhage (SAH) — ruptured berry aneurysm (85%). Modifiable risk factors: hypertension (most important — present in 70-80% of stroke patients), atrial fibrillation, smoking (doubles risk), diabetes, hyperlipidaemia, obesity, excess alcohol, physical inactivity, obstructive sleep apnoea, and cocaine/amphetamines (vasospasm).

Use the FAST acronym to recognize stroke: Face — sudden facial drooping or asymmetry (smile test); Arms — sudden unilateral arm weakness (cannot raise both arms equally); Speech — sudden slurred speech, word-finding difficulty, or inability to understand; Time — time to call emergency services immediately. Additional sudden onset features: visual loss in one eye (amaurosis fugax), half visual field loss (hemianopia), double vision (diplopia), severe dizziness and imbalance (posterior circulation stroke), sudden severe 'thunderclap' headache ('worst headache of my life' — SAH until proven otherwise), loss of consciousness. The key characteristic is SUDDEN ONSET — symptoms come on in seconds to minutes. Stroke symptoms never build up gradually over hours (which would suggest another diagnosis). Neurological examination: hemiplegia, hemisensory loss, aphasia, dysarthria, hemineglect, gaze deviation, ataxia, and Homer's syndrome (posterior circulation).

Non-contrast CT head is performed immediately on arrival — available 24/7 in any acute hospital — to exclude haemorrhage before administering thrombolysis (alteplase causes fatal haemorrhage in haemorrhagic stroke). CT angiography of head and neck (CTA) identifies large vessel occlusion (LVO) suitable for thrombectomy. CT perfusion (CTP) shows ischaemic core (irreversibly damaged) vs. penumbra (salvageable tissue) — guides treatment eligibility in late or wake-up presentations. MRI with diffusion-weighted imaging (DWI) detects ischaemic changes within minutes of onset (more sensitive than CT for early infarction and posterior fossa/brainstem strokes). ECG: identifies atrial fibrillation (most common embolic cause). Blood glucose: hypoglycaemia is a stroke mimic — correct immediately. FBC, coagulation screen, renal function urgently. Echocardiography (TTE/TOE) and 72-hour Holter monitoring for source of embolism in cryptogenic stroke. Carotid Doppler ultrasound for carotid artery stenosis. NIHSS score quantifies neurological deficit severity.

The goal is rapid reperfusion: 'time is brain.' IV alteplase (tissue plasminogen activator, tPA) 0.9 mg/kg IV (max 90mg) within 4.5 hours of symptom onset in eligible ischaemic stroke patients — reduces death and disability by 30%. Tenecteplase (single bolus IV) is increasingly used as an equivalent or superior alternative. Absolute contraindications: haemorrhagic stroke (hence CT first), anticoagulation, recent major surgery, severe thrombocytopaenia, uncontrolled hypertension. Mechanical thrombectomy (endovascular clot retrieval) is the major advance in ischaemic stroke treatment — removes LVO clots via catheter under fluoroscopy, up to 24 hours from onset in selected patients with demonstrated penumbra on imaging; reduces death and severe disability by 40-50%. Stroke unit care (dedicated ward with specialist multidisciplinary team) reduces death and disability by 20% — independent of reperfusion therapy. Haemorrhagic stroke: aggressive BP control (SBP <140 mmHg within 1 hour — INTERACT trial); reverse anticoagulation (Vitamin K + PCC for warfarin; andexanet for apixaban/rivaroxaban); neurosurgical evacuation for select patients; avoid antiplatelets and anticoagulants acutely. SAH: nimodipine 60mg 4-hourly for 21 days (prevents vasospasm); emergency coiling (neurointerventional radiology) or surgical clipping of ruptured aneurysm. Secondary prevention: aspirin 300mg immediately (after haemorrhage excluded); long-term antiplatelet (clopidogrel) or anticoagulation (DOAC for AF); statin; antihypertensive; carotid endarterectomy for symptomatic 70-99% stenosis.

Permanent neurological disability is the most common complication of ischaemic stroke — 50–70% of survivors have some residual deficit at 6 months: hemiplegia or hemiparesis (most common), hemisensory loss, dysphasia (expressive, receptive, or global — depending on hemisphere involvement), homonymous hemianopia, dysphagia (30–50% acutely — requiring nasogastric feeding to prevent aspiration pneumonia), and cognitive impairment or vascular dementia. Cerebral oedema peaks at 48–72 hours in large MCA territory infarcts — massive 'malignant' MCA oedema with midline shift causes transtentorial herniation and death; decompressive hemicraniectomy within 48 hours reduces mortality by 50% and improves functional outcome (DESTINY, HAMLET, and HAMLET trials). Haemorrhagic transformation (petechial haemorrhage into the infarcted territory) occurs in 10–40% of ischaemic strokes, particularly after thrombolysis in large territory infarcts — symptomatic haemorrhagic transformation causing clinical deterioration (sICH) occurs in 3–6% after IV alteplase; 4.5% after thrombectomy alone. Seizures occur in 5–10% within 2 weeks; epilepsy develops in 10% long-term. Aspiration pneumonia from dysphagia affects 25–30% and is the leading cause of early in-hospital stroke mortality. Deep vein thrombosis (DVT) and pulmonary embolism from immobility occur in 20–30% without prophylaxis (LMWH or mechanical devices). Depression is the most prevalent neuropsychiatric complication — affecting 30–50% at 1 year. Stroke recurrence risk is 10% at 1 year and 25–35% at 5 years without secondary prevention; aggressive risk factor modification and antiplatelet/anticoagulant therapy are essential.

Primary stroke prevention: aggressively treat hypertension to below 130/80 mmHg (most impactful intervention — reduces stroke risk 40%). Anticoagulate atrial fibrillation with DOACs (apixaban, rivaroxaban, dabigatran, edoxaban) when CHA2DS2-VASc score is 2+ in men or 3+ in women — reduces AF stroke risk by 64%. Statins for LDL above 3.0 mmol/L or established cardiovascular disease. Quit smoking. Control diabetes. Healthy weight and regular exercise. Limit alcohol to under 14 units weekly. TIA is a medical emergency — urgent same-day assessment and secondary prevention (dual antiplatelet therapy for 21 days, then single antiplatelet; anticoagulation for AF; statin; antihypertensive; CEA for high-grade carotid stenosis) reduces 90-day stroke risk from 10-15% to under 2%.

CALL EMERGENCY SERVICES (999/911/112) IMMEDIATELY if you witness any FAST symptom — facial drooping, arm weakness, or speech difficulty — even if symptoms appear to improve. Do not drive — time wasted reaching hospital independently can mean the difference between thrombolysis eligibility and permanent disability. Note the EXACT time symptoms began (for thrombolysis eligibility) — if the patient woke up with symptoms, last known well time is when they went to sleep. TIA (symptoms fully resolved) is also a medical emergency: go to the emergency department the same day — do NOT wait to see your GP. Severe 'thunderclap' headache (worst ever, instantaneous onset) requires emergency assessment for subarachnoid haemorrhage. Every minute matters in acute stroke.