Acute Ischaemic Stroke
Also known as: Stroke, CVA, Cerebrovascular accident

Sudden focal neurological deficit due to interruption of cerebral blood supply, most commonly from thromboembolic occlusion of a cerebral artery. Time-critical emergency; approximately 1.9 million neurons lost per minute of untreated large vessel occlusion.
Classified by mechanism (TOAST classification): large artery atherosclerosis, cardioembolism (notably atrial fibrillation), small vessel occlusion (lacunar), other determined cause (dissection, vasculitis, hypercoagulable states), undetermined cause.
Sudden onset focal neurological deficit; presentation depends on vascular territory:
Anterior circulation (MCA most common): contralateral hemiparesis/hemisensory loss (face/arm > leg), aphasia (dominant hemisphere), neglect/visuospatial dysfunction (non-dominant), homonymous hemianopia
Anterior cerebral artery: contralateral leg > arm weakness, behavioral changes
Posterior circulation: vertigo, diplopia, ataxia, dysarthria, crossed sensory/motor deficits, reduced consciousness, visual field defects; can be subtle and easily misattributed to benign vertigo
Lacunar syndromes: pure motor, pure sensory, ataxic hemiparesis, sensorimotor stroke; typically no cortical signs
FAST recognition tool: Face drooping, Arm weakness, Speech difficulty, Time to call emergency services
NIHSS: standardized severity assessment, guides treatment decisions and prognostication
Onset time is CRITICAL ; establish "last known well" time precisely (not "time found") ; determines eligibility for thrombolysis/thrombectomy
Immediate non-contrast CT head: primary role is excluding hemorrhage (mandatory before thrombolysis); early ischemic changes may be subtle/absent in first few hours
CT angiography: identifies large vessel occlusion; essential if considering mechanical thrombectomy
CT perfusion: assesses core infarct vs. penumbra (salvageable tissue) ; valuable for extended time-window thrombectomy decisions (6-24h)
MRI (diffusion-weighted imaging): more sensitive for early ischemia, useful when onset time unclear (DWI-FLAIR mismatch can suggest stroke <4.5h old)
ECG: identify AF or other arrhythmia as embolic source
Bloods: glucose (exclude hypoglycemia as stroke mimic ; mandatory first check), FBC, coagulation profile (essential before thrombolysis), U&E, troponin
Carotid Doppler/CT angiography neck: assess for carotid stenosis once acute phase managed
Echocardiography: assess cardioembolic source
Differentials (stroke mimics ; up to 30% of suspected strokes): hypoglycemia, seizure with post-ictal (Todd's) paresis, migraine with aura, functional neurological disorder, intracranial mass lesion, hypertensive encephalopathy, syncope, sepsis unmasking old deficit, Bell's palsy.
Hyperacute; time-critical pathway:
Immediate CT head on arrival, glucose check, NIHSS assessment
IV thrombolysis (alteplase or tenecteplase): within 4.5 hours of symptom onset in eligible patients; alteplase 0.9mg/kg (max 90mg), 10% as bolus then remainder over 60 minutes
Key contraindications: hemorrhage on CT, recent major surgery/trauma, active bleeding, anticoagulation with elevated INR/therapeutic DOAC levels, recent ischemic stroke (<3 months), severe uncontrolled hypertension (>185/110 despite treatment), platelet count <100
Extended window (4.5-9h, or wake-up stroke): may be considered with advanced imaging showing salvageable tissue
Mechanical thrombectomy: for confirmed large vessel occlusion, within 6 hours routinely, extended to 24 hours in selected patients with favorable perfusion imaging; can be combined with thrombolysis or standalone
BP management: permissive hypertension generally (do NOT aggressively lower BP ; risk of extending infarct) UNLESS thrombolysis/thrombectomy planned (target <185/110 pre-treatment, <180/105 for 24h post) or BP >220/120 without reperfusion planned
Maintain normoglycemia, normothermia, adequate oxygenation
Post-acute/stroke unit care:
Swallow assessment before any oral intake ; NBM until formally assessed
Antiplatelet therapy: aspirin 300mg started 24 hours after thrombolysis (or immediately if not thrombolysed, once hemorrhage excluded) ; dual antiplatelet for 21 days in minor stroke/high-risk TIA, then single antiplatelet long-term
Anticoagulation for cardioembolic stroke (AF): typically delayed 4-14 days depending on infarct size; DOAC preferred over warfarin in most cases
Statin therapy: high-intensity, started early
VTE prophylaxis: mechanical preferred initially over pharmacological
Long-term BP management: gradual introduction after acute phase
Malignant MCA syndrome: decompressive hemicraniectomy in selected patients
Multidisciplinary rehabilitation: early mobilization, physiotherapy, occupational therapy, speech and language therapy, stroke unit admission (proven mortality/disability benefit).
Secondary prevention: carotid endarterectomy/stenting for significant symptomatic stenosis, anticoagulation for AF, risk factor modification.
Referral: stroke team/neurology immediately on suspicion, neurosurgery for hemorrhagic transformation/malignant edema, cardiology for embolic source workup.


