Acute ischaemic stroke

Large-artery atherosclerosis

Carotid or intracranial stenosis with thrombosis or artery-to-artery embolism

Cardioembolic

Atrial fibrillation, recent MI with LV thrombus, endocarditis, prosthetic valve, patent foramen ovale

Small-vessel disease

Lipohyalinosis of penetrating arteries causing lacunar infarcts

Other determined

Arterial dissection, vasculitis, sickle cell disease, thrombophilia, reversible cerebral vasoconstriction

Undetermined (cryptogenic)

No cause after full work-up — consider prolonged rhythm monitoring for occult AF

Drug-related

Cocaine, amphetamines, oestrogen-containing contraceptives with additional risk factors

• Stroke is the second leading cause of death and a leading cause of acquired adult disability worldwide.
• Approximately 62% of incident strokes are ischaemic.
• Incidence is rising in younger adults, with hypertension, diabetes and smoking the dominant drivers.

• Hypertension (the single largest attributable risk), atrial fibrillation, diabetes, dyslipidaemia, smoking, obesity, physical inactivity, harmful alcohol, obstructive sleep apnoea, prior TIA or stroke, carotid stenosis, CKD, sickle cell disease.

Normal physiology → mechanism → tissue change → clinical picture

1. 1Normal physiology: cerebral blood flow is autoregulated at roughly 50 mL/100 g/min across a wide pressure range.
2. 2Mechanism: arterial occlusion drops flow below 10-12 mL/100 g/min in the core and 12-20 in the penumbra.
3. 3Tissue change: ATP failure, ionic pump failure, glutamate excitotoxicity, calcium influx, free radical injury and cytotoxic oedema.
4. 4Penumbra biology: electrically silent but structurally viable tissue that is salvageable until collateral flow fails — the target of reperfusion.
5. 5Clinical manifestation: territory-specific deficit; later vasogenic oedema may cause mass effect and herniation.

Gross timeline

Pale soft swollen tissue (12-24 h) → liquefactive necrosis (3-7 d) → cystic cavity with gliosis (weeks-months)

Microscopic

Red neurons at 12 h, neutrophils 1-3 d, macrophages 3-7 d, reactive astrocytosis from 1-2 weeks

Haemorrhagic transformation

Petechial to confluent haemorrhage in reperfused infarct, higher risk after thrombolysis

Imaging correlate

Restricted diffusion within minutes; hypodensity on CT after 3-6 h; loss of insular ribbon early sign

• Sudden unilateral weakness or numbness of face, arm or leg
• Sudden speech disturbance — expressive or receptive aphasia, dysarthria
• Sudden visual loss, hemianopia or diplopia
• Sudden vertigo with ataxia (posterior circulation)
• Onset is abrupt and maximal at onset; progressive onset over hours suggests an alternative diagnosis

• Facial asymmetry, pronator drift, hemiparesis with upper motor neuron pattern
• Hemisensory loss, neglect, gaze deviation, homonymous hemianopia
• Dysarthria or aphasia; NIHSS quantifies severity
• Posterior circulation: nystagmus, crossed signs, Horner syndrome, dysphagia, limb ataxia
• Irregular pulse suggesting atrial fibrillation; carotid bruit

1. 1Establish exact time of onset or last-known-well — this defines eligibility.
2. 2Assess airway, breathing, circulation, glucose (hypoglycaemia is a common mimic) and NIHSS.
3. 3Non-contrast CT head immediately to exclude haemorrhage; add CT angiography to detect large-vessel occlusion.
4. 4Use CT perfusion or MRI diffusion/FLAIR mismatch for late-window or wake-up stroke selection.
5. 5Screen thrombolysis contraindications while imaging is being reviewed.
6. 6Deliver thrombolysis and/or transfer for thrombectomy without waiting for other results.
7. 7Complete aetiological work-up in the stroke unit: ECG and rhythm monitoring, echocardiography, carotid imaging, lipids, HbA1c.

Initial

• Capillary glucose, non-contrast CT head, ECG, FBC, coagulation screen, electrolytes, creatinine, troponin.

Confirmatory / selection

• CT angiography head and neck, CT perfusion or MRI with DWI, carotid duplex.

Severity

• NIHSS, ASPECTS score on CT, swallow screen, repeat imaging at 24 h before starting antithrombotics after thrombolysis.

Aetiology

• Prolonged cardiac monitoring for occult AF, transthoracic echo (TOE if young or embolic pattern), HbA1c, lipids, thrombophilia and vasculitis screen in young stroke.

Intracerebral haemorrhage

Rule in: CT hyperdensity — indistinguishable clinically. Rule out: only by imaging.

Hypoglycaemia

Rule in: low capillary glucose, resolves with glucose. Rule out: normal glucose.

Seizure / Todd paresis

Rule in: witnessed convulsion, postictal state, gradual resolution. Rule out: persistent deficit with matching vascular territory.

Migraine with aura

Rule in: spreading positive visual symptoms, headache, prior similar episodes. Rule out: abrupt maximal negative deficit.

Functional neurological disorder

Rule in: inconsistent examination, Hoover sign. Rule out: cortical signs and imaging correlate.

Sepsis / metabolic encephalopathy

Rule in: global confusion, infection, deranged biochemistry. Rule out: focal territorial deficit.

NIHSS 0-4

Minor stroke

NIHSS 5-15

Moderate

NIHSS 16-20

Moderate-severe

NIHSS ≥ 21

Severe

ASPECTS

10-point CT score of early ischaemic change; low scores predict poorer thrombectomy outcome

TOAST classification

Large-artery, cardioembolic, small-vessel, other determined, undetermined

Immediate

• Airway protection and oxygen only if SpO2 < 94%
• Treat hypoglycaemia; avoid hyperglycaemia (target 7.8-10 mmol/L)
• Do not lower blood pressure unless > 220/120 mmHg, or > 185/110 mmHg if thrombolysis is planned
• IV thrombolysis (alteplase or tenecteplase) if eligible and within window
• Mechanical thrombectomy for large-vessel occlusion per imaging selection

Early secondary prevention

• Aspirin 300 mg once haemorrhage excluded (delay 24 h after thrombolysis), then long-term antiplatelet
• Short-course dual antiplatelet therapy for minor stroke or high-risk TIA per guideline
• Anticoagulation for atrial fibrillation, timed by infarct size
• High-intensity statin, blood-pressure lowering after the acute phase, glycaemic optimisation

Procedural

• Decompressive hemicraniectomy for malignant MCA oedema in selected patients ≤ 60-70 years.
• Carotid endarterectomy or stenting for symptomatic ≥ 50-70% stenosis, ideally within 2 weeks.

Supportive

• Stroke unit care, dysphagia screening before oral intake, VTE prophylaxis with intermittent pneumatic compression, early mobilisation, pressure-area care, mood and cognition screening, multidisciplinary rehabilitation.

Monitoring

• Neuro-observations hourly initially, repeat imaging for deterioration, blood pressure trend, glucose, swallow re-assessment, rehabilitation goal review.

Early

• Haemorrhagic transformation, malignant cerebral oedema, seizures, aspiration pneumonia, urinary retention and infection.

Intermediate

• Deep vein thrombosis, pressure ulcers, shoulder pain, spasticity, depression, malnutrition.

Late

• Persistent disability, post-stroke cognitive impairment and dementia, central post-stroke pain, epilepsy, recurrent stroke.

• Roughly a third of patients recover to functional independence, a third are left dependent and a third die within a year in unselected cohorts — reperfusion therapy shifts this substantially.
• Number needed to treat for thrombectomy to reduce disability by one level is around 2.6 in selected large-vessel occlusion.
• Predictors: age, baseline NIHSS, infarct volume, collateral status, time to reperfusion, glucose and comorbidity.
• Recurrence risk is highest in the first 90 days, greatly reduced by early secondary prevention.

• Blood pressure control is the single most effective intervention
• Anticoagulation for atrial fibrillation using a validated stroke-risk score
• Statin therapy, smoking cessation, diabetes control, physical activity, salt reduction
• Carotid intervention for symptomatic significant stenosis
• Public FAST awareness campaigns to shorten onset-to-door time

• Stroke clinic review at 4-6 weeks: risk factors, medication adherence, mood, cognition, driving and work
• Confirm anticoagulation start date and adherence for atrial fibrillation
• Ongoing rehabilitation with measurable functional goals
• Annual review of blood pressure, lipids, HbA1c and lifestyle

Pregnancy

Thrombolysis is not absolutely contraindicated — individualise with obstetric and neurology input

Elderly

Age alone does not exclude thrombolysis or thrombectomy; assess premorbid function

Anticoagulated patients

Thrombolysis contraindicated with therapeutic anticoagulation; thrombectomy remains an option

Young stroke (< 50 y)

Investigate dissection, PFO, thrombophilia, vasculitis, substance use, infective endocarditis

CKD

Careful contrast use with hydration; adjust anticoagulant dosing

Sickle cell disease

Exchange transfusion is a key acute therapy; transcranial Doppler screening in children

• AHA/ASA early management of acute ischaemic stroke (2019 update)
• National stroke pathway and thrombectomy network protocol for your region

• Late-window thrombectomy trials (DAWN, DEFUSE-3) established selection by imaging mismatch rather than clock alone.
• Tenecteplase is a non-inferior, single-bolus alternative to alteplase in several trials.
• Thrombectomy benefit has been extended to large-core infarcts in recent randomised trials.

• AHA/ASA 2019 acute ischaemic stroke guideline (guideline, USA).
• DrZep editorial summary, demo dataset v0.1.