Lucan · Conditions

Acute ischaemic stroke

Australian guidance: Stroke Foundation Clinical Guidelines for Stroke Management 2022

1. Definition and epidemiology

Acute ischaemic stroke is a sudden-onset focal neurological deficit caused by interruption of blood supply to a defined region of the brain, lasting more than 24 hours or resulting in imaging evidence of infarction. In Australia, stroke affects approximately 50,000 people annually, with ischaemic stroke accounting for around 80% of all strokes; it is a leading cause of death and acquired adult disability. Aboriginal and Torres Strait Islander Australians experience stroke at roughly twice the rate of non-Indigenous Australians, with onset occurring at younger ages.

2. Pathophysiology

Per Robbins Ch 28 CNS, ischaemic stroke results from cessation of cerebral perfusion below the threshold required to maintain neuronal function and viability. The ischaemic core (perfusion below approximately 10 mL/100 g/min) undergoes irreversible necrosis within minutes, involving both neurones and glia in a pattern termed pan-necrosis. Surrounding the core is the ischaemic penumbra, where perfusion is reduced but sufficient to maintain cell membrane integrity transiently; this tissue is the therapeutic target. Energy failure drives failure of the Na/K ATPase pump, leading to intracellular sodium and water influx (cytotoxic oedema), glutamate-mediated excitotoxicity, calcium influx, and free radical generation. Reperfusion injury can paradoxically accelerate cell death through oxidative and inflammatory mechanisms. The main aetiological categories (TOAST classification) are large artery atherosclerosis, cardioembolism (most commonly from atrial fibrillation), small vessel lacunar disease, other determined aetiology, and cryptogenic.

3. Clinical presentation and diagnostic criteria

The FAST mnemonic (Face drooping, Arm weakness, Speech difficulty, Time to call 000) covers the most common presentations. Focal deficits reflect the vascular territory involved: middle cerebral artery occlusion produces contralateral hemiplegia, hemianopia, and aphasia (dominant) or neglect (non-dominant); posterior circulation strokes present with diplopia, vertigo, ataxia, dysarthria, or altered consciousness. Symptom onset is typically abrupt and maximal at onset. Stroke severity is quantified using the National Institutes of Health Stroke Scale (NIHSS), which should be recorded by a trained clinician on admission. A key diagnostic pitfall is hypoglycaemia, which can mimic stroke and must be excluded by urgent blood glucose measurement before assuming a neurological aetiology.

4. Investigations and AU-specific cutoffs

The order of investigation is driven by urgency of reperfusion eligibility assessment:

1. Urgent brain imaging: All patients who are reperfusion candidates should have imaging immediately; all others should have brain CT or MRI within 60 minutes of arrival. MRI diffusion-weighted imaging is more sensitive than non-contrast CT for early ischaemia and is preferred when diagnostic confirmation is required. If CT is used to identify hyperdense thrombus, thin-slice imaging below 2 mm should be used rather than the standard 5 mm protocol to improve sensitivity for vessel occlusion.
2. CT perfusion: May be added to improve diagnostic and prognostic accuracy, and is required to establish perfusion mismatch criteria for extended thrombolysis windows up to 9 hours.
3. Vascular imaging: CT angiography or MR angiography from aortic arch to cerebral vertex should be performed in all potential thrombectomy candidates to identify large vessel occlusion, and in all patients with carotid territory symptoms for stenosis assessment. Carotid imaging in TIA patients should not be delayed beyond 2 days.
4. ECG: All patients should have ECG on arrival. For embolic stroke of uncertain source, prolonged ambulatory or implantable cardiac monitoring is indicated.
5. Bloods: Full blood count, coagulation screen, electrolytes, renal function, glucose, and lipids. Blood glucose must be checked immediately to exclude hypoglycaemia as a mimic.
6. Echocardiography: Transoesophageal echocardiography is more sensitive than transthoracic for valvular, left atrial, and aortic arch pathology and should be considered where aetiology remains unclear.

Pre-thrombolysis blood pressure cutoff: below 185/110 mmHg is required before and for 24 hours after intravenous thrombolysis. Intensive blood pressure lowering to a target systolic below 140 mmHg in the acute phase is not recommended for ischaemic stroke (strong recommendation against, June 2025 update).

5. Management

Pre-hospital: Suspected stroke with reperfusion potential is a time-critical emergency; ambulance services must dispatch immediately, pre-notify the receiving hospital, and preferably transport directly to a reperfusion-capable stroke unit. In major metropolitan areas, pre-hospital treatment via a mobile stroke unit is recommended.

Stroke unit care: All stroke patients must be admitted to a dedicated stroke unit with an interdisciplinary team, preferably within three hours of onset. Standardised protocols covering fever control, blood glucose management, and swallowing assessment are mandatory.

Reperfusion: For disabling ischaemic stroke within 4.5 hours of onset without contraindications, intravenous tenecteplase 0.25 mg/kg (maximum 25 mg) is first line; if tenecteplase is unavailable, alteplase 0.9 mg/kg (maximum 90 mg) is used. This represents a June 2025 strong recommendation update. Thrombolysis for non-disabling stroke is not recommended. For patients meeting perfusion mismatch criteria, the treatment window extends to 9 hours. Patients with large vessel occlusion of the internal carotid artery, proximal middle cerebral artery (M1 and proximal or dominant M2), or basilar artery should undergo endovascular thrombectomy within 24 hours where feasible, taking into account brain injury extent, premorbid function, and patient and family preferences. Thrombolysis and thrombectomy are not mutually exclusive and should proceed concurrently without either delaying the other.

Acute antithrombotic therapy: Antiplatelet therapy should begin as soon as haemorrhage has been excluded on imaging, unless thrombolysis was given, in which case antiplatelet therapy starts after the 24-hour post-thrombolysis brain scan. For minor ischaemic stroke or high-risk TIA, dual antiplatelet therapy with aspirin plus clopidogrel should be commenced within 24 hours and continued for three weeks. Routine anticoagulation in patients without cardioembolism is not recommended.

Dysphagia: Swallowing must be screened with a validated tool within four hours of hospital arrival and before oral intake; failed screening requires formal assessment by a speech pathologist.

Surgical: Patients aged 60 years and under with malignant middle cerebral artery territory infarction should be considered for decompressive hemicraniectomy within 48 hours.

6. Pharmacology and AU PBS notes

Thrombolytics: - Tenecteplase (Metalyse) 0.25 mg/kg IV bolus, max 25 mg. First-line per June 2025 update. PBS: listed for ST-elevation myocardial infarction; stroke use is currently off-label on the PBS but widely available in stroke centres. - Alteplase (Actilyse) 0.9 mg/kg IV (10% bolus, remainder over 60 minutes), max 90 mg. Use when tenecteplase is unavailable.

Antiplatelet therapy (secondary prevention): - Aspirin 100 mg daily plus clopidogrel 75 mg daily for three weeks post-minor stroke or high-risk TIA, then transition to monotherapy. Both listed on PBS. - Long-term monotherapy options: aspirin 100 mg, clopidogrel 75 mg (PBS Streamlined Authority code 1424 post-stroke/TIA), or combined low-dose aspirin and modified-release dipyridamole.

Anticoagulation for atrial fibrillation: - Direct oral anticoagulants (DOACs) preferred over warfarin for non-valvular AF (PBS Streamlined Authority codes apply: apixaban, rivaroxaban, dabigatran). For valvular AF or inadequate renal function, warfarin targeting INR 2.0 to 3.0. - DOAC may commence within 48 hours of minor to moderate stroke and from day 6 to 7 for major stroke.

Statins: High-potency statin (e.g. atorvastatin 40 to 80 mg, PBS unrestricted) targeting LDL below 1.8 mmol/L for all ischaemic stroke with possible atherosclerotic contribution.

Blood pressure: ACE inhibitors, angiotensin receptor blockers, calcium channel blockers, or thiazide diuretics are acceptable long-term agents; beta-blockers are not first line unless ischaemic heart disease is present.

7. Complications and monitoring

Haemorrhagic transformation: Occurs in up to 40% of ischaemic strokes, more commonly after thrombolysis or thrombectomy. Routine brain imaging at approximately 24 hours post-reperfusion is required to assess this and guide antithrombotic decisions and DVT prophylaxis.

Cerebral oedema: Peak at 48 to 72 hours for large infarcts. Corticosteroids are not recommended. Osmotherapy and hyperventilation may be used as bridging treatment pending neurosurgical consultation. Malignant middle cerebral artery infarction with midline shift requires early neurosurgical review for hemicraniectomy.

Aspiration pneumonia: Consequent on dysphagia; prevented by early swallowing screening and speech pathology referral.

Deep vein thrombosis and pulmonary embolism: DVT prophylaxis decisions are guided by the 24-hour imaging findings; early mobilisation within the stroke unit reduces risk.

Stroke recurrence: Highest risk in the first 48 to 72 hours, particularly after TIA. Early antiplatelet therapy, secondary blood pressure control, statin initiation, and cardiac rhythm monitoring are the primary preventive levers.

Monitoring schedule: NIHSS at admission and 24 hours; blood pressure every 15 minutes during thrombolysis and hourly for the first 24 hours; swallowing screen within 4 hours; brain imaging at 24 hours post-reperfusion; rehabilitation needs assessment within 24 to 48 hours of stroke unit admission.

Written for Australian practice and grounded in the guidance named above. Study material only — not medical advice. Always check against current guidelines.