Malignant Middle Cerebral Artery Infarction

Malignant middle cerebral artery infarction is infarction of at least two thirds of the middle cerebral artery territory with progressive cerebral oedema, midline shift and herniation. Mortality with medical care alone approaches 80%.

It affects about 1 to 10% of patients with supratentorial infarction, mostly after internal carotid or proximal middle cerebral artery occlusion. Younger patients are more at risk because of limited brain atrophy.

Time course. Swelling begins on day 1, peaks between days 2 and 5, and declining consciousness precedes herniation.

Predictors. Early CT hypodensity in over 50% of the territory, NIHSS over 15 for a dominant and over 20 for a non-dominant hemisphere, diffusion weighted imaging volume of 145 cm3 or more within 14 hours, and involvement of other territories.

Pathophysiology.

Cytotoxic oedema evolves into vasogenic oedema with disrupted blood brain barrier, expanding the infarcted hemisphere within a rigid skull. Rising pressure shifts midline structures, compresses the contralateral hemisphere and causes uncal and subfalcine herniation.

Impaired venous outflow and hypoxia worsen swelling and neuronal injury.

• Severe hemiplegia, gaze deviation, hemianopia and hemisensory loss, with global aphasia (dominant) or neglect (non-dominant).
• Progressive drowsiness, headache, vomiting, a dilated pupil and posturing as swelling develops.
• Cushing response and respiratory change late.

Red flags.

• Fall in consciousness in the first 48 to 96 hours.
• New pupillary dilatation or asymmetry.
• Midline shift on repeat imaging.

• Non-contrast CT showing extensive hypodensity and mass effect; repeat CT at 12 to 24 hours and with any deterioration.
• MRI with diffusion weighted imaging volume when available; CT angiography showing proximal occlusion.
• Intracranial pressure monitoring is optional and does not replace repeated clinical assessment.
• Early assessment of life expectancy, premorbid function and preferences for surgery.

Differential diagnosis. Haemorrhagic transformation, space occupying haemorrhage, hydrocephalus, seizure, hyponatraemia, hypoxia and sedative effect.

• Admit to a neurocritical or stroke unit with hourly neurological observations; eligible patients have thrombolysis and thrombectomy before swelling develops.
• Medical measures: head elevation to 30 degrees, avoid hypotonic fluids, hypoxia, hypercapnia, hyperthermia and hyponatraemia, and keep normoglycaemia. Corticosteroids are not effective for infarct oedema, and prophylactic hypothermia is not proven.
• Mannitol 0.25 to 0.5 g/kg intravenously over 15 to 20 minutes, repeated every 4 to 6 hours as needed for up to 48 to 72 hours, as a bridge to surgery. Maximum 1.5 g/kg in 24 hours. Monitor serum sodium and osmolality (stop if over 320 mOsm/kg), renal function and fluid balance. Avoid in anuria, severe dehydration and heart failure; use caution in renal impairment.
• Decompressive haemicraniectomy within 48 hours of onset in patients aged 18 to 60 years with deterioration: it reduces mortality from about 70 to 80% to about 20 to 30% and improves survival with moderate disability.
• Patients over 60 years: surgery increases survival, but most survivors have severe disability, so the decision is individualised through discussion with the family and the patient's wishes.
• Complications: seizures (levetiracetam 500 mg orally or intravenously twice daily, increased as needed to a maximum of 1500 mg twice daily; reduce dose when creatinine clearance is 50 to 80 mL/min to 500 to 1000 mg twice daily, 30 to 50 mL/min to 250 to 750 mg twice daily and under 30 mL/min to 250 to 500 mg twice daily; monitor mood and renal function), aspiration, infection and venous thromboembolism.
• Rehabilitation with early mobilisation, speech therapy and long term support.

Monitoring. Neurological observations hourly for 5 days; repeat CT at 24 hours and with any change; intracranial pressure monitoring only in selected cases.

Referral and escalation. Early neurosurgical referral for any large infarct at risk, before herniation; palliative care input when surgery is declined or not suitable.

Special groups. Older adults: discuss expected disability before surgery. Dominant hemisphere lesions: aphasia affects consent and rehabilitation.