Erfan Bashar
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Stroke Management

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Educational scope notice: This is a study note for medical students, not medical advice, diagnosis, or treatment guidance. Clinical management should follow local protocols and current guidelines.

Acute stroke care is organized around saving the ischemic penumbra, the hypoperfused but still viable tissue around the infarct core. That tissue dies progressively over hours, so every step from arrival to reperfusion is timed. The commonly cited door-to-needle target of under 60 minutes for thrombolysis reflects this physiology rather than an administrative goal.

The emergency pathway

Suspected stroke is triaged with the urgency of major trauma or myocardial infarction. Immediate steps include intravenous access, blood glucose to exclude hypoglycemia as a mimic, electrocardiography, and direct transfer to CT, with blood work drawn in parallel without delaying imaging. Non-contrast CT comes first because it rapidly excludes haemorrhage: blood contraindicates thrombolysis and redirects the pathway toward haemorrhage care, while a blood-free scan with a compatible focal deficit supports a working diagnosis of ischemic stroke.

The National Institutes of Health Stroke Scale, scored out of 42 in current use, standardizes severity across consciousness, gaze, visual fields, facial movement, limb strength, ataxia, sensation, language, dysarthria, and neglect. Higher scores suggest larger or multiple-territory involvement and help weigh reperfusion benefit against risk, alongside time from onset, premorbid status, and imaging. Lack of early improvement suggests persisting occlusion with penumbra still at risk.

Mimics, contraindications, and eligibility windows that gate reperfusion are set out under eligibility and safety (/notes/neurology/stroke-eligibility-safety/).

Thrombolysis

Intravenous alteplase converts plasminogen to plasmin, which degrades fibrin within the thrombus and restores flow. The widely used regimen is 0.9 mg per kg up to a 90 mg maximum, with 10% as a bolus and the remainder infused over 60 minutes, within 4.5 hours of symptom onset. Earlier treatment within that window gives better outcomes. When onset time is uncertain, such as waking with a deficit, imaging of the diffusion-perfusion mismatch may identify patients who can still benefit.

The major risk is symptomatic intracranial haemorrhage in roughly 6–7% of treated patients. Alteplase acts systemically rather than only at the cerebral clot, and the ischemic bed with its injured endothelium is prone to bleed once reperfused. Every decision balances that risk against the penumbra at stake.

Mechanical thrombectomy

Catheter-based thrombectomy retrieves or aspirates clot from proximal arteries, usually reached through femoral or brachial access into the carotid or cerebral circulation. It is often combined with intravenous thrombolysis and extends the treatable window for large-vessel occlusion beyond thrombolysis alone. For large anterior-circulation occlusion at 6 to 24 hours, selection rests on clinical-imaging mismatch as in the DAWN and DEFUSE-3 criteria. Follow-up CT checks for re-occlusion or hemorrhagic transformation, with repeat angiography when indicated.

Blood pressure: two competing risks

Elevated pressure risks hemorrhagic transformation, especially after thrombolysis, while the penumbra depends on mean arterial pressure for collateral perfusion. Targets therefore stay permissive: approximately 160–180 mmHg systolic and 90–110 mmHg diastolic in patients not receiving thrombolysis, with lower targets once a lytic state exists. When intracranial edema is present, pressure is kept toward the higher end to preserve cerebral perfusion against rising intracranial pressure.

Edema, hemorrhagic transformation, and surgery

Cerebral edema typically peaks 3–5 days after onset, and roughly 10–20% of ischemic strokes develop edema needing intervention. Care focuses on factors that raise intracranial pressure, including hypo-osmolarity, hyperthermia, hypercapnia, and hypoxia. The head of the bed stays above 30 degrees to aid venous drainage, and cerebral vasodilators are avoided. Osmotic therapy with mannitol or glycerol is reserved for rising pressure, herniation, or deterioration rather than given prophylactically. Corticosteroids have no demonstrated benefit for cytotoxic stroke edema and are not recommended. When medical measures fail, hemicraniectomy can be life-saving, particularly for malignant middle cerebral artery edema, and ventricular drainage addresses hydrocephalus.

Spontaneous hemorrhagic transformation occurs in roughly 4% after ischemic stroke and rises with larger infarcts, markedly elevated pressure, and antithrombotic or lytic use. Reperfused capillaries with damaged endothelium leak under normal pressure, which is why deterioration after treatment prompts repeat CT.

Stroke-unit care and seizures

Dedicated stroke units improve outcomes through continuous neurological monitoring, early mobilization, swallowing assessment, venous thromboembolism prophylaxis, and prevention of pressure injury and infection. Early detection of deterioration with rapid imaging and neurosurgical input is the mechanism behind the benefit. Mobilization follows a supervised physiotherapist-led exercise model for patients with deficits. Venous thromboembolism needs real prophylaxis rather than stockings alone. Mood is screened and treated because intervention improves long-term outcome.

Early seizures after ischemic stroke are reported in a wide range across studies, in low single digits in unselected cohorts and higher with cortical or haemorrhagic involvement, with roughly 50–78% of those early seizures occurring within the first 24 hours, arising from electrically unstable penumbral neurons, and they worsen outcome by raising metabolic demand during limited supply. Prophylactic anti-epileptic drugs are not recommended without a seizure; recurrent seizures are typically treated, often with levetiracetam.

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