8.1 Ischemic and Hemorrhagic Stroke Management

Neurocritical care demands rapid assessment and precise pharmacological interventions, particularly in the setting of acute cerebrovascular events. The management of stroke hinges fundamentally on its etiology—ischemic versus hemorrhagic—as the treatment pathways are diametrically opposed.

Acute Ischemic Stroke (AIS)

Acute ischemic stroke results from thrombotic or embolic occlusion of a cerebral artery, leading to a core of irreversibly infarcted brain tissue surrounded by the ischemic penumbra—tissue that is hypoperfused but potentially salvageable. The primary goal of medical therapy is rapid recanalization to restore perfusion to this penumbra.

Thrombolytic Therapy

Intravenous thrombolysis remains a cornerstone for eligible patients within 4.5 hours of symptom onset. While Alteplase (tPA) has historically been the standard, Tenecteplase (TNK) has increasingly become the preferred agent at many comprehensive stroke centers due to its higher fibrin specificity, longer half-life, and ease of administration (single bolus versus bolus plus infusion).

Dosing

• Alteplase: 0.9 mg/kg (maximum 90 mg). Administer 10% as an IV bolus over 1 minute, and the remaining 90% as a continuous infusion over 60 minutes.
• Tenecteplase: 0.25 mg/kg (maximum 25 mg) given as a single IV bolus over 5 seconds. (Note: A 0.4 mg/kg dose has also been studied, particularly prior to thrombectomy, but 0.25 mg/kg is standard for AIS).

Blood Pressure Management in AIS

Blood pressure control is critical to minimize the risk of hemorrhagic conversion of the ischemic infarct.

• Prior to thrombolytics: Blood pressure MUST be < 185/110 mmHg. If elevated, agents like IV Labetalol, Nicardipine, or Clevidipine are utilized.
• During and after thrombolytics: Blood pressure MUST be strictly maintained at < 180/105 mmHg for at least 24 hours post-administration.
• No thrombolytics given: In the absence of thrombolytic therapy or endovascular intervention, permissive hypertension is generally allowed up to 220/120 mmHg for the first 48-72 hours to maintain cerebral perfusion to the penumbra.

Endovascular Thrombectomy (EVT)

For patients with a large vessel occlusion (LVO) in the anterior circulation, EVT is indicated up to 24 hours from last known normal, depending on specific imaging criteria (e.g., DAWN or DEFUSE-3 trials). Thrombolytics should be given prior to EVT if the patient presents within the appropriate time window; they should not delay the procedure.

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Hemorrhagic Stroke

Hemorrhagic stroke encompasses intracerebral hemorrhage (ICH) and subarachnoid hemorrhage (SAH). These carry higher mortality rates than ischemic stroke and require aggressive medical and surgical management.

Intracerebral Hemorrhage (ICH)

ICH involves bleeding directly into the brain parenchyma. The primary concern in the hyperacute phase is hematoma expansion, which is strongly associated with clinical deterioration and death.

Blood Pressure Control

For spontaneous ICH presenting with systolic blood pressure (SBP) between 150 and 220 mmHg, acute lowering of SBP to a target of 140 mmHg is generally recommended and has been shown to be safe, aiming to reduce hematoma expansion. Continuous infusions of nicardipine or clevidipine are preferred for precise titration.

Reversal of Anticoagulation

If the ICH is secondary to anticoagulant use, emergent reversal is paramount:

• Warfarin: 4-factor Prothrombin Complex Concentrate (4F-PCC, Kcentra) is preferred over Fresh Frozen Plasma (FFP) due to faster correction, smaller volume, and lack of requirement for blood typing. Vitamin K (IV, 10 mg) should be co-administered to sustain the reversal.
• Dabigatran: Idarucizumab (Praxbind) 5 grams IV.
• Factor Xa Inhibitors (Apixaban, Rivaroxaban): Andexanet alfa is FDA-approved for reversal. Alternatively, 4F-PCC is frequently used in clinical practice (often at an off-label dose of 50 units/kg) due to the high cost and logistical challenges of Andexanet alfa.

Subarachnoid Hemorrhage (SAH)

Most commonly caused by the rupture of a cerebral aneurysm, aSAH presents classically as a "thunderclap" headache.

Delayed Cerebral Ischemia (DCI) and Vasospasm

Following the initial hemorrhage, patients are at high risk for angiographic vasospasm and delayed cerebral ischemia, typically peaking between days 4 and 14.

To improve neurological outcomes, Nimodipine, a dihydropyridine calcium channel blocker that is highly lipophilic and crosses the blood-brain barrier, is the standard of care.

• Dose: 60 mg PO or via enteral tube every 4 hours for 21 days.
• Crucial Warning: Nimodipine must NEVER be administered intravenously; IV administration has resulted in fatal cardiovascular collapse.
• If hypotension occurs, the dose may be reduced to 30 mg every 2 hours, though the 60 mg every 4 hour regimen is the evidence-based standard.

Management of clinical vasospasm involves maintaining euvolemia and inducing hypertension (often with vasopressors like norepinephrine) to force blood flow through the narrowed vessels, though "Triple-H" therapy (hypervolemia, hemodilution, hypertension) has largely been abandoned in favor of euvolemic hypertension.