9.1 Acute Stroke, TIA, & Neurovascular Emergencies

Introduction & Hyperacute Assessment

Acute neurovascular events are medical emergencies where rapid recognition, imaging, and intervention directly dictate long-term functional recovery. In Canada, stroke is a leading cause of adult disability and mortality. The clinical approach to acute neurovascular disease centers on rapid differentiation between ischemic stroke, hemorrhagic stroke, and stroke mimics, followed by time-critical reperfusion therapies.

Initial Triage & Emergency Workup

Upon presentation with hyperacute neurological deficits (onset of focal weakness, facial drooping, speech disturbance, or sensory loss):

1. Stabilize Airway, Breathing, and Circulation (ABCs): Ensure adequate oxygenation ($SpO_2 \ge 94%$) and continuous cardiac monitoring.
2. Check Capillary Blood Glucose Immediately: Hypoglycemia ($<2.8\text{ mmol/L}$) is the most critical and easily reversible stroke mimic. Severe hyperglycemia can also exacerbate ischemic brain injury.
3. Perform Focused Neurological Assessment: Calculate the National Institutes of Health Stroke Scale (NIHSS) score to quantify stroke severity and establish baseline function.
4. STAT Non-Contrast Computed Tomography (NCCT) Head: NCCT must be performed immediately. The primary objective of hyperacute NCCT is not to visualize early ischemic changes, but to rule out intracranial hemorrhage (ICH) prior to initiating antiplatelet or thrombolytic therapy.
5. Computed Tomography Angiography (CTA): CTA of the head and neck (from aortic arch to vertex) should be performed concurrently with NCCT in all acute stroke candidates to detect Large Vessel Occlusions (LVO) eligible for Endovascular Thrombectomy (EVT).

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Ischemic Stroke Thrombolysis & Endovascular Thrombectomy

Ischemic stroke accounts for approximately 85% of all stroke presentations, resulting from thromboembolic arterial occlusion. Canadian Stroke Best Practice Recommendations (CSBPR) emphasize rapid door-to-needle (DTN target $<30\text{ minutes}$) and door-to-groin-puncture times.

Intravenous Thrombolysis

Intravenous thrombolysis degrades fibrin clots by activating plasminogen to plasmin. CSBPR recommends Tenecteplase (TNK) $0.25\text{ mg/kg}$ IV single bolus (maximum $25\text{ mg}$) or Alteplase (tPA) $0.9\text{ mg/kg}$ IV (10% bolus, 90% infusion over 60 minutes, maximum $90\text{ mg}$). Tenecteplase is increasingly preferred in Canadian stroke centers due to rapid single-bolus administration and superior fibrin specificity.

Absolute Contraindications to Intravenous Thrombolysis

• Active internal bleeding or acute bleeding diathesis.
• Prior intracranial hemorrhage (ICH) at any time.
• Known intracranial neoplasm, arteriovenous malformation (AVM), or aneurysm.
• Severe head trauma or intracranial/intraspinal surgery within the preceding 3 months.
• Uncontrolled severe hypertension (SBP $>185\text{ mmHg}$ or DBP $>110\text{ mmHg}$ unresponsive to acute IV antihypertensive therapy).
• Platelet count $<100 \times 10^9\text{/L}$, INR $>1.7$, or elevated aPTT.
• Direct Oral Anticoagulant (DOAC) ingestion within the last 48 hours (unless specific lab assays show no anticoagulant activity or specific reversal agent available).

Endovascular Thrombectomy (EVT)

EVT involves mechanical intra-arterial clot retrieval using stent retrievers or aspiration catheters. It provides dramatic functional benefits for large vessel occlusions.

• Indications: Occlusion of the internal carotid artery (ICA) or proximal middle cerebral artery (MCA M1/M2 segment), pre-stroke modified Rankin Scale (mRS) score 0–1, age $\ge 18$, and NIHSS $\ge 6$.
• Standard Time Window: Within 6 hours of symptom onset.
• Extended Time Window (6 to 24 Hours): Select patients presenting between 6 and 24 hours after last known well (including wake-up strokes) are eligible for EVT if CT Perfusion (CTP) or diffusion-weighted MRI demonstrates a small ischemic core with a large salvageable ischemic penumbra (DAWN and DEFUSE-3 trial criteria).

Exam Trap: Do NOT delay EVT administration while waiting to observe clinical response to IV thrombolysis. If a patient is eligible for both IV thrombolysis and EVT, initiate IV tenecteplase/alteplase immediately and simultaneously dispatch the patient to the angiography suite for EVT ("bridge therapy").

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Permissive Hypertension & BP Management in Acute Stroke

Blood pressure management in hyperacute ischemic stroke requires balancing perfusion of the ischemic penumbra against the risk of cerebral edema or hemorrhagic transformation.

Management Rules

1. Patients Eligible for IV Thrombolysis / EVT: Lower BP to $<185/110\text{ mmHg}$ prior to bolus using short-acting IV agents (Labetalol $10\text{--}20\text{ mg}$ IV, Nicardipine infusion, or Hydralazine). Maintain $<180/105\text{ mmHg}$ for 24 hours.
2. Patients NOT Eligible for Thrombolysis / EVT: Allow permissive hypertension up to $220/120\text{ mmHg}$ for the first 24 to 48 hours. Do not lower blood pressure unless SBP $>220\text{ mmHg}$ or DBP $>120\text{ mmHg}$, or if acute concomitant end-organ damage is present (e.g., acute aortic dissection, acute myocardial infarction, acute pulmonary edema, or hypertensive encephalopathy). When lowering is required, reduce mean arterial pressure (MAP) by no more than 15% in the first 24 hours.

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TIA & Secondary Stroke Prevention

A Transient Ischemic Attack (TIA) is defined as a brief episode of neurological dysfunction caused by focal brain, spinal cord, or retinal ischemia, without acute infarction on tissue imaging (neuroimaging negative). TIA represents an urgent warning sign; up to 10% of TIA patients suffer an ischemic stroke within 90 days, with the highest risk occurring in the first 48 hours.

ABCD2 Risk Stratification Score

• Age $\ge 60$ years (1 point)
• Blood Pressure $\ge 140/90\text{ mmHg}$ at initial evaluation (1 point)
• Clinical Features: Unilateral motor weakness (2 points), Speech impairment without weakness (1 point)
• Duration of Symptoms: $\ge 60$ minutes (2 points), $10\text{--}59$ minutes (1 point)
• Diabetes Mellitus history (1 point)

Patients with high-risk TIA (ABCD2 score $\ge 4$, motor weakness, speech deficit, or fluctuating symptoms) require immediate workup within 24 hours at a rapid-access TIA clinic or emergency department.

Acute Secondary Prevention Protocols

• Dual Antiplatelet Therapy (DAPT): For non-cardioembolic high-risk TIA or minor ischemic stroke (NIHSS $\le 3$), initiate Aspirin $81\text{ mg}$ + Clopidogrel $75\text{ mg}$ daily (following loading doses of Aspirin $160\text{--}325\text{ mg}$ and Clopidogrel $300\text{--}600\text{ mg}$) for 21 to 90 days (based on CHANCE and POINT trials), followed by monotherapy (Clopidogrel or Aspirin). DAPT beyond 90 days increases bleeding risk without incremental benefit.
• High-Intensity Statin: Initiate Atorvastatin $80\text{ mg}$ daily immediately regardless of baseline LDL-C.
• Vascular Imaging: Perform urgent CTA or carotid Doppler ultrasound. If symptomatic carotid artery stenosis is $70%\text{--}99%$, perform Carotid Endarterectomy (CEA) within 14 days of the index event.
• Cardioembolic Workup: Holter monitoring to detect occult Atrial Fibrillation. If atrial fibrillation is identified, initiate Direct Oral Anticoagulant (DOAC: Apixaban, Rivaroxaban, Dabigatran, or Edoxaban) therapy. Delay initiation by 3 to 14 days post-stroke depending on stroke size and hemorrhagic risk.

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Hemorrhagic Neurovascular Emergencies

Intracerebral Hemorrhage (ICH)

Intracerebral hemorrhage results from rupture of small penetrating arteries damaged by chronic hypertension (Charcot-Bouchard microaneurysms) or amyloid angiopathy.

• Clinical Presentation: Sudden focal neurological deficit accompanied by headache, vomiting, rapid elevation of BP, and declining level of consciousness.
• Acute Interventions:
  • BP Reduction: Rapidly lower SBP to a target of $130\text{--}140\text{ mmHg}$ using IV labetalol or nicardipine (avoiding SBP $<110\text{ mmHg}$).
  • Anticoagulation Reversal:
    • Warfarin: IV Vitamin K $10\text{ mg}$ + 4-factor Prothrombin Complex Concentrate (PCC).
    • Dabigatran: Idarucizumab $5\text{ g}$ IV.
    • Factor Xa Inhibitors (Apixaban/Rivaroxaban): Andexanet alfa or 4-factor PCC ($50\text{ units/kg}$).
    • Heparin: Protamine sulfate.
  • Neurosurgical Consultation: Indicated for cerebellar hemorrhage $>3\text{ cm}$ with neurological deterioration, brainstem compression, or hydrocephalus.

Subarachnoid Hemorrhage (SAH)

Subarachnoid hemorrhage is most commonly caused by rupture of a saccular ("berry") aneurysm in the Circle of Willis (most frequent site: Anterior Communicating Artery).

• Clinical Features: Sudden, catastrophic "thunderclap" headache ("worst headache of my life"), reaching peak intensity within seconds, accompanied by vomiting, meningismus (nuchal rigidity, Kernig/Brudzinski signs), photophobia, and transient loss of consciousness.
• Diagnostic Algorithm:
  1. Non-Contrast Head CT: Highly sensitive ($>95%$) within the first 6 hours of headache onset.
  2. Lumbar Puncture (LP): If NCCT is negative or equivocal and clinical suspicion remains high, LP is mandatory. Inspect CSF for xanthochromia (yellowish discoloration of CSF supernatant caused by bilirubin from RBC breakdown), which requires 12 hours from headache onset to reliably develop. Spectrophotometry or centrifuge visual inspection confirms SAH.
  3. Cerebral Angiography (CTA or Digital Subtraction Angiography): Performed to identify the ruptured aneurysm.
• Complications & Management:
  • Vasospasm Prevention: Oral Nimodipine $60\text{ mg}$ q4h for 21 days improves neurological outcomes by preventing delayed cerebral ischemia.
  • Aneurysm Repair: Endovascular coiling or surgical clipping within 24–72 hours to prevent rebleeding.
  • Hydrocephalus: Managed with External Ventricular Drain (EVD).

Clinical Scenario: A 48-year-old female presents to the ED with a severe, instantaneous headache that began 8 hours ago. Her non-contrast CT head is completely normal. The candidate must recognize that a normal CT at 8 hours DOES NOT rule out subarachnoid hemorrhage. The mandatory next step is a lumbar puncture to assess for xanthochromia.