6.2 Acute Ischemic Stroke, Hemorrhagic Stroke & Subarachnoid Hemorrhage
Key Takeaways
- Intravenous thrombolysis with alteplase (0.9 mg/kg) or tenecteplase (0.25 mg/kg) is indicated within 4.5 hours of last known normal (LKN) in acute ischemic stroke.
- Blood pressure thresholds depend on thrombolytic eligibility: $< 185/110 \text{ mmHg}$ prior to thrombolysis ($< 180/105 \text{ mmHg}$ post-tPA) versus $< 220/120 \text{ mmHg}$ in non-candidates.
- Continuous anti-hypertensive infusions for stroke emergencies include nicardipine (-15 \text{ mg/hr}$), clevidipine (-21 \text{ mg/hr}$), or labetalol boluses/infusion.
- Acute spontaneous intracerebral hemorrhage (ICH) requires rapid SBP reduction to $< 140 \text{ mmHg}$ and immediate anticoagulant reversal (Idarucizumab for Dabigatran, Andexanet alfa or 4F-PCC for Factor Xa inhibitors, 4F-PCC + Vitamin K for Warfarin, Protamine for Heparin).
- Subarachnoid hemorrhage (SAH) management utilizes Hunt-Hess and Fisher grading, enteral Nimodipine ( \text{ mg}$ q4h) for vasospasm prevention, and euvolemic hypertension.
6.2 Acute Ischemic Stroke, Hemorrhagic Stroke & Subarachnoid Hemorrhage
Cerebrovascular emergencies rank among the most time-sensitive conditions encountered in critical care transport. Rapid neurological assessment, precise blood pressure titration, timely administration of thrombolytic agents, urgent reversal of anticoagulation, and prevention of secondary vasospasm are vital to preserving viable brain tissue and preventing permanent disability.
Acute Ischemic Stroke (AIS) & Reperfusion Therapy
Acute Ischemic Stroke accounts for approximately 87% of all strokes. Ischemic tissue surrounding the dense infarcted core is known as the ischemic penumbra—a region of hypoperfused but metabolically active, potentially salvageable brain tissue.
Thrombolytic Time Windows & Dosing
- Intravenous Recombinant Tissue Plasminogen Activator (rtPA / Alteplase):
- Treatment Window: Within 4.5 hours of "Last Known Normal" (LKN).
- Dosing: $0.9 \text{ mg/kg}$ IV (maximum total dose $90 \text{ mg}$). Administer $10%$ of total dose as an initial IV bolus over 1 minute, followed by the remaining $90%$ as a continuous infusion over 60 minutes.
- Tenecteplase (TNK-tPA):
- Treatment Window: Within 4.5 hours of LKN (increasingly preferred due to single IV bolus administration).
- Dosing: $0.25 \text{ mg/kg}$ IV single bolus (maximum total dose $25 \text{ mg}$).
- Endovascular Thrombectomy (EVT): Indicated up to 24 hours from LKN for patients with Large Vessel Occlusions (LVO) in the anterior circulation, determined by CT angiogram and perfusion mismatch.
Blood Pressure Management Thresholds in AIS
Blood pressure management in acute ischemic stroke is tightly regulated based on whether the patient is eligible to receive intravenous thrombolysis.
| Clinical Scenario | Initial BP Threshold to Start Treatment | Post-Treatment Maintenance BP Target |
|---|---|---|
| tPA / TNK Candidate | MUST lower BP to $< 185/110 \text{ mmHg}$ prior to initiating thrombolytic infusion. | Maintain BP $< 180/105 \text{ mmHg}$ for at least 24 hours post-thrombolysis to prevent intracerebral hemorrhage. |
| Non-tPA Candidate | Allow Permissive Hypertension. Treat ONLY if SBP $> 220 \text{ mmHg}$ or DBP $> 120 \text{ mmHg}$. | Reduce MAP by $15%$ over the first 24 hours. Avoid abrupt BP drops to maintain penumbral perfusion. |
Rationale for Permissive Hypertension: In non-thrombolytic candidates, elevated blood pressure is a compensatory reflex maintaining collateral arterial perfusion through cerebral vessel networks into the ischemic penumbra. Precipitous lowering of BP collapses collateral flow, enlarging the stroke infarct size.
First-Line Anti-Hypertensive Infusions
Continuous IV infusions are mandatory for acute blood pressure control in neurocritical emergencies due to their rapid onset and precise titratability.
| Antihypertensive Agent | Class & Mechanism | Standard Dosing & Titration | Clinical Pearls & Contraindications |
|---|---|---|---|
| Nicardipine (Cardene) | Dihydropyridine Calcium Channel Blocker (causes arterial vasodilation) | Start $5 \text{ mg/hr}$ IV; titrate by $2.5 \text{ mg/hr}$ every 5–15 min to max $15 \text{ mg/hr}$. | Excellent cerebral selectivity. Does not increase ICP. Requires large peripheral or central line (venous irritant). |
| Clevidipine (Cleviprex) | Ultra-short-acting Dihydropyridine CCB (metabolized by blood esterases) | Start $1-2 \text{ mg/hr}$ IV; double every 90 sec; titrate by $1-2 \text{ mg/hr}$ q5-10min (max $21 \text{ mg/hr}$). | Ultra-rapid onset ($2-4 \text{ min}$) and offset. Contraindicated in soy/egg allergies or lipid metabolism disorders. |
| Labetalol (Trandate) | Combined $\alpha_1$ and non-selective $\beta$-blocker ($1:7 \ \alpha:\beta$ ratio IV) | $10-20 \text{ mg}$ IV push over 1–2 min; double dose q10min (max $300 \text{ mg}$), or infusion $2-8 \text{ mg/min}$. | Avoid in severe bradycardia ($HR < 60$), 2nd/3rd degree heart block, decompensated heart failure, or severe asthma. |
Acute Spontaneous Intracerebral Hemorrhage (ICH)
Intracerebral hemorrhage involves primary bleeding into the brain parenchyma, most commonly caused by chronic hypertension, cerebral amyloid angiopathy, or vascular malformations. Hematoma expansion occurs rapidly within the first 3–6 hours.
Blood Pressure Reduction in ICH
- Target Systolic Blood Pressure: Rapidly lower and maintain SBP to $< 140 \text{ mmHg}$ (specifically target SBP between $130 - 140 \text{ mmHg}$).
- Clinical Objective: Lowering SBP reduces hydrostatic pressure driving ongoing capillary bleeding, significantly decreasing hematoma expansion without inducing peri-hematomal cerebral ischemia.
Urgent Anticoagulant Reversal Protocols
For patients presenting with acute ICH while on anticoagulant therapy, immediate reversal is paramount prior to or during transport.
| Anticoagulant Agent | Reversal Antidote / Agent | Specific Dosing & Administration Protocol |
|---|---|---|
| Warfarin (Coumadin) | 4-Factor Prothrombin Complex Concentrate (4F-PCC / Kcentra) + Vitamin K | 4F-PCC $25 - 50 \text{ units/kg}$ IV based on baseline INR and body weight + Vitamin K $10 \text{ mg}$ slow IV infusion in $50-100 \text{ mL}$ NS over 30 min. |
| Dabigatran (Pradaxa) | Idarucizumab (Praxbind) | $5 \text{ g}$ IV total, administered as two consecutive $2.5 \text{ g}$ bolus doses (humanized monoclonal antibody fragment). |
| Factor Xa Inhibitors (Rivaroxaban, Apixaban) | Andexanet Alfa (Andexxa) or 4F-PCC (Kcentra) | Andexxa IV bolus followed by a 2-hour continuous infusion (recombinant modified human Factor Xa). Alternatively, high-dose 4F-PCC ($50 \text{ units/kg}$ IV). |
| Unfractionated Heparin (UFH) | Protamine Sulfate | $1 \text{ mg}$ Protamine per $100 \text{ units}$ UFH given in the past 2–3 hours (max single dose $50 \text{ mg}$ slow IV over 10 min). |
| LMWH (Enoxaparin) | Protamine Sulfate | $1 \text{ mg}$ Protamine per $1 \text{ mg}$ Enoxaparin administered within the preceding 8 hours. |
Subarachnoid Hemorrhage (SAH) & Vasospasm Management
Aneurysmal Subarachnoid Hemorrhage (aSAH) results from the rupture of an intracranial saccular ("berry") aneurysm into the subarachnoid space. Patients present with classic "thunderclap headache" ("worst headache of life"), vomiting, nuchal rigidity, photophobia, and rapid loss of consciousness.
SAH Clinical & Radiographic Grading
| Grading System | Parameter Assessed | Clinical & Radiographic Criteria |
|---|---|---|
| Hunt-Hess Scale | Clinical Severity & Surgical Mortality | Grade 1: Asymptomatic or mild headache.<br>Grade 2: Moderate-to-severe headache, nuchal rigidity, no neural deficit.<br>Grade 3: Drowsy, confused, mild focal deficit.<br>Grade 4: Stuporous, moderate-to-severe hemiparesis.<br>Grade 5: Deep coma, decerebrate posturing. |
| Fisher Grade | Non-contrast CT Blood Burden & Vasospasm Risk | Grade 1: No subarachnoid blood detected.<br>Grade 2: Diffuse thin layer of blood ($< 1 \text{ mm}$ thick).<br>Grade 3: Localized clot and/or thick layer of blood ($> 1 \text{ mm}$ thick) — High Risk of Vasospasm.<br>Grade 4: Intracerebral or intraventricular blood with diffuse or no SAH. |
Delayed Cerebral Ischemia (DCI) & Vasospasm Prevention
Cerebral vasospasm typically develops between days 4 and 14 post-hemorrhage as blood breakdown products irritate cerebral arteries.
- Enteral Nimodipine: Oral/nasogastric calcium channel blocker administered as $60 \text{ mg}$ PO/NG every 4 hours for 21 consecutive days. Nimodipine improves neurological outcomes through neuroprotective actions. Warning: Nimodipine must NEVER be administered intravenously; IV administration causes severe refractory vasodilation and fatal cardiac arrest.
- Euvolemic Hypertension vs. Historical Triple-H Therapy: Historical "Triple-H Therapy" (Hypervolemia, Arterial Hypertension, Hemodilution) has been abandoned due to high risks of pulmonary edema, myocardial infarction, and hyponatremia. Current critical care standard dictates maintaining strict EUVOLEMIA using isotonic crystalloids ($0.9%$ NaCl) and initiating induced arterial hypertension (using norepinephrine infusion to target MAP $90 - 110 \text{ mmHg}$) ONLY if symptomatic cerebral vasospasm occurs.
A 62-year-old female presents with acute left-sided hemiparesis and a confirmed ischemic stroke. Her last known normal was 2 hours ago. Her initial blood pressure is 200/115 mmHg. The team plans to administer IV alteplase (tPA). What is the mandatory blood pressure threshold prior to starting tPA, and which agent is most appropriate?
A critical care transport team is transferring an 70-year-old male with an acute spontaneous intracerebral hemorrhage (ICH) who was taking Dabigatran (Pradaxa) for atrial fibrillation. What is the target Systolic Blood Pressure for acute ICH, and what specific reversal agent is indicated?
Which medical regimen is indicated for preventing delayed cerebral ischemia (DCI) and managing vasospasm in a patient with a Grade 3 Fisher Subarachnoid Hemorrhage (SAH)?