Initial Workup - Code Red, Brain Bleed
- ABCs first: Secure airway, breathing, circulation.
- Immediate non-contrast CT head: The single most important initial test.
- Vitals & Neuro Exam: Glasgow Coma Scale (GCS), NIH Stroke Scale (NIHSS).
- Key Labs: Stat coagulation panel (PT/INR, aPTT), CBC, platelets, glucose.
- Blood Pressure: Keep SBP <160 mmHg initially; use IV labetalol or nicardipine.

⭐ Non-contrast CT is paramount. Thrombolytics (for ischemic stroke) are absolutely contraindicated in hemorrhagic stroke and would be catastrophic.
Acute BP & Coags - The First Hour
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Immediate Goal: Aggressively lower BP and reverse any coagulopathy to limit hematoma expansion, the primary driver of early neurological deterioration.
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Blood Pressure Control:
- Target Systolic BP <140 mmHg.
- Use easily titratable IV agents like Labetalol or Nicardipine.
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Coagulopathy Reversal:
- Warfarin: Vitamin K + 4-factor Prothrombin Complex Concentrate (4F-PCC).
- DOACs: Use specific reversal agents (Idarucizumab for Dabigatran; Andexanet Alfa for Xa inhibitors).
- Antiplatelets: Platelet transfusions are generally not recommended but may be considered for patients requiring neurosurgery.
⭐ For warfarin reversal, 4F-PCC is superior to FFP. It provides faster INR correction with a lower infusion volume, minimizing the risk of fluid overload.
ICH vs. SAH - Two Flavors of Trouble
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Intracerebral Hemorrhage (ICH)
- Cause: Chronic hypertension → Charcot-Bouchard microaneurysms; cerebral amyloid angiopathy.
- Presentation: Focal neurological deficits that worsen over minutes to hours.
- CT Finding: Blood within the brain parenchyma.
- Management: Strict BP control (target SBP <140 mmHg), reverse anticoagulation.
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Subarachnoid Hemorrhage (SAH)
- Cause: Ruptured saccular (berry) aneurysm (85%).
- Presentation: Sudden, explosive "worst headache of my life"; meningeal signs.
- CT Finding: Blood in cisterns and sulci.
- Management: Nimodipine for vasospasm prevention; surgical clipping or endovascular coiling.

⭐ Nimodipine in SAH does not prevent re-bleeding but is critical to prevent delayed cerebral ischemia from vasospasm, a major cause of morbidity/mortality days after the initial event.
Complications - Watching for Waves
- Re-bleeding: Highest risk in first 24h; sudden neurological decline, ↑ mortality.
- Vasospasm: Peaks 4-14 days post-SAH. Causes delayed cerebral ischemia. Prevent with nimodipine.
- Hydrocephalus: Obstructive/communicating due to blood in ventricles/cisterns. May require external ventricular drain (EVD).
- Seizures: Can occur due to cortical irritation from blood. Prophylaxis is controversial.
- Hyponatremia: From SIADH or cerebral salt wasting.
⭐ Nimodipine is the only drug shown to improve outcomes in SAH by preventing vasospasm-related ischemia, but it does not reduce the incidence of vasospasm itself.

High-Yield Points - ⚡ Biggest Takeaways
- Immediate BP control is the first crucial step; aggressively lower to SBP < 140 mmHg.
- Urgently reverse any anticoagulation; use Vitamin K, FFP, or prothrombin complex concentrates (PCC).
- Secure emergent neurosurgical consultation for potential hematoma evacuation.
- Manage elevated intracranial pressure (ICP) with head elevation, mannitol, and hyperventilation.
- Seizure prophylaxis is often indicated, particularly for lobar hemorrhages.
- Non-contrast CT is the essential first diagnostic step to differentiate from ischemic stroke.
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