Cerebral Stroke Cheatsheet

Cheatsheet Content

1. Introduction to Stroke Definition: A stroke occurs when blood flow to a part of the brain is interrupted, leading to brain cell death. Synonyms: Cerebrovascular accident (CVA), "brain attack." Impact: Leading cause of long-term disability and a major cause of death worldwide. 2. Types of Stroke 2.1. Ischemic Stroke (87% of strokes) Cause: Blockage of a blood vessel supplying the brain. Mechanisms: Thrombotic: Clot forms in an artery supplying the brain (e.g., atherosclerosis). Embolic: Clot travels from another part of the body (e.g., heart, carotid artery) to the brain. Risk Factors: Atrial fibrillation, carotid artery disease, hypercoagulable states, patent foramen ovale (PFO). 2.2. Hemorrhagic Stroke (13% of strokes) Cause: Bleeding into the brain tissue or surrounding spaces. Types: Intracerebral Hemorrhage (ICH): Bleeding directly into brain tissue. Often due to uncontrolled hypertension, amyloid angiopathy, arteriovenous malformations (AVMs). Subarachnoid Hemorrhage (SAH): Bleeding into the subarachnoid space (between arachnoid and pia mater). Most commonly caused by ruptured aneurysms, AVMs, trauma. Risk Factors: Hypertension, anticoagulation, illicit drug use (e.g., cocaine), brain aneurysms. 2.3. Transient Ischemic Attack (TIA) Definition: "Mini-stroke," temporary blockage of blood flow to the brain, without permanent brain damage. Symptoms: Similar to stroke, but resolve within minutes to 24 hours. Significance: A warning sign; significantly increases risk of future stroke. Requires urgent evaluation. 3. Pathophysiology Ischemic Penumbra: Area of brain tissue surrounding the infarct core that is hypoperfused but still viable. Target for therapeutic intervention. Excitotoxicity: Ischemia leads to release of excitatory neurotransmitters (e.g., glutamate), causing neuronal damage. Inflammation: Immune response contributes to secondary brain injury. Blood-Brain Barrier Disruption: Can lead to vasogenic edema. 4. Clinical Presentation (FAST) F ace drooping: One side of the face droops or is numb. A rm weakness: One arm is weak or numb. S peech difficulty: Slurred speech, inability to speak, or difficulty understanding speech. T ime to call emergency services: Call 911 immediately if any of these symptoms appear. Other Symptoms: Sudden severe headache (especially SAH), sudden vision changes, sudden dizziness/loss of balance, confusion. 5. Diagnosis Clinical Assessment: Neurological exam (NIH Stroke Scale), history. Imaging: Non-contrast CT Scan: Primary imaging to differentiate ischemic from hemorrhagic stroke. Rapidly identifies hemorrhage. CT Angiography (CTA): Visualizes cerebral arteries, identifies large vessel occlusions, aneurysms, AVMs. CT Perfusion (CTP): Measures blood flow, volume, and transit time to identify penumbra. MRI (DWI, FLAIR, MRA): More sensitive for acute ischemia, identifies smaller infarcts, can estimate age of infarct. Lab Tests: CBC, electrolytes, glucose, coagulation studies (PT/INR, PTT), cardiac enzymes, toxicology screen. ECG/Cardiac Monitoring: To detect atrial fibrillation or other cardiac sources of emboli. 6. Acute Management (Ischemic Stroke) 6.1. Reperfusion Therapy Intravenous Thrombolysis (alteplase/tPA): Mechanism: Converts plasminogen to plasmin, dissolving clots. Time Window: Within 4.5 hours of symptom onset (strict criteria apply). Contraindications: Prior ICH, active bleeding, recent surgery, uncontrolled hypertension, etc. Endovascular Thrombectomy: Mechanism: Mechanical removal of large vessel clots. Time Window: Up to 6-24 hours for selected patients with large vessel occlusion in anterior circulation. 6.2. General Supportive Care Blood Pressure Management: Carefully manage BP to optimize cerebral perfusion and prevent hemorrhagic transformation. Glucose Control: Maintain euglycemia. Temperature Control: Treat fever. Swallowing Assessment: Prevent aspiration pneumonia (NPO until swallow screen passed). DVT Prophylaxis: Early mobilization, intermittent pneumatic compression devices, or anticoagulants. 7. Acute Management (Hemorrhagic Stroke) Blood Pressure Control: Aggressive BP management to prevent further bleeding. Reversal of Anticoagulation: If patient is on anticoagulants, reverse immediately (e.g., Vitamin K, PCC, idarucizumab, andexanet alfa). Neurosurgical Intervention: ICH: May be indicated for large, superficial hematomas with neurological deterioration. SAH: Clipping or coiling of ruptured aneurysms to prevent re-bleeding; external ventricular drain (EVD) for hydrocephalus. Cerebral Vasospasm (SAH complication): Prophylaxis with nimodipine, close monitoring. 8. Stroke Prevention 8.1. Primary Prevention Lifestyle Modifications: Healthy diet, regular exercise, smoking cessation, limit alcohol. Medical Management: Hypertension: Antihypertensive medications. Diabetes: Glycemic control. Dyslipidemia: Statins. Atrial Fibrillation: Anticoagulation (e.g., DOACs, warfarin). 8.2. Secondary Prevention (After Stroke/TIA) Antiplatelet Therapy: Aspirin, clopidogrel, aspirin + dipyridamole for ischemic stroke. Anticoagulation: For cardioembolic stroke (e.g., AFib). Carotid Endarterectomy/Stenting: For significant carotid artery stenosis. Lifestyle & Medical Management: As in primary prevention. 9. Complications of Stroke Neurological: Seizures, cognitive impairment, depression, spasticity, central post-stroke pain. Medical: Aspiration pneumonia, DVT/PE, urinary tract infection, pressure ulcers, cardiac complications. 10. Rehabilitation Multidisciplinary Team: Physical therapy, occupational therapy, speech therapy, physiatrist, social work, nursing. Goals: Maximize functional recovery, improve quality of life, prevent recurrence. Early Mobilization: Crucial for better outcomes.