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Emergency And Acute Medicine – Cerebral Reperfusion Therapy
Cerebral reperfusion therapy is indicated for acute ischemic stroke, defined as a sudden interruption of regional cerebral blood flow resulting in focal neurologic deficits. Reperfusion strategies include intravenous thrombolysis to dissolve thromboembolic occlusion, intra-arterial thrombolysis, and mechanical thrombectomy. The primary goal is rapid restoration of cerebral perfusion to salvage ischemic penumbra and reduce long-term disability. “Time is brain,” and treatment decisions are highly time dependent.
Ischemic stroke may be thrombotic, embolic, or due to other vascular occlusive processes. Thrombotic stroke results from in situ thrombosis, often at an ulcerated atherosclerotic plaque or from hypercoagulable states such as antithrombin III, protein C, or protein S deficiency. Sludging syndromes such as sickle cell disease or polycythemia vera may also contribute. Embolic stroke commonly arises from cardiac sources including atrial fibrillation, mural thrombus after myocardial infarction, cardiomyopathy, ventricular aneurysm, or prosthetic valves. Arterial sources include aortic or carotid atherosclerotic plaques. Other causes include vascular dissection and vasospasm from subarachnoid hemorrhage or vasoconstrictive agents such as cocaine.
Patients typically present with acute focal neurologic deficits within 4.5 hours of onset. Determining the exact time of symptom onset is critical. If unknown, the time last known well is used. Symptoms correspond to vascular territories. Middle cerebral artery involvement may cause contralateral hemiplegia (face and arm more than leg), hemisensory loss, homonymous hemianopsia, aphasia in the dominant hemisphere, or neglect. Posterior cerebral artery infarction may cause visual field deficits or visual agnosia. Vertebrobasilar strokes can present with vertigo, nystagmus, dysarthria, cranial nerve deficits, ataxia, and crossed sensory findings. Anterior cerebral artery infarction typically affects the contralateral leg more than the arm and may produce apraxia or behavioral changes. Lacunar infarcts may produce pure motor or pure sensory syndromes. Stroke severity is quantified using the National Institutes of Health Stroke Scale (NIHSS), which standardizes neurologic assessment and helps predict prognosis and hemorrhagic risk.
Initial evaluation includes immediate bedside glucose testing to exclude hypoglycemia. Laboratory studies include CBC and coagulation studies (PT/PTT) to assess bleeding risk prior to thrombolysis. A noncontrast head CT scan must be obtained emergently to exclude intracranial hemorrhage. Early ischemic changes may be subtle or absent in the first hours. Additional studies may include ECG to assess for arrhythmia or myocardial ischemia, serum electrolytes, renal function, pregnancy testing, and toxicology screening when indicated. Advanced imaging such as diffusion-weighted MRI, CT perfusion, CT angiography, or MR angiography may identify salvageable tissue and vascular occlusion but should not delay timely thrombolysis when indicated.
Intravenous alteplase (tPA) is indicated in eligible patients aged 18 years or older with clearly defined symptom onset within 4.5 hours and no evidence of hemorrhage on CT. Absolute contraindications include recent stroke or intracranial surgery within 3 months, prior intracranial hemorrhage, suspected subarachnoid hemorrhage, active bleeding, severe uncontrolled hypertension (>185/110 mm Hg), coagulopathy, thrombocytopenia, elevated INR, recent heparin with elevated aPTT, hypoglycemia <50 mg />L, or large established infarction involving more than one third of a cerebral hemisphere. Between 3 and 4.5 hours, additional exclusion criteria apply, including age over 80 years, oral anticoagulant use, NIHSS greater than 25, large MCA territory involvement, or history of both stroke and diabetes.
Blood pressure must be controlled to ≤185/110 mm Hg before thrombolysis and maintained below 180/105 mm Hg after treatment. Labetalol or nicardipine are commonly used. Alteplase is administered at 0.9 mg/kg (maximum 90 mg), with 10% given as an initial bolus over 1 minute and the remainder infused over 60 minutes. Antiplatelet and anticoagulant agents should be withheld for 24 hours. Blood pressure and neurologic status must be monitored frequently during and after infusion. Complications include intracranial hemorrhage, which occurs in up to 6% of treated patients and more commonly in those with severe strokes. If hemorrhage is suspected, tPA should be discontinued and emergent CT performed. Management includes reversal with cryoprecipitate, fibrinogen, platelets, and neurosurgical consultation.
Mechanical thrombectomy or intra-arterial therapy may be considered in selected patients with large vessel occlusion, often within 6 hours of onset, and sometimes beyond in specialized centers based on advanced imaging criteria. These approaches are particularly valuable in patients who are ineligible for IV thrombolysis or who have persistent large vessel occlusion despite treatment.
All patients receiving reperfusion therapy must be admitted to an intensive care or dedicated stroke unit for close neurologic and hemodynamic monitoring. Rapid recognition, precise determination of symptom onset, strict adherence to inclusion and exclusion criteria, and careful blood pressure management are critical. Even brief delays in therapy can significantly reduce the likelihood of meaningful neurologic recovery.
Cerebral reperfusion therapy is indicated for acute ischemic stroke, defined as a sudden interruption of regional cerebral blood flow resulting in focal neurologic deficits. Reperfusion strategies include intravenous thrombolysis to dissolve thromboembolic occlusion, intra-arterial thrombolysis, and mechanical thrombectomy. The primary goal is rapid restoration of cerebral perfusion to salvage ischemic penumbra and reduce long-term disability. “Time is brain,” and treatment decisions are highly time dependent.
Ischemic stroke may be thrombotic, embolic, or due to other vascular occlusive processes. Thrombotic stroke results from in situ thrombosis, often at an ulcerated atherosclerotic plaque or from hypercoagulable states such as antithrombin III, protein C, or protein S deficiency. Sludging syndromes such as sickle cell disease or polycythemia vera may also contribute. Embolic stroke commonly arises from cardiac sources including atrial fibrillation, mural thrombus after myocardial infarction, cardiomyopathy, ventricular aneurysm, or prosthetic valves. Arterial sources include aortic or carotid atherosclerotic plaques. Other causes include vascular dissection and vasospasm from subarachnoid hemorrhage or vasoconstrictive agents such as cocaine.
Patients typically present with acute focal neurologic deficits within 4.5 hours of onset. Determining the exact time of symptom onset is critical. If unknown, the time last known well is used. Symptoms correspond to vascular territories. Middle cerebral artery involvement may cause contralateral hemiplegia (face and arm more than leg), hemisensory loss, homonymous hemianopsia, aphasia in the dominant hemisphere, or neglect. Posterior cerebral artery infarction may cause visual field deficits or visual agnosia. Vertebrobasilar strokes can present with vertigo, nystagmus, dysarthria, cranial nerve deficits, ataxia, and crossed sensory findings. Anterior cerebral artery infarction typically affects the contralateral leg more than the arm and may produce apraxia or behavioral changes. Lacunar infarcts may produce pure motor or pure sensory syndromes. Stroke severity is quantified using the National Institutes of Health Stroke Scale (NIHSS), which standardizes neurologic assessment and helps predict prognosis and hemorrhagic risk.
Initial evaluation includes immediate bedside glucose testing to exclude hypoglycemia. Laboratory studies include CBC and coagulation studies (PT/PTT) to assess bleeding risk prior to thrombolysis. A noncontrast head CT scan must be obtained emergently to exclude intracranial hemorrhage. Early ischemic changes may be subtle or absent in the first hours. Additional studies may include ECG to assess for arrhythmia or myocardial ischemia, serum electrolytes, renal function, pregnancy testing, and toxicology screening when indicated. Advanced imaging such as diffusion-weighted MRI, CT perfusion, CT angiography, or MR angiography may identify salvageable tissue and vascular occlusion but should not delay timely thrombolysis when indicated.
Intravenous alteplase (tPA) is indicated in eligible patients aged 18 years or older with clearly defined symptom onset within 4.5 hours and no evidence of hemorrhage on CT. Absolute contraindications include recent stroke or intracranial surgery within 3 months, prior intracranial hemorrhage, suspected subarachnoid hemorrhage, active bleeding, severe uncontrolled hypertension (>185/110 mm Hg), coagulopathy, thrombocytopenia, elevated INR, recent heparin with elevated aPTT, hypoglycemia <50 mg />L, or large established infarction involving more than one third of a cerebral hemisphere. Between 3 and 4.5 hours, additional exclusion criteria apply, including age over 80 years, oral anticoagulant use, NIHSS greater than 25, large MCA territory involvement, or history of both stroke and diabetes.
Blood pressure must be controlled to ≤185/110 mm Hg before thrombolysis and maintained below 180/105 mm Hg after treatment. Labetalol or nicardipine are commonly used. Alteplase is administered at 0.9 mg/kg (maximum 90 mg), with 10% given as an initial bolus over 1 minute and the remainder infused over 60 minutes. Antiplatelet and anticoagulant agents should be withheld for 24 hours. Blood pressure and neurologic status must be monitored frequently during and after infusion. Complications include intracranial hemorrhage, which occurs in up to 6% of treated patients and more commonly in those with severe strokes. If hemorrhage is suspected, tPA should be discontinued and emergent CT performed. Management includes reversal with cryoprecipitate, fibrinogen, platelets, and neurosurgical consultation.
Mechanical thrombectomy or intra-arterial therapy may be considered in selected patients with large vessel occlusion, often within 6 hours of onset, and sometimes beyond in specialized centers based on advanced imaging criteria. These approaches are particularly valuable in patients who are ineligible for IV thrombolysis or who have persistent large vessel occlusion despite treatment.
All patients receiving reperfusion therapy must be admitted to an intensive care or dedicated stroke unit for close neurologic and hemodynamic monitoring. Rapid recognition, precise determination of symptom onset, strict adherence to inclusion and exclusion criteria, and careful blood pressure management are critical. Even brief delays in therapy can significantly reduce the likelihood of meaningful neurologic recovery.
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