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Emergency And Acute Medicine – Intracerebral Hemorrhage
Basics
Description Intracerebral hemorrhage is bleeding into the brain parenchyma causing direct compression of brain tissue. Secondary injury results from cerebral edema, rising intracranial pressure, and risk of brain herniation.
Etiology
Intracerebral hemorrhage may be spontaneous or traumatic. Common causes include uncontrolled or acute hypertension (most common), vascular malformations (arteriovenous malformations, venous angiomas), ruptured cerebral aneurysms, intracranial neoplasms (especially melanoma and glioma), anticoagulant or thrombolytic therapy, illicit drug use (cocaine, amphetamines), bleeding disorders, cerebral amyloid angiopathy, and blunt or penetrating head trauma.
Diagnosis
Signs and symptoms Sudden severe headache, seizures, vomiting, neck stiffness, altered mental status, or coma. Neurologic deficits depend on hemorrhage location. Putaminal hemorrhage causes contralateral hemiparesis and sensory loss. Lobar hemorrhage causes variable focal deficits. Cerebellar hemorrhage presents with vomiting, ataxia, and nystagmus. Thalamic hemorrhage causes motor and sensory deficits with eye movement abnormalities. Pontine hemorrhage presents with quadriplegia and pinpoint pupils.
Essential workup
Secure airway if indicated and obtain immediate noncontrast CT of the head, which shows acute hemorrhage as a hyperdense lesion.
Diagnosis tests and interpretation
Lab CBC, electrolytes, BUN/creatinine, coagulation studies (PT, PTT, INR, platelets), pregnancy test when appropriate, ECG, and toxicology screen if indicated.
Imaging Noncontrast CT is diagnostic. CT angiography may identify an underlying vascular lesion and contrast extravasation (“spot sign”), which predicts hematoma expansion and worse outcomes. MRI may be useful later but is not first line in the ED.
Differential diagnosis
Seizure with postictal paralysis, ischemic stroke, CNS infection, intracranial mass, electrolyte or metabolic abnormalities, intoxication, migraine, transient ischemic attack, and traumatic intracranial hemorrhages.
Treatment
Prehospital Maintain cervical spine precautions if trauma suspected, elevate head with spinal alignment, and document neurologic deficits for comparison.
Initial stabilization Manage airway and breathing aggressively. Early neurosurgical and neurologic consultation is essential.
Emergency department management Control blood pressure cautiously to avoid reducing cerebral perfusion. Gradually lower diastolic blood pressure by approximately 10%, avoiding rapid normalization. Treat elevated intracranial pressure with head elevation, controlled ventilation, osmotic therapy, and fluid management. Reverse coagulopathies promptly using vitamin K, fresh frozen plasma, platelets, or prothrombin complex concentrates as indicated. Consider anticonvulsants for seizure management or prophylaxis.
Medication
Common agents include labetalol, nicardipine, esmolol, or enalapril for blood pressure control; mannitol or furosemide for intracranial pressure; phenytoin or fosphenytoin for seizures; and appropriate blood products for anticoagulation reversal.
Follow-up and disposition
Admission criteria All patients with intracerebral hemorrhage require admission. ICU care is indicated for altered mental status, intubation, or continuous blood pressure infusions.
Discharge criteria Discharge is not appropriate for intracerebral hemorrhage.
Follow-up recommendations Long-term blood pressure control, smoking and substance cessation, and rehabilitation planning are critical to reduce recurrence and improve functional recovery.
Key points
Early brain imaging is essential in patients with headache, hypertension, or altered mental status. Blood pressure reduction must be cautious to preserve cerebral perfusion. Delayed hemorrhage should be considered in anticoagulated patients with head trauma.
Basics
Description Intracerebral hemorrhage is bleeding into the brain parenchyma causing direct compression of brain tissue. Secondary injury results from cerebral edema, rising intracranial pressure, and risk of brain herniation.
Etiology
Intracerebral hemorrhage may be spontaneous or traumatic. Common causes include uncontrolled or acute hypertension (most common), vascular malformations (arteriovenous malformations, venous angiomas), ruptured cerebral aneurysms, intracranial neoplasms (especially melanoma and glioma), anticoagulant or thrombolytic therapy, illicit drug use (cocaine, amphetamines), bleeding disorders, cerebral amyloid angiopathy, and blunt or penetrating head trauma.
Diagnosis
Signs and symptoms Sudden severe headache, seizures, vomiting, neck stiffness, altered mental status, or coma. Neurologic deficits depend on hemorrhage location. Putaminal hemorrhage causes contralateral hemiparesis and sensory loss. Lobar hemorrhage causes variable focal deficits. Cerebellar hemorrhage presents with vomiting, ataxia, and nystagmus. Thalamic hemorrhage causes motor and sensory deficits with eye movement abnormalities. Pontine hemorrhage presents with quadriplegia and pinpoint pupils.
Essential workup
Secure airway if indicated and obtain immediate noncontrast CT of the head, which shows acute hemorrhage as a hyperdense lesion.
Diagnosis tests and interpretation
Lab CBC, electrolytes, BUN/creatinine, coagulation studies (PT, PTT, INR, platelets), pregnancy test when appropriate, ECG, and toxicology screen if indicated.
Imaging Noncontrast CT is diagnostic. CT angiography may identify an underlying vascular lesion and contrast extravasation (“spot sign”), which predicts hematoma expansion and worse outcomes. MRI may be useful later but is not first line in the ED.
Differential diagnosis
Seizure with postictal paralysis, ischemic stroke, CNS infection, intracranial mass, electrolyte or metabolic abnormalities, intoxication, migraine, transient ischemic attack, and traumatic intracranial hemorrhages.
Treatment
Prehospital Maintain cervical spine precautions if trauma suspected, elevate head with spinal alignment, and document neurologic deficits for comparison.
Initial stabilization Manage airway and breathing aggressively. Early neurosurgical and neurologic consultation is essential.
Emergency department management Control blood pressure cautiously to avoid reducing cerebral perfusion. Gradually lower diastolic blood pressure by approximately 10%, avoiding rapid normalization. Treat elevated intracranial pressure with head elevation, controlled ventilation, osmotic therapy, and fluid management. Reverse coagulopathies promptly using vitamin K, fresh frozen plasma, platelets, or prothrombin complex concentrates as indicated. Consider anticonvulsants for seizure management or prophylaxis.
Medication
Common agents include labetalol, nicardipine, esmolol, or enalapril for blood pressure control; mannitol or furosemide for intracranial pressure; phenytoin or fosphenytoin for seizures; and appropriate blood products for anticoagulation reversal.
Follow-up and disposition
Admission criteria All patients with intracerebral hemorrhage require admission. ICU care is indicated for altered mental status, intubation, or continuous blood pressure infusions.
Discharge criteria Discharge is not appropriate for intracerebral hemorrhage.
Follow-up recommendations Long-term blood pressure control, smoking and substance cessation, and rehabilitation planning are critical to reduce recurrence and improve functional recovery.
Key points
Early brain imaging is essential in patients with headache, hypertension, or altered mental status. Blood pressure reduction must be cautious to preserve cerebral perfusion. Delayed hemorrhage should be considered in anticoagulated patients with head trauma.
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