Nontraumatic intracerebral hemorrhage

Key Points
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By Ravindra Kumar Garg MD

Nontraumatic intracerebral hemorrhage is also known as or subsumes Acute spontaneous brain hemorrhage and Intracranial hematoma. -ed.

Intracerebral hemorrhage is much less common than ischemic stroke but is associated with a significantly high mortality and morbidity. Intracerebral hemorrhage frequently affects the basal ganglia, thalamus, cerebral lobes, pons, and cerebellum. Hypertension, cerebral amyloid angiopathy, and anticoagulation are major causes of intracerebral hemorrhage. Carriers of apolipoprotein E2 and E4 have an increased risk of intracerebral hemorrhage in lobar locations, presumably because of the effects of these gene variants on risk of cerebral amyloid angiopathy. Genetic studies identify 1q22 as a susceptibility locus for intracerebral hemorrhage. Hematoma expansion is an accurate predictor of poor outcome of intracerebral hemorrhage. "Spot sign" on CT angiography has been reported to predict hematoma expansion. Strict blood pressure control may prevent further enlargement of hematoma. Anticoagulation-related intracerebral hemorrhage is often fatal, and rapid reversal of anticoagulation is the most effective therapy currently available. Surgical evacuation of hematoma for supratentorial intracerebral hemorrhage was not shown to be beneficial. Considering a high rate of early neurologic deterioration in the first few hours, the American Heart Association recommends identifying patients at high risk of hematoma expansion. Advanced imaging is recommended to identify underlying lesions in patients with unusual appearance of the hematoma, such as subarachnoid hemorrhage, unusual shape or location, significant early edema, or suggestion of a mass. In this article, the author reviews in detail the different aspects of intracerebral hemorrhage.

Key Points

  • Intracerebral hemorrhage is a common cause of stroke.
  • It results from hypertensive damage to blood vessels, rupture of an aneurysm or arteriovenous malformations, cerebral amyloid angiopathy, altered hemostasis (like thrombolysis and anticoagulation), hemorrhagic necrosis (like tumor and infection), or substance abuse (cocaine).
  • Common sites for involvement include the basal ganglia, lobes of cerebral hemispheres, thalamus, pons, cerebellum, and other brainstem sites.
  • Computed tomography readily demonstrates acute hemorrhage.
  • Initial management is focused on maintaining breathing, circulation, and fluid and electrolyte balance.
  • Quick hemostasis to prevent hematoma expansion, surgical removal of clot, removal of intraventricular blood, and prompt blood pressure control improve outcomes.

In This Article

Key Points
Introduction
Clinical manifestations
Etiology
Pathogenesis and pathophysiology
Epidemiology
Diagnostic workup
Prognosis and complications
Management
References cited
Contributors