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Anticoagulant-related hemorrhage in acute cerebral embolism
Insights
Early anticoagulant therapy for nonseptic cerebral embolism can lead to dangerous hemorrhage into brain infarcts. This study highlights the risks, especially with large infarcts, suggesting caution with anticoagulation post-stroke.
Area of Science:
- Neurology
- Cardiology
- Radiology
Background:
- Nonseptic cerebral embolism of cardiac origin poses a risk for stroke.
- Early treatment strategies are crucial for patient outcomes.
Observation:
- Five patients with cardiac-embolic strokes experienced clinical deterioration or death.
- Hemorrhage into acute infarcts was confirmed by serial CT scans.
- All patients had large infarcts in the right middle cerebral artery territory.
Findings:
- Early anticoagulant therapy (heparin or warfarin) was administered to all five patients.
- Clinical deterioration occurred hours to days after initiating anticoagulation.
- Hemorrhage into the infarcted brain tissue was the cause of deterioration.
Implications:
- Early anticoagulant therapy may be dangerous in acute nonseptic cerebral embolism.
- Caution is advised when using anticoagulants, particularly with large cerebral infarcts.
- Further research is needed to determine optimal timing and safety of anticoagulation.
Abstract:
Five patients with nonseptic cerebral embolism of cardiac origin are reported in whom early anticoagulant therapy resulted in clinical deterioration or death from frank hemorrhage into the acute infarct. In each patient an initial CT scan excluded the presence of intracerebral hemorrhage and a second CT scan, after clinical deterioration had occurred, documented frank hemorrhage into the infarcted zone. All five patients had large infarctions in the right middle cerebral artery territory and three patients were mildly hypertensive. Four patients received heparin within 36 hours of their stroke and one was on warfarin at time of the embolism. Clinical deterioration occurred after intervals of several hours (2 cases), 5-6 days (2 cases) and 30 days (1 case). In only 2 patients was anticoagulant activity excessive at time of clinical deterioration. This report illustrates the danger of early anticoagulant therapy of acute nonseptic cerebral embolism, particularly in the setting of large infarction.