JOURNAL ARTICLE
Intracerebral hemorrhage after carotid endarterectomy associated with asymptomatic perioperative cerebral ischemia detected by cerebral perfusion imaging: case report.
Surgical Neurology 2004 October
BACKGROUND: Risk factors for intracerebral hemorrhage following carotid endarterectomy (CEA) include perioperative cerebral ischemia, postoperative cerebral hyperperfusion, and postoperative anticoagulation therapy, and at least 2 of these risk factors are typically present in the context of intracerebral hemorrhage (ICH).
CASE DESCRIPTION: A 75-year-old man with severe bilateral cervical internal carotid artery stenosis and a minor stroke resulting in left motor weakness underwent a right CEA. The operation was uneventful, and the patient did not experience new neurologic deficits upon recovery from anesthesia. Brain single photon emission computed tomography (SPECT) obtained immediately after CEA showed a perfusion defect in the right parietal lobe and absence of cerebral hyperperfusion. A computed tomography (CT) scan showed no new abnormal findings. Aspirin therapy was instituted postoperatively. On the second postoperative day, the patient experienced abrupt worsening of left hemiparesis, and subsequent CT imaging demonstrated a hematoma in the right parietal lobe. Cerebral hyperperfusion was absent on repeat SPECT.
CONCLUSION: Perioperative cerebral ischemia can result in intracerebral hemorrhage after CEA even in the absence of cerebral hyperperfusion and/or anticoagulation therapy. Further, cerebral perfusion imaging performed immediately after CEA is a useful modality for the identification of occult cerebral ischemia or hyperperfusion that may lead to intracerebral hemorrhage.
CASE DESCRIPTION: A 75-year-old man with severe bilateral cervical internal carotid artery stenosis and a minor stroke resulting in left motor weakness underwent a right CEA. The operation was uneventful, and the patient did not experience new neurologic deficits upon recovery from anesthesia. Brain single photon emission computed tomography (SPECT) obtained immediately after CEA showed a perfusion defect in the right parietal lobe and absence of cerebral hyperperfusion. A computed tomography (CT) scan showed no new abnormal findings. Aspirin therapy was instituted postoperatively. On the second postoperative day, the patient experienced abrupt worsening of left hemiparesis, and subsequent CT imaging demonstrated a hematoma in the right parietal lobe. Cerebral hyperperfusion was absent on repeat SPECT.
CONCLUSION: Perioperative cerebral ischemia can result in intracerebral hemorrhage after CEA even in the absence of cerebral hyperperfusion and/or anticoagulation therapy. Further, cerebral perfusion imaging performed immediately after CEA is a useful modality for the identification of occult cerebral ischemia or hyperperfusion that may lead to intracerebral hemorrhage.
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