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Published on: July 9, 2020
Case report: Aggressive blood pressure management for carotid endarterectomy hyperperfusion syndrome
James Scozzafava1, Muhammad S Hussain, Tom Yeo
1Division of Neurology, University of Alberta, Edmonton, Alberta, Canada.
Insights
Aggressive blood pressure control is crucial for managing cerebral hyperperfusion syndrome (CHS) after revascularization. Lowering systolic blood pressure to 90-140 mmHg successfully treated a severe CHS case, preventing stroke and hemorrhage.
Area of Science:
- Neurology
- Neurosurgery
- Vascular Surgery
Background:
- Cerebral hyperperfusion syndrome (CHS) is a rare but serious complication after cerebral revascularization procedures.
- It arises from impaired cerebral autoregulation following chronic hypoperfusion, leading to potential stroke or hemorrhage.
Observation:
- A 67-year-old male developed seizures and right-sided weakness post-carotid endarterectomy, indicative of CHS.
- Imaging revealed significant vasogenic edema without infarction, prompting aggressive management.
Findings:
- A strict systolic blood pressure target of 90-140 mmHg was implemented, lower than standard stroke protocols.
- This aggressive blood pressure management led to rapid clinical improvement and resolution of edema on follow-up imaging.
Implications:
- This case highlights the critical importance of tailored, lower blood pressure targets in managing CHS.
- Awareness and prompt intervention are key to preventing devastating neurological outcomes in patients undergoing cerebral revascularization.
Purpose:
Cerebral hyperperfusion syndrome (CHS) is a rare but potentially devastating complication following cerebral revascularization. Management of CHS requires aggressive blood pressure control to prevent stroke and intracerebral hemorrhage. This case report documents a severe case of CHS, and outlines a successful outcome associated with aggressive blood pressure control.
Clinical Features:
A 67-yr-old gentleman, nine days post left carotid endarterectomy, required tracheal intubation and intensive care unit admission following seizures and acute right-sided weakness. A computed tomography scan and magnetic resonance imaging revealed significant vasogenic edema in the left middle cerebral artery territory, without evidence of infarction. The history and radiographic findings suggested CHS. As such, a systolic blood pressure target was set at 90-140 mmHg. This blood pressure parameter was lower than typically targeted following acute ischemic or hemorrhagic stroke. Rapid clinical improvements were seen by day five, and tight blood pressure control was maintained throughout. Repeat computed tomography and magnetic resonance imaging revealed improved edema and no evidence of infarct or hemorrhage.
Conclusion:
Cerebral hyperperfusion syndrome is believed to occur following restoration of blood flow to a brain with impaired autoregulation due to chronic hypoperfusion. Massive brain edema and hemorrhage can result from higher pressures. Clinicians should be aware of this potential complication following cerebral revascularization procedures, and the importance of establishing blood pressure targets which are considerably lower than for other patients with similar clinical presentations.
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