DP28: ACUTE ONSET OF CEREBRAL HYPERPERFUSION SYNDROME UPON EMERGENCE AFTER CAROTID ENDARTERECTOMY
Matthew D Witkin, MD; Miguel Abalo, MD
University of Miami/Jackson Health System
Introduction/Background: Cerebral hyperperfusion syndrome (CHS) is a rare but potentially devastating complication following carotid endarterectomy (CEA) with an incidence ranging from 1-3%. Its postoperative peak presentation occurs on POD#6 and is characterized by symptoms of severe uni/ipsilateral headache, seizure, focal neurological signs, brain edema, and intracranial hemorrhage (ICH) (1-4). Possible risk factors include chronic HTN and reduced cerebral vasculature reserve (2). The pathophysiology of the syndrome is primarily believed to be due to impaired cerebral blood flow autoregulation secondary to a chronic ischemic/low-flow state with maximally dilated vessels unable to acutely adjust to the new reperfusion state.
Methods: A 63-year-old male with a PMH significant for bilateral carotid stenosis, CAD c/b STEMI s/p CABG x4, severe PAD, HTN, HLD, T2M, and moderate AS presented for a right CEA. The patient underwent an uneventful induction and intubation. A left radial arterial line was placed for close hemodynamic monitoring. Upon surgical incision, the patient demonstrated labile blood pressures requiring repeated boluses of nicardipine and nitroglycerine as well as a dexmedetomidine gtt. The patient underwent a right carotid clamping time of 34 minutes with no evidence of baseline deviation utilizing NIRS neuromonitoring. Upon extubation, the patient displayed left-sided hemiplegia and hemi-neglect for which a stroke alert was called. There was concern for possible formation of an intimal flap vs thrombosis vs seizure vs CHS. After his initial imaging was obtained, the patient was admitted to the CVICU for strict blood pressure management.
Results: The patient’s initial CT Brain w/o contrast demonstrated no evidence of acute ICH or acute territorial infarct. His CTA neck/head displayed no evidence of hemodynamically significant stenosis of the R ICA and no new large vessel occlusion or critical intracranial arterial stenosis. An MRI Brain also supported no acute ischemic infarct or ICH. On POD#1, an EEG demonstrated no seizure/epileptiform discharges but did indicate moderate to severe encephalopathy, worse on the right hemisphere. Also on POD#1, his transcranial doppler (TCD) showed evidence of increased mean flow velocities of the right terminal ICA, siphon, and MCA - suggestive of CHS. On POD#3, his TCD showed evidence of interval improvement, however on POD#5 his mean flow velocities were increased, despite tight blood pressure control. His MRI Brain on POD#3 showed diffuse right hemispheric cortical DWI abnormality with FLAIR correlate, suggesting of cytogenic an mixed vasogenic edema – again supporting CHS. Our patient spent 11 days in the CVICU until he was discharged to a rehab facility. Unfortunately, the patient continues to suffer from left-sided hemiplegia.
Discussion/Conclusion: Our patient displayed a unique acute presentation of CHS. Most acute complications of CEA are usually ischemic in nature (1). Due to its rare presentation, CHS remains poorly understood. As of now, the best management strategy is to maintain strict blood pressure (systolic BP <150mmHg) control during the post-operative period to allow time for cerebral autoregulation to reactivate and to prevent the most devastating sequela of ICH. Labetalol and clonidine are the therapies of choice as other vasodilating medications can potentially worsen CHS(5).