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Cerebral hyperperfusion syndrome after carotid endarterectomy: predictive factors and hemodynamic changes
Enrico Ascher1, Natalia Markevich, Richard W Schutzer
1Division of Vascular Surgery, Department of Surgery, Maimonides Medical Center, Brooklyn, NY, USA. eascher@maimonides.org
Insights
Cerebral hyperperfusion syndrome (CHS) is not strongly linked to severe carotid disease or hypertension. Recent contralateral carotid endarterectomy (CEA) appears to be a significant predictor of CHS development.
Area of Science:
- Neurology
- Vascular Surgery
Background:
- Cerebral hyperperfusion syndrome (CHS) is often attributed to impaired cerebral autoregulation following chronic ischemia.
- Preoperative factors like increased intraoperative cerebral blood flow, carotid artery disease, and hypertension are commonly implicated in CHS development.
Purpose of the Study:
- To investigate the clinical experience with CHS following carotid endarterectomy (CEA).
- To evaluate the correlation between CHS and commonly believed causative factors, including carotid disease severity and hypertension.
Main Methods:
- A retrospective analysis of 455 CEA procedures performed between March 2000 and February 2002.
- Detailed review of patient demographics, surgical history, preoperative and intraoperative findings, and postoperative outcomes.
- Carotid artery duplex scanning was performed intraoperatively and postoperatively to assess blood flow and stenosis.
Main Results:
- Nine patients (2%) developed CHS postoperatively, presenting with symptoms such as severe headache, seizures, and stroke.
- Intraoperative cerebral blood flow and the severity of ipsilateral or contralateral carotid stenosis were not significantly different in CHS patients compared to controls.
- Patients who developed CHS had significantly higher mean ICA volume flow and peak systolic velocity at symptom onset.
- Only 3 CHS patients had elevated blood pressure (>160 mm Hg) at symptom onset.
Conclusions:
- The study findings do not support the prevailing belief that severe carotid disease or hypertension are primary drivers of CHS.
- A history of recent contralateral CEA (within 3 months) emerged as a potential predictive factor for CHS development.
- Further research is warranted to elucidate the precise mechanisms and risk factors associated with CHS post-CEA.
Purpose:
It is believed that cerebral hyperperfusion syndrome (CHS) is caused by loss of cerebral autoregulation resulting from chronic cerebral ischemia and that factors including increased intraoperative cerebral blood flow, ipsilateral or contralateral carotid disease, and postoperative hypertension may cause CHS. We describe our experience with CHS, which diverges from published reports.
Materials And Methods:
From March 2000 to February 2002 we performed 455 carotid endarterectomy (CEA) procedures in 404 patients at our institution. CHS developed 1 to 8 days (mean, 3.2 +/- 2.5 days) postoperatively in 9 patients (2%), 6 women and 3 men, whose age ranged from 52 to 84 years (mean, 69 +/- 8 years). Indications for surgery in 8 patients without neurologic symptoms were ipsilateral internal carotid artery (ICA) stenoses ranging from 70% to 99% (mean, 80% +/- 7%); the remaining patient had an ipsilateral stroke, with good clinical recovery, 7 weeks before CEA. Only 1 patient had significant contralateral ICA stenosis (70%). However, 5 patients had undergone contralateral CEA within the previous 3 months. CHS symptoms were severe headache in 5 patients, seizures in 3 patients (1 stroke), and visual disturbance and ataxia in 1 patient. All 404 patients (455 cases) underwent intraoperative and early (2 weeks) postoperative carotid artery duplex scanning. The 9 patients with CHS also underwent carotid artery duplex scanning at the time of the neurologic event.
Results:
Mean intraoperative ICA volume flow (MICAVF) in the 9 CHS cases was not significantly different from that in the other 446 cases (170 +/- 47 mL/min and 182 +/- 81 mL/min, respectively). However, mean ICA volume flow (481 +/- 106 mL/min) and peak systolic velocity (PSV) (108 +/- 33 cm/s) for the 9 CHS cases measured at onset of symptoms were higher than those for the remaining 446 cases (267 +/- 87 mL/min and 80 +/- 26 cm/s, respectively) (P <.01). Of the 9 patients with CHS, only 3 had systolic blood pressures more than 160 mm Hg at onset of symptoms. Severity of ipsilateral and contralateral ICA stenoses was not significantly different between the 9 CHS cases and the remaining 446 cases.
Conclusions:
These data do not corroborate the common belief that CHS occurs preferentially in patients with severe ipsilateral or contralateral carotid disease, increased intraoperative cerebral perfusion, or severe hypertension. Recently performed contralateral CEA (<3 months) appears to be predictive of CHS.