Clinical risk predictors for cerebral hyperperfusion syndrome after carotid endarterectomy
- 1Division of Critical Care Neurology, Department of Neurology, Northwestern University, Chicago, Illinois, USA
- 2Division of Vascular and Critical Care Neurology, Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA
- 3Division of Vascular and Endovascular Surgery, Department of Surgery, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA
- 4Division of Interventional Neuroradiology, Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA
- 5Section of Vascular Medicine, Division of Cardiology, Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA
- Correspondence to Dr Matthew Brandon Maas, Division of Critical Care Neurology, Department of Neurology, Northwestern University, 710 N Lake Shore Drive, 11th Floor, Chicago, IL 60611, USA;
- Received 11 July 2012
- Revised 5 September 2012
- Accepted 20 November 2012
- Published Online First 15 December 2012
Background Cerebral hyperperfusion syndrome (CHS) is an important complication of carotid endarterectomy (CEA), yet prior research has been limited to small cohorts and retrospective analyses, or studies using radiographic rather than clinical definitions.
Methods A prospective monitoring system was implemented to monitor CEA outcomes at a major academic medical centre. Independent, trained monitors from the neurology department examined all patients undergoing CEA preoperatively and postoperatively at 24 h and 30 days. Clinical variables were analysed to identify risk factors for CHS, which was defined as cases with postoperative development of a severe headache, new neurological deficits without infarction, seizure or intracerebral haemorrhage.
Results Between 2008 and 2010, 841 CEAs were monitored and CHS occurred in 14 (1.7%) subjects, including seizures in 5 (0.6%) and intracerebral haemorrhage in 4 (0.5%). Univariate analysis identified a history of dyslipidaemia, coronary artery disease, diastolic blood pressure, intraoperative shunt use and non-elective CEA (performed during hospitalisation for a symptomatic ipsilateral stroke, transient ischaemic attack or amaurosis fugax) as potential risks for CHS (all p≤0.15); other variables—including the degree of ipsilateral and contralateral stenosis, operative time, intraoperative EEG slowing, history of prior CEA or carotid stent and time from prior carotid interventions— were not significant. Logistic regression confirmed the risk association between non-elective CEA and CHS (p=0.046).
Conclusions Independent, prospective monitoring of a large cohort of CEA cases identified a brief time interval between ischaemic symptoms and endarterectomy as the clearest risk factor for CHS.