Intracranial hemorrhage associated with cerebral hyperperfusion syndrome following carotid endarterectomy and carotid artery stenting: retrospective review of 4494 patients

Author:

Ogasawara Kuniaki1,Sakai Nobuyuki2,Kuroiwa Terumasa3,Hosoda Kohkichi4,Iihara Koji5,Toyoda Kazunori6,Sakai Chiaki2,Nagata Izumi7,Ogawa Akira1,_ _

Affiliation:

1. Department of Neurosurgery, Iwate Medical University, Morioka;

2. Department of Neurosurgery, Kobe City General Hospital;

3. Department of Neurosurgery, Asahikawa Red Cross Hospital, Asahikawa;

4. Department of Neurosurgery, Hyogo Emergency Medical Center/Kobe Red Cross Hospital, Kobe;

5. Department of Neurosurgery, National Cardiovascular Center;

6. Cerebrovascular Division, Department of Medicine, National Cardiovascular Center, Osaka; and

7. Department of Neurosurgery, Nagasaki University School of Medicine, Nagasaki, Japan

Abstract

Object Intracranial hemorrhage associated with cerebral hyperperfusion syndrome (CHS) following carotid endarterectomy (CEA) or carotid artery stenting (CAS) is a rare but potentially devastating complication. In the present study the authors evaluated 4494 patients with carotid artery stenosis who had undergone CEA or CAS to clarify the clinicopathological features and outcomes of those with CHS and associated intracranial hemorrhage. Methods Patients with postoperative CHS were retrospectively selected, and clinicopathological features and outcomes were studied. Results Sixty-one patients with CHS (1.4%) were identified, and intracranial hemorrhage developed in 27 of them (0.6%). The onset of CHS peaked on the 6th postoperative day in those who had undergone CEA and within 12 hours in those who had undergone CAS. Results of logistic regression analysis demonstrated that poor postoperative control of blood pressure was significantly associated with the development of intracranial hemorrhage in patients with CHS after CEA (p = 0.0164). Note, however, that none of the tested variables were significantly associated with the development of intracranial hemorrhage in patients with CHS after CAS. Mortality (p = 0.0010) and morbidity (p = 0.0172) rates were significantly higher in patients with intracranial hemorrhage than in those without. Conclusions Cerebral hyperperfusion syndrome after CEA and CAS occurs with delayed classic and acute presentations, respectively. Although strict control of postoperative blood pressure prevents intracranial hemorrhage in patients with CHS after CEA, there appears to be no relationship between blood pressure control and intracranial hemorrhage in those with CHS after CAS. Finally, the prognosis of CHS in patients with associated intracerebral hemorrhage is poor.

Publisher

Journal of Neurosurgery Publishing Group (JNSPG)

Subject

Genetics,Animal Science and Zoology

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