title: Acute hypoperfusion immediately after subarachnoid hemorrhage: a xenon contrast-enhanced CT study.
abstract: The acute neurological deficit present immediately after subarachnoid hemorrhage (SAH) correlates with overall outcome. Only limited data are available to quantify changes in cerebral perfusion in this acute phase, and this study sought to characterize those changes within the first 12 h post-SAH. Xenon contrast-enhanced CT scanning was performed in 17 patients (Hunt and Hess grade [HH] 1-3, n = 9; HH 4-5, n = 8) within 12 h after SAH. Cerebral blood flow (CBF) was analyzed in all cortical and central vascular regions of interest (ROI), as well as infratentorial ROI. Hemodynamic stress distribution (central/cortical ROI) was also calculated. Asymptomatic patients without perfusion deficits served as controls (n = 5), and Glasgow Outcome Scale score (GOS) was determined 3 months after the event. Intracranial pressure (ICP) and cerebral perfusion pressure (CPP) were within normal limits in all patients. CBF was significantly reduced in all patients with SAH (34 mL/100 g x min) compared to controls (67 mL/100 g x min; p < 0.001). Patients in better clinical condition (HH 1-3) presented with significantly less reduction of CBF (41 mL/100 g x min) compared to patients with more severe hemorrhage (HH 4-5: 24 mL/100 g x min; p < 0.001), and had better outcomes. Changes in perfusion were more pronounced in supratentorial than in infratentorial ROI. Hemodynamic stress distribution was most pronounced in patients with higher HH grade (p < 0.05). The first 12 h after SAH are characterized by persistent, severe reduction of CBF, which in turn correlates with HH grade, but is independent of ICP or CPP. Acute peripheral vasospasm of the microvasculature, not detectable by conventional angiography, may account for this early phase of prolonged hypoperfusion.
authors.affiliation: Department of Neurosurgery, Universitätsmedizin Mannheim, University of Heidelberg , Mannheim, Germany. gerrit.schubert@gmx.net
authors.forename: Gerrit Alexander
authors.initials: GA
authors.lastname: Schubert
authors.forename: Marcel
authors.initials: M
authors.lastname: Seiz
authors.forename: Aldemar Andrés
authors.initials: AA
authors.lastname: Hegewald
authors.forename: Jérôme
authors.initials: J
authors.lastname: Manville
authors.forename: Claudius
authors.initials: C
authors.lastname: Thomé
mesh_terms: D000208:Acute Disease; D000328:Adult; D000368:Aged; D001794:Blood Pressure / Q000502:physiology; D001921:Brain / Q000098:blood supply / Q000000981:diagnostic imaging / Q000503:physiopathology; D002545:Brain Ischemia / Q000000981:diagnostic imaging* / Q000209:etiology / Q000503:physiopathology*; D002536:Cerebral Arteries / Q000503:physiopathology; D002560:Cerebrovascular Circulation / Q000502:physiology; D003287:Contrast Media; D005260:Female; D023261:Glasgow Outcome Scale; D006439:Hemodynamics / Q000502:physiology; D006801:Humans; D007427:Intracranial Pressure / Q000502:physiology; D008297:Male; D008833:Microcirculation / Q000502:physiology; D008875:Middle Aged; D012720:Severity of Illness Index; D013312:Stress, Physiological / Q000502:physiology; D013345:Subarachnoid Hemorrhage / Q000150:complications / Q000000981:diagnostic imaging* / Q000503:physiopathology*; D014057:Tomography, X-Ray Computed / Q000379:methods*; D020301:Vasospasm, Intracranial / Q000000981:diagnostic imaging / Q000209:etiology / Q000503:physiopathology; D014978:Xenon
chemical_list: D003287:Contrast Media; D014978:Xenon