CEREBRAL HEMODYNAMIC AND METABOLIC CHANGES CAUSED BY BRAIN RETRACTIONAFTER ANEURYSMAL SUBARACHNOID HEMORRHAGE

OBJECTIVE: The cerebral hemodynamic and metabolic effects of aneurysma l subarachnoid hemorrhage are complex. To investigate the impact of su rgical retraction, we analyzed positron emission tomography (PET) stud ies that measured the regional cerebral metabolic rate for oxygen, reg ional oxygen extraction fraction, and regional cerebral blood flow in four patients before and after right frontotemporal craniotomies for c lipping of ruptured anterior circulation aneurysms. METHODS: Preoperat ive studies were conducted 1 day before surgery and postoperative stud ies 6 to 17 days after surgery. No patient had hydrocephalus or intrac erebral hematoma. At the time of the second PET study, none of the pat ients had signs of clinical vasospasm. Regional measurements were obta ined from the right ventrolateral frontal and anterior temporal region s corresponding to the area of retraction and compared to the same reg ions in the opposite hemisphere. To establish a quantitative means to differentiate between hemodynamic and metabolic changes related to art erial vasospasm and those caused by brain retraction, we studied a sec ond group of preoperative patients, who had undergone PET during angio graphic and clinical vasospasm. RESULTS: There was a 45% reduction in regional cerebral metabolic rate for oxygen (1.87 +/- 0.22 to 1.04 +/- 0.28 mi 100 g(-1) min(-1)) and 32% reduction in regional oxygen extra ction fraction (0.41 +/- 0.04 to 0.28 +/- 0.03) in the region of retra ction but no change in the opposite hemisphere (paired t test; P = 0.0 42 and 0.003, respectively). There was no change in regional cerebral blood flow in any region. Brain retraction produced a focal area of ti ssue injury at the site of retractor blade placement, as compared to m ore diffuse vascular territory changes produced by vasospasm. CONCLUSI ON: This reduction in the cerebral metabolic rate of oxygen and the ox ygen extraction fraction indicates a primary reduction in metabolism a nd uncoupling of flow and metabolism (luxury perfusion). Similar findi ngs of luxury perfusion have been reported after ischemic stroke and t raumatic brain injury. Further studies will be necessary to fully unde rstand the clinical and pathophysiological significance of these obser vations.