title: Continuous monitoring of cerebrovascular autoregulation after subarachnoid hemorrhage by brain tissue oxygen pressure reactivity and its relation to delayed cerebral infarction.
abstract: OBJECTIVE
  Disturbances of cerebrovascular autoregulation are thought to be involved in delayed cerebral ischemia and infarction after aneurysmal subarachnoid hemorrhage (SAH). We hypothesized that the continuous monitoring of brain tissue oxygen (PtiO(2)) pressure reactivity enables the detection of impaired autoregulation after SAH and that impaired autoregulation is associated with delayed infarction.
  
  
  METHODS
  In 67 patients after severe SAH, continuous monitoring of cerebral perfusion pressure (CPP) and PtiO(2) was performed for an average of 7.4 days. For assessment of autoregulation, the index of PtiO(2) pressure reactivity (ORx) was calculated as a moving correlation coefficient between values of CPP and PtiO(2). Higher ORx values indicate disturbed autoregulation, whereas lower ORx values signify intact autoregulation.
  
  
  RESULTS
  Twenty patients developed delayed cerebral infarction, and 47 did not. Mean ORx was significantly higher in the infarction group compared with the noninfarction group (0.43+/-0.09 vs 0.23+/-0.14, respectively; P<0.0001). In a day-by-day analysis, ORx did not differ between groups from days 1 to 4 after SAH but was significantly higher from day 5 onward in the infarction group, indicating a deficit of autoregulatory capacity. In a logistic-regression model, ORx values from days 5 and 6 after SAH carried predictive value for the occurrence of delayed infarction but before this event ultimately occurred (P=0.003).
  
  
  CONCLUSIONS
  ORx indicates impaired autoregulation in patients who develop delayed infarction after SAH. Furthermore, this index may distinguish between patients who finally develop delayed infarction and those who do not.
authors.affiliation: Department of Neurosurgery, University of Leipzig, Leipzig, Germany. jaem@medizin.uni-leipzig.de
authors.forename: Matthias
authors.initials: M
authors.lastname: Jaeger
authors.forename: Martin U
authors.initials: MU
authors.lastname: Schuhmann
authors.forename: Martin
authors.initials: M
authors.lastname: Soehle
authors.forename: Christoph
authors.initials: C
authors.lastname: Nagel
authors.forename: Jürgen
authors.initials: J
authors.lastname: Meixensberger
mesh_terms: D000328:Adult; D000368:Aged; D001921:Brain / Q000502:physiology*; D002544:Cerebral Infarction / Q000209:etiology / Q000503:physiopathology*; D005260:Female; D006706:Homeostasis / Q000502:physiology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D008991:Monitoring, Physiologic; D010100:Oxygen / Q000502:physiology*; D011312:Pressure; D013345:Subarachnoid Hemorrhage / Q000150:complications / Q000503:physiopathology*; D013997:Time Factors
chemical_list: D010100:Oxygen