title: Cerebral extraction of oxygen and intracranial hypertension in severe, acute, pediatric brain trauma: preliminary novel management strategies.
abstract: OBJECTIVE
  To evaluate long-term clinical outcomes after severe, acute, pediatric brain trauma, in relation to cerebral extraction of oxygen (CEO(2)) and intracranial pressure abnormalities treated with a protocol to simultaneously normalize both parameters.
  
  
  METHODS
  Forty-five acutely comatose children who had sustained severe, non-missile brain trauma were prospectively evaluated and treated according to a protocol to maintain normalized values not only for intracranial pressure and perfusion pressure but also for CEO(2) (the arteriojugular oxyhemoglobin saturation difference). Six-month clinical outcomes were assessed in relation to physiological abnormalities observed during the acute phase of injury.
  
  
  RESULTS
  At 6 months after injury, 37 children (82.2%) had achieved favorable clinical outcomes, whereas eight children (17.8%) had not. The mortality rate was 4.4% (two children only). For the overall series, intracranial hypertension was closely associated with the development of relative cerebral hyperperfusion (decreased CEO(2)), especially after postinjury Day 1. A comparison of data for children with favorable versus unfavorable clinical outcomes revealed statistically significant between-group differences for high intracranial pressure and low CEO(2) values, both of which were more prominent in the unfavorable outcome group. No significant within- or between-group differences with respect to blood pressure were observed.
  
  
  CONCLUSIONS
  In severe, acute, non-missile pediatric brain trauma, phasic physiological patterns demonstrated an association between the development of intracranial hypertension and relative cerebral hyperperfusion (decreased global CEO(2)), especially after postinjury Day 1. Unfavorable clinical outcomes were significantly related to more pronounced intracranial hypertension and more profound concomitant decreases in CEO(2), indicating hyperoxic uncoupling between global cerebral consumption of oxygen and cerebral blood flow.
authors.affiliation: The Comprehensive International Center for Neuroemergencies, Federal University of São Paulo, and Clean Field Hospital, São Paulo, Brazil.
authors.forename: Julio
authors.initials: J
authors.lastname: Cruz
authors.forename: Patricia
authors.initials: P
authors.lastname: Nakayama
authors.forename: Janete H
authors.initials: JH
authors.lastname: Imamura
authors.forename: Karl G W
authors.initials: KG
authors.lastname: Rosenfeld
authors.forename: Helena S
authors.initials: HS
authors.lastname: de Souza
authors.forename: Gina Valéria F
authors.initials: GV
authors.lastname: Giorgetti
mesh_terms: D000208:Acute Disease; D001921:Brain / Q000378:metabolism*; D001930:Brain Injuries / Q000150:complications / Q000503:physiopathology* / Q000628:therapy; D002560:Cerebrovascular Circulation; D002648:Child; D002675:Child, Preschool; D003128:Coma / Q000209:etiology; D006801:Humans; D019586:Intracranial Hypertension / Q000503:physiopathology*; D007427:Intracranial Pressure; D010101:Oxygen Consumption; D011446:Prospective Studies; D012720:Severity of Illness Index