Cerebral extraction of oxygen and intracranial hypertension in severe, acute, pediatric brain trauma: Preliminary novel management strategies

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Cruz, J.
Nakayama, P.
Imamura, J. H.
Rosenfeld, KGW
Souza, H. S. de
Giorgetti, GVF
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OBJECTIVE: To evaluate long-term clinical outcomes after severe, acute, pediatric brain trauma, in relation to cerebral extraction of oxygen (CEO2) 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 CEO2 (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 CEO2), 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 CEO2 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.CONCLUSION: 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 CEO2), especially after postinjury Day 1. Unfavorable clinical outcomes were significantly related to more pronounced intracranial hypertension and more profound concomitant decreases in CEO2, indicating hyperoxic uncoupling between global cerebral consumption of oxygen and cerebral blood flow.
Neurosurgery. Philadelphia: Lippincott Williams & Wilkins, v. 50, n. 4, p. 774-779, 2002.