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Cerebral electrophysiologic effects of resuscitation with hypertonic saline-dextran after hemorrhage
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1990
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Trauma ResuscitationTraumatic Brain InjuryVascular TraumaHypertonic SalineSocial SciencesCerebral Vascular RegulationCardiopulmonary ResuscitationStrokeIntracranial PressureBrain InjuryNeurologyNeurorehabilitationSpinal Cord InjuryCerebral Blood FlowTraumatic Cardiac ArrestReperfusion InjuryHypertonic Saline-dextranSsep ResponseNeurophysiologyBrain ElectrophysiologyElectrophysiologyConcussionAnesthesiaMedicineFluid InfusionEmergency Medicine
When brain injury accompanies hemorrhage, resuscitation with hypertonic saline (HS) improves intracranial pressure (ICP) and elastance; however, its effect on brain function after a traumatic or ischemic insult has not been assessed. This study compares the electrophysiologic response to hemorrhage and resuscitation with 7.5% NaCl + 6% dextran (HSD), 6% hetastarch (HE), or 0.9% NaCl (NS) using somatosensory evoked potentials (SSEP). Resuscitation with HE resulted in a better return of electrocortical function than with either HSD or NS (SSEP grade 2.0 +/- 0.2 for HE vs. 3.2 +/- 0.3 for HSD and 2.9 +/- 0.3 for NS; p less than .01). SSEP response correlated closet with mean arterial pressure (MAP) (r = -.53). There was no correlation between the SSEP response and cardiac index (r = .06) or ICP (r = -.04). HSD blunted the usual early increase in ICP after fluid infusion, and resulted in a lower ICP throughout resuscitation. However, the restoration of MAP and cerebral perfusion pressure (CPP) after HSD infusion was poor. The vasodilatory properties of hypertonic saline have been well described, both in the systemic and in the pulmonary vascular bed. While these characteristic usually are cited as advantages of this solution, in the case of ischemic cerebral dysfunction, this diminished vascular tone prevents early restoration of the MAP and CPP. The result is suboptimal electrocortical recovery after hemorrhage.