Hypertonic fluid resuscitation improves cerebral oxygen delivery and reduces intracranial pressure after hemorrhagic shock.

Prospective clinical studies have shown that hypotension from hemorrhage contributes to increased morbidity and mortality in patients with traumatic brain injury. It is implied that poorer outcome is the result of secondary brain injury from impaired cerebral oxygen delivery (cO2del). We studied the early and late effects of hypertonic sodium lactate (HSL: 500 mOsm/L) resuscitation on mean arterial pressure (MAP), cardiac output (CO), systemic oxygen delivery (sO2del), cerebral perfusion pressure (CPP), intracranial pressure (ICP), cO2del, cerebral blood flow (CBF), serum osmolality, and cortical water content (CWC) in a porcine model of hemorrhagic shock. Swine were randomized to receive a bolus (4 mL/kg) of either lactated Ringer's solution (LR: 274 mOsm/L) or HSL after shock, followed by either LR or HSL to return MAP to baseline levels. Shed blood was returned 1 hour after resuscitation, and all animals were studied for 24 hours. Control animals were instrumented only. The HSL resuscitation significantly increased cO2del and CBF for 24 hours postresuscitation when compared with LR. The ICP in the HSL-treated animals was significantly lower throughout the postresuscitation phase when compared with the LR-treated animals (p less than 0.05). The CWC was significantly lower in the HSL-treated animals (p less than 0.05). We attribute these effects to hypertonic dehydration of both the brain parenchyma and the cerebrovascular endothelium. These data suggest that by decreasing ICP and improving cO2del after shock, HSL could decrease secondary brain injury when brain injury and shock occur together.