Brain Edema and Neurologic Status Following Head Trauma in the Rat

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Abstract
Disagreement exists regarding the need to restrict the administration of fluid and glucose following head injury to prevent cerebral edema and neurologic deterioration. We examined whether blood osmolality and glucose, neurologic outcome, and the development of brain edema following head trauma were altered by intravenous infusion of large volumes of isotonic or hypertonic fluids that contained or did not contain glucose. Fifty-five rats that survived ether anesthesia and closed head trauma (delivered using a weight drop device) were assigned to one of five groups. In the first group no fluid was infused. In the second group minimal volumes of saline were infused during placement of a jugular vein catheter. In the three remaining groups 10 ml.kg-1.h-1 of either total parenteral nutrition (TPN) (glucose 25%, amino acids 4.25%, 40 mEq/l sodium and 40 mEq/l potassium, 1935 mOsm/kg), dextrose 5% in 0.45% saline (495 mOsm/kg), or Haemaccel (isotonic plasma expander, 298 mOsm/kg) was infused via the jugular vein. Following head trauma and cannula placement, ether was discontinued. Neurologic severity score at 1 and 18 h after head trauma was used to assess neurologic outcome. A score between 0 and 6 was assigned by an observer who was blinded as to the experimental groups, with 0 representing no neurologic damage and 6 representing severe damage. Specific gravity of brain tissue samples containing gray matter and subcortical white matter from the traumatized and contralateral hemispheres was measured at 18 h after head trauma to determine the development of brain edema. There were no statistically significant differences in neurologic outcome and brain edema between the groups.(ABSTRACT TRUNCATED AT 250 WORDS)

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