HYPERTONIC SALINE DOES NOT IMPROVE CEREBRAL OXYGEN DELIVERY AFTER HEAD-INJURY AND MILD HEMORRHAGE IN CATS

Objectives: To investigate the effects of hypertonic saline for resusc itation after mild hemorrhagic hypotension combined with fluid percuss ion traumatic brain injury. Specifically, the effects of hypertonic sa line on intracranial pressure, cerebral blood flow (radioactive micros phere method), cerebral oxygen delivery (cerebral oxygen delivery = ce rebral blood flow x arterial oxygen content), and electroencephalograp hic activity were studied. Design: Randomized, controlled, interventio n trial. Setting: University laboratory. Subjects: Thirty four mongrel cats of either sex, anesthetized with 1.0% to 1.5% isoflurane in nitr ous oxide/oxygen (70:30). Interventions: Anesthetized (isoflurane) cat s were prepared for traumatic brain injury, and then randomly assigned to the following groups: moderate traumatic brain injury only (2.7 +/ - 0.2 atmospheres [atm], group 1); mild hemorrhage (18 mL/kg) only, fo llowed immediately by resuscitation with 10% hydroxyethyl starch in 0. 9% saline in a volume equal to shed blood (group 2); or both traumatic brain injury (2.7 +/- 0.1 atm) and mild hemorrhage, followed immediat ely by replacement of a volume equal to shed blood of 10% hydroxyethyl starch in 0.9% saline (group 3); or 3.0% saline (group 4). Measuremen ts and Main Results: Data were collected at baseline, at the end of he morrhage, and at 0, 60, and 120 mins after resuscitation (or at compar able time points in group 1). Intracranial pressure in group 1 was sig nificantly increased by traumatic brain injury at the end of hemorrhag e, immediately after resuscitation, and 60 mins after resuscitation (p < .02 vs. baseline). In group 2, intracranial pressure increased sign ificantly only immediately after resuscitation (p < .0001 vs. baseline ). Groups 3 and 4 exhibited higher, although statistically insignifica nt, intracranial pressure increases at 60 and 120 mins after resuscita tion. During resuscitation, cerebral blood flow increased significantl y (p < .02 vs, baseline) in the uninjured cats. In contrast, cerebral blood flow failed to increase during resuscitation in the cats subject ed to traumatic brain injury before hemorrhage and resuscitation. Alth ough cerebral oxygen delivery in group 2 decreased significantly immed iately, 60 mins, and 120 mins after resuscitation (p < .001 vs. baseli ne) both groups 3 and 4 had significantly lower cerebral oxygen delive ry at 60 and 120 mins after resuscitation (p < .01 and p < .005, respe ctively, vs. group 1 at 60 mins after resuscitation, and p < .01 and p < .01, respectively, vs. group 1 at 120 mins after resuscitation). Co nclusions: After a combination of hemorrhage and traumatic brain injur y, neither 10% hydroxyethyl starch nor 3.0% hypertonic saline restored cerebral oxygen delivery. Although neither trauma alone nor hemorrhag e alone altered electroencephalographic activity, the combination prod uced significant decreases in electroencephalographic activity at 60 a nd 120 mins after resuscitation in groups 3 and 4, suggesting that cer ebral oxygen delivery is inadequately restored by either resuscitation fluid. Therefore, traumatic brain injury abolished compensatory cereb ral blood flow increases to hemodilution, and neither hydroxyethyl sta rch nor 3.0% hypertonic saline restored cerebral blood flow, cerebral oxygen delivery, or electroencephalographic activity after hemorrhagic hypotension after traumatic brain injury.