Abstract
Resuscitation from hemorrhagic shock by infusion of isotonic (normal) saline (NS) is accompanied by a transient elevation in intracranial pressure (ICP), although cerebral edema, as measured by brain weights at 24 hours, is prevented by adequate volume resuscitation. The transient increase in ICP is not observed during hypertonic saline (HS) resuscitation. The effect of colloid resuscitation on ICP is unknown. Beagles were anesthetized, intubated, and ventilated, maintaining pCO2 between 30-45 torr. Femoral artery, pulmonary artery, and urethral catheters were positioned. ICP was measured with a subarachnoid bolt. Forty per cent of the dog's blood volume was shed and the shock state maintained for 1 hour. Resuscitation was done with shed blood and a volume of either NS (n = 5), 3% HS (n = 5), or 10% dextran-40 (D-40, n = 5) equal to the amount of shed blood. Intravascular volume was then maintained with NS. ICP fell from baseline values (4.7 +/- 3.13 mmHg) during the shock state and increased greatly during initial fluid resuscitation in NS and D-40 groups, to 16.0 +/- 5.83 mmHg and 16.2 +/- 2.68 mmHg, respectively. ICP returned to baseline values of 3.0 +/- 1.73 mmHg in the HS group with initial resuscitation and remained at baseline values throughout resuscitation. NS and D-40 ICP were greater than HS ICP at 1 hour (p less than .001) and 2 hours (p less than .05) after resuscitation. These results demonstrate that NS or colloid resuscitation from hemorrhagic shock elevates ICP and that HS prevents elevated ICP.