The relationship of fluid balance and sodium administration to cerebral edema formation and intracranial pressure in a porcine model of brain injury.
BACKGROUND
Fluid and sodium restriction have been advocated after brain injury as a means of controlling intracranial pressure (ICP). Recent clinical data showing no significant relationships between the amount of fluid infused or sodium administered (Na) and ICP question this practice.


OBJECTIVE
To analyze the relationship of amount of fluid, Na, and fluid balance to cerebral edema formation and ICP.


METHODS
A cryogenic brain injury with and without hemorrhagic shock was studied after 24 hours in swine (n = 35) randomized to receive either lactated Ringer's solution (LR) or hypertonic sodium lactate (HSL). Cerebral edema formation as indicated by cortical water content (CWC) was determined by measurement of specific gravity.


RESULTS
There was a significant positive correlation between the following variables: (1) amount of fluid and ICP (r = 0.598; p < 0.01); (2) fluid balance and ICP (r = 0.684; p < 0.01); and (3) free water and ICP (r = 0.614; p < 0.01). There was a significant negative correlation between serum osmolarity and ICP (r = -0.654; p < 0.01). The study failed to demonstrate a significant correlation between Na and ICP, amount of fluid and CWC, or fluid balance and CWC.


CONCLUSIONS
These data suggest that both the volume of fluid infused and the fluid balance do affect the ICP, but the amount of Na infused does not. The lack of a significant correlation between any of the independent variables and CWC suggests that their effect on ICP is not related to cerebral edema formation. These findings, combined with the observed significant positive correlation between free H2O infused and ICP, and the significant negative correlation between serum osmolarity and ICP, suggest that HSL resuscitation increases intracranial compliance after brain injury while LR decreases it. The data also suggest that free water restriction is warranted in patients with head injuries.
Ramming
S
S
Department of Surgery, University of Vermont, College of Medicine, Burlington.
Shackford
S R
SR
Zhuang
J
J
Schmoker
J D
JD
D000818:Animals; D001834:Body Water / Q000378:metabolism; D001929:Brain Edema / Q000209:etiology / Q000503:physiopathology*; D001930:Brain Injuries / Q000150:complications / Q000503:physiopathology / Q000628:therapy*; D002540:Cerebral Cortex / Q000378:metabolism; D005440:Fluid Therapy; D006439:Hemodynamics; D007427:Intracranial Pressure; D007552:Isotonic Solutions / Q000008:administration & dosage; D012151:Resuscitation; D000077325:Ringer's Lactate; D012462:Saline Solution, Hypertonic / Q000008:administration & dosage*; D013046:Specific Gravity; D013552:Swine; D014882:Water-Electrolyte Balance
D007552:Isotonic Solutions; D000077325:Ringer's Lactate; D012462:Saline Solution, Hypertonic