BACKGROUND: Recent work suggests that increased intracranial pressure (ICP) following brain injury and shock is related to increased central venous pressure (CVP) following resuscitation. OBJECTIVE: To analyze the relationship of intravascular pressures to edema formation and ICP in an experimental model. METHODS: In a porcine model of cryogenic brain injury and hemorrhagic shock, we studied CVP, mean arterial pressure (MAP), ICP, and cortical water content (CWC, as cortical specific gravity) at baseline (BL), 45 minutes after shock (H45), and 1, 3, 6, 12, and 24 hours (H) after resuscitation. Group 1 was the control group, group 2 brain injury only, group 3 shock only, and group 4 brain injury and shock. RESULTS: Brain injury significantly increased ICP and CWC. Mean arterial pressure significantly correlated with ICP (r = 0.54, p = 0.02) and with CWC (r = -0.48, p = 0.03) in group 4 at 24H but not in the other groups at any time period. There was no significant correlation between CVP and ICP or CWC in any group at any time interval. CONCLUSIONS: These data suggest that brain edema formation in the injured hemisphere is related to MAP and not CVP, but variability in MAP accounts for only 29% of the variability in CWC and ICP, suggesting the importance of factors other than hydrostatic pressure in determining the amount of edema and the ICP after brain injury. Previous work demonstrating the significant correlation of polymorphonuclear leukocyte infiltration with ICP (r = 0.71, p < 0.001) and with CWC (r = -0.63, p < 0.001) suggests that inflammation may be one of these factors.
BACKGROUND: Recent work suggests that increased intracranial pressure (ICP) following brain injury and shock is related to increased central venous pressure (CVP) following resuscitation. OBJECTIVE: To analyze the relationship of intravascular pressures to edema formation and ICP in an experimental model. METHODS: In a porcine model of cryogenic brain injury and hemorrhagic shock, we studied CVP, mean arterial pressure (MAP), ICP, and cortical water content (CWC, as cortical specific gravity) at baseline (BL), 45 minutes after shock (H45), and 1, 3, 6, 12, and 24 hours (H) after resuscitation. Group 1 was the control group, group 2 brain injury only, group 3 shock only, and group 4 brain injury and shock. RESULTS:Brain injury significantly increased ICP and CWC. Mean arterial pressure significantly correlated with ICP (r = 0.54, p = 0.02) and with CWC (r = -0.48, p = 0.03) in group 4 at 24H but not in the other groups at any time period. There was no significant correlation between CVP and ICP or CWC in any group at any time interval. CONCLUSIONS: These data suggest that brain edema formation in the injured hemisphere is related to MAP and not CVP, but variability in MAP accounts for only 29% of the variability in CWC and ICP, suggesting the importance of factors other than hydrostatic pressure in determining the amount of edema and the ICP after brain injury. Previous work demonstrating the significant correlation of polymorphonuclear leukocyte infiltration with ICP (r = 0.71, p < 0.001) and with CWC (r = -0.63, p < 0.001) suggests that inflammation may be one of these factors.