Gt. Trevisani et al., BRAIN EDEMA FORMATION AFTER BRAIN INJURY, SHOCK, AND RESUSCITATION - EFFECTS OF VENOUS AND ARTERIAL-PRESSURE, The journal of trauma, injury, infection, and critical care, 37(3), 1994, pp. 452-458
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 br
ain injury and hemorrhagic shock, we studied CVP, mean arterial pressu
re (MAP), ICP, and cortical water content (CWC, as cortical specific g
ravity) at baseline (BL), 45 minutes after shock (H45), and 1, 3, 6, 1
2, 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 inj
ury and shock. Results: Brain injury significantly increased ICP and C
WC. 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 n
ot in the other groups at any time period. There was no significant co
rrelation between CVP and ICP or CWC in any group at any time interval
. Conclusions: These data suggest that brain edema formation in the in
jured hemisphere is related to MAP and not CVP, but variability in MAP
accounts for only 29% of the variability in CWC and ICP, suggesting t
he importance of factors other than hydrostatic pressure in determinin
g the amount of edema and the ICP after brain injury. Previous work de
monstrating 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.