Rj. Hariri et al., TRAUMATIC BRAIN INJURY, HEMORRHAGIC-SHOCK, AND FLUID RESUSCITATION - EFFECTS ON INTRACRANIAL-PRESSURE AND BRAIN COMPLIANCE, Journal of neurosurgery, 79(3), 1993, pp. 421-427
Intracranial hypertension following traumatic brain injury is associat
ed with considerable morbidity and mortality. Hemorrhagic hypovolemia
commonly coexists with head injury in this population of patients. The
rapy directed at correcting hypovolemic shock includes vigorous volume
expansion with crystalloid' solutions. It is hypothesized that, follo
wing traumatic brain injury, cerebrovascular dysfunction results in ra
pid loss of brain compliance, resulting in increased sensitivity to ce
rebrovascular venous pressure. Increased central venous pressure (CVP)
occurring with vigorous crystalloid resuscitation may therefore contr
ibute to the loss of brain compliance and the development of intracran
ial hypertension. The authors tested this hypothesis in miniature swin
e subjected to traumatic brain injury, hemorrhage, and resuscitation.
Elevated CVP following resuscitation from hemorrhage to a high CVP sig
nificantly worsened intracranial hypertension in animals with concurre
nt traumatic brain injury, as compared to animals subjected to traumat
ic brain injury alone (mean +/- standard error of the mean: 33.0 +/- 2
.0 vs. 20.0 +/- 2.0 mm Hg, p < 0.05) or to animals subjected to the co
mbination of traumatic brain injury, hemorrhage, and resuscitation to
a low CVP (33.0 +/- 2.0 vs. 24.0 +/- 2.0 mm Hg, p < 0.05). These data
support the hypothesis that reduction in brain compliance can occur se
condary to elevation of CVP following resuscitation from hemorrhagic s
hock. This may worsen intracranial hypertension in patients with traum
atic brain injury and hemorrhagic shock.