TRAUMATIC BRAIN INJURY, HEMORRHAGIC-SHOCK, AND FLUID RESUSCITATION - EFFECTS ON INTRACRANIAL-PRESSURE AND BRAIN COMPLIANCE

Citation
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
Citations number
34
Categorie Soggetti
Neurosciences,Surgery
Journal title
ISSN journal
00223085
Volume
79
Issue
3
Year of publication
1993
Pages
421 - 427
Database
ISI
SICI code
0022-3085(1993)79:3<421:TBIHAF>2.0.ZU;2-2
Abstract
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.