Citation

Sparks JL, Bolte JH, Dupaix RB, Jones KH, Steinberg SM, Herriott RG, Stammen JA, Donnelly BR. Stapp Car Crash J. 2007; 51: 401-432.

Affiliation

The Ohio State University, USA. jsparks@wfubmc.edu

Copyright

(Copyright © 2007, Society of Automotive Engineers SAE)

DOI

unavailable

PMID

18278606

Abstract

Liver trauma research suggests that rapidly increasing internal pressure plays a role in causing blunt liver injury. Knowledge of the relationship between pressure and the likelihood of liver injury could be used to enhance the design of crash test dummies. The objectives of this study were (1) to characterize the relationship between impact-induced pressures and blunt liver injury in an experimental model to impacts of ex vivo organs; and (2) to compare human liver vascular pressure and tissue pressure in the parenchyma with other biomechanical variables as predictors of liver injury risk. Test specimens were 14 ex vivo human livers. Specimens were perfused with normal saline solution at physiological pressures, and a drop tower applied blunt impact at varying energies. Impact-induced pressures were measured by transducers inserted into the hepatic veins and the parenchyma (caudate lobe) of ex vivo specimens. Experimentally induced liver injuries were consistent with those documented in the Crash Injury Research and Engineering Network (CIREN) database. Binary logistic regression analysis demonstrated that injury predictors associated with tissue pressure measured in the parenchyma were the best indicators of serious liver injury risk. The best injury predictor overall was the product of the peak rate of tissue pressure increase and the peak tissue pressure, P T max * P T max (pseudo-R2 = .82, p = .001). A burst injury mechanism directly related to hydrostatic pressure is postulated for the ex vivo liver loaded dynamically in a drop test experiment.

Language: en