Outcome after Hemorrhagic Shock in Trauma Patients

Heckbert, Susan R.; Vedder, Nicholas B.; Hoffman, Wilma; Winn, Robert K.; Hudson, Leonard D.; Jurkovich, Gregory J.; Copass, Michael K.; Harlan, John M.; Rice, Charles L.; Maier, Ronald V.

doi:10.1097/00005373-199809000-00022

Cited by 336 publications

(192 citation statements)

References 12 publications

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“…These complications result in an increase in mortality even after successful resuscitation [1,[9][10][11]. Avoiding this lethal cascade requires hemorrhage control prior to arrival at the hospital minimizing blood loss and allowing for earlier resuscitation [12][13][14]15].…”

Section: Introductionmentioning

confidence: 99%

The Effects of BleedArrest, Celox, and TraumaDex on Hemorrhage Control in a Porcine Model

Gegel

Burgert

Cooley

et al. 2010

Journal of Surgical Research

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Background. Hemorrhage is the second leading cause of death in civilian trauma and the leading cause of preventable death in military trauma. The purpose of this study was to examine the effectiveness of three hemostatic agents: BleedArrest, TraumaDex, and Celox.Materials and Methods. This was a prospective, experimental study using male Yorkshire swine. The pigs (n [ 5 per group) were randomly assigned to one of the following: BleedArrest, TraumaDex, Celox, or control. To simulate a trauma injury, the investigators generated a complex groin injury with transection of the femoral artery and vein in all pigs. After 1 min of uncontrolled hemorrhage, one of the hemostatic agents was poured into the wound, followed by standard wound packing. The control group underwent the same procedures with the exception of the hemostatic agents. In all groups, 5 min of direct manual pressure was applied to the wound followed by a standard pressure dressing. After 30 min, dressings were removed, and the amount of bleeding was determined.Results. There were significant differences between the BleedArrest (mean [ 21.2, SD ± 36.6 mL) TraumaDex (mean [ 68, SD ± 103.5 mL) and Celox (mean [ 18.l6, SD ± 41.6 mL) groups compared with Control group (mean [ 230, SD ± 154 mL) (P < 0.05). However, there were no statistically significant difference between BleedArrest, TraumaDex, and Celox groups (P [ 0.478).Conclusions. BleedArrest, Celox, and TraumaDex were statistically and clinically superior at controlling hemorrhage compared with the standard pressure dressing in the control group. Published by Elsevier Inc.

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Section: Introductionmentioning

confidence: 99%

The Effects of BleedArrest, Celox, and TraumaDex on Hemorrhage Control in a Porcine Model

Gegel

Burgert

Cooley

et al. 2010

Journal of Surgical Research

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“…The liver with its important metabolic and homeostasis functions is among the most frequently affected organs after hemorrhage-induced hypotension in humans (12). Although the liver tolerates prolonged periods of diminished oxygen delivery, primary (hypoxic) or secondary (ischemia and reperfusion) hepatocellular injury may occur and is associated with metabolic changes, inflammation, and eventually cell death (13).…”

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confidence: 99%

Liver apoptosis is age dependent and is reduced by activation of peroxisome proliferator-activated receptor-γ in hemorrhagic shock

Zingarelli

Chima

O’Connor

et al. 2010

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…Hemorrhagic shock and subsequent resuscitation are frequently associated with endotoxemia in animals and humans (41). The liver, with its crucial involvement in metabolism and homeostasis, is among the most frequently affected organs after hemorrhage-induced hypotension in humans (17). The liver also acts to clear and detoxify toxins and bacterial products entering via the portal vein from the gut.…”

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confidence: 99%

Lipopolysaccharide-binding protein modulates hepatic damage and the inflammatory response after hemorrhagic shock and resuscitation

Lehnert¹,

Uehara²,

Bradford³

et al. 2006

American Journal of Physiology-Gastrointestinal and Liver Physi

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Lipopolysaccharide-binding protein modulates hepatic damage and the inflammatory response after hemorrhagic shock and resuscitation. Am J Physiol Gastrointest Liver Physiol 291: G456 -G463, 2006. First published May 18, 2006 doi:10.1152/ajpgi.00480.2005.-Hemorrhagic shock and resuscitation cause endotoxemia and hepatocellular damage. Because lipopolysaccharide-binding protein (LBP) enhances cellular responses to endotoxin, our aim was to determine whether LBP contributes to hemorrhage/resuscitation-induced injury by comparing LBP knockout and wild-type mice. Under pentobarbital anaesthesia, wild-type and LBP-deficient mice were hemorrhaged to 30 mmHg for 3 h and then resuscitated with shed blood plus half the volume of lactated Ringer solution. Serum alanine aminotransferase (ALT) necrosis, neutrophil infiltration, and 4-hydroxynonenal by histology/ cytochemistry and stress kinase activation by immunoblot analysis were then determined. ALT in wild-type mice was 2,461 Ϯ 383 and 1,418 Ϯ 194 IU/l (means Ϯ SE), respectively, at 2 and 6 h after resuscitation versus sham ALT of 102 Ϯ 6 IU/l. In LBP-deficient mice, ALT was blunted at both time points to 1,108 Ϯ 340 and 619 Ϯ 171 IU/l (P Ͻ 0.05). Liver necrosis after 6 h was also attenuated from 3.5 Ϯ 0.8% in wild-type mice to 1.3 Ϯ 0.5% in LBP-deficient mice (P Ͻ 0.05). After hemorrhage/resuscitation, neutrophil infiltration increased 71% more in wild-type than LBP knockout mice. Similarly, hepatic 4-hydroxynonenal staining, indicative of lipid peroxidation, decreased from 33.8 Ϯ 4.5% in wild-type mice to 11.6 Ϯ 1.9% in knockout mice (P Ͻ 0.05).

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Outcome after Hemorrhagic Shock in Trauma Patients

Abstract: Hemorrhage-induced hypotension in trauma patients is predictive of high mortality (54%) and morbidity. The requirement for large volumes of crystalloid was associated with increased mortality.

Cited by 336 publications

References 12 publications

The Effects of BleedArrest, Celox, and TraumaDex on Hemorrhage Control in a Porcine Model

The Effects of BleedArrest, Celox, and TraumaDex on Hemorrhage Control in a Porcine Model

Liver apoptosis is age dependent and is reduced by activation of peroxisome proliferator-activated receptor-γ in hemorrhagic shock

Lipopolysaccharide-binding protein modulates hepatic damage and the inflammatory response after hemorrhagic shock and resuscitation

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