Journal articles: 'Trauma hemorrhagic shock'

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Horton, J. W. "Cardiac contractile effects of ethanolism and hemorrhagic shock." American Journal of Physiology-Heart and Circulatory Physiology 262, no. 4 (April 1, 1992): H1096—H1103. http://dx.doi.org/10.1152/ajpheart.1992.262.4.h1096.

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Moderate ethanol consumption, associated with cardiac depression, occurs in greater than 50% of trauma. Hemorrhagic shock, a significant component of trauma in the clinical setting, causes intrinsic cardiac contractile dysfunction. In this study, we used an isolated heart model to determine whether acute ethanolism increases the cardiovascular risk associated with hemorrhagic shock. We hypothesized that hemorrhagic shock in the acutely intoxicated subject would cause significantly greater cardiac dysfunction compared with that observed in a nonintoxicated subject. A total of 116 guinea pigs was divided into four groups: control (no ethanol, no shock), ethanol intoxication alone (1 mg/kg iv), hemorrhagic shock alone (mean arterial blood pressure, 30 mmHg for 2 h), and a combination of hemorrhagic shock plus ethanol. Half of the hearts in each group were used for isolated heart studies, and half were used to assess myocardial cell membrane integrity. Ethanol alone reduced peak isovolumic pressure by 36%, maximal rate of left ventricular pressure (LVP) rise by 27%, and maximal rate of LVP fall by 35%; however, contractile depression was significantly greater in the intoxicated, hemorrhaged, group compared with the nonintoxicated, hemorrhaged, group (P less than 0.05). Both ethanol and hemorrhage independently altered myocardial cell volume regulation; however, abnormalities in myocardial cell volume regulation induced by hemorrhage were similar in the intoxicated and nonintoxicated groups. Our data show that hemorrhagic shock causes significantly greater cardiac contractile dysfunction in the intoxicated subject.

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D'Alessandro, Angelo, Hunter B. Moore, Ernest E. Moore, Matthew Wither, Travis Nemkov, Eduardo Gonzalez, Anne Slaughter, et al. "Early hemorrhage triggers metabolic responses that build up during prolonged shock." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 308, no. 12 (June 15, 2015): R1034—R1044. http://dx.doi.org/10.1152/ajpregu.00030.2015.

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Metabolic staging after trauma/hemorrhagic shock is a key driver of acidosis and directly relates to hypothermia and coagulopathy. Metabolic responses to trauma/hemorrhagic shock have been assayed through classic biochemical approaches or NMR, thereby lacking a comprehensive overview of the dynamic metabolic changes occurring after shock. Sprague-Dawley rats underwent progressive hemorrhage and shock. Baseline and postshock blood was collected, and late hyperfibrinolysis was assessed (LY30 >3%) in all of the tested rats. Extreme and intermediate time points were collected to assay the dynamic changes of the plasma metabolome via ultra-high performance liquid chromatography-mass spectrometry. Sham controls were used to determine whether metabolic changes could be primarily attributable to anesthesia and supine positioning. Early hemorrhage-triggered metabolic changes that built up progressively and became significant during sustained hemorrhagic shock. Metabolic phenotypes either resulted in immediate hypercatabolism, or late hypercatabolism, preceded by metabolic deregulation during early hemorrhage in a subset of rats. Hemorrhagic shock consistently promoted hyperglycemia, glycolysis, Krebs cycle, fatty acid, amino acid, and nitrogen metabolism (urate and polyamines), and impaired redox homeostasis. Early dynamic changes of the plasma metabolome are triggered by hemorrhage in rats. Future studies will determine whether metabolic subphenotypes observed in rats might be consistently observed in humans and pave the way for tailored resuscitative strategies.

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GODINHO, MAURICIO, PEDRO PADIM, PAULO ROBERTO B. EVORA, and SANDRO SCARPELINI. "Curbing Inflammation in hemorrhagic trauma: a review." Revista do Colégio Brasileiro de Cirurgiões 42, no. 4 (August 2015): 273–78. http://dx.doi.org/10.1590/0100-69912015004013.

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Trauma is one of the world's leading causes of death within the first 40 years of life and thus a significant health problem. Trauma accounts for nearly a third of the lost years of productive life before 65 years of age and is associated with infection, hemorrhagic shock, reperfusion syndrome, and inflammation. The control of hemorrhage, coagulopathy, optimal use of blood products, balancing hypo and hyperperfusion, and hemostatic resuscitation improve survival in cases of trauma with massive hemorrhage. This review discusses inflammation in the context of trauma-associated hemorrhagic shock. When one considers the known immunomodulatory effects of traumatic injury, allogeneic blood transfusion, and the overlap between patient populations, it is surprising that so few studies have assessed their combined effects on immune function. We also discuss the relative benefits of curbing inflammation rather than attempting to prevent it.

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Napolitano, Lena M. "Resuscitation following trauma and hemorrhagic shock." Critical Care Medicine 23, no. 5 (May 1995): 795–97. http://dx.doi.org/10.1097/00003246-199505000-00001.

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Laserna, Anna Karen Carrasco, Yiyang Lai, Guihua Fang, Rajaseger Ganapathy, Mohamed Shirhan Bin Mohamed Atan, Jia Lu, Jian Wu, Mahesh Uttamchandani, Shabbir M. Moochhala, and Sam Fong Yau Li. "Metabolic Profiling of a Porcine Combat Trauma-Injury Model Using NMR and Multi-Mode LC-MS Metabolomics—A Preliminary Study." Metabolites 10, no. 9 (September 16, 2020): 373. http://dx.doi.org/10.3390/metabo10090373.

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Profiles of combat injuries worldwide have shown that penetrating trauma is one of the most common injuries sustained during battle. This is usually accompanied by severe bleeding or hemorrhage. If the soldier does not bleed to death, he may eventually succumb to complications arising from trauma hemorrhagic shock (THS). THS occurs when there is a deficiency of oxygen reaching the organs due to excessive blood loss. It can trigger massive metabolic derangements and an overwhelming inflammatory response, which can subsequently lead to the failure of organs and possibly death. A better understanding of the acute metabolic changes occurring after THS can help in the development of interventional strategies, as well as lead to the identification of potential biomarkers for rapid diagnosis of hemorrhagic shock and organ failure. In this preliminary study, a metabolomic approach using the complementary platforms of nuclear magnetic resonance (NMR) spectroscopy and liquid chromatography coupled with mass spectrometry (LC-MS) was used to determine the metabolic changes occurring in a porcine model of combat trauma injury comprising of penetrating trauma to a limb with hemorrhagic shock. Several metabolites associated with the acute-phase reaction, inflammation, energy depletion, oxidative stress, and possible renal dysfunction were identified to be significantly changed after a thirty-minute shock period.

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Liu, Fu-Chao, Chih-Wen Zheng, and Huang-Ping Yu. "Maraviroc-Mediated Lung Protection following Trauma-Hemorrhagic Shock." BioMed Research International 2016 (2016): 1–8. http://dx.doi.org/10.1155/2016/5302069.

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Objectives.The peroxisome proliferator-activated receptor gamma (PPARγ) pathway exerts anti-inflammatory effects in response to injury. Maraviroc has been shown to have potent anti-inflammatory effects. The aim of this study was to investigate whether PPARγplays an important role in maraviroc-mediated lung protection following trauma-hemorrhage.Methods.Male Sprague-Dawley rats underwent trauma-hemorrhage (mean blood pressure maintained at approximately 35–40 mmHg for 90 minutes), followed by fluid resuscitation. During resuscitation, a single dose of maraviroc (3 mg/kg, intravenously) with and without a PPARγinhibitor GW9662 (1 mg/kg, intravenously), GW9662, or vehicle was administered. Lung water content, tissue histology, and other various parameters were measured (n=8rats/group) 24 hours after resuscitation. One-way ANOVA and Tukey’s testing were used for statistical analysis.Results.Trauma-hemorrhage significantly increased lung water content, myeloperoxidase activity, intercellular adhesion molecule-1, interleukin-6, and interleukin-1βlevels. These parameters significantly improved in the maraviroc-treated rats subjected to trauma-hemorrhage. Maraviroc treatment also decreased lung tissue damage as compared to the vehicle-treated trauma-hemorrhaged rats. Coadministration of GW9662 with maraviroc abolished the maraviroc-induced beneficial effects on these parameters and lung injury.Conclusion.These results suggest that PPARγmight play a key role in maraviroc-mediated lung protection following trauma-hemorrhage.

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Chu, Xiaogang, Kumar Subramani, Marie Warren, and Raghavan Pillai Raju. "Innate immune response in acute lung injury following hemorrhagic shock." Journal of Immunology 198, no. 1_Supplement (May 1, 2017): 70.9. http://dx.doi.org/10.4049/jimmunol.198.supp.70.9.

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Abstract Trauma is the major cause of death for Americans under the age of 46 years. Hemorrhagic shock accounts for up to 40% of trauma-related deaths. Hemorrhagic shock evokes an acute, non-specific, systemic inflammatory response syndrome (SIRS) resulting in the damage to multiple organs. Acute lung injury (ALI) is one of the most serious complications in traumatic patients, however, the immunological mechanisms in ALI are still not well understood. Recently studies suggest that mitochondria play an important role in physical injury, leading to the onset of the SIRS. In order to address the mechanistic basis of ALI following hemorrhagic shock, we subjected rats to severe hemorrhage and shock (hemorrhagic injury - HI) or sham procedure and lung tissue was tested. We demonstrate that NLRX1, a mitochondria-targeted protein, that negatively regulates innate immunity and cell death responses, was markedly decreased in HI lung. The decrease of NLRX1 was concomitant with the activation of NF/κB and TBK1 signaling pathways. Lung histochemistry was used to establish pathologic effect on the lung. Significant increases in pulmonary expression of inflammatory signaling molecules IL-6, IL-1β, IL-10, TNF-α and MIP-1α further confirmed HI induced pulmonary inflammation and injury. Our results suggest NLRX1 participate in the pathogenesis of HI related pulmonary diseases and support its important role in the regulation of innate immune response following hemorrhagic shock.

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Schneider, Christian P., Martin G. Schwacha, T. S. Anantha Samy, Kirby I. Bland, and Irshad H. Chaudry. "Androgen-mediated modulation of macrophage function after trauma-hemorrhage: central role of 5α-dihydrotestosterone." Journal of Applied Physiology 95, no. 1 (July 2003): 104–12. http://dx.doi.org/10.1152/japplphysiol.00182.2003.

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Androgens have been implicated as the causative factor for the postinjury immune dysfunction in males; however, it remains unknown whether androgens directly affect macrophages. To study this, male mice were sham operated or subjected to trauma (i.e., midline laparotomy) and hemorrhagic shock (mean arterial pressure, 30 ± 5 mmHg for 90 min and then resuscitated). The mice received the 5α-reductase inhibitor 4-hydroxyandrostenedione (4-OHA) before resuscitation. Plasma TNF-α, IL-6, and IL-10 levels were elevated after trauma-hemorrhage and normalized by 4-OHA. TNF-α and IL-6 production by splenic macrophages was decreased after injury, whereas Kupffer cell production of these mediators was enhanced. 4-OHA normalized cytokine production. Androgens suppressed cytokine production by splenic macrophages from hemorrhaged mice, whereas it enhanced TNF-α and IL-6 production by Kupffer cells. The addition of 4-OHA in vitro normalized cytokine production by cells treated with testosterone, but it had no effect on dihydrotestosterone-treated cells. These results indicate that androgens directly affect macrophage function in males after trauma and hemorrhagic shock and that the intracellular conversion of testosterone to dihydrotestosterone is of particular importance in mediating the androgen-induced effects.

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Gauss, Tobias, Justin E. Richards, Costanza Tortù, François-Xavier Ageron, Sophie Hamada, Julie Josse, François Husson, et al. "Association of Early Norepinephrine Administration With 24-Hour Mortality Among Patients With Blunt Trauma and Hemorrhagic Shock." JAMA Network Open 5, no. 10 (October 7, 2022): e2234258. http://dx.doi.org/10.1001/jamanetworkopen.2022.34258.

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ImportanceHemorrhagic shock is a common cause of preventable death after injury. Vasopressor administration for patients with blunt trauma and hemorrhagic shock is often discouraged.ObjectiveTo evaluate the association of early norepinephrine administration with 24-hour mortality among patients with blunt trauma and hemorrhagic shock.Design, Setting, and ParticipantsThis retrospective, multicenter, observational cohort study used data from 3 registries in the US and France on all consecutive patients with blunt trauma from January 1, 2013, to December 31, 2018. Patients were alive on admission with hemorrhagic shock, defined by prehospital or admission systolic blood pressure less than 100 mm Hg and evidence of hemorrhage (ie, prehospital or resuscitation room transfusion of packed red blood cells, receipt of emergency treatment for hemorrhage control, transfusion of &gt;10 units of packed red blood cells in the first 24 hours, or death from hemorrhage). Blunt trauma was defined as any exposure to nonpenetrating kinetic energy, collision, or deceleration. Statistical analysis was performed from January 15, 2021, to February 22, 2022.ExposureContinuous administration of norepinephrine in the prehospital environment or resuscitation room prior to hemorrhage control, according to European guidelines.Main Outcomes and MeasuresThe primary outcome was 24-hour mortality, and the secondary outcome was in-hospital mortality. The average treatment effect (ATE) of early norepinephrine administration on 24-hour mortality was estimated according to the Rubin causal model. Inverse propensity score weighting and the doubly robust approach with 5 distinct analytical strategies were used to determine the ATE.ResultsA total of 52 568 patients were screened for inclusion, and 2164 patients (1508 men [70%]; mean [SD] age, 46 [19] years; median Injury Severity Score, 29 [IQR, 17-36]) presented with acute hemorrhage and were included. A total of 1497 patients (69.1%) required emergency hemorrhage control, 128 (5.9%) received a prehospital transfusion of packed red blood cells, and 543 (25.0%) received a massive transfusion. Norepinephrine was administered to 1498 patients (69.2%). The 24-hour mortality rate was 17.8% (385 of 2164), and the in-hospital mortality rate was 35.6% (770 of 2164). None of the 5 analytical strategies suggested any statistically significant association between norepinephrine administration and 24-hour mortality, with ATEs ranging from –4.6 (95% CI, –11.9 to 2.7) to 2.1 (95% CI, –2.1 to 6.3), or between norepinephrine administration and in-hospital mortality, with ATEs ranging from –1.3 (95% CI, –9.5 to 6.9) to 5.3 (95% CI, –2.1 to 12.8).Conclusions and RelevanceThe findings of this study suggest that early norepinephrine infusion was not associated with 24-hour or in-hospital mortality among patients with blunt trauma and hemorrhagic shock. Randomized clinical trials that study the effect of early norepinephrine administration among patients with trauma and hypotension are warranted to further assess whether norepinephrine is safe for patients with hemorrhagic shock.

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Rushing, G. D., R. C. Britt, J. N. Collins, F. J. Cole, L. J. Weireter, and L. D. Britt. "Adrenal Insufficiency in Hemorrhagic Shock." American Surgeon 72, no. 6 (June 2006): 552–54. http://dx.doi.org/10.1177/000313480607200619.

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Adrenal insufficiency during sepsis is well documented. The association between hemorrhagic shock and adrenal insufficiency is unclear and may be related to ischemia, necrosis, or resuscitation. This study was designed to determine the incidence of relative adrenal insufficiency in hemorrhagic shock. A retrospective review of a prospectively gathered database for patients admitted to the trauma intensive care unit with hemorrhagic shock was undertaken. A random serum cortisol of <25 mcg/dL defined relative adrenal insufficiency. All of the cortisol levels were drawn within the first 24 hours of admission. Data analyzed included demographics, length of stay, injury mechanism, infections, and mortality. Fifteen patients presented with hemorrhagic shock, with 14 of 15 meeting the criteria for relative adrenal insufficiency. The average serum cortisol level was 15.8 (9–26.8). The average APACHE II score was 18.3 (4–33), and the average Injury Severity Score was 22.5 (8–41). The mechanism was blunt trauma in 10 patients and penetrating trauma in 5. The average intensive care unit and hospital length of stay were 13.2 and 27.4 days, respectively. There were five urinary tract infections, four blood stream infections, and two wound infections. Two of the 15 patients died. Relative adrenal insufficiency appears to be common in hemorrhagic shock. Future research is warranted to elucidate the pathophysiology, as well as to prospectively determine which patients may benefit from steroid replacement.

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Karavdić, K., A. Firdus, L. Kapetanović-Zametica, D. Anić, N. Kulenović-Spahović, N. Begić, and S. Begić. "Hemorrhagic Shock Caused by Mesenteric Injury - Ski Pediatric Blunt Abdominal Trauma case report." Journal of Clinical Surgery and Research 3, no. 3 (March 18, 2022): 01–08. http://dx.doi.org/10.31579/2768-2757/040.

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Trauma is the leading cause of pediatric mortality and abdominal injury is a significant contributor to morbidity. Abdominal trauma in the population of injured children, is the third leading cause of death in this population, after head and thoracic injuries. It is the most common cause of death owing to unrecognized injury. They most often occur in traffic accidents, games and sports. The clinical presentation depends on the severity of the injury, the injured organ and the associated injuries. Mesenteric injury from blunt abdominal trauma is uncommon and can be difficult to diagnose. It is known that seatbelt trauma from motor vehicle accidents is the most common mechanism of mesenteric injury and that the mesentery of the small bowel is injured more frequently than that of the colon. We present an unusual case, a seven-year-old boy who was injured while skiing. The patient was in a state of hemorrhagic shock and underwent emergency surgery after an urgent diagnosis. During the operation, the leading trauma and the reason for the hemorrhagic shock were found to be a mesenteric injury, and bleeding from the branches of the superior mesenteric artery. Early transport, monitoring and diagnostics significantly contribute to reducing morbidity and mortality. The standard in surgery is non-operative treatment of injured parenchymal organs. A multidisciplinary approach that includes doctors of various specialties (pediatric surgeons, pediatricians, neurosurgeons, anesthesiologists and radiologists) who contribute to the diagnosis and treatment of injured children through diagnostic and therapeutic procedures has a key role. At the end, the decision regarding surgical treatment is responsibility of pediatric surgeon.

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Larraga-García, Blanca, Aurora Pérez-Jiménez, Santiago Ros-Dopico, Javier Rubio-Bolívar, Manuel Quintana-Diaz, and Álvaro Gutiérrez. "Design and Development of a Hemorrhagic Trauma Simulator for Lower Limbs: A Pilot Study." Sensors 21, no. 11 (May 31, 2021): 3816. http://dx.doi.org/10.3390/s21113816.

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One of the main preventable leading causes of death after a trauma injury is the hemorrhagic shock. Therefore, it is extremely important to learn how to control hemorrhages. In this paper, a hemorrhagic trauma simulator for lower limb has been developed and a pilot study has been accomplished to trail the simulator. Four different bleeding scenarios have been tested per participant, gathering information about the manual pressure exerted to control the bleeding. Data, altogether, from 54 hemorrhagic scenarios managed by final year medical students and doctors were gathered. Additionally, a post-simulation questionnaire, related to the usability of the simulator, was completed. All the participants managed to control the simulated bleeding scenarios, but the pressure exerted to control the four different scenarios is different depending if the trainee is a student or a doctor, especially in deep venous hemorrhages. This research has highlighted the different approach to bleeding control treatment between medical students and doctors. Moreover, this pilot study demonstrated the need to deliver a more effective trauma treatment teaching for hemorrhagic lesions and that hemorrhagic trauma simulators can be used to train and evaluate different scenarios.

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Fishman, Jordan E., Gal Levy, Vamsi Alli, Sharvil Sheth, Qu Lu, and Edwin A. Deitch. "Oxidative modification of the intestinal mucus layer is a critical but unrecognized component of trauma hemorrhagic shock-induced gut barrier failure." American Journal of Physiology-Gastrointestinal and Liver Physiology 304, no. 1 (January 1, 2013): G57—G63. http://dx.doi.org/10.1152/ajpgi.00170.2012.

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Recent studies demonstrate that mechanisms underlying gut barrier failure include systemic processes and less studied luminal processes. We thus tested the hypothesis that mucus layer oxidation is a component of trauma/hemorrhagic shock-induced gut injury and dysfunction. Male Sprague-Dawley rats underwent trauma/hemorrhagic shock. Controls underwent trauma only. Mucus from the terminal 30 cm of the ileum was collected, processed, and analyzed for reactive nitrogen intermediates (RNI)-mediated damage, reactive oxygen species (ROS)-induced damage, and total antioxidant capacity. The distal ileum was stained to quantify the mucus layer; gut permeability was assessed physiologically. A time course study was conducted to determine the temporal sequence of mucus layer damage. The role of free radical-mediated damage to the gut barrier was investigated by the effect of the free radical scavenger dimethyl sulfoxide on trauma/hemorrhagic shock-induced changes on the mucus and on gut permeability. Trauma/hemorrhagic shock increased intestinal permeability, which was associated with evidence of loss of the unstirred mucus layer. These changes correlated with increased ROS- and RNI-mediated mucus damage and loss of mucus total antioxidant capacity. Based on the time course study, ROS-mediated mucus damage and loss of total antioxidant capacity were present immediately following shock, whereas RNI-mediated damage was delayed for 3 h. Dimethyl sulfoxide ameliorated gut barrier loss, ROS-mediated changes to the mucus layer, and loss of total antioxidant capacity. There was no change in RNI-induced changes to the mucus layer. These results support the hypothesis that trauma/hemorrhagic shock leads to mucus damage and gut dysfunction through the generation of free radical species.

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Ba, Zheng F., Joachim F. Kuebler, Loring W. Rue, Kirby I. Bland, Ping Wang, and Irshad H. Chaudry. "Gender dimorphic tissue perfusion response after acute hemorrhage and resuscitation: role of vascular endothelial cell function." American Journal of Physiology-Heart and Circulatory Physiology 284, no. 6 (June 1, 2003): H2162—H2169. http://dx.doi.org/10.1152/ajpheart.00724.2002.

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Proestrous female rodents are protected from the deleterious effects of trauma-hemorrhage that are observed in males. We hypothesized that the gender dimorphic outcome after trauma-hemorrhage might be related to gender differences in endothelial function and organ perfusion under such conditions. Male and cycle-matched proestrous female Sprague-Dawley rats underwent a midline laparotomy, hemorrhagic shock (40 mmHg for ∼90 min), and resuscitation (Ringer lactate, 4× shed blood volume over 60 min). Various parameters were measured 2 h after completion of resuscitation. In the first set of animals, the left ventricle was cannulated and heart performance (maximal rate of left ventricular pressure increase) as well as cardiac output and organ perfusion rates were determined with 85Sr microspheres. In the second set of animals, aortic vessel rings were harvested and relaxation in response to acetylcholine and nitroglycerin was measured. In the third set of animals, in situ isolated small intestine was perfused to measure the response of the splanchnic vessel bed to acetylcholine and nitroglycerin. After trauma-hemorrhage and resuscitation, females maintained cardiac output and demonstrated increased splanchnic and cardiac perfusion compared with males. Moreover, female intestines did not manifest the endothelial dysfunction that was observed in male intestines after hemorrhagic shock. We conclude that proestrous females show improved endothelial function and tissue perfusion patterns after hemorrhagic shock and that this gender-specific response might be a potential mechanism contributing to the beneficial effects of the proestrus stage under such conditions.

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Hoen, Sophie, Karim Asehnoune, Sylvie Brailly-Tabard, Jean-Xavier Mazoit, Dan Benhamou, Pierre Moine, and Alain R. Edouard. "Cortisol Response to Corticotropin Stimulation in Trauma Patients." Anesthesiology 97, no. 4 (October 1, 2002): 807–13. http://dx.doi.org/10.1097/00000542-200210000-00010.

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Background An abnormal adrenocortical function and a vasopressor dependency have been demonstrated during septic shock. Because trauma and hemorrhage are the leading causes of noninfectious inflammatory syndromes, the goal of this study was to assess the adrenal reserve of trauma patients and its relation with clinical course. Methods Cortisol response to an intravenous corticotropin bolus was obtained in 34 young trauma patients (Injury Severity Score =29.1 +/- 7.3) at the end of the resuscitative period ("early phase") and at the end of the first posttraumatic week ("late period"). Cortisol response less than +9 g/dl defined an impaired adrenal function, and the corresponding patient was called a nonresponder. According to the early response, hemorrhagic shock, circulating interleukin-6, need for vasopressor therapy, subsequent organ dysfunction and infection, and outcomes were studied. Results Sixteen patients (47%) were nonresponders at the end of the early phase. Hemorrhagic shock was more frequent (69 vs. 28%; = 0.037) and interleukin-6 concentrations were higher (728 +/- 589 vs. 311 +/- 466 pg/ml; = 0.048) in these patients. The early cortisol responses were negatively correlated with the concomitant interleukin-6 serum concentrations (r(2) = 0.298; = 0.003). Four early nonresponders (and shock patients) remained nonresponders during the late phase (25%). Morbidity and mortality were similar in early nonresponders and responders. The duration of norepinephrine treatment and the total amount of infused drug were significantly higher in early nonresponders. Conclusions A sustained impairment of adrenal reserve is frequently observed in trauma patients. This abnormal cortisol response to corticotropin stimulation is related with the inflammatory consequences of hemorrhagic shock and is followed by a prolonged vasopressor dependency.

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Xu, Ying Xin, Alfred Ayala, and Irshad H. Chaudry. "Prolonged Immunodepression after Trauma and Hemorrhagic Shock." Journal of Trauma: Injury, Infection, and Critical Care 44, no. 2 (February 1998): 335–41. http://dx.doi.org/10.1097/00005373-199802000-00018.

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Heckbert, Susan R., Nicholas B. Vedder, Wilma Hoffman, Robert K. Winn, Leonard D. Hudson, Gregory J. Jurkovich, Michael K. Copass, John M. Harlan, Charles L. Rice, and Ronald V. Maier. "Outcome after Hemorrhagic Shock in Trauma Patients." Journal of Trauma: Injury, Infection, and Critical Care 45, no. 3 (September 1998): 545–49. http://dx.doi.org/10.1097/00005373-199809000-00022.

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DEITCH, EDWIN A. "THE ROLE OF GENDER ON GUT BARRIER FUNCTION FOLLOWING TRAUMA-HEMORRHAGI TRAUMA-HEMORRHAGIC SHOCK." Shock 21, Supplement (March 2004): 74. http://dx.doi.org/10.1097/00024382-200403001-00293.

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Mileski, W. J., R. K. Winn, J. M. Harlan, and C. L. Rice. "Sensitivity to endotoxin in rabbits is increased after hemorrhagic shock." Journal of Applied Physiology 73, no. 3 (September 1, 1992): 1146–49. http://dx.doi.org/10.1152/jappl.1992.73.3.1146.

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The immunoinflammatory response following trauma and hemorrhage may predispose to the development of sepsis and multiple-organ failure syndrome. Cardiac output (CO), arterial pressure, arterial PO2, and pulmonary permeability index were measured. We examined the sensitivity of rabbits to infusions of lipopolysaccharide (LPS) after hemorrhagic shock. Shock was produced by reducing CO to 40% of baseline for 90 min, followed by resuscitation with shed blood and then with lactated Ringer solution to maintain CO near baseline. Animals were assigned to three groups: 1) hemorrhagic shock only, 2) LPS only, and 3) hemorrhagic shock + LPS. Groups 1 and 3 were subjected to hemorrhagic shock on day 1. Escherichia coli LPS was infused (1.0 microgram/kg i.v.) into groups 2 and 3 on day 2. Fluid resuscitation with lactated Ringer solution was continued in an effort to maintain CO at baseline. Five hours after LPS infusion, 125I-albumin was injected intravenously, and rabbits were killed 1 h later for measurement of pulmonary permeability index. LPS infusion after shock (group 3) caused significant decreases in CO, arterial pressure, and PO2 and an increase in pulmonary permeability. These changes were not seen in the groups 1 and 2. We conclude that hemorrhagic shock and resuscitation result in a proinflammatory state, leading to increased sensitivity to subsequent exposure to LPS.

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Franco, Derek F., and Steven M. Zangan. "Interventional Radiology in Pelvic Trauma." Seminars in Interventional Radiology 37, no. 01 (March 2020): 044–54. http://dx.doi.org/10.1055/s-0039-3401839.

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AbstractTraumatic pelvic injuries are associated with high injury severity scores and significant morbidity and mortality. As fractures and ligamentous disruption result in increased pelvic volume, retroperitoneal hemorrhage can spiral and progress to hemorrhagic shock. Due to the extensive collateral supply and limitations of surgery for pelvic hematomas, angiographic treatment is at the forefront of pelvic trauma management. This article will discuss typical injuries seen in pelvic trauma, treatment modalities available to the interventional radiologist, and common angiographic treatment strategies and techniques.

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van Wessem, Karlijn J. P., and Luke P. H. Leenen. "Does Liberal Prehospital and In-Hospital Tranexamic Acid Influence Outcome in Severely Injured Patients? A Prospective Cohort Study." World Journal of Surgery 45, no. 8 (April 29, 2021): 2398–407. http://dx.doi.org/10.1007/s00268-021-06143-y.

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Abstract Background Early hemorrhage control is important in trauma-related death prevention. Tranexamic acid (TXA) has shown to be beneficial in patients in hemorrhagic shock, although widespread adoption might result in incorrect TXA administration leading to increased morbidity and mortality. Methods A 7-year prospective cohort study with consecutive trauma patients admitted to a Level-1 Trauma Center ICU was performed to investigate administration of both pre- and in-hospital TXA and its relation to morbidity and mortality. Indication for prehospital and in-hospital TXA administration was (suspicion of) hemorrhagic shock, and/or systolic blood pressure (SBP) ≤ 90 mmHg. Demographics, data on physiology, resuscitation and outcomes were prospectively collected. Results Four hundred and twenty-two patients (71% males, median ISS 29, 95% blunt injuries) were included. Even though TXA patients were more severely injured with more deranged physiology, no differences in outcome were noted. Overall, thrombo-embolic complication rate was 8%. In half the patients, hemorrhagic shock was the indication for prehospital TXA, whereas 79% of in-hospital TXA was given based on suspicion of hemorrhagic shock. Thirteen percent of patients with SBP ≤ 90 mmHg in ED received no TXA at all. Based on SBP alone, 22% of prehospital TXA and 25% of in-hospital TXA were justified. Conclusions Despite being more severely injured, TXA patients had similar outcome compared to patients without TXA. Thrombo-embolic complication rate was low despite liberal use of both prehospital and in-hospital TXA. Caution should be exercised in selecting patients for TXA, although this might be challenging based on SBP alone in patients who do not yet show signs of deranged physiology on arrival in ED.

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Marjanović, Vesna, and Ivana Budić. "Fluid Resuscitation and Massive Transfusion Protocol in Pediatric Trauma." Acta Facultatis Medicae Naissensis 33, no. 2 (June 1, 2016): 91–99. http://dx.doi.org/10.1515/afmnai-2016-0010.

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Summary Trauma is the leading cause of morbidity and mortality in children due to the occurrence of hemorrhagic shock. Hemorrhagic shock and its consequences, anemia and hypovolemia, decrease oxygen delivery, due to which appropriate transfusion and volume resuscitation are critical. Guidelines for massive transfusion, in the pediatric trauma, have not been defined yet. Current data indicate that early identification of coagulopathy and its treatment with RBSs, plasma and platelets in a 1:1:1 unit ratio, and limited use of crystalloids may improve survival in pediatric trauma patients.

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Rajani, Ravi R., Chad G. Ball, David V. Feliciano, and Gary A. Vercruysse. "Vasopressin in Hemorrhagic Shock: Review Article." American Surgeon 75, no. 12 (December 2009): 1207–12. http://dx.doi.org/10.1177/000313480907501212.

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Trauma with resultant hypovolemic shock remains both prevalent and difficult to treat. Standard strategies using volume resuscitation and catecholamine support have historically yielded poor results. Vasopressin has emerged as a possible pharmacologic adjunct, particularly in patients with shock refractory to the administration of fluids and catecholamines. Much of the data regarding vasopressin is extrapolated from its usefulness in cases of nonhypovolemic human shock, which are supported by convincing animal studies. It is true that humans show a deficiency in vasopressin minutes after significant hemorrhage that can respond to administration of exogenous vasopressin. When given in physiological dosing regimens, vasopressin appears to be a safe adjunct to other therapy. Definite recommendations regarding indications for use, recommended dose, and long-term outcome in patients with hemorrhagic shock await a much needed prospective, randomized, controlled trial.

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Schmand, Jochen F., Alfred Ayala, Mary H. Morrison, and Irshad H. Chaudry. "Effects of hydroxyethyl starch after trauma-hemorrhagic shock." Critical Care Medicine 23, no. 5 (May 1995): 806–14. http://dx.doi.org/10.1097/00003246-199505000-00006.

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Gonzalez, E., E. E. Moore, M. V. Wohlauer, A. Ghasabyan, M. Carr, J. Harr, A. Banerjee, and C. C. Silliman. "The Acute Endothelial Response to Trauma/Hemorrhagic Shock." Journal of Surgical Research 172, no. 2 (February 2012): 326–27. http://dx.doi.org/10.1016/j.jss.2011.11.593.

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Franchin, Marilyn, Daniel Jost, Hugues Lefort, Stephane Travers, and Jean-Pierre Tourtier. "Utility of shock index calculation in hemorrhagic trauma." American Journal of Emergency Medicine 33, no. 7 (July 2015): 978. http://dx.doi.org/10.1016/j.ajem.2015.04.001.

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Wohlauer, Max, Ernest E. Moore, Miguel Fragoso, Frank Wright, Carlton C. Barnett, Eduardo Gonzalez, James Haenel, John Eun, and Anirban Banerjee. "Isoflurane suppresses inflammation following trauma and hemorrhagic shock." Journal of the American College of Surgeons 211, no. 3 (September 2010): S47. http://dx.doi.org/10.1016/j.jamcollsurg.2010.06.122.

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Caldwell, Nicole W., Mithun Suresh, Tricia Garcia-Choudary, and Christopher A. VanFosson. "CE: Trauma-Related Hemorrhagic Shock: A Clinical Review." AJN, American Journal of Nursing 120, no. 9 (September 2020): 36–43. http://dx.doi.org/10.1097/01.naj.0000697640.04470.21.

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Kumar, Manoj, and Sanjeev Bhoi. "Impaired hematopoietic progenitor cells in trauma hemorrhagic shock." Journal of Clinical Orthopaedics and Trauma 7, no. 4 (October 2016): 282–85. http://dx.doi.org/10.1016/j.jcot.2016.05.013.

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Kuebler, Joachim F., Balazs Toth, Yukihiro Yokoyama, Kirby I. Bland, Loring W. Rue, and Irshad H. Chaudry. "Alpha1-acid-glycoprotein protects against trauma-hemorrhagic shock." Journal of Surgical Research 119, no. 1 (June 2004): 21–28. http://dx.doi.org/10.1016/j.jss.2003.07.007.

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Angele, Martin K., Alfred Ayala, William G. Cioffi, Kirby I. Bland, and Irshad H. Chaudry. "Testosterone: the culprit for producing splenocyte immune depression after trauma hemorrhage." American Journal of Physiology-Cell Physiology 274, no. 6 (June 1, 1998): C1530—C1536. http://dx.doi.org/10.1152/ajpcell.1998.274.6.c1530.

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Studies indicate that, whereas immune functions in males are depressed, they are enhanced in females after trauma hemorrhage. Moreover, castration of male mice (i.e., androgen depletion) before trauma hemorrhage prevented the depression of cell-mediated immunity. Nonetheless, it remains unknown whether or not testosterone per se is responsible for producing the immune depression. To study this, female C3H/HeN mice ( n = 7 animals/group) were pretreated with 5α-dihydrotestosterone (DHT) or vehicle for 19 days, then subjected to laparotomy (e.g., trauma) and hemorrhagic shock (blood pressure 35 ± 5 mmHg for 90 min) followed by fluid resuscitation or sham operation. Nontreated males underwent either trauma hemorrhage or sham operation. Twenty-four hours thereafter, splenocyte immune functions as well as plasma DHT, estradiol, and corticosterone levels were measured. DHT-pretreated females had significantly ( P < 0.05) increased DHT levels, comparable to those seen in males. Conversely, estradiol levels in such females were similar to control males. Splenocyte proliferation as well as interleukin-2 and interleukin-3 release were not depressed in vehicle-treated females, whereas it was in DHT-treated females after trauma hemorrhage, comparable to hemorrhaged males. Thus high testosterone and/or low estradiol levels appear to be responsible for producing splenocyte immune depression in males after trauma hemorrhage. Agents that block testosterone receptors or increase estradiol levels may therefore be helpful in improving depressed immune functions in male trauma patients.

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Smith, Jennifer, Scott Bricker, and Brant Putnam. "Tissue Oxygen Saturation Predicts the Need for Early Blood Transfusion in Trauma Patients." American Surgeon 74, no. 10 (October 2008): 1006–11. http://dx.doi.org/10.1177/000313480807401027.

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Near-infrared spectroscopy (NIRS) has been used to measure regional tissue oxygen saturation (StO2) in skeletal muscle as an indicator of perfusion in trauma patients. In an effort to prospectively examine the usefulness of StO2 in identifying trauma patients in hemorrhagic shock, we evaluated the need for blood transfusion within 24 hours of injury as a marker of significant hemorrhage. A 6-month prospective, observational study was conducted at a university-affiliated, urban Level I trauma center using a convenience sample of 26 trauma patients thought to be at high risk for hemorrhagic shock. Baseline demographic data, vital signs, laboratory values, and amounts of fluid and blood products administered were collected. NIRS-derived StO2 values were measured for 1 hour after arrival to the trauma bay and the minimum value noted. A minimum StO2 less than 70 per cent correlated with the need for blood transfusion with a sensitivity of 88 per cent and a specificity of 78 per cent. The positive predictive value was 64 per cent and the negative predictive value was 93 per cent. The need for blood transfusion within 24 hours of arrival was not predicted by hypotension, tachycardia, arterial lactate, base deficit, or hemoglobin. StO2 may represent an important screening tool for identifying trauma patients who require blood transfusion or other limited medical resources.

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R. Doelle, Morrison, and Benjamin M. Predmore. "SARM1mediates TLR9-induced vascular hyperpermeability following hemorrhagic shock." American Journal of BioMedicine 6, no. 3 (August 30, 2018): 264–79. http://dx.doi.org/10.18081/2333-5106/015-10/644-657.

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Hemorrhagic shock (HS) result in multiple organ dysfunction syndrome (MODS) and inflammatory response. It is one of the world's leading causes of death within the first 40 years of life and thus a significant health problem. The exact mechanism is not clear. TLRs are stimulated both by pathogen-associated molecular patterns as well as by damage-associated molecular patterns, including trauma and hemorrhagic shock. In the present study, we investigated whether the SARM1 responsible for mediats-TLR9-induces inflammatory process and vascular hyperpermeability following hemorrhagic shock. Here we produced an in vivo model of severe hemorrhagic shock in adult wild type mice (40 ± 2 mmHg for 90 min, fluid resuscitation for 30 min) was employed. Mesenteric postcapillary venules were examined for changes in hyperpermeability by intravital microscopy. Blood samples were collected for measurement of tumor necrosis factor (TNF) using ELISA. Biopsies were obtained from organs for light microscopic examination. Our data suggest that SARM1 promising a new mechanisim of TLR9 involved in regulation of hemorrhagic shock and therapeutic target for the treatment of hemorrhagic shock.

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Sloan, Edward P., Max Koenigsberg, James M. Clark, and Amol Desai. "The Use of the Revised Trauma Score as an Entry Criterion in Traumatic Hemorrhagic Shock Studies: Data from the DCLHb Clinical Trials." Prehospital and Disaster Medicine 27, no. 4 (July 30, 2012): 330–44. http://dx.doi.org/10.1017/s1049023x12000970.

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AbstractIntroductionThe Revised Trauma Score (RTS) has been proposed as an entry criterion to identify patients with mid-range survival probability for traumatic hemorrhagic shock studies.Hypothesis/ProblemDetermination of which of four RTS strata (1-3.99, 2-4.99, 1-4.99, and 2-5.99) identifies patients with predicted and actual mortality rates near 50% for use as an entry criterion in traumatic hemorrhagic shock clinical trials.MethodsExisting database analysis in which demographic and injury severity data from two prior international Diaspirin Cross-Linked Hemoglobin (DCLHb) clinical trials were used to identify an RTS range that could be an optimal entry criterion in order to find the population of trauma patients with mid-range predicted and actual mortality rates.ResultsOf 208 study patients, the mean age was 37 years, 65% sustained blunt trauma, 49% received DCLHb, and 57% came from the European Union study arm. The mean values were: ISS, 31 (SD = 18); RTS, 5.6 (SD = 1.8); and Glasgow Coma Scale (GCS), 10.4 (SD = 4.8). The mean TRISS-predicted mortality was 34% and the actual 28-day mortality was 35%. The initially proposed 1-3.99 RTS range (n = 41) had the highest predicted (79%) and actual (71%) mortality rates. The 2-5.99 RTS range (n = 79) had a 62% predicted and 53% actual mortality, and included 76% blunt trauma patients. Removal of GCS <5 patients from this RTS 2-5.99 subgroup caused a 48% further reduction in eligible patients, leaving 41 patients (20% of 208 total patients), 66% of whom sustained a blunt trauma injury. This subgroup had 54% predicted and 49% actual mortality rates. Receiver operator curve (ROC) analysis found the GCS to be as predictive of mortality as the RTS, both in the total patient population and in the RTS 2-5.99 subgroup.ConclusionThe use of an RTS 2-5.99 inclusion criterion range identifies a traumatic hemorrhagic shock patient subgroup with predicted and actual mortality that approach the desired 50% rate. The exclusion of GCS <5 from this RTS 2-5.99 subgroup patients yields a smaller, more uniform patient subgroup whose mortality is more likely related to hemorrhagic shock than traumatic brain injury. Future studies should examine whether the RTS or other physiologic criteria such as the GCS score are most useful as traumatic hemorrhagic shock study entry criteria.Sloan EP, Koenigsberg M, Clark JM, Desai A. The use of the Revised Trauma Score as an entry criterion in traumatic hemorrhagic shock studies: data from the DCLHb clinical trials. Prehosp Disaster Med. 2012;27(4):1-15.

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Carrick, Matthew M., Jan Leonard, Denetta S. Slone, Charles W. Mains, and David Bar-Or. "Hypotensive Resuscitation among Trauma Patients." BioMed Research International 2016 (2016): 1–8. http://dx.doi.org/10.1155/2016/8901938.

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Hemorrhagic shock is a principal cause of death among trauma patients within the first 24 hours after injury. Optimal fluid resuscitation strategies have been examined for nearly a century, more recently with several randomized controlled trials. Hypotensive resuscitation, also called permissive hypotension, is a resuscitation strategy that uses limited fluids and blood products during the early stages of treatment for hemorrhagic shock. A lower-than-normal blood pressure is maintained until operative control of the bleeding can occur. The randomized controlled trials examining restricted fluid resuscitation have demonstrated that aggressive fluid resuscitation in the prehospital and hospital setting leads to more complications than hypotensive resuscitation, with disparate findings on the survival benefit. Since the populations studied in each randomized controlled trial are slightly different, as is the timing of intervention and targeted vitals, there is still a need for a large, multicenter trial that can examine the benefit of hypotensive resuscitation in both blunt and penetrating trauma patients.

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Tait, S. M., P. Wang, Z. F. Ba, and I. H. Chaudry. "Downregulation of hepatic beta-adrenergic receptors after trauma and hemorrhagic shock." American Journal of Physiology-Gastrointestinal and Liver Physiology 268, no. 5 (May 1, 1995): G749—G753. http://dx.doi.org/10.1152/ajpgi.1995.268.5.g749.

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Although it is well known that sympathoadrenal activity increases under various adverse circulatory conditions, it is not known whether there are any alterations in hepatic plasma membrane beta-adrenergic receptors after trauma-hemorrhage and crystalloid resuscitation. To study this, rats underwent a 5-cm midline laparotomy (i.e., trauma induced) and were bled to and maintained at a mean arterial pressure of 40 mmHg until 40% of the maximal bleedout (MB) volume was returned in the form of Ringer lactate. The animals were then resuscitated with four times the volume of MB in the form of Ringer lactate over 60 min. Hepatic plasma membranes were isolated using discontinuous Percoll gradient centrifugation. The maximal binding capacity and dissociation constant (i.e., 1/affinity) of [125I]iodopindolol binding to beta-adrenergic receptors were determined using a membrane filtration assay and Scatchard analysis. The results indicate that there was a significant decrease in the maximal binding capacity at the time of MB, which persisted despite crystalloid resuscitation after hemorrhage. However, there were no significant changes in the dissociation constant at any time point during this study. The downregulation of beta-adrenergic receptor binding capacity may be responsible for metabolic abnormalities observed after hemorrhagic shock.

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Angeli, Anastasia Pearl, Soni Sunarso Sulistiawan, Jimmy Yanuar Annas, and Pesta Parulian Maurid Edwar. "The Use of O Universal Profile Within Hemorrhagic Shock Post-partum Bleeding Patients in Dr. Soetomo General Hospital’s Emergency Installation." JAI (Jurnal Anestesiologi Indonesia) 14, no. 1 (March 9, 2022): 13–18. http://dx.doi.org/10.14710/jai.v0i0.41691.

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Background: Hemorrhagic shock is one of the most common types of shock in trauma patients, and it is defined as acute blood volume loss. One of the causes of hemorrhagic shock is post-childbirth bleeding or post-partum bleeding. The most important management for patients who experience post-partum bleeding is blood transfusions. Type-O blood is known as a universal donor, because someone with type- O blood can transfuse theirs to recipients with blood types other than O. Giving blood transfusions to pos-tpartum bleeding patients is expected to extend their life expectancy, however it cannot be denied that there are quite a several patients who died after receiving transfusions from universal type O blood.Objective: This study aims to determine the profile and effect of universal O use on hemorrhagic shock within post-partum bleeding patients at IGS RSUD Dr. Soetomo Surabaya.Methods: This research was conducted by a descriptive retrospective method by observing the patient's medical record data in the central medical record room of Dr. Soetomo Hospital, Surabaya.Result: There were 17 patients with hemorrhagic shock due to post-partum hemorrhage who received blood transfusions from universal O donors at Dr. Soetomo Surabaya. From the obtained data, the patient age group was dominated by the 28 years old group (23,5%). Transfusion history within patients with the most hemorrhagic shock due to post-partum bleeding were patients who received transfusions with packed red cell (PRC) O + (76,5%). As for transfusion reactions that occur within patients, there are no data on transfusion reactions.Conclusion: The 28 years old group was the largest one that received transfusions from the universal group O blood. History transfusion of hemorrhagic shock due to post-partum bleeding patients shows that most of them are those who received PRC O + transfusions. There are no data regarding the transfusion reactions which occurred in these patients.

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Simovic, Milomir O., James Bynum, Bin Liu, Jurandir J. Dalle Lucca, and Yansong Li. "Impact of Immunopathy and Coagulopathy on Multi-Organ Failure and Mortality in a Lethal Porcine Model of Controlled and Uncontrolled Hemorrhage." International Journal of Molecular Sciences 25, no. 5 (February 21, 2024): 2500. http://dx.doi.org/10.3390/ijms25052500.

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Uncontrolled hemorrhage is a major preventable cause of death in patients with trauma. However, the majority of large animal models of hemorrhage have utilized controlled hemorrhage rather than uncontrolled hemorrhage to investigate the impact of immunopathy and coagulopathy on multi-organ failure (MOF) and mortality. This study evaluates these alterations in a severe porcine controlled and uncontrolled hemorrhagic shock (HS) model. Anesthetized female swine underwent controlled hemorrhage and uncontrolled hemorrhage by partial splenic resection followed with or without lactated Ringer solution (LR) or Voluven® resuscitation. Swine were surveyed 6 h after completion of splenic hemorrhage or until death. Blood chemistry, physiologic variables, systemic and tissue levels of complement proteins and cytokines, coagulation parameters, organ function, and damage were recorded and assessed. HS resulted in systemic and local complement activation, cytokine release, hypocoagulopathy, metabolic acidosis, MOF, and no animal survival. Resuscitation with LR and Voluven® after HS improved hemodynamic parameters (MAP and SI), metabolic acidosis, hyperkalemia, and survival but resulted in increased complement activation and worse coagulopathy. Compared with the LR group, the animals with hemorrhagic shock treated with Voluven® had worse dilutional anemia, coagulopathy, renal and hepatic dysfunction, increased myocardial complement activation and renal damage, and decreased survival rate. Hemorrhagic shock triggers early immunopathy and coagulopathy and appears associated with MOF and death. This study indicates that immunopathy and coagulopathy are therapeutic targets that may be addressed with a high-impact adjunctive treatment to conventional resuscitation.

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Torres Filho, Ivo P., David Barraza, Kim Hildreth, Charnae Williams, and Michael A. Dubick. "Cremaster muscle perfusion, oxygenation, and heterogeneity revealed by a new automated acquisition system in a rodent model of prolonged hemorrhagic shock." Journal of Applied Physiology 127, no. 6 (December 1, 2019): 1548–61. http://dx.doi.org/10.1152/japplphysiol.00570.2019.

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Local blood flow/oxygen partial pressure (Po2) distributions and flow-Po2 relationships are physiologically relevant. They affect the pathophysiology and treatment of conditions like hemorrhagic shock (HS), but direct noninvasive measures of flow, Po2, and their heterogeneity during prolonged HS are infrequently presented. To fill this void, we report the first quantitative evaluation of flow-Po2 relationships and heterogeneities in normovolemia and during several hours of HS using noninvasive, unbiased, automated acquisition. Anesthetized rats were subjected to tracheostomy, arterial/venous catheterizations, cremaster muscle exteriorization, hemorrhage (40% total blood volume), and laparotomy. Control animals equally instrumented were not subjected to hemorrhage/laparotomy. Every 0.5 h for 4.5 h, noninvasive laser speckle contrast imaging and phosphorescence quenching were employed for nearly 7,000 flow/Po2 measurements in muscles from eight animals, using an automated system. Precise alignment of 16 muscle areas allowed overlapping between flow and oxygenation measurements to evaluate spatial heterogeneity, and repeated measurements were used to estimate temporal heterogeneity. Systemic physiological parameters and blood chemistry were simultaneously assessed by blood samplings replaced with crystalloids. Hemodilution was associated with local hypoxia, but increased flow prevented major oxygen delivery decline. Adding laparotomy and prolonged HS resulted in hypoxia, ischemia, decreased tissue oxygen delivery, and logarithmic flow/Po2 relationships in most regions. Flow and Po2 spatial heterogeneities were higher than their respective temporal heterogeneities, although this did not change significantly over the studied period. This quantitative framework establishes a basis for evaluating therapies aimed at restoring muscle homeostasis, positively impacting outcomes of civilian and military trauma/HS victims. NEW & NOTEWORTHY This is the first study on flow-Po2 relationships during normovolemia, hemodilution, and prolonged hemorrhagic shock using noninvasive methods in multiple skeletal muscle areas of monitored animals. Automated flow/Po2 measurements revealed temporal/spatial heterogeneities, hypoxia, ischemia, and decreased tissue oxygen delivery after trauma/severe hemorrhage. Hemodilution was associated with local hypoxia, but hyperemia prevented a major decline in oxygen delivery. This framework provides a quantitative basis for testing therapeutics that positively impacts muscle homeostasis and outcomes of trauma/hemorrhagic shock victims.

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Akhsan, Alfie Barkah, Nurhayat Usman, and Reno Rudiman. "The Relationship Between Initial Hematocrit and Base Excess For Signs Of Hemorrhagic Shock In Patients With Blunt Abdominal Trauma." Jurnal llmu Bedah Indonesia 45, no. 1 (June 9, 2020): 3–15. http://dx.doi.org/10.46800/jibi-ikabi.v45i1.38.

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Introduction: Trauma abdominal and pelvic part of the largest causes of death and, if diagnosed early, the deaths could have been prevented. By increasing the capacity for early detection and prompt and appropriate action, will produce a satisfactory outcome. In patients with bleeding, hemodilution appear within a few minutes to obtain a decrease in hematocrit. BE decline is the result of pyruvic acid metabolism occurring anaerobic tissue hypoperfusion due to bleeding unresolved. There is a strong correlation between the decrease in hematocrit and BE with shock because of intra-abdominal haemorrhage. To analyze the relationship between decreased hematocrit and BE in bleeding patients we investigated the relationship between the initial value of hematocrit and BE against any signs of shock because of intra-abdominal hemorrhage in patients with blunt abdominal trauma. Methods: cross-sectional of the 34 subjects. The research data obtained from history taking, physical examination, investigation, and medical records. Conducted a comparative analysis of Kruskal-Wallis. Test for normality by Kolmogorov-Smirnov test. A p value <0.05 indicates a significant relationship between variables. Data were analyzed using SPSS version 19. Result: It was found an average increase in the pulse (P) frequency with decreasing hematocrit (Ht) is 92.67 ± 6.43x / min for group Ht> 40%, 95.5 ± 16.52x / min for group Ht 37-40%, and 112.89 ± 19.23x / min for group Ht <37%. Obtained an average increase of P frequency with decreasing Base Excess (BE) is 88.0 ± 0x / min for groups BE> 2, 92.33 ± 7.84x / min for BE Group 2 - (- 2), and 112.81 ± 19.22x / min for groups BE < -2. This means that there is a significant relationship between hematocrit decrease with increased of P frequency as one of the signs of hemorrhagic shock with p value = 0.046 and significant correlation between the decrease in BE with increased P frequency as one of the signs of hemorrhagic shock with p value = 0.028. Conclusion: There is a significant correlation between the value of the initial hematocrit and BE with signs of hemorrhagic shock due to intra-abdominal hemorrhage in patients with blunt abdominal trauma.

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Zaets, S., T. Berezina, E. Deitch, and G. Machiedo. "TRAUMA-HEMORRHAGIC SHOCK CAUSES INCREASED RED BLOOD CELL AGGREGATION." Shock 21 (June 2004): 51–52. http://dx.doi.org/10.1097/00024382-200406002-00151.

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SINGH, GURDEV, KHALIL I. CHAUDRY, LOREN C. CHUDLER, and IRSHAD H. CHAUDRY. "Depressed Gut Absorptive Capacity Early After Trauma-Hemorrhagic Shock." Annals of Surgery 214, no. 6 (December 1991): 712–18. http://dx.doi.org/10.1097/00000658-199112000-00011.

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Wang, Weiyang, Ping Wang, and Irshad H. Chaudry. "Pentoxifylline increases gut ketogenesis following trauma and hemorrhagic shock." Critical Care Medicine 26, no. 1 (January 1998): 101–7. http://dx.doi.org/10.1097/00003246-199801000-00023.

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Vogt, Nina, Christiane Herden, Elke Roeb, Martin Roderfeld, Daphne Eschbach, Thorsten Steinfeldt, Hinnerk Wulf, Steffen Ruchholtz, Eberhard Uhl, and Karsten Schöller. "Cerebral Alterations Following Experimental Multiple Trauma and Hemorrhagic Shock." SHOCK 49, no. 2 (February 2018): 164–73. http://dx.doi.org/10.1097/shk.0000000000000943.

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Feinman, Rena, Edwin A. Deitch, Virginie Aris, Hung B. Chu, Billy Abungu, Francis J. Caputo, Anthony Galante, et al. "MOLECULAR SIGNATURES OF TRAUMA-HEMORRHAGIC SHOCK-INDUCED LUNG INJURY." Shock 28, no. 3 (September 2007): 360–68. http://dx.doi.org/10.1097/shk.0b013e318048565b.

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Jacob, Mathews, and Praveen Kumar. "The challenge in management of hemorrhagic shock in trauma." Medical Journal Armed Forces India 70, no. 2 (April 2014): 163–69. http://dx.doi.org/10.1016/j.mjafi.2014.03.001.

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Klöss, T., U. B. Brückner, and H. Leinberger. "Pulmonary pressure-flow relation after trauma and hemorrhagic shock." Research in Experimental Medicine 186, no. 5 (September 1986): 325–36. http://dx.doi.org/10.1007/bf01852098.

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Farooq, Nauman, Panagis Galiatsatos, Jasmine K. Aulakh, Christopher Higgins, and Anthony Martinez. "Massive transfusion practice in non-trauma related hemorrhagic shock." Journal of Critical Care 43 (February 2018): 65–69. http://dx.doi.org/10.1016/j.jcrc.2017.08.033.

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Anand, Tanya, Angelica Alvarez Reyes, Michael C. Sjoquist, Louis Magnotti, and Bellal Joseph. "Resuscitating the Endothelial Glycocalyx in Trauma and Hemorrhagic Shock." Annals of Surgery Open 4, no. 3 (June 28, 2023): e298. http://dx.doi.org/10.1097/as9.0000000000000298.

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Lichte, Philipp, Philipp Kobbe, Roman Pfeifer, Graeme C. Campbell, Rainer Beckmann, Mersedeh Tohidnezhad, Christian Bergmann, et al. "Impaired Fracture Healing after Hemorrhagic Shock." Mediators of Inflammation 2015 (2015): 1–7. http://dx.doi.org/10.1155/2015/132451.

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Impaired fracture healing can occur in severely injured patients with hemorrhagic shock due to decreased soft tissue perfusion after trauma. We investigated the effects of fracture healing in a standardized pressure controlled hemorrhagic shock model in mice, to test the hypothesis that bleeding is relevant in the bone healing response. Male C57/BL6 mice were subjected to a closed femoral shaft fracture stabilized by intramedullary nailing. One group was additionally subjected to pressure controlled hemorrhagic shock (HS, mean arterial pressure (MAP) of 35 mmHg for 90 minutes). Serum cytokines (IL-6, KC, MCP-1, and TNF-α) were analyzed 6 hours after shock. Fracture healing was assessed 21 days after fracture. Hemorrhagic shock is associated with a significant increase in serum inflammatory cytokines in the early phase. Histologic analysis demonstrated a significantly decreased number of osteoclasts, a decrease in bone quality, and more cartilage islands after hemorrhagic shock.μCT analysis showed a trend towards decreased bone tissue mineral density in the HS group. Mechanical testing revealed no difference in tensile failure. Our results suggest a delay in fracture healing after hemorrhagic shock. This may be due to significantly diminished osteoclast recruitment. The exact mechanisms should be studied further, particularly during earlier stages of fracture healing.

Journal articles on the topic 'Trauma hemorrhagic shock'

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