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"Traumatic shock."
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Modulating the Biologic Activity of Mesenteric Lymph after Traumatic Shock Decreases Systemic Inflammation and End Organ Injury
Trauma/hemorrhagic shock (T/HS) causes the release of pro-inflammatory mediators into the mesenteric lymph (ML), triggering a systemic inflammatory response and acute lung injury (ALI). Direct and pharmacologic vagal nerve stimulation prevents gut barrier failure and alters the biologic activity of ML after injury. We hypothesize that treatment with a pharmacologic vagal agonist after T/HS would attenuate the biologic activity of ML and prevent ALI.
ML was collected from male Sprague-Dawley rats after T/HS, trauma-sham shock (T/SS) or T/HS with administration of the pharmacologic vagal agonist CPSI-121. ML samples from each experimental group were injected into naïve mice to assess biologic activity. Blood samples were analyzed for changes in STAT3 phosphorylation (pSTAT3). Lung injury was characterized by histology, permeability and immune cell recruitment.
T/HS lymph injected in naïve mice caused a systemic inflammatory response characterized by hypotension and increased circulating monocyte pSTAT3 activity. Injection of T/HS lymph also resulted in ALI, confirmed by histology, lung permeability and increased recruitment of pulmonary macrophages and neutrophils to lung parenchyma. CPSI-121 attenuated T/HS lymph-induced systemic inflammatory response and ALI with stable hemodynamics and similar monocyte pSTAT3 levels, lung histology, lung permeability and lung immune cell recruitment compared to animals injected with lymph from T/SS.
Treatment with CPSI-121 after T/HS attenuated the biologic activity of the ML and decreased ALI. Given the superior clinical feasibility of utilizing a pharmacologic approach to vagal nerve stimulation, CPSI-121 is a potential treatment strategy to limit end organ dysfunction after injury.
Journal Article
MKK3 depletion attenuates intestinal injury after traumatic hemorrhagic shock by restoring mitochondrial function
Background
Traumatic hemorrhagic shock (THS) is a complex pathophysiological process resulting in multiple organ failure. Intestinal barrier dysfunction is one of the mechanisms implicated in multiple organ failure. The present study aimed to explore the regulatory role of mitogen-activated protein kinase kinase 3 (MKK3) in THS-induced intestinal injury and to elucidate its potential mechanism.
Methods
Rats were subjected to trauma and hemorrhage to establish a THS animal model. MKK3-targeted lentiviral vectors were injected via the tail vein 72 h before modeling. Twelve hours post-modeling, the mean arterial pressure (MAP) and heart rate (HR) were monitored, and histological injury to the intestine was assessed via H&E staining and transmission electron microscopy. Mitochondrial function and mitochondrial reactive oxygen species (ROS) were evaluated. IEC-6 cells were exposed to hypoxia to mimic intestinal injury following THS in vitro.
Results
MKK3 deficiency alleviated intestinal injury and restored mitochondrial function in intestinal tissues from THS-induced rats and hypoxia-treated IEC-6 cells. In addition, MKK3 deficiency promoted Sirt1/PGC-1α-mediated mitochondrial biogenesis and restricted Pink1/Parkin-mediated mitophagy in the injured intestine and IEC-6 cells. Furthermore, the protective effect of MKK3 knockdown against hypoxia-induced mitochondrial damage was strengthened upon simultaneous LC3B/Pink1/Parkin knockdown or weakened upon simultaneous Sirt1 knockdown.
Conclusion
MKK3 deficiency protected against intestinal injury induced by THS by promoting mitochondrial biogenesis and restricting excessive mitophagy.
Journal Article
Local hemostasis, immunothrombosis, and systemic disseminated intravascular coagulation in trauma and traumatic shock
Knowing the pathophysiology of trauma-induced coagulopathy is important for the management of severely injured trauma patients. The aims of this review are to provide a summary of the recent advances in our understanding of thrombosis and hemostasis following trauma and to discuss the pathogenesis of disseminated intravascular coagulation (DIC) at an early stage of trauma. Local hemostasis and thrombosis respectively act to induce physiological wound healing of injuries and innate immune responses to damaged-self following trauma. However, if overwhelmed by systemic inflammation caused by extensive tissue damage and tissue hypoperfusion, both of these processes foster systemic DIC associated with pathological fibrin(ogen)olysis. This is called DIC with the fibrinolytic phenotype, which is characterized by the activation of coagulation, consumption coagulopathy, insufficient control of coagulation, and increased fibrin(ogen)olysis. Irrespective of microvascular thrombosis, the condition shows systemic thrombin generation as well as its activation in the circulation and extensive damage to the microvasculature endothelium. DIC with the fibrinolytic phenotype gives rise to oozing-type non-surgical bleeding and greatly affects the prognosis of trauma patients. The coexistences of hypothermia, acidosis, and dilution aggravate DIC and lead to so-called trauma-induced coagulopathy.
He that would know what shall be must consider what has been.
The Analects of Confucius.
Journal Article
Prognostic accuracy of the CMPMIT-ICD-10, APACHE Ⅱ, SOFA, ISS, and AIS for in-hospital death among patients with traumatic hemorrhagic shock
The China Mortality Prediction Model in Trauma, which is based on the International Classification of Disease Disorders (ICD)-10-CM lexicon (CMPMIT-ICD-10),is a new trauma scoring system. Our objective was to compare the prognostic performance of the CMPMIT-ICD10 with that of the Acute Physiology and Chronic Health Evaluation II (APACHEII), Sequential Organ Failure Assessment (SOFA), Injury Severity Score (ISS), and Abbreviated Injury Scale (AIS) for in-hospital mortality in patients with traumatic hemorrhagic shock(THS).This retrospective observational cohort study was conducted at a tertiary teaching hospital from May 1, 2013, to May 31, 2023.The area under the receiver operating characteristic curve (AUC), sensitivity, specificity, accuracy, and associations with outcomes of theCMPMIT-ICD-10, APACHE II, SOFA, ISS, and AIS scores for the prediction of in-hospital death were assessed. A total of 420 patients with THS were included. Forty-one (9.8%) patients died during hospitalization. For the prediction of in-hospital death, the CMPMIT-ICD-10 (0.8757) and APACHE II(0.8709) had greater AUCs compared with the AIS (0.6243), SOFA (0.7669), and ISS (0.6601). With the best cut-off value of 59.5, the CMPMIT-ICD10 had a highest sensitivity (85.4%) and good specificity(79.9%) and overall accuracy (80.4%). The CMPMIT-ICD10 (OR 1.057, 95% CI 1.028–1.087, p < 0.001) and APACHE II (OR 1.125, 95% CI 1.045–1.211, p = 0.002) were independently associated with in-hospital death. Comparable to the APACHE II but significantly better than the SOFA, ISS, and AIS, the CMPMIT-ICD-10 performed well in predicting the short-term mortality of patients with THS. These findings suggest that the CMPMIT-ICD-10 may have superior utility for predicting short-term death in THS patients.
Journal Article
Incidence and risk factors for acute kidney injury after traumatic hemorrhagic shock: A 10-year retrospective cohort study
Background
Acute kidney injury (AKI) is a common complication of traumatic hemorrhagic shock. The risk factors for AKI after traumatic hemorrhagic shock remain unclear. The aim of this study was to investigate the risk factors for AKI after traumatic hemorrhagic shock.
Methods
This was a ten-year retrospective cohort study of patients who experienced traumatic hemorrhagic shock between January 2013 and April 2023. Patient characteristics and clinical data were recorded for 417 patients. The outcome was the occurrence of AKI, defined as a serum creatinine increase of ≥ 0.3 mg/dL (≥ 26.5 μmol/L) within 48 h, or an increase to 1.5 times the baseline, or a urine volume of < 0.5 mL/(kg h.). Risk factors for AKI were tested by logistic regression models.
Results
The incidence of AKI after traumatic hemorrhagic shock was 29.3% (122/417 patients). Multivariable analysis revealed that the independent risk factors for AKI included age (OR, 1.048; 95% CI, 1.022–1.074;
p
< 0.001), B-type natriuretic peptide (OR, 1.002; 95% CI, 1.000–1.004;
p
= 0.041), sepsis (OR, 4.536; 95% CI, 1.651–12.462;
p
= 0.030) and acute myocardial injury (OR, 2.745; 95% CI, 1.027–7.342;
p
= 0.044). Road traffic accidents (OR, 0.202; 95% CI, 0.076–0.541;
p
= 0.001), mean arterial pressure (OR, 0.972; 95% CI, 0.950–0.995;
p
= 0.017), and base excess (OR, 0.842; 95% CI, 0.764–0.929;
p
= 0.001) were negatively correlated with AKI. The area under the receiver operating characteristic (ROC) curve for prediction by this model was 0.85 (95% CI, 0.81–0.90).
Conclusion
The incidence of AKI after traumatic hemorrhagic shock was 29.3% in our series. Indicators of blood perfusion, sepsis and acute myocardial injury may be independent risk factors for AKI after traumatic hemorrhagic shock. Early detection and effective intervention on these risk factors could reduce the occurrence of AKI and improve outcomes.
Graphical abstract
Journal Article
Organ-Specific Oxidative Events under Restrictive Versus Full Reperfusion Following Hemorrhagic Traumatic Shock in Rats
Background aim: Reperfusion after hemorrhagic traumatic shock (HTS) is often associated with complications that are partly ascribed to the formation of reactive oxygen species (ROS). The aim of our study was to compare the effects of restrictive reperfusion (RR) to rapid full reperfusion (FR) on ROS formation and/or oxidative events. Materials and methods: Anesthetized male rats were randomly subjected to HTS followed by FR (75 mL/kg/h) or RR (30 mL/kg/h for 40 min, followed by 75 mL/kg/h) with Ringer’s solution (n = 8/group). Compartment-specific ROS formation was determined by infusion of ROS scavenger 1-hydroxy-3-carboxy-2,2,5,5-tetramethyl-pyrrolidine hydrochloride (CP-H) during resuscitation, followed by electron paramagnetic resonance spectroscopy. Sham-operated animals (n = 8) served as controls. The experiment was terminated 100 min post-shock. Results: Mean arterial pressure was significantly higher in the FR compared to the RR group during early reperfusion. Only RR animals, not FR animals, showed significantly higher ROS concentrations in erythrocytes (1951 ± 420 vs. 724 ± 75 AU) and in liver (474 ± 57 vs. 261 ± 21 AU) compared to sham controls. This was accompanied by elevated alanine aminotransferase and creatinine levels in RR animals compared to both shams and FR animals, while lipid peroxidation products (thiobarbituric acid reactive substances) were significantly increased only in the kidney in the FR group (p < 0.05). RR animals showed significantly higher plasma peroxiredoxin-4 values when compared to the FR group (20 ± 2 vs. 14 ± 0.5 RLU). Conclusion: Restrictive reperfusion after HTS is associated with increased ROS formation in erythrocytes and liver compared to sham controls. Moreover, the restrictive reperfusion is associated with a more pronounced injury to the liver and kidney, which is likely mediated by other than lipid peroxidation process and/or oxidative stress reactions.
Journal Article
Corticotropin-releasing factor is present in intestinal tissue of patients with gastrointestinal dysfunction following shock and abdominal surgery
Corticotropin-releasing factor (CRF) is implicated in stress-related gastrointestinal dysfunction, possibly causing gut dysfunction following trauma and surgery. We investigated plasma and intestinal tissue CRF levels and gut function in patients with traumatic shock or those undergoing elective abdominal surgery.
In a prospective, parallel, observational study in a university hospital surgical intensive care unit (ICU), 8 shocked patients (systolic blood pressure <90 mmHg and/or acidosis and/or urine output <1 mL/kg/hr and/or requiring >2 L of intravenous fluid resuscitation) undergoing small bowel resection during emergency laparotomy following abdominal injury and 17 stable patients undergoing elective hepatobiliary surgery were included if they required postoperative ICU management. Serial plasma and intestinal CRF was measured and postoperative gastric emptying and intestinal permeability were evaluated.
Plasma CRF was significantly increased in the shocked patients compared with the elective surgery patients at all times. CRF peptide was quantified in intestinal tissue at similar levels in both groups. Intestinal permeability was increased and associated with shock and resuscitation fluid volume. Gastric emptying was retarded and correlated significantly with shock but not with plasma CRF. Delayed gastric emptying in shocked patients was associated with longer ICU stay.
The novel finding is the presence of CRF in the small bowel of both elective and emergency gastrointestinal surgery patients with concomitant gastrointestinal dysfunction. Circulating CRF is associated with poor gastric emptying, which prolongs ICU stay, whereas shock significantly impairs gastric emptying and gut permeability.
Journal Article
Venoarterial extracorporeal life support in post-traumatic shock and cardiac arrest: lessons learned
Objectives
Venoarterial extracorporeal life support (VA-ECLS) is an effective support of acute hemodynamic collapse caused by miscellaneous diseases. However, using VA-ECLS for post-traumatic shock is controversial and may induce a disastrous hemorrhage. To investigate the feasibility of using VA-ECLS to treat post-traumatic shock or cardiac arrest (CA), a single-center experience of VA-ECLS in traumatology was reported.
Materials and methods
This retrospective study included nine patients [median age: 37 years, interquartile range (IQR): 26.5-46] with post-traumatic shock/CA who were treated with VA-ECLS in a single institution between November 2003 and October 2012. The causes of trauma were high-voltage electrocution (n = 1), penetrating chest trauma (n = 1), and blunt chest or poly-trauma (n = 7). Medians of the injury severity score and the maximal chest abbreviated injury scale were 34 (IQR: 15.5-41) and 4 (IQR: 3-4), respectively. All patients received peripheral VA-ECLS without heparin infusion for at least 24 hours.
Results
The median time from arrival at our emergency department (ED) to VA-ECLS was 6 h (IQR: 4-47.5). The median duration of VA-ECLS was 91 h (IQR: 43-187) with a duration < 24 h in 2 patients. Among the 9 patients, 5 received VA-ECLS to treat the post-traumatic shock/CA presenting during (n = 2) or following (n = 3) damage-control surgeries for initial trauma, and another 4 patients were supported for non-surgical complications associated with initial trauma. VA-ECLS was terminated in 2 non-survivors owing to uncontrolled hemothorax or retroperitoneal hemorrhage. Three patients survived to hospital discharge. All of them received damage-control surgeries for initial trauma and experienced a complicated hospitalization after weaning off VA-ECLS.
Conclusion
Using VA-ECLS to treat post-traumatic shock/CA is challenging and requires multidisciplinary expertise.
Journal Article
Resuscitation strategies with different arterial pressure targets after surgical management of traumatic shock
Introduction
Hypotensive fluid resuscitation has a better effect before and during surgical intervention for multiple trauma patients with haemorrhagic shock. However, it is questionable whether hypotensive fluid resuscitation is suitable after surgical intervention for these patients, and whether resuscitation with different mean arterial pressure (MAP) targets after surgical intervention can obtain different results. The aim of this study was to investigate these questions and to explore the underlying mechanisms.
Methods
A total of 30 anesthetized piglets were randomly divided into 3 groups (n = 10 per group): low MAP, middle MAP, and high MAP, which had MAP targets of 60, 80, and 100 mmHg, respectively. All animals underwent femur fracture, intestine and liver injury, haemorrhagic shock, early hypotensive resuscitation, and surgical intervention. Then, the animals received fluid resuscitation with different MAP targets as mentioned above for 24 hours. Hemodynamic parameters and vital organ functions were evaluated.
Results
Fluid resuscitation in the 80 mmHg MAP group maintained haemodynamic stability, tissue perfusion, and organ function better than that in the other groups. The 60 mmHg MAP group presented with profound metabolic acidosis and organ histopathologic damage. In addition, animals in the 100 mmHg MAP group exhibited severe tissue oedema, organ function failure, and histopathologic damage.
Conclusions
In our porcine model of resuscitation, targeting high MAP by fluid administration alone resulted in a huge increase in the infusion volume, severe tissue oedema, and organ dysfunction. Meanwhile, targeting low MAP resulted in persistent tissue hypoperfusion and metabolic stress. Hence, a resuscitation strategy of targeting appropriate MAP might be compatible with maintaining haemodynamic stability, tissue perfusion, and organ function.
Journal Article