Shock : molecular, cellular, and systemic pathobiological aspects and therapeutic approaches : the official journal the Shock Society, the European Shock Society, the Brazilian Shock Society, the International Federation of Shock Societies
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Hemorrhagic shock with tissue trauma (HS/T) leads to the activation of a system-wide immune-inflammatory response that involves all organs and body compartments. Recent advances in single-cell analysis permit the simultaneous assessment of transcriptomic patterns in a large number of cells making it feasible to survey the landscape of immune cell responses across numerous anatomic sites. Here, we used single-cell RNA sequencing of leukocytes from the blood, liver, and spleen to identify the major shifts in gene expression by cell type and compartment in a mouse HS/T model. ⋯ The dominant pattern across all compartments for B and T cells was a suppression of genes associated with cell activation and signaling after HS/T. Using complement factor 3 (C3) knockout mice we unveiled a role for C3 in the suppression of monocyte Major Histocompatibility Complex class II expression and activation of gene expression associated with migration, phagocytosis and cytokine upregulation, and an unexpected role in promoting interferon-signaling in a subset of B and T cells across all three compartments after HS/T. This transcriptomic landscape study of immune cells provides new insights into the host immune response to trauma, as well as a rich resource for further investigation of trauma-induced immune responses and complement in driving interferon signaling.
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Pediatric shock has a high mortality rate because many of the early clinical signs are subtle and have poor sensitivity and specificity. Pediatric shock was categorized either: compensated with normal blood pressure, poor skin perfusion (CRT >2 s, mottled, cool peripheries, peripheral cyanosis), weak peripheral pulse, age specific tachycardia, tachypnoea, and oliguria or decompensated with hypotension (SBP < 70 + (2× age in years) mm Hg and decreased mental status. The perfusion index is a non-invasive method for assessing peripheral perfusion and may be a useful marker for identifying shock early in pediatric patients. ⋯ Perfusion index (PI), lactate, and lactate clearance provided comparable sensitivity and specificity for predicting outcomes among pediatric patients with shock Therefore, we suggest that the PI is an inexpensive, rapid, and non-invasive tool that can be used to predict illness severity and mortality in busy pediatric intensive care units and emergency departments. This tool may guide better patient triage and an earlier diagnosis of shock in this setting.
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Exsanguination remains a leading cause of preventable death in traumatically injured patients. To better treat hemorrhagic shock, hospitals have adopted massive transfusion protocols (MTPs) which accelerate the delivery of blood products to patients. There has been an increase in mass casualty events (MCE) worldwide over the past two decades. These events can overwhelm a responding hospital's supply of blood products. Using a computerized model, this study investigated the ability of US trauma centers (TCs) to meet the blood product requirements of MCEs. ⋯ Assuming a TC's ability to treat patients is limited only by their supply of blood products, US level-1 TCs lack the on-hand blood products required to adequately treat patients following a MCE. Use of non-traditional blood products, which have a longer shelf life, may allow TCs to better meet the blood product requirement needs of patients following larger MCEs.
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The Surviving Sepsis Campaign published the Hour-1 Sepsis Bundle in 2018. The first-hour management of patients with sepsis in the emergency department (ED) is important, as suggested in the Hour-1 Sepsis Bundle. The objectives of the present study were to evaluate 28-day mortality and delayed septic shock with use of a complete and incomplete Hour-1 Sepsis Bundle in the ED. ⋯ The complete Hour-1 Sepsis Bundle treatment in the ED was not significantly associated with 28-day mortality and delayed septic shock.