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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Review
« Immunosuppression » is Inappropriately Qualifying the Immune Status of Septic and Sirs Patients.
Immunosuppression is the most commonly used concept to qualify the immune status of patients with either sterile systemic inflammatory response syndrome (SIRS) or sepsis. In this review we attempt to demonstrate that the concept of immunosuppression is an oversimplification of the complex anti-inflammatory response that occurs in patients dealing with a severe sterile or infectious insult. ⋯ This juxtaposition illustrates that there is no global defect. The mechanisms called reprogramming or trained innate immunity are probably aimed at preventing a generalized deleterious inflammatory reaction, and work to maintain the defense mechanisms at their due levels.
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Prolonged low blood pressure <40 mmHg in hemorrhagic shock (HS) causes irreversible heart dysfunction, 'Shock Heart Syndrome' (SHS), which is associated with lethal arrhythmias (ventricular tachycardia or ventricular fibrillation [VT/VF]) leading to a poor prognosis. ⋯ Ventricular structural remodeling after HS causes VT/VF in the presence of APDd. Transfusion of HbV prevents VT/VF, similarly to transfusion of wRBCs, by preventing electrical remodeling and preserving myocardial structures in HS-induced SHS.
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Intestinal ischemia/reperfusion (I/R)-induced systemic inflammation leads to multiple organ dysfunction syndrome. Previous studies have indicated that the NOD-like receptor protein (NLRP)3 inflammasome modulates intestinal inflammation; however, the pathophysiological mechanisms remain unclear. Autophagy is a critical metabolic mechanism that promotes cellular survival following ischemic injury. ⋯ Subsequently, we demonstrated a critical role for autophagy in suppressing intestinal I/R-induced NLRP3 inflammasome activation in vivo. Furthermore, we showed that the loss of autophagy activates inflammasome-mediated IL-1β secretion, which aggravates H/R injury, and NLRP3 knockdown reverses these effects. Collectively, these results directly implicated the homeostatic process of autophagy and NLRP3 inflammasome in ischemic bowel disease and identified a novel pathway for therapeutic intervention in intestinal I/R.
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Early differential diagnosis of an infection in a trauma patient is likely to have a significant influence on the prognosis. In the present study, we evaluated the early differential value of plasma presepsin, procalcitonin (PCT), C-reactive protein (CRP), and white blood cells (WBCs) on infection in trauma patients. ⋯ Presepsin might be a superior biomarker for early differentiation of infection in trauma patients; however, trauma stress elevates PCT, CRP, and WBCs even in the absence of infection; therefore, caution is advised when using these indicators to diagnose infection.
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Uncontrolled bleeding is the main cause of the potential preventable death in trauma patients. Accordingly, we reviewed all the existing scores for massive transfusion posttraumatic hemorrhage and summarized their characteristics, thus making it easier for the reader to have a global view of these scores-how they were created, their accuracy and to which population they apply. ⋯ The current prevailing practice that is best described as institutional or provider centered should be supplemented with score-based protocol with auditing and monitoring tools to refine it. This review summarizes the current scoring models in predicting the need for MT in civilian and military trauma. Several questions remain open; i.e., do we need to develop new score, merge scores, modify scores, or adopt existing score for certain trauma setting?