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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Platelets are subcellular anucleate components of blood primarily responsible for initiating and maintaining hemostasis. After injury to a blood vessel, platelets can be activated via several pathways, resulting in changed shape, adherence to the injury site, aggregation to form a plug, degranulation to initiate activation in other nearby platelets, and acceleration of thrombin formation to convert fibrinogen to fibrin before contracting to strengthen the clot. Platelet function assays use agonists to induce and measure one or more of these processes to identify alterations in platelet function that increase the likelihood of bleeding or thrombotic events. ⋯ We review the pros, cons, and evidence for use of many of the popular assays in trauma, discuss limitations of their use in this patient population, and present approaches that can be taken to develop improved functional assays capable of elucidating mechanisms of trauma-induced platelet dysfunction. Platelet dysfunction in trauma has been associated with need for transfusions and mortality; however, most of the current platelet function assays were not designed for evaluating trauma patients, and there are limited data regarding their use in this population. New or improved functional assays will help define the mechanisms by which platelet dysfunction occurs, as well as help optimize future treatment.
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Background: Current means of diagnosis of acute kidney injury (AKI) based on serum creatinine have poor sensitivity and may miss possible therapeutic windows in subclinical kidney injury, especially in septic AKI. Kidney injury molecule-1 (KIM-1) may be a valuable biomarker to improve diagnostic algorithms for AKI. The understanding of septic AKI is still insufficient, and knowledge about KIM-1 kinetics in inflammation is scarce. ⋯ This outlines the insufficiency of the current diagnostic approach regarding AKI and the urgency to develop novel diagnostic algorithms including markers of kidney injury. Clinical Trial Registration:www.clinicaltrials.gov. Unique identifier: NCT03392701 (August 1, 2018).
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Resuscitation of trauma patients after hemorrhagic shock causes global I/R, which may contribute to organ dysfunction. Oxidative stress resulting from I/R is known to induce signaling pathways leading to the production of inflammatory molecules culminating in organ dysfunction/injury. Our recent work demonstrated that oxidative stress was able to induce activation of the mitochondrial antiviral signaling protein (MAVS), a protein known to be involved in antiviral immunity, in an in vitro model. ⋯ Further, in vitro silencing of MAVS by specific siRNA in RAW 264.7 and exposure of the cells to H/R caused activation of mitophagy. This may represent a compensatory response to increased liver inflammation. We conclude that activation of MAVS by hypoxia/reoxygenation dampens inflammation, potentially suggesting a novel target for intervention.
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Objective: We previously identified two transcriptomic subtypes (Signature Groups: SG1 vs. SG2) in trauma patients at 12 hours postinjury, with SG1 associated with worse outcomes. In this study, we aimed to further characterize the changes in SG subtype categorization of trauma patients over time after injury and define the corresponding association with outcomes based on the timing of the subtype designation. ⋯ SG1 assignment, regardless of time point, was associated consistently with slower recovery. Further analysis revealed that additional prognostic information could be obtained by assessing SG subtype at both 12 hours and 1 day. Conclusions: This study provides a proof of concept that immune status can worsen after admission and highlights the benefit of longitudinally monitoring SG subtypes in trauma patients.
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Clinical Trial
Value of corrected flow time in common carotid artery in predicting volume responsiveness under mechanical ventilation.
Objective: The present study aimed to investigate whether corrected flow time (FTc) in common carotid artery could predict volume responsiveness under mechanical ventilation and to further explore whether the sensitivity and specificity would be influenced by positive end-expiratory pressure (PEEP). Methods: The first stage of this study included 80 patients from the general surgery department undergoing laparotomy. After induction of general anesthesia, FTc in the common carotid artery was measured when hemodynamic indicators, such as blood pressure, heart rate, and cardiac output (CO), were stabilized. ⋯ The area under the receiver operating characteristic curve for FTc in predicting volume responsiveness was 0.921, 0.805, and 0.719 when PEEP was 0, 5, and 10 cmH 2 O ( P < 0.05), respectively, and the cutoff value of FTc for diagnosing volume responsiveness was 323.42 milliseconds, 326.69 milliseconds, and 312.03 milliseconds, respectively. Conclusion: Corrected flow time in the common carotid artery can predict volume responsiveness under mechanical ventilation, and the predictive performance is not influenced by PEEP. Clinical Trial Registration Clinical register number: ChicTR2000029519.