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Life-threatening organ dysfunction/failure in critically ill patients suffering from sepsis or trauma is caused by a dysregulated host response to infection and/or inflammation. Despite significant advances in our understanding of some of the key signaling pathways involved in the excessive inflammation associated with sepsis/trauma, the translation of our current understanding of the underlying pathophysiology into organ-protective therapeutic strategies is still very limited. Current therapeutic approaches, hence, continue to rely on source control, antibiotics and supportive care, and particularly early goal-directed therapy.
Trauma represents a leading cause of death, particularly in the younger population. Traumatic brain injury and hemorrhage are the most common causes of early death, whereas complications such as infections, (multi-)organ failure and “persistent inflammation, immunosuppression, and catabolism syndrome” (PICS) represent relevant factors for late adverse outcomes. Pre- and intra-hospital diagnostic and therapeutic standard operating procedures have been shown to beneficially influence posttraumatic outcome. However, development of patient-specific diagnostic and therapeutic strategies remains challenging due to uncertainties regarding the assessment of the individual risk profile. Furthermo...
Sepsis remains a leading cause of morbidity and mortality in critically ill patients, posing a major challenge to modern medicine. Despite advancements in treatment, the complexity of sepsis—characterized by a dysregulated immune response to infection—continues to resist definitive therapeutic solutions. Central to this challenge is the delicate balance between pro-inflammatory and anti-inflammatory responses, which can either clear pathogens or lead to damaging immunopathology. Recent research has highlighted the critical role of endogenous regulators in modulating innate immunity during sepsis. These naturally occurring molecules have the potential to either amplify or suppress immune ...
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