Abstract

A dysfunctional innate immune response to injury or infection often leads to sepsis, multiple organ failure, and fulminant death. As treatment of the critically ill patient has improved significantly over the past two decades, many high acuity patients in intensive care units (ICU) survive in a state of chronic critical illness (CCI)—characterized by high resource utilization, prolonged ICU stay, incapacitating functional outcomes, and dismal long-term survival. These patients are described by many different terms, including but not limited to, “Post-Sepsis Syndrome” and “Post Intensive Care Unit Syndrome.” However, these terms describe a clinical phenotype and do not necessarily describe or lend insight into the pathophysiology of these patients. The Persistent Inflammation, Immunosuppression, and Catabolism Syndrome, which will be delineated as PICS in this chapter, has been hypothesized as an important driver of CCI patient outcomes. The self-perpetuating and persistent cycle of inflammation is induced by the release of endogenous alarmins and danger-associated molecular patterns (DAMPs). As the incidence of CCI cases continues to escalate, a better understanding of the mechanisms driving PICS and propagating CCI is necessary.

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