Abstract

Multiple organ failure (MOF) emerged in the early 1970s with the advent of intensive care units (ICUs). Sepsis and trauma were recognized to be the primary inciting events. MOF was initially viewed to be “fatal expression of uncontrolled infection” caused by intra-abdominal infection. As a result, research focused on preventing IAIs as well and stress formula TPN to prevent the resulting “septic auto-cannibalism”. In the mid-1980s, it was shown that blunt trauma frequently induced a non-infectious “sepsis syndrome” phenotype. Research efforts focused on identifying the driving mechanisms. Unrecognized shock was identified and it became a common ICU practice to maximize oxygen delivery to eliminate “oxygen debt”. In the late 1980s, tremendous advances in trauma care resulted in decreased early deaths. However, an epidemic of iatrogenic abdominal compartment syndrome (ACS) emerged as a new phenotype. Simultaneously, “sepsis syndrome” was replaced by the SIRS/CARS paradigm to explain the bimodal presentation on early and late MOF. In the late 1990s, again fundamental advances in trauma care reduced early deaths, but largely eliminated ACS. In the 2000s, implementing the Glue Grant trauma and the Surviving Sepsis Campaign evidence based guidelines in surgical ICU substantially decreased ICU deaths from MOF. However, MOF had evolved into a lingering phenotype of chronic critical illness (CCI). The term persistent inflammation, immunosuppression, and catabolism syndrome (PICS) was coined to describe the new phenotype and to provide a mechanistic framework in which to study CCI in surgical ICU patients. A recently completed 5 year prospective study of surgical ICU sepsis demonstrated that while ICU deaths were surprising low, over a 1/3rd of patients progressed into CCI. Roughly, 80% of CCI patients had a poor discharge disposition suffering from severe disabilities and a 1 year mortality of 40%. Serial biomarkers out to 28 days validated the PICS–CCI paradigm.

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