Molecular mechanisms of postintensive care syndrome

Effectiveness of intensive care must be evaluated not only by short-term survival after a critical illness, but also by the recovery to an adequate quality of life. The increased evidence of long-term functional disabilities in intensive care survivors led to the definition of post-intensive care syndrome (PICS) Early diagnosis and effective treatments for these newly recognized conditions are warranted. However, most of the initial efforts to limit long-term sequelae have not yielded satisfactory results The objective of this review is to identify the molecular mechanisms that lead to organ dysfunction after intensive care and to summarize them into several plausible unifying hypotheses. From these mechanisms, novel therapeutic targets with the potential to prevent PICS may arise [3], allowing for earlier interventions during acute organ failure aimed to improve the quality of life of intensive care unit (ICU) survivors. Cost-effective strategies based on growing pathogenetic evidence on PICS would hence allocate research efforts and funding to implement preventive treatments, to impede pathogenetic mechanisms triggered during ICU stay, rather than exclusively rehabilitate long-term sequelae when they are already established.