Metabolic and Endocrine Changes in Sepsis and the Catabolic State

Sepsis and critical illness constitute severe physical stress, associated with a characteristic physiological response. Historically, the metabolic and endocrine components of this response have been considered part of a uniform and (should the situation go on) sometimes persisting physiological adaptation. More recently, this model has been challenged on two fronts. Firstly, the metabolic and endocrine responses to sepsis and critical illness are not uniform and persistent. Rather, acute and chronic phases (where they occur) are associated with responses that are both distinct and discordant. Secondly, the interpretation that these responses are somehow adaptive has been rechallenged. Specifi c patterns of metabolic and endocrine response have prognostic value. Furthermore, recent clinical studies have demonstrated the benefi t of intervention targeting specific metabolic and endocrine endpoints. Both of these observations challenge the simple assumption that these responses are a positive design feature. Natural selection could have resulted in metabolic adaptation to acute severe illness built, in part, on the physiological responses to other stressors. However, the same process could not have produced metabolic adaptation to persisting critical illness—an entity that has only existed following developments in organ support and critical care units. What is adaptive in the short term may not be thereafter. Rather, these responses may go on to form part of the pathophysiological cascade that characterizes multiple organ failure.