Endocrine Aspects of Acute and Prolonged Critical Illness

Critical illness is characterized by modifications involving the autonomic nervous system, the endocrine system, the immune system, the inflammatory response, and the coagulation pathway. The purpose of such a chain of events, also defined as the “stress response,” is to maintain body homeostasis and promote survival in the acute phase of critical illness. The magnitude of this response is proportional to the severity of the acute illness, and it may change during the evolution of the illness itself. The development of modern treatments in the intensive care unit has certainly improved the chances of survival, leading to a prolonged or “chronic” phase of critical illness. The exact time of the transition from the acute to the chronic phase cannot be established but is probably around 10 days of illness. This prolonged phase is characterized by specific neuroendocrine alterations that are no longer aimed at the survival of the patient. The alterations in mitochondrial function associated with hypoxia and hypoperfusion, especially in the acute phase, have been more recently investigated. Such mitochondrial dysfunction is associated with a sort of metabolic and bioenergetic hibernation of the cell, a phenomenon that may also have an adaptive and protective purpose, with the aim of preventing deterioration and cell death in the acute phase of critical illness. The fact that mitochondria at this stage are not capable of utilizing substrates for energetic purposes could explain why aggressive nutrition in the early hyperacute phase of critical illness may be detrimental, increasing oxidative stress and worsening the clinical outcome. In this chapter, we aimed to provide an overview of the current understanding of the endocrine aspects of acute and prolonged critical illness.