ABSTRACT

The role of surgical critical care, including resuscitation and/ or organ support, must be to work alongside the metabolic effects of injury while the patient is restored to a situation from which homeostatic mechanisms can achieve a return to normality. Impaired immunity as part of the metabolic response compounds this risk and explains why sepsis and MODS/ failure is a key part of perioperative care and a leading mode of death among our patients. This chapter reviews the mediators of the stress response, the physiological and biochemical pathway changes associated with surgical injury and the changes in body composition that occur following surgical injury. Patients also respond rapidly to injury by the classical neuroendocrine pathways of the stress response, consisting of afferent nociceptive neurones, the spinal cord, thalamus, hypothalamus and pituitary.