The metabolic and nutritional response to critical illness

The metabolic response to critical illness is complex and affects every body system. The first phase of this response is characterized by increased hypothalamic pituitary activity and resistance (decreased response) to effector hormones in many target tissues. Cytokines released in the early stages of such illness may be important as they appear to stimulate the hypothalamic pituitary axis directly as part of this ‘stress response’. This phase is considered ‘adaptive’ (helpful), increasing the availability of glucose, free fatty acids, and amino acids as substrates for vital organs. However, in prolonged illness, the neuroendocrine response is very different with damped hypothalamic responses, leading to a state in which catabolism predominates, leading to what might be termed the critical illness wasting syndrome. The gastrointestinal (GI) failure often associated with prolonged critical illness appears to be due, at least in part, to an altered neuroendocrine environment. The poor nutritional state associated with GI failure exacerbates the catabolic response, prolonging illness and the period of intensive care management required by the patient. The result is increased mortality and, in survivors, a more prolonged recovery/rehabilitation process.