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ABSTRACT
Glucose metabolism and homeostasis change considerably during the course of critical illness. The hyperglycemic response to stress is thought to be an adaptive change to restore the glucose supply of poorly perfused tissues. Endogenous glucose production is severely impaired in sepsis, and the resultant hypoglycemia is a significant cause of death in many cases. The neuroendocrine changes during the acute and chronic phases of severe illness are differentially regulated. The initial changes consist primarily of activated anterior pituitary function, the peripheral anabolic pathways being inactivated. In prolonged critical illness, however, there is a uniform reduction in the pulsatile secretion of pituitary hormones. In this phase, the pulsatility may be reestablished by the administration of relevant combinations of releasing factors. In the existence of partial adrenocortical insufficiency, treatment with high doses of glucocorticoids remains controversial, but physiological doses might be beneficial. Similarly, there is no adequate data concerning the beneficial effect of treatment of thyroid hormone abnormalities, the so-called euthyroid sick syndrome. In the acute phase of critical illness, high dose growth hormone administration is not recommended due to increased mortality and morbidity. It remains plausible that growth hormone/insulin-like growth factor-I provided in conjunction with appropriate nutritional support would be of benefit in appropriately selected groups particularly in the chronic phase of critical illness.
Glucose metabolism and homeostasis change considerably during the course of critical illness. The hyperglycemic response to stress is thought to be an adaptive change to restore the glucose supply of poorly perfused tissues. Endogenous glucose production is severely impaired in sepsis, and the resultant hypoglycemia is a significant cause of death in many cases. The neuroendocrine changes during the acute and chronic phases of severe illness are differentially regulated. The initial changes consist primarily of activated anterior pituitary function, the peripheral anabolic pathways being inactivated. In prolonged critical illness, however, there is a uniform reduction in the pulsatile secretion of pituitary hormones. In this phase, the pulsatility may be reestablished by the administration of relevant combinations of releasing factors. In the existence of partial adrenocortical insufficiency, treatment with high doses of glucocorticoids remains controversial, but physiological doses might be beneficial. Similarly, there is no adequate data concerning the beneficial effect of treatment of thyroid hormone abnormalities, the so-called euthyroid sick syndrome. In the acute phase of critical illness, high dose growth hormone administration is not recommended due to increased mortality and morbidity. It remains plausible that growth hormone/insulin-like growth factor-I provided in conjunction with appropriate nutritional support would be of benefit in appropriately selected groups particularly in the chronic phase of critical illness.