Hyperglycaemia is common during critical illness and may be viewed teleologically as a means of ensuring an adequate supply of glucose for the brain and phagocytic cells. Under normal conditions, euglycaemia is maintained by neural, hormonal and hepatic autoregulatory mechanisms. Critical illness promotes hyperglycaemia through an activation of the hypothalamic-pituitary-adrenal axis, which in turn increases hepatic glucose production and inhibits insulin-mediated glucose uptake to skeletal muscle. Sustained hyperglycaemia is associated with adverse consequences that demand its control. Appropriate management includes discontinuing causative drugs, correcting hypokalaemia, treating infection and administering insulin. Insulin therapy also appears to be useful for promoting an anabolic response in skeletal muscle.
Copyright 2001 Harcourt Publishers Ltd.