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 …