Blood glucose control within critical care – a review of literature influencing practice

Journal of Diabetes Nursing Vol 16 No 8 2012 The effects of hyperglycaemia within critical care are profound, as critically ill individuals are in a hypermetabolic state as a result of either major surgery or acute illness. The causes of this metabolic response are the intense activation of the counter-regulatory hormones – cortisol, glucagon, epinephrine and growth hormone. These hormones increase blood glucose by stimulating the synthesis of glucose from amino acids (gluconeogenesis) and by breaking down glycogen into glucose (glycogenolysis; Bilous and Donnelly, 2010). These metabolic processes cause insulin resistance, where there is the appropriate level of insulin produced but the body is unable to use the insulin and is therefore unable to maintain normoglycaemia (Knieriem et al, 2007). Hyperglycaemia in the critically ill person, also documented as “stress hyperglycaemia”, was deemed a beneficial, adaptive response that provided essential glucose to vital organs such as the brain, skeletal muscles and heart during critical illness (Marik, 2009). In addition to the metabolic responses, hyperglycaemia may also be induced by some medical interventions, such as total parenteral nutrition (TPN), anaesthetic agents and dextrose supplements (McCowan et al, 2005). However, evidence suggests that stress hyperglycaemia may also be associated with increased mortality and morbidity in the intensive-care setting (Knieriem et al, 2007; Shultz et al, 2010). Studies have shown that increased blood glucose circulation has detrimental effects, such as increased inflammation, immune system dysfunction, stimulation of coagulation and modulation of the endothelium (Knieriem et al, 2007). High blood glucose levels are also suggested to be acutely toxic – cellular glucose Blood glucose control within critical care – a review of literature influencing practice