Hyperglycemia in the surgical intensive care unit

Abstract

Hyperglycemia is the most common metabolic disturbance seen in the postoperative, intensive care patient. It can occur in patients with previously diagnosed diabetes mellitus, with undiagnosed diabetes, 1 and in patients without diabetes under the acute stress of trauma, surgery, or myocardial infarction. 2 Critical illness induces insulin resistance at the cellular level, which coupled with relative insulin inadequacy and unabated hepatic glucose release, leads to persistent elevation in blood glucose. A number of factors released during acute illness and stress act as mediators for this response, including cytokines, growth hormone, glucagon, catecholamines, and cortisol.3 Impairment of insulin action leads to lipolysis and protein catabolism that produce substrates for additional glucose production by the liver. Glycogenolysis is promoted by release or administration of catecholamines. Insulin-mediated glucose uptake by heart and skeletal muscle is impaired and further worsens glucose homeostasis. To some extent, the resultant increase in blood glucose can be adaptive to provide increased substrate to organs that do not require insulin for glucose uptake such as brain and blood cells. Not surprisingly, when pushed to the extreme by critical illness these accommodations can lead to untoward consequences requiring interventions in order to reverse this metabolic derangement. © 2010 Springer-Verlag US.