The role of hyperglycemia in burned patients: evidence-based studies

Abstract

Severely burned patients typically experience a systemic response expressed as increased metabolism, inflammation, alteration of cardiac and immune function, and associated hyperglycemia. Hyperglycemia has been associated with an increased risk of morbidity and mortality in critically ill patients. Until recently and for many years, hyperglycemia has been expectantly managed and considered a normal and desired response of an organism to stress. However, findings reported from recent studies now suggest beneficial effects of intensive insulin treatment of critically ill patients. The literature on the management of hyperglycemia in severely burned patients is sparse, with most of the available studies involving only small numbers of burned patients. The purpose of this article is to describe the pathophysiology of hyperglycemia after severe burns and to review the available literature on the outcome of intensive insulin treatment and other anti-hyperglycemic modalities in burned patients in an evidence-based medical approach.

Fig. 1

Determination of glucose concentration in plasma. A. Plasma glucose levels are determined by production/external load and uptake of glucose from peripheral tissues. B. An increased production/load, decreased uptake or both causes increased glucose levels.

Fig. 1

Determination of glucose concentration in plasma. A. Plasma glucose levels are determined by production/external load and uptake of glucose from peripheral tissues. B. An increased production/load, decreased uptake or both causes increased glucose levels.

Fig. 2

Insulin independent tissues (i.e. erythrocyte) do not require insulin to uptake glucose. Insulin-dependent tissues require insulin binding to insulin receptor to activate the insulin signaling, leading to expression of the GLUT-4 transporter permitting glucose uptake and further oxidation by mitochondria.

Fig. 3

Burned patients typically had impaired insulin signaling, decreasing insulin uptake by the cells, and affecting the mitochondrial oxidation. Metformin primarily acts by reducing hepatic glucose production. Fenofibrate attenuates insulin resistance by acting in the insulin signaling, and increasing mitochondrial oxidation of intracellular glucose. Metformin decreases hepatic gluconeogenesis and improves insulin sensitivity.