Acute Hyperglycemia

The cellular effects of acute hyperglycemia are poorly understood, but reports have begun to shed some light on alterations in normal cell functions at the molecular level. One study^[96] showed that acutely elevated glucose levels depress endothelin-induced calcium signaling in rat mesangial cells, thereby depressing the contractile state of glomerular cells. Such information supports the hypothesis that acute hyperglycemia can affect cellular functions and may lead to clinically evident pathology.

Acute consequences of elevated serum glucose levels include impaired wound healing, dehydration, impaired immune system response, and proteolysis. The dehydration seen during acute hyperglycemia results from the osmotic diuretic effect of high serum glucose levels. Patients with diabetes are well known for having poor wound healing, which is commonly believed to be caused by impaired blood flow to the wound. However, there is evidence that acute hyperglycemia may impair fibroblast activity and impair vitamin C uptake by cells, thereby inhibiting new collagen synthesis. ^[97]

In addition to delayed wound healing, elevated glucose levels also inhibit immune function, and increase the risk of postoperative infection. One study^[98] suggests that continuous insulin infusions, used to control intraoperative and postoperative glucose levels, decrease the incidence of sternal wound infections after cardiac surgery. A second study^[99] found that aggressive glucose control intraoperatively significantly increased neutrophil activity in vitro. Alveolar macrophages from normal hosts demonstrate impaired respiratory burst when exposed in vitro to elevated glucose concentrations.^[100] Taken together, these data indicate that tight glucose control intraoperatively may significantly influence the ability of patients to recover more quickly from surgery.