Hyperglycemia and outcomes in patients with sepsis

van Vught and coworkers studied the relationship between admission glucose levels greater than 70 mg/dL and outcomes in critically ill patients with sepsis (1). This study included 987 patients; the distribution of admission glucose values measured in the time frame of 4 h before admission to 4 h after admission included 519 patients with euglycemia (71–140 mg/dL), 267 patients with mild hyperglycemia (140–199 mg/dL), and 201 patients with severe hyperglycemia (≥200 mg/dL). These glucose measurements were obtained early in the sepsis course and presumably reflect glucose regulation before treatment of infection and of elevated glucose levels. Patients with mild and severe hyperglycemia were older, had higher body mass indices, and had more chronic co-morbidity. In addition, 53.7% of patients with severe hyperglycemia had a history of diabetes. The proportion of patients with organ failure was similar in the three groups, but shock on ICU admission was significantly more frequent in patients admitted with normal glucose levels. Patients with severe hyperglycemia developed acute kidney injury and acute myocardial infarction more frequently while in the ICU. Multivariable Cox regression analysis demonstrated that patients with severe hyperglycemia had an increased risk for mortality by day 30 compared to patients with euglycemia (hazard ratio =1.66; 95% CI, 1.24–2.23). This adverse effect of severe hyperglycemia was present in both patients with and without diabetes. There appeared to be a complex interaction between glucose levels and lactate levels in this study. In the overall cohort and in patients with diabetes, hyperglycemia was associated with increased mortality after correction for the highest lactate value obtained during the first 24 h. However, hyperglycemia was not associated with increased mortality in patients without diabetes after adjustment for lactate. Patients with sepsis had increased acute phase protein responses and activation of cytokine networks, the vascular endothelium, and coagulation pathways. There was no increase in these levels suggesting unregulated cytokine production, and these responses were reduced or blunted in patients with both mild and severe hyperglycemia. This information on inflammatory responses is relevant to both host defense responses to infection and to dysregulated host defense responses and organ dysfunction associated with sepsis