Pathophysiological aspects of hyperglycemia in children with meningococcal sepsis and septic shock: a prospective, observational cohort study

Abstract

IntroductionThe objective of this study was to investigate the occurrence of hyperglycemia and insulin response in critically ill children with meningococcal disease in the intensive care unit of an academic children's hospital.MethodsSeventy-eight children with meningococcal disease were included. The group was classified into shock non-survivors, shock survivors and sepsis survivors. There were no sepsis-only non-survivors. The course of laboratory parameters during 48 hours was assessed. Insulin sensitivity and β-cell function on admission were investigated by relating blood glucose level to insulin level and C-peptide level and by homeostasis model assessment (HOMA) [β-cell function (HOMA-%B) and insulin sensitivity (HOMA-%S)].ResultsOn admission, hyperglycemia (glucose >8.3 mmol/l) was present in 33% of the children. Shock and sepsis survivors had higher blood glucose levels compared with shock non-survivors. Blood glucose level on admission correlated positively with plasma insulin, C-peptide, cortisol, age and glucose intake. Multiple regression analysis revealed that both age and plasma insulin on admission were significantly related to blood glucose. On admission, 62% of the hyperglycemic children had overt insulin resistance (glucose >8.3 mmol/l and HOMA-%S <50%); 17% had β-cell dysfunction (glucose >8.3 mmol/l and HOMA-%B <50%) and 21% had both insulin resistance and β-cell dysfunction. Hyperglycemia was present in 11% and 8% of the children at 24 and 48 hours after admission, respectively.ConclusionsChildren with meningococcal disease often show hyperglycemia on admission. Both insulin resistance and β-cell dysfunction play a role in the occurrence of hyperglycemia. Normalization of blood glucose levels occurs within 48 hours, typically with normal glucose intake and without insulin treatment.

CD64-Neutrophil expression and stress metabolic patterns in early sepsis and severe traumatic brain injury in children

“…It has been recently reported that 62% of hyperglycemic septic children had overt insulin resistance on admission and 17% had β-cell dysfunction [48] and that the endotoxin activity was significantly associated with 52% increased risk for incident diabetes [49]. Further studies are needed to examine the cross talk between hormonal and inflammatory responses in the development of SIRS in sepsis, since the metabolic and immune systems are closely involved in inflammation and may significantly contribute to the critically illness pathology [1].…”

Surviving Sepsis Campaign: International Guidelines for Management of Severe Sepsis and Septic Shock, 2012

“…An RCT of strict glycemic control compared to moderate control using insulin in a pediatric ICU population found a reduction in mortality with an increase in hypoglycemia. Insulin therapy should only be conducted with frequent glucose monitoring in view of the risks for hypoglycemia which can be greater in newborns and children due to a) relative lack of glycogen stores and muscle mass for gluconeogenesis, and b) the heterogeneity of the population with some excreting no endogenous insulin and others demonstrating high insulin levels and insulin resistance [622][623][624][625][626][627][628].…”

Surviving Sepsis Campaign

“…Insulin therapy should only be conducted with frequent glucose monitoring in view of the risks for hypoglycemia which can be greater in newborns and children due to a) relative lack of glycogen stores and muscle mass for gluconeogenesis, and b) the heterogeneity of the population with some excreting no endogenous insulin and others demonstrating high insulin levels and insulin resistance (622)(623)(624)(625)(626)(627)(628). In general, infants are at risk for developing hypoglycemia when they depend on intravenous fluids.…”