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Crit Care. 2011;15(1):R44. doi: 10.1186/cc10006. Epub 2011 Jan 31.

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

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Department of Intensive Care, Erasmus MC - Sophia Children's Hospital, Dr, Molewaterplein 60, Rotterdam 3015 GJ, The Netherlands.



The 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.


Seventy-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)].


On 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.


Children 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.

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