A strong association exists between hyperglycemia and outcome in pediatric traumatic brain injury (TBI). Herein, we describe observations of serum markers of glucose metabolism in a cohort of pediatric TBI patients and how these variables are related to parameters of intracranial pathophysiology.
A retrospective analysis was performed on pediatric severe TBI patients admitted to Addenbrookes Hospital Paediatric Intensive Care Unit (PICU) between January 2001 and December 2013. Demographic, outcome, systemic physiological, and cerebral autoregulatory data were extracted for patients who had received continuous invasive monitoring (ICM+, Cambridge Enterprise, Cambridge, UK). Data were analyzed using a mixed linear model.
Forty-four patients with an average age of 12.2 years were admitted to the PICU with a TBI requiring invasive neurosurgical monitoring. Thirty-two patients (73%) survived, with favorable outcomes in 62%. The mean (SD) intracranial pressure (ICP) was 17.6 + 9.0 mmHg, MAP was 89.7 + 9.0 mmHg, and pressure-reactivity index (PRx) was −0.01 + 0.23 a.u. The mean (SD) serum lactate was 2.2 (3.3) mmol/L. and the mean (SD) serum glucose was 6.1 (1.6) mmol/L. Early hyperglycemia was strongly associated with both PRx (Pearson correlation 0.351,
Increases in systemic glucose are associated with impaired cerebrovasular autoregulation after severe pediatric TBI. Moreover, deranged blood glucose is a marker of poor prognosis. Further studies are required to delineate putative mechanisms of hyperglycemia induced cerebral harm.