Review: Traumatic brain injury and hyperglycemia, a potentially modifiable risk factor

Abstract

Hyperglycemia after severe traumatic brain injury (TBI) occurs frequently and is associated with poor clinical outcome and increased mortality. In this review, we highlight the mechanisms that lead to hyperglycemia and discuss how they may contribute to poor outcomes in patients with severe TBI. Moreover, we systematically review the proper management of hyperglycemia after TBI, covering topics such as nutritional support, glucose control, moderated hypothermia, naloxone, and mannitol treatment. However, to date, an optimal and safe glycemic target range has not been determined, and may not be safe to implement among TBI patients. Therefore, there is a mandate to explore a reasonable glycemic target range that can facilitate recovery after severe TBI.

Previous physical exercise alters the hepatic profile of oxidative‐inflammatory status and limits the secondary brain damage induced by severe traumatic brain injury in rats

“…; Shi et al . ). Indeed, our experimental protocol of exercise training protected against blood glucose, insulin and HOMA‐2%S increases, as well as hepatic immunoreactivity of pJNK increase, and also pIRS and pAKT decreases after neuronal injury.…”

“…Recently, considerable evidence has demonstrated that hyperglycaemia (both peak glucose and persistent hyperglycaemia) is one of the most common secondary complications of severe TBI (Shi et al . ). In line with this view, the present study shows that blood glucose, insulin and HOMA‐2%S were significantly elevated following acute neuronal injury in sedentary rats.…”

A Cross-sectional Observational Analysis of Preoperative Blood Glucose Levels in Nondiabetic Patients presenting for Surgery

“…Perioperative dysglycemia is recognized as one of the risk factors of increased morbidity and mortality during and after surgery. 23 Preoperative hypoglycemia results in neuroendocrine stimulation and may lead to behavioral changes, confusion, seizure, palpitation, tremor, anxiety, diaphoresis, pallor, etc. On the contrary, preoperative hyperglycemia prolongs wound healing and increases the chances of surgical site infection.…”

Brain Trauma Disrupts Hepatic Lipid Metabolism: Blame It on Fructose?

“…GH can also stimulate hepatic glucose production, such that change of GH production can affect insulin sensitivity and glucose homeostasis. Reduced sensitivity to the action of insulin is considered a predictor of poor clinical outcome in TBI patients . Posttraumatic neuroendocrine abnormalities particularly in the somatotrophic axis are commonly observed in TBI patients, which are also likely affected by fructose consumption.…”