Cerebral traumatic injury and glucose metabolism: a scoping review

Objective To review the influence of metabolic dysfunction of glucose after traumatic brain injury on patient mortality. Materials and methods We searched PubMed, Scopus, EBSCOhost, Medline, and Embase electronic databases, involving publications from 1980 to August 2017 in English and Spanish. Results The glucose metabolism in brain involved in brain signal conduction, neurotransmission, synaptic plasticity, and cognitive function. Insulin levels traverse the blood–brain barrier by utilizing an insulin receptor protein as a carrier, playing a pivotal role in various cognitive functions while also regulating energy metabolism. TBI causes elevated blood glucose levels. Hyperglycemia is attributed to an acute sympatho-adrenomedullary response, resulting in elevated catecholamines, increased levels of cortisol, and IL-6. Moreover, there is a potential association with hypothalamic involvement. Additionally, hyperglycemia is linked to lactic acidosis at the tissue level, ultimately contributing to higher mortality rates. Conclusions The monitoring and control of glucose should be an important part of multimodal monitoring in patients with moderate to severe traumatic brain injury managed in neurocritical care units. A management protocol should ensure normoglycemia and early detection and correction of glucose abnormalities since it improves patients' clinical outcomes.