Nutrition Therapy, Glucose Control, and Brain Metabolism in Traumatic Brain Injury: A Multimodal Monitoring Approach

Abstract

The goal of neurocritical care in patients with traumatic brain injury (TBI) is to prevent secondary brain damage. Pathophysiological mechanisms lead to loss of body mass, negative nitrogen balance, dysglycemia, and cerebral metabolic dysfunction. All of these complications have been shown to impact outcomes. Therapeutic options are available that prevent or mitigate their negative impact. Nutrition therapy, glucose control, and multimodality monitoring with cerebral microdialysis (CMD) can be applied as an integrated approach to optimize systemic immune and organ function as well as adequate substrate delivery to the brain. CMD allows real-time bedside monitoring of aspects of brain energy metabolism, by measuring specific metabolites in the extracellular fluid of brain tissue. Sequential monitoring of brain glucose and lactate/pyruvate ratio may reveal pathologic processes that lead to imbalances in supply and demand. Early recognition of these patterns may help individualize cerebral perfusion targets and systemic glucose control following TBI. In this direction, recent consensus statements have provided guidelines and recommendations for CMD applications in neurocritical care. In this review, we summarize data from clinical research on patients with severe TBI focused on a multimodal approach to evaluate aspects of nutrition therapy, such as timing and route; aspects of systemic glucose management, such as intensive vs. moderate control; and finally, aspects of cerebral metabolism. Research and clinical applications of CMD to better understand the interplay between substrate supply, glycemic variations, insulin therapy, and their effects on the brain metabolic profile were also reviewed. Novel mechanistic hypotheses in the interpretation of brain biomarkers were also discussed. Finally, we offer an integrated approach that includes nutritional and brain metabolic monitoring to manage severe TBI patients.

Nutrition in the Neurocritical Care Unit: a New Frontier

“…Neurologic injury triggers a hypercatabolic state, primarily mediated by glucocorticoids, catecholamines, and glucagon [15]. Resting energy expenditure (REE) has been found to be as high as 200% of usual needs in two-thirds of patients during the first 2 to 4 weeks following brain trauma [1, 10,16].…”

“…Elevated REE in patients with higher grade aneurysmal subarachnoid hemorrhage (SAH) has been associated with higher incidence of vasospasm [18][19][20]. Additionally, metabolic demands may vary throughout the ICU course as various therapies common in neurocritical care influence metabolic demands including the use of barbiturates, sedation, normothermia, and hypothermia [15,21].…”

“…In addition to an increase in REE, metabolic processes such as glycogenolysis and gluconeogenesis result in concomitant hyperglycemia and increased skeletal protein catabolism [15]. This elevated protein catabolism in the setting of inadequate nutritional intake or delivery may result in a negative nitrogen balance, reflecting the loss of total body protein [16].…”

“…Cerebral microdialysis (CMD) is an invasive parenchymal monitor that provides insight into the nuances of cerebral metabolism, and allows for the study of real-time substance concentrations within brain tissue and can be implemented as a tool for multimodal monitoring [15].…”

“…Limitations often discussed in using CMD are whether or not data from these catheters reflect a regional versus global picture, or if any interventions equally effect normal brain tissue [17]. Despite limitations, CMD research has allowed for the understanding that there are pathologic patterns, such as high CMD lactate-to-pyruvate ratio (LPR) and low CMD glucose, which are associated with increased mortality [15]. Only a few studies describe the effects of nutritional interventions on these markers.…”