The optimal range of blood glucose levels in neurosurgical and neurocritically ill patients has not been determined and remains controversial. No consensus exists on blood glucose level goals for the perioperative period; however, several organizations have established general targets for neurocritically ill and neurosurgery patients [12
]. The question of optimal blood glucose goals cannot be answered with certainty, especially in neurocritically ill patients [12
]. The brain is very vulnerable to extreme blood glucose level variations. It was demonstrated that an energy crisis may even occur with blood glucose levels within normal range [59
]. Therefore, it would be essential to know what the safe lower limit is. However, neither PET scanners nor microdialysis are available in every ICU. The American Diabetes Association and the American Association of Clinical Endocrinologists [8
], based on the available evidence, set an upper limit at 180
mmol/L), at which insulin therapy should be started. This would also propose to maintain blood glucose levels between 140 and 180
] in critically ill patients and in the perioperative period. The available clinical data do not support tight glucose control with IIT in this critically ill subpopulation [12
]. Two meta-analyses of all patient types treated with IIT drew similar conclusions [81
outlines where blood sugar levels should be kept in patients with acute brain injury, while shows our proposal for an algorithm in hyperglycemia management to use in neurocritically ill patients.
Suggested glycemic targets during acute brain injury/neurosurgery. Where L/P: Lactate/Pyruvate and BBB: Blood–brain barrier.
Algorithm proposed for hyperglycemic management.
Ongoing and future research promises to clarify the present muddled picture. Examples include stratification of neurologic-injury-based protein and biochemical biomarkers and identifying potential high-throughput strategies that will allow one to individualize disease management.
Further studies on the multimodal effects of insulin via modulation of signaling pathways, such as inflammation, cell adhesion, and activity of glucose transporters and pyruvate metabolism enzymes, will have to be conducted. Investigation of agents other than insulin, such as glucagon-like peptide-1 (GLP-1), for glucose-lowering effects may demonstrate a reduced rate of hypoG or other beneficial metabolic effects. Microdialysis studies in patients undergoing IIT therapy could provide important insight into regional alterations of glucose metabolism in injured brain tissue. Neurocritically ill patient populations are heterogeneous, and data interpretation and generalization has to be done with caution. We need a better understanding of all these pathophysiological processes before adoption of IIT.
Finally, special attention should be drawn to the optimal technology for accurate, reliable, and rapid glucose measurement. Closed-loop continuous glucose control systems should be developed. New technologies may facilitate the avoidance of hypoG under an IIT regimen and the development of IIT protocols that can be individualized to the specific metabolic state of the patient under treatment.