Glucose Control in the (Neuro) Intensive Care Unit

Abstract

Introduction The vexing question of optimal glucose level in the intensive care unit has long perplexed intensivists. Hyperglycemia is a natural response to physiologic stress,1 and in the critically ill patient has been attributed to inflammatory processes, insulin counter-regulatory hormones, organ dysfunction, iatrogenic carbohydrate or medication related hyperglycemia, and insulin resistance as evidenced by concurrently elevated insulin levels.1 Hyperglycemia occurs in 50-75% of patients admitted to an ICU, and has been associated with various adverse outcomes including increased mortality, organ dysfunction, susceptibility to infections, and neurological complications.1,2 On the cellular level, tissue/organ damage is theorized to be mediated via the production of toxic polyol metabolites and reactive oxygen species,3 with compromise of mitochondrial/cellular function.1 At the opposite extreme, hypoglycemia is acutely detrimental and clearly mandates avoidance. Glucose variability has also been linked to adverse outcomes,4 and insulin administration itself has been associated with increased mortality.5 As such, it is believed that resolution of hypoglycemia, and not insulin administration, is the determinant of improved outcomes.5