Incidence and Course of Stress Hyperglycemia in Critically Ill Children Admitted to PICU of Assiut University Children Hospital

Critically ill patients often develop endocrine and metabolic changes, particularly disruptions of glucose homeostasis that result in hyperglycemia and hypoglycemia.Stress hyperglycemia commonly occurs in children with critical illnesses.

Stress hyperglycemia results from increased gluconeogenesis relative to the clearance of glucose as well as from the development of insulin resistance affecting glucose uptake. These mechanisms are mediated through increased production of counteracting hormones (i.e., epinephrine, norepinephrine, cortisol, glucagon, and growth hormone). Furthermore, stress hyperglycemia is associated with pro-inflammatory cytokines, oxidative stress, and therapeutic interventions. Those factors in turn inhibit the secretion of insulin by pancreatic β cells through α-adrenergic receptor stimulation, interfere with insulin receptor signaling and/or insulin-regulated glucose channels, and directly interfere with proper glucose transport and utilization in peripheral cells.

Several studies have demonstrated the association of stress hyperglycemia in critically ill children with mortality. Specifically, peak and duration of stress hyperglycemia appear to be associated with mortality. Peak blood glucose concentrations tend to be much higher in non survivors compared with survivors. Similarly, non survivors tend to have exposure to longer duration of stress hyperglycemia compared with survivors. This association of stress hyperglycemia with mortality appears across different pediatric disease states, including septic shock, burns, traumatic brain injury, post cardiac surgery, and trauma. Additionally, stress hyperglycemia is associated with longer periods of ICU and hospital stay and more frequent nosocomial infections, including surgical site infections in critically ill children. While all these studies demonstrate strong associations between stress hyperglycemia and poor clinical outcomes, they do not necessarily demonstrate a cause and effect relationship.