Role Of Stress Induced Hyperglycemia On The Outcome Of Trauma Patients

Intensive glucose control is vital for prognosis and preservation of normal physiologic status in trauma patients. The acute effects of severe trauma, infection, and surgery result in remarkable metabolic stress on the human body. Hyperglycemia is a normal metabolic response to stress and injury [1]. Irrespective of the involved injury mechanism, post-traumatic metabolic changes occur due to stress in terms of an increased glucose production, decreased insulin production, and insulin resistance in the peripheral tissues and eventually lead to a state of hyperglycemia. Traumatic injury also induces changes in endogenous hormone production and enhanced utilization of metabolites that usually lead to stress related hyperglycemia. Measurement of HbA1c levels can be used as a screening tool to discriminate unknown diabetes mellitus from stress-induced hyperglycemia (SIH). Published studies that have evaluated the association between presenting hyperglycemia and worse outcomes in trauma patients have all consistently showed higher mortality and infection rates in patients presented with elevated serum glucose levels of 200 mg/dL or more [2-5]. A recent study evaluated the differential effect of SIH in comparison to diabetic hyperglycemia (DH) on outcomes in trauma victims. The authors observed that as opposed to DH, SIH is associated with a higher mortality rate after injury [4]. A prospective study of patients with severe traumatic brain injury demonstrated that admission glucose levels >11.1 mmol/L were associated with increased mortality and poor neurologic outcomes [6]. Stress associated with critical illness is characterized by the activation of inflammatory cellular mediators [7]. During acute illness there is an increase in the systemic inflammatory response that is characterized by increased production of pro-inflammatory cytokines. Importantly, there is relationship between abnormal cytokine production and hyperglycemia in severe sepsis patients which aggravates the immune response leading to poor clinical outcomes. Recent studies suggested that interleukin-6 (IL-6) is involved in glucose metabolism and insulin action. The proinflammatory IL-6 is normally released upon infection; however, it induces insulin resistance during conditions of hyperglycemia [8]. Moreover, IL-18 levels are significantly elevated in diabetic patients with microalbuminuria as compared with patients with normoalbuminuria [9]. This might indicate that certain interleukins (IL) are involved in the pathogenesis of SIH. Though, the clinical relevance of the observed SIH in trauma patients remains unclear. The earlier studies suggested the implications of cytokines in SIH and outcomes after trauma. To date, there is little information regarding the effect of diabetic hyperglycemia (occult or known) on the clinical outcomes after trauma and whether these patients represent a distinct group with differential outcomes when compared to those with SIH. The purpose of this study is to identify the incidence of SIH as well as diabetic hyperglycemia in trauma patients and to investigate the association between the proinflammatory cytokine levels and hyperglycemia in trauma population.

Primary objective:

• To evaluate the outcomes of stress induced hyperglycemia in patients presented with traumatic injury.

Secondary objectives:

• To investigate the association between pro-inflammatory cytokine levels and SIH in trauma patients.
• To identify the incidence of SIH and occult diabetes mellitus in trauma population.