Abstract
Background: Admission hyperglycemia is associated with higher morbidity and mortality in patients with traumatic brain injury (TBI). Stress-induced hyperglycemia (SIH), a form of hyperglycemia induced by the stress response, is associated with increased patient mortality following TBI. However, admission hyperglycemia occurs not only in SIH but also in patients with diabetic hyperglycemia (DH). Current information regarding whether trauma patients with SIH represent a distinct group with differential outcomes compared to those with DH remains limited. Methods: Serum glucose concentration ≥200 mg/dL upon arrival at the emergency department was defined as hyperglycemia. Presence of diabetes mellitus (DM) was determined by patient history and/or admission glycated hemoglobin (HbA1c) level ≥6.5%. In the present study, the patient cohort included those with moderate and severe TBI, as defined by an Abbreviated Injury Scale (AIS) score ≥3 points in the head, and excluded those who had additional AIS scores ≥3 points in any other region of the body. A total of 1798 adult patients with isolated moderate to severe TBI were allocated into four groups: SIH (n = 140), DH (n = 187), diabetic normoglycemia (DN, n = 186), and non-diabetic normoglycemia (NDN, n = 1285). Detailed patient information was retrieved from the Trauma Registry System at a level I trauma center between 1 January 2009, and 31 December 2015. Unpaired Student's t- and Mann-Whitney U-tests were used to analyze normally and non-normally distributed continuous data, respectively. Categorical data were compared using the Pearson chi-square or two-sided Fisher's exact tests. Matched patient populations were allocated in a 1:1 ratio according to propensity scores calculated by NCSS software. Logistic regression was used to evaluate the effect of SIH and DH on the adjusted mortality outcome. Results: In patients with isolated moderate to severe TBI, the presence of SIH and DH led to 9.1-fold and 2.3-fold higher odds of mortality, respectively, than patients with NDN. After adjusting for confounding factors, including sex and age, pre-existing co-morbidities, existence of different kinds of intracerebral hemorrhage, and injury severity, patients with SIH still had 6.6-fold higher odds of mortality than those with NDN; however, DH did not present significantly higher adjusted mortality odds. SIH and DH presented different effects on outcomes after TBI. The results also suggested that the pathophysiological effect associated with SIH was different from that of DH. Conclusions: This study demonstrated that patients with SIH and DH had significantly higher mortality than patients with NDN. However, the adjusted mortality was significantly higher only in the selected propensity score-matched patients with SIH and not in those with DH.