Troponin Increases in the Critically Injured Patient: Mechanical Trauma or Physiologic Stress?

Abstract

Serum troponin (Tn) is a sensitive and specific marker of myocardial injury. Tn increase after injury is usually attributed to mechanical chest trauma, but this relationship remains unproven. We sought to examine the etiologic factors and prognostic significance of increased Tn levels in a widely screened trauma population. We reviewed all trauma intensive care unit (ICU) admissions over a 5-year period with serial Tn I (TnI) measurements as part of a screening protocol. TnI was categorized as normal (0-1.2 microg/L), intermediate (1.3-5 microg/L), or high (>5 microg/L), and mortality rates were compared between groups. Multivariate regression analysis was used to identify independent predictors of TnI increase and mortality. There were 1,081 patients identified. An increased TnI was found in 29% of patients. Mortality significantly increased from 16% in the normal group to 33 and 44% in the intermediate and high TnI groups, respectively. Independent predictors of an increased TnI were admission base excess (p = 0.04), Injury Severity Score (ISS) (p < 0.001), and Acute Physiology and Chronic Health Evaluation score (p < 0.001). Chest Abbreviated Injury Scale score and the presence or absence of severe chest injury did not independently predict TnI increase (p = 0.5 and 0.83). Any increase of TnI (>1.2 microg/L) was a strong independent predictor of mortality (odds ratio, 2.1; 95% confidence interval, 1.4-3.1) after controlling for age, sex, mechanism, base excess, Glasgow Coma Scale score, and ISS. Beta-blocker use was associated with a 50% reduction in mortality among patients with an increased Tn (38 versus 16%; p < 0.01). Increased serum TnI after trauma is related to the degree of overall injury and physiologic stress and not mechanical chest trauma. Intermediate and high TnI increases are associated with increased mortality, which may be improved by selective use of beta-blockade.