Troponin increases in the critically injured patient

Mechanical trauma or physiologic stress?

Matthew Martin, Philip Mullenix, Peter M Rhee, Howard Belzberg, Demetrios Demetriades, Ali Salim

Research output: Contribution to journalArticle

41 Citations (Scopus)

Abstract

Background: 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. Methods: 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 μg/ L), intermediate (1.3-5 μg/L), or high (>5 μg/L), and mortality rates were compared between groups. Multivariate regression analysis was used to identify independent predictors of TnI increase and mortality. Results: 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 μg/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). Conclusions: Increased serum TnI after trauma is related to the degree of over-all 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.

Original languageEnglish (US)
Pages (from-to)1086-1091
Number of pages6
JournalJournal of Trauma
Volume59
Issue number5
DOIs
StatePublished - Nov 2005
Externally publishedYes

Fingerprint

Troponin
Wounds and Injuries
Mortality
Injury Severity Score
Thorax
Glasgow Coma Scale
Mechanical Stress
Troponin I
Serum
Intensive Care Units
Multivariate Analysis
Odds Ratio
Regression Analysis
Confidence Intervals

Keywords

  • Blunt injury
  • Cardiac injury
  • Myocardial contusion
  • Penetrating injury
  • Troponin

ASJC Scopus subject areas

  • Surgery

Cite this

Troponin increases in the critically injured patient : Mechanical trauma or physiologic stress? / Martin, Matthew; Mullenix, Philip; Rhee, Peter M; Belzberg, Howard; Demetriades, Demetrios; Salim, Ali.

In: Journal of Trauma, Vol. 59, No. 5, 11.2005, p. 1086-1091.

Research output: Contribution to journalArticle

Martin, Matthew ; Mullenix, Philip ; Rhee, Peter M ; Belzberg, Howard ; Demetriades, Demetrios ; Salim, Ali. / Troponin increases in the critically injured patient : Mechanical trauma or physiologic stress?. In: Journal of Trauma. 2005 ; Vol. 59, No. 5. pp. 1086-1091.
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title = "Troponin increases in the critically injured patient: Mechanical trauma or physiologic stress?",
abstract = "Background: 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. Methods: 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 μg/ L), intermediate (1.3-5 μg/L), or high (>5 μg/L), and mortality rates were compared between groups. Multivariate regression analysis was used to identify independent predictors of TnI increase and mortality. Results: 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 μg/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). Conclusions: Increased serum TnI after trauma is related to the degree of over-all 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.",
keywords = "Blunt injury, Cardiac injury, Myocardial contusion, Penetrating injury, Troponin",
author = "Matthew Martin and Philip Mullenix and Rhee, {Peter M} and Howard Belzberg and Demetrios Demetriades and Ali Salim",
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T1 - Troponin increases in the critically injured patient

T2 - Mechanical trauma or physiologic stress?

AU - Martin, Matthew

AU - Mullenix, Philip

AU - Rhee, Peter M

AU - Belzberg, Howard

AU - Demetriades, Demetrios

AU - Salim, Ali

PY - 2005/11

Y1 - 2005/11

N2 - Background: 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. Methods: 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 μg/ L), intermediate (1.3-5 μg/L), or high (>5 μg/L), and mortality rates were compared between groups. Multivariate regression analysis was used to identify independent predictors of TnI increase and mortality. Results: 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 μg/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). Conclusions: Increased serum TnI after trauma is related to the degree of over-all 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.

AB - Background: 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. Methods: 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 μg/ L), intermediate (1.3-5 μg/L), or high (>5 μg/L), and mortality rates were compared between groups. Multivariate regression analysis was used to identify independent predictors of TnI increase and mortality. Results: 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 μg/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). Conclusions: Increased serum TnI after trauma is related to the degree of over-all 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.

KW - Blunt injury

KW - Cardiac injury

KW - Myocardial contusion

KW - Penetrating injury

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