DOI: 10.1097/01.sa.0000177136.64166.01
,
Issn Print: 0039-6206
Publication Date: 2005/10/01
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Excerpt
Alain R. Edouard, Marie-Louise Felten, Jean-Louis Hebert, Claudine Cosson, Laurent Martin, and Dan Benhamou
(Anesthesiology, 101:1262-1268, 2004)
Service d'Anesthésie-Réanimation, Hôpital de Bicêtre, Le Kremlin Bicêtre, France.
The routine repeated assessment of cardiac enzymes for detecting a blunt cardiac or myocardial injury is controversial during the treatment of patients with trauma. The incidence and significance of troponin I release and its mechanism are unknown in severe trauma patients. The characteristics of this release were prospectively studied in trauma patients and correlated with the presence of shock, existence of myocardial contusion, and outcome.
During a 24-month period, serial electrocardiographic recordings and troponin I measurements were performed at admission and again between 6 and 12 hours after admission in all trauma patients admitted to a surgical intensive care unit. Additional troponin I concentrations and electrocardiograms were repeated as long as the troponin I concentration remained increased, the electrocardiogram remained abnormal, or both. Electrocardiographic criteria were used to make the diagnosis of myocardial contusion. Three groups of patients were defined, based on the time course of troponin I: very transient (≤12 hours) and limited release (troponin I <2 μg/L), transient (≤36 hours) and significant release (troponin I ≥2 μg/L), and sustained (>36 hours) and significant release (troponin I >2 μg/L). In the last group, coronary artery angiography was performed as soon as possible. The limit of detection of troponin I was 0.04 μg/L; the threshold for a diagnosis of myocardial necrosis was 1.5 μg/L.
During the study period, 728 patients were admitted with trauma. They were young, aged 37 ± 19 years, with significant trauma with physiopathologic consequences. Brain and chest injuries were noted in 240 and 169 patients, respectively. An abnormal electrocardiogram leading to a diagnosis of significant myocardial contusion was found in 35 patients; 23 of these patients underwent emergency surgery. Shock was seen in 149 patients, and the mortality rate for the whole group was 17%.
Troponin I release was observed in 86 patients, attributed to "medical" myocardial ischemia in 7 patients. Of these 86 patients, 25 were early nonsurvivors (brain death, exsanguination, or early multiorgan failure), and 17 of these 25 were among the 642 patients without troponin I release. Troponin I release was observed in 54 early survivors without preexisting coronary artery disease. Brain injury, blunt cardiac trauma, and shock were more frequent in these patients than in the 625 early survivors without troponin I release. Mortality was similar in early survivors with and without troponin I release (15% and 12%, respectively). Among the 54 patients with troponin I release, a very transient and limited release of troponin I was seen in 22 hemodynamically unstable patients. In the 15 patients with significant but transient troponin I release, there was a high incidence of brain injury and shock. Sustained and significant troponin I release occurred in 17 patients and was often associated with chest trauma and constantly associated with electrocardiographic abnormalities. On the basis of electrocardiographic abnormalities, the sensitivity, specificity, and positive and negative predictive values of troponin I release over time for the diagnosis of significant myocardial contusion were 63%, 98%, and 40% and 98%, respectively.
Coronary angiography was not done in 2 of the 17 patients with prolonged release of troponin I because of renal failure or ongoing sepsis. In the other 15 patients, a coronary artery injury was found in 7. Two patients had a major vascular injury, and 5 had only minor vascular injuries. The 7 patients were given β-adrenergic blockers and salicylate as soon as possible.
