The use of cardiac biomarkers in the setting of BCI is so for not very clearly supported in literature. There are several reasons for this including the lack of a gold standard for BCI, highly variable clinical outcomes, and the use of different biomarkers.
The use of cardiac biomarkers may not affect the management of blunt trauma patients with hemodynamic instability or an abnormal ECG that does not demonstrate myocardial infarction.
In one prospective study of 187 patients with blunt chest trauma, an increased troponin at admission or within six hours of arrival correlated with increasing risk of arrhythmia and decreased ejection fraction. In another prospective study, no adverse outcomes occurred in a subgroup of 16 patients with some initial ECG abnormality but no elevation in troponin at four to six hours. Patients with a normal ECG and normal serial measurements of serial cTnI had no significant blunt cardiac injury–related complications in one study.
In the absence of hemodynamic instability, signs of severe injury, or an abnormal ECG, several observational studies suggest that an elevated CK-MB or cardiac troponin is nonspecific for the presence of a clinically significant BCI and has little prognostic value. Moreover, abnormally elevated troponins occur more frequently among patients with significant nonthoracic trauma. This latter finding may stem from catecholamine-induced stress, hypovolemic shock with reperfusion injury, oxidative injury, bacterial or viral toxins, or microcirculatory dysfunction.
For these reasons, it is not routine to obtain cardiac biomarkers in patients without hemodynamic instability, signs of severe injury, or an ECG with significant abnormalities. Concerning ECG abnormalities include arrhythmias other than mild sinus tachycardia, a new conduction block, and ST or T wave abnormalities suggestive of ischemia.
The sensitivity of an abnormal ECG and elevated cTnI for clinically significant blunt cardiac injury (cardiogenic shock, dysrhythmias requiring intervention, or structural cardiac abnormalities related to trauma) was 100%, with a PPV of 62%.Clinically significant blunt cardiac injury can occur without elevation of troponins, but there is usually an abnormality of the ECG. Isolated serum troponin elevation should be monitored and followed serially. Marked elevations have been associated with ventricular dysrhythmias and left ventricular dysfunction.
In summary, while these studies are limited, they suggest that troponin measurements may have some utility in patients with ECG abnormalities. However, with a markedly abnormal ECG or complex arrhythmia, it is doubtful a negative troponin provides reassurance that further complications will not occur, and such patients should be admitted for further evaluation. In place of biomarkers, repeat examinations, serial ECGs, and cardiac monitoring should be used during a brief course of observation (four to six hours) to screen for BCI, if concern exists. The use of biomarkers has not been shown to be more accurate than this approach. While some studies suggest that biomarkers are sensitive indicators of BCI, whether such injuries are significant in patients without clinical signs or symptoms remains unclear.
In the rare case of the blunt thoracic trauma patient with evidence of myocardial infarction on ECG, serial biomarkers should be measured and consultation with both cardiology and cardiac surgery urgently obtained.
References:
2 Jackson L, Stewart A. Best evidence topic report. Use of troponin for the diagnosis of myocardial contusion after blunt chest trauma. Emerg Med J 2005; 22:193.http://www.uptodate.com/contents/cardiac-injury-from-blunt-trauma/abstract/50
3 Salim A, Velmahos GC, Jindal A, et al: Clinically significant blunt cardiac trauma: role of serum troponin levels combined with electrocardiographic findings. J Trauma 50: 237, 2001
4 Rajan GP, Zellweger R: Cardiac troponin I as a predictor of arrhythmia and ventricular dysfunction in trauma patients with myocardial contusion. J Trauma 57: 801, 2004; discussion 808
This post from Dr. Mohammed Sabit
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