Blunt cardiac injury (BCI) includes a wide spectrum of clinical symptoms. The decelerating force leads to mechanical cardiac injuries, including valvular, septal, ventricular, atrial, or septal wall damage. Additionally, relatively mild myocardial contusion may lead to other adverse cardiac events, such as mild arrhythmias [1–3]. Considering the numerosity of complications, careful monitoring is warranted in patients with suspected BCIs. However, diagnosing BCI remains a challenge due to the absence of a clear definition and a gold standard diagnostic test [1–3, 10–12]. Managing physicians should be aware that chest injuries including pulmonary contusion, sternum fracture, and multiple rib fractures are possible indicators for BCI. Therefore, the role of complete diagnosis after typical trauma mechanisms should not be underestimated even in patients whose clinical condition is not indicative of severe injury [1].
BCI arises from a variety of injuries, often due to high-speed impact. The most common causes of injury is motor vehicle accidents; in addition, bicycle accidents, falls, sports-related injuries, and even assaults can also result in BCI [2, 3, 13, 14].
Few clinical signs or symptoms are specific for BCI. The most common clinical signs associated with BCI is chest pain. This pain may or may not be anginal in nature, and it is usually a result of associated chest trauma [15]. Echocardiography and ECG may indicate damage to the tissue architecture and subsequent complications, however, information on specific cellular damage within the heart muscle requires measurement of cardiac muscle-specific proteins such as Tn-T, Tn-I, or creatine kinase muscle [1, 6, 16]. Tissue damage always occurs with cellular damage, but cellular damage does not require tissue damage; therefore, a combination of tests is usually used [1]. However, ECG, cardiac enzymes, and echocardiography in the diagnosis of BCI remains controversial [3]. Level I evidence supports that all patients with suspicious BCI should obtain 12-lead ECG upon admission or at the emergency room [8]. The use of ECG changes has demonstrated a sensitivity, specificity, and negative predictive value of 100%, 47%, and 90% in the detection of BCI-related complications that require treatment; these changes include sinus tachycardia, bradycardia, conduction delays, or atrial or ventricular dysrhythmias [10]. Additionally, Tn-I and Tn-T have been recently used to screen for BCIs. In 26 patients diagnosed with BCI using ECG or echocardiographic criteria, the sensitivity of Tn-I and Tn-T was 23% and 12%, respectively, while the specificity was 97% and 100%, respectively [17]. A report by Salim et al. [7] found that patients with normal ECG and serial values of Tn-I had no significant BCI-related complications. Furthermore, they found that abnormal ECG and elevated Tn-I had 100% sensitivity and 62% positive predictive value in diagnosing clinically significant BCI. Through these studies, the value of Tn-I increased when it was simultaneously performed with ECG. Though, there are still no definite guidelines, the ECG-based AAST Cardiac Injury Scale is widely used.
To develop a diagnostic tool for BCI, additional insight regarding the diagnostic properties of available tests is warranted. Yasue et al. [18] determined that NT pro-BNP is secreted mainly from the left ventricle in healthy adults and in patients with left ventricular dysfunction. Additionally, the authors found an increased rate of NT pro-BNP secretion when the left ventricular tension increased. Considering this relationship, Yasue et al. proposed the use of increased serum NT pro-BNP level as a diagnostic and prognostic marker of cardiac dysfunction in patients with congestive heart failure, and ischemic heart disease [19].
Previous studies have investigated the relationship between NT pro-BNP and trauma [4, 6, 19]. Kirchhoff et al. [19] reported the significant correlation of NT pro-BNP levels with clinical signs of multiple organ dysfunction syndrome after multiple injuries at a level 1 trauma center. Additionally, a relationship was observed between NT pro-BNP levels and decreased C.I. The data of this pilot study may indicate the potential value of NT pro-BNP in the diagnosis of post-traumatic cardiac impairment. In 60 patients diagnosed with major trauma, serum NT pro-BNP levels helped predict mortality in patients with major trauma [6]. Dogan et al. [4] reported the potential of NT pro-BNP as a marker of BCI in an experimental study of rats with blunt chest trauma; they found a significant increase in NT pro-BNP levels in rats with BCI at 5 hour after blunt chest trauma. This study suggested the benefits of using NT pro-BNP in the diagnosis of BCI as an adjunct to other tests including Tn-I, ECG, and echocardiogram.
Traumatic sternal fractures indicate a high risk of the presence of BCI [12]. Based this risk, our study was limited to patients with sternal fractures from among a wide range of patients admitted to the TICU. Absolute bed rest was the principle for accurate monitoring. We investigated the adjunct to other diagnostic tests of BCI through serial monitoring and biomarkers.
In this study, no significant difference was observed in the length of stay between the two groups; however, significant differences were observed in total TICU stay and total ventilator care. No significant difference was observed between the ISS of the two groups; however, the BCI group may require more cardiac monitoring and long-term intensive care compared to the non-BCI group. In addition, no patient underwent additional procedures. These results indicate a favorable prognosis for patients diagnosed with BCI without intra-cardiac injury.
No relationship was observed between NT pro-BNP and BCI which was inconsistent with the results of previous studies. However, a significant decrease in C.I was observed in the BCI group on admission and on HD 3. However, no significant difference in C.I value was observed on HD 2. Therefore, this study does not show the concordance of consecutive results; it cannot be concluded that there is a relationship between value of C.I and BCI. Further studies are needed to determine the relationship between NT pro-BNP, C.I and BCI.
Additionally, no difference was found in the ISS of the two groups; however, the results showed a correlation between BCI and lactate levels. Therefore, future researches should focus on the relationship between BCI and lactate levels.
This study has some limitations. First, it was a single-center retrospective study that included a small number of patients. Second, since no accurate diagnostic criteria for BCI exist, the diagnostic criterion of BCI was the AAST cardiac injury scale except for patients with emergency surgical procedures. Therefore, this study seems to be meaningful only for the association between mild traumatic cardiac injury focused on ECG changes and the values presented in this study. Third, the postoperative results are highly influenced by other accompanying injuries as the criteria were based on major trauma patients who admitted the TICU with an ISS score of 15 or higher. Finally, this study investigated diagnostic adjuvant tools; therefore, it does not influence the treatment of patients and has no influence on patient survival and treatment direction.