Trauma patients with thoracic aortic injury (TAI) suffer blunt cardiac injury (BCI) at variable frequencies. This investigation aimed to determine the frequency of BCI in trauma patients with TAI and compare with those without TAI. All trauma patients with TAI who had admission electrocardiography (ECG) and serum creatine kinase-MB (CK-MB) from January 1999 to May 2009 were included as a study group at a level I trauma center. BCI was diagnosed if there was a positive ECG with either an elevated CK-MB or abnormal echocardiography. There were 26 patients (19 men, mean age 45.1 years, mean ISS 34.4) in the study group; 20 had evidence of BCI. Of 52 patients in the control group (38 men, mean age 46.9 years, mean ISS 38.7), eighteen had evidence of BCI. There was a significantly higher rate of BCI in trauma patients with TAI versus those without TAI (77% versus 35%, ). 1. Introduction Blunt cardiac injury (BCI) is a very rare, but potentially fatal, condition that accounts for 12%–32% of trauma-related fatality [1–3]. Ruptured cardiac cavities, coronary arteries, or intrapericardial portion of major vessels typically result in death at the scene of the collision [2, 4]. Victims of relatively less severe cardiac injuries such as myocardial contusion, hemopericardium due to contusions or lacerations, valvular regurgitation, or myocardial infarction due to coronary artery injury may survive the initial trauma and thus present to the emergency department (ED) for evaluation [1, 5, 6]. Among those who arrived alive at the ED, BCI is associated with a high mortality rate of 89% [7]. The frequency of reported BCI in trauma patients is difficult to determine. It varies widely from 0.045% to 86%, depending on patient population, subpopulation, and a variety of factors that were considered to make the diagnosis [1, 4, 5, 7–10]. Patients who suffer BCI usually have multiple severe concomitant injuries of other organs, including the thoracic aorta. By itself, thoracic aortic injury (TAI) is considered a potentially fatal condition if left untreated [1, 11–15]. Therefore, a surgical or endovascular intervention is usually performed as a definitive treatment if the patient’s condition allows. When an open thoracotomy or endovascular repair is expected, it is critical for treating physicians to evaluate all associated injuries to determine the need for immediate interventions and for preoperative risk assessment [16]. With the widespread use of CT in polytrauma patients, the diagnosis of TAI and coexisting injuries to the lungs, pleura, chest wall, and abdomen can
References
[1]
R. Prêtre and M. Chilcott, “Blunt trauma to the heart and great vessels,” New England Journal of Medicine, vol. 336, no. 9, pp. 626–632, 1997.
[2]
P. G. R. Teixeira, C. Georgiou, K. Inaba et al., “Blunt cardiac trauma: lessons learned from the medical examiner,” Journal of Trauma, vol. 67, no. 6, pp. 1259–1264, 2009.
[3]
A. A. Turan, F. A. Karayel, E. Akyildiz et al., “Cardiac injuries caused by blunt trauma: an autopsy based assessment of the injury pattern,” Journal of Forensic Sciences, vol. 55, no. 1, pp. 82–84, 2010.
[4]
L. F. Parmley, W. C. Manion, and T. W. Mattingly, “Nonpenetrating traumatic injury of the heart,” Circulation, vol. 18, no. 3, pp. 371–396, 1958.
[5]
G. Fulda, C. E. M. Brathwaite, A. Rodriguez, S. Z. Turney, C. M. Dunham, and R. A. Cowley, “Blunt traumatic rupture of the heart and pericardium: a ten-year experience (1979–1989),” Journal of Trauma, vol. 31, no. 2, pp. 167–173, 1991.
[6]
K. Kato, S. Kushimoto, K. Mashiko et al., “Blunt traumatic rupture of the heart: an experience in Tokyo,” Journal of Trauma, vol. 36, no. 6, pp. 859–864, 1994.
[7]
P. G. R. Teixeira, K. Inaba, D. Oncel et al., “Blunt cardiac rupture: a 5-year NTDB analysis,” Journal of Trauma, vol. 67, no. 4, pp. 788–791, 2009.
[8]
R. M. Shorr, M. Crittenden, and M. Indeck, “Blunt thoracic trauma. Analysis of 515 patients,” Annals of Surgery, vol. 206, no. 2, pp. 200–205, 1987.
[9]
S. Santavirta and E. Arajarvi, “Ruptures of the heart in seatbelt wearers,” Journal of Trauma, vol. 32, no. 3, pp. 275–279, 1992.
[10]
M. F. El-Chami, W. Nicholson, and T. Helmy, “Blunt cardiac trauma,” Journal of Emergency Medicine, vol. 35, no. 2, pp. 127–133, 2008.
[11]
T. C. Fabian, J. D. Richardson, M. A. Croce et al., “Prospective study of blunt aortic injury: multicenter trial of the American Association for the Surgery of Trauma,” Journal of Trauma, vol. 42, no. 3, pp. 374–382, 1997.
[12]
D. McGillicuddy and P. Rosen, “Diagnostic dilemmas and current controversies in blunt chest trauma,” Emergency Medicine Clinics of North America, vol. 25, no. 3, pp. 695–711, 2007.
[13]
S. E. Mirvis and K. Shanmuganathan, “Diagnosis of blunt traumatic aortic injury 2007: still a nemesis,” European Journal of Radiology, vol. 64, no. 1, pp. 27–40, 2007.
[14]
J. Cook, C. Salerno, B. Krishnadasan, S. Nicholls, M. Meissner, and R. Karmy-Jones, “The effect of changing presentation and management on the outcome of blunt rupture of the thoracic aorta,” Journal of Thoracic and Cardiovascular Surgery, vol. 131, no. 3, pp. 594–600, 2006.
[15]
L. F. Parmley, T. W. Mattingly, W. C. Manion, et al., “Nonpenetrating traumatic injury of the aorta,” Circulation, vol. 17, no. 6, pp. 1086–1101, 1958.
[16]
H. B. Kram, P. L. Appel, and W. C. Shoemaker, “Increased incidence of cardiac contusion in patients with traumatic thoracic aortic rupture,” Annals of Surgery, vol. 208, no. 5, pp. 615–618, 1988.
[17]
C. J. Ng, J. C. Chen, L. J. Wang et al., “Diagnostic value of the helical CT scan for traumatic aortic injury: correlation with mortality and early rupture,” Journal of Emergency Medicine, vol. 30, no. 3, pp. 277–282, 2006.
[18]
R. L. Maenza, D. Seaberg, and F. D'Amico, “A meta-analysis of blunt cardiac trauma: ending myocardial confusion,” American Journal of Emergency Medicine, vol. 14, no. 3, pp. 237–241, 1996.
[19]
P. Kaye and I. O'Sullivan, “Myocardial contusion: emergency investigation and diagnosis,” Emergency Medicine Journal, vol. 19, no. 1, pp. 8–10, 2002.
[20]
K. C. Sybrandy, M. J. M. Cramer, and C. Burgersdijk, “Diagnosing cardiac contusion: old wisdom and new insights,” Heart, vol. 89, no. 5, pp. 485–489, 2003.
[21]
E. E. Moore, M. A. Malangoni, T. H. Cogbill et al., “Organ injury scaling IV: thoracic vascular, lung, cardiac, and diaphragm,” Journal of Trauma, vol. 36, no. 3, p. 299, 1994.
[22]
M. Pasquale and T. C. Fabian, “Practice management guidelines for trauma from the Eastern Association for the Surgery of Trauma,” Journal of Trauma, vol. 44, no. 6, pp. 941–957, 1998.
[23]
N. T. Feghali and L. M. Prisant, “Blunt myocardial injury,” Chest, vol. 108, no. 6, pp. 1673–1677, 1995.
[24]
S. H. Tsung, “Creatine kinase isoenzyme patterns in human tissue obtained at surgery,” Clinical Chemistry, vol. 22, no. 2, pp. 173–175, 1976.
[25]
K. A. Illig, M. J. Swierzewski, D. V. Feliciano, and J. H. Morton, “A rational screening and treatment strategy based on the electrocardiogram alone for suspected cardiac contusion,” American Journal of Surgery, vol. 162, no. 6, pp. 537–544, 1991.
[26]
W. L. Biffl, F. A. Moore, E. E. Moore et al., “Cardiac enzymes are irrelevant in the patient with suspected myocardial contusion,” American Journal of Surgery, vol. 168, no. 6, pp. 523–528, 1994.
[27]
R. C. Hendel, S. Cohn, G. Aurigemma et al., “Focal myocardial injury following blunt chest trauma: a comparison of indium-111 antimyosin scintigraphy with other noninvasive methods,” American Heart Journal, vol. 123, no. 5, pp. 1208–1215, 1992.
[28]
A. Salim, G. C. Velmahos, A. Jindal et al., “Clinically significant blunt cardiac trauma: role of serum troponin levels combined with electrocardiographic findings,” Journal of Trauma, vol. 50, no. 2, pp. 237–243, 2001.
[29]
J. P. Bertinchant, A. Polge, D. Mohty et al., “Evaluation of incidence, clinical significance, and prognostic value of circulating cardiac troponin II and T elevation in hemodynamically stable patients with suspected myocardial contusion after blunt chest trauma,” Journal of Trauma, vol. 48, no. 5, pp. 924–931, 2000.
[30]
J. E. Adams III, V. G. Davilla-Roman, P. Q. Bessey, D. P. Blake, J. H. Ladenson, and A. S. Jaffe, “Improved detection of cardiac contusion with cardiac troponin I,” American Heart Journal, vol. 131, no. 2, pp. 308–312, 1996.
[31]
G. C. Velmahos, M. Karaiskakis, A. Salim et al., “Normal electrocardiography and serum troponin I levels preclude the presence of clinically significant blunt cardiac injury,” Journal of Trauma, vol. 54, no. 1, pp. 45–51, 2003.
[32]
M. Lindstaedt, A. Germing, T. Lawo et al., “Acute and long-term clinical significance of myocardial contusion following blunt thoracic trauma: results of a prospective study,” Journal of Trauma, vol. 52, no. 3, pp. 479–484, 2002.
