© 2014, Wiley Periodicals, Inc. DOI: 10.1111/echo.12801
Echocardiography
CASE REPORTS Section Editor: Brian D. Hoit, M.D.
Blunt Chest Trauma Resulting in Both Atrial and Ventricular Septal Defects Yahaira Ortiz, M.D.,* Adam J. Waldman, M.D.,† Jeff N. Bott, M.D.,† Steve J. Carlan, M.D.,‡ and Mario Madruga, M.D.* *Department of Internal Medicine, Orlando Regional Healthcare, Orlando, Florida; †The Orlando Health Heart Institute, Orlando Regional Healthcare, Orlando, Florida; and ‡Academic Center, Orlando Regional Healthcare, Orlando, Florida
Cardiac septal defects are known complications to blunt chest trauma. The incidence of a traumatic isolated atrial septal defect is unknown and the concurrent occurrence of nonlethal ventricular and atrial septal defects has not been reported. A healthy male sustained violent blunt chest trauma resulting in traumatic cardiac septal disruption in the atrium and ventricle. The defects were detected by echocardiography within 14 hours of the accident. The extent of damage was confirmed at the time of surgical repair. The patient recovered uneventfully. The diagnosis and management of concurrent ASD and VSD is similar to single septal injury. (Echocardiography 2015;32:592–594) Key words: blunt chest trauma, ventricular septal defect, atrial septal defect
Cardiac septal disruption is a known complication of violent blunt chest trauma.1 Traumatic ventricular septal defects (VSD) are reported in 5.5% of cases of severe blunt chest trauma2,3 and atrial septal defects (ASD) are less common.4 To date no reports of nonlethal traumatic concurrent VSDs and ASDs have been reported. We describe a case of a combined traumatic ASD and VSD discovered by transthroacic echocardiography within 14 hours of the injury and confirmed at the time of surgical repair. A 20-year-old previously healthy male presented after a single car crash into a tree. He was an unrestrained driver and no air bag was deployed. On arrival he was awake with a Glasgow Coma Scale of 15. His initial blood pressure was 88/47 mmHg and heart rate was 82 beats/min. His initial physical examination was unrevealing. He did have an abrasion over his forehead and left side of his chest, and a minor laceration on his left lower extremity. No murmurs were appreciated. Abdominal examination showed no liver enlargement, normal bowel sounds, no tenderness or guarding. Pulses were palpable, symmetric, and normal. Computed tomography (CT) (SOMATOM Sensation 64, Siemens, Forchheim, Germany) of the head and entire spine was normal except for bilateral pars fracture at L5. CT of chest, abdomen, and pelvis Address for correspondence and reprint requests: S. J. Carlan, M.D., 1401 Lucerne Terrace, 2nd floor, Orlando, FL 32806. Fax: 321-481-0182; E-mail: [email protected]
592
showed small left-sided pneumothorax, pulmonary contusions, mediastinal hematoma, and small splenic laceration. Initial electrocardiogram (MAC 5500, GE Healthcare, Bangalore, India) demonstrated incomplete right bundle branch block with ST depression in inferior leads and lateral leads and ST elevations in anteroseptal leads. His cardiac markers were elevated CK-MB 23.7 ng/mL (normal: 0.1–4), troponin I 7.63 ng/ mL (normal: 0–0.05). Within 2 hours he became tachypneic and hypoxic requiring endotracheal intubation. Follow-up chest x-ray showed progression of bilateral pulmonary contusions. At this point he was transferred to the intensive care unit for further care. Fourteen hours after admission a new harsh holosystolic murmur 4/6 was noted over the left lower sternal border with a thrill. Emergent transthoracic echocardiogram (Philips iE33 xMatrix, Philips, Uster, Switzerland) followed by transesophageal echocardiograms (Philips iE33 xMatrix) were performed which revealed a secundum-type atrial septal defect (Figs. 1 and 2) and a ventriculoseptal defect (Fig. 3) toward the apical portion of the septum with left to right shunt, septal dyskinesia and an ejection fraction of 55%. On the second day he was extubated and he remained hemodynamically stable. He had sinus tachycardia requiring an esmolol drip to control the heart rate. During the days that followed he underwent extensive cardiac evaluation by cardiology, interventional pediatric cardiology, and cardiothoracic surgeon
Blunt Chest Trauma and Cardiac Septal Defects
Figure 1. Two-dimensional transesophageal echocardiogram, bicaval view. The left ventricle (LA) is the left atrium and the arrow shows complete disruption of the interatrial septum.
to determine the approach and appropriate timing for surgical intervention. A repeat echocardiograph showed slight progression of the VSD. Right and left heart catheterization confirmed left-to-right shunt with pulmonary-to-systemic flow ratio of 1.6 and normal coronaries. On day 6, he was taken to the operating room. The septum secundum which was completely avulsed and shredded was repaired with autologous pericardium (Fig. 4). The lower two-thirds of the ventricular septum was shredded with multiple defects (Fig. 5). It was repaired with a bovine pericardial patch. He was extubated within a few hours after surgery and successfully recovered. He was discharged home 7 days after surgery. Two months after discharge patient reported doing well. A year later, transthoracic echocardi-
Figure 2. Transesophageal echocardiogram, color Doppler of the interatrial septal disruption. Arrow shows the turbulence from the left-to-right shunting across the defect.
Figure 3. Transesophageal echocardiogram, apical fourchamber view. Image shows the LV (left ventricle) and the apical ventricular septal defects at the arrows.
ography showed a confirmed repair and no evidence of residual shunting. Discussion: This case is unique for several reasons. First, this combination of cardiac injuries in a survivor is unreported. A detailed search of the published literature discovered no cases of posttraumatic ASD and VSD in the same patient secondary to blunt chest trauma. Second, the characteristics of the forces applied to the heart in our case may have been
Figure 4. Completed repair of atrial septal defect utilizing autogenous pericardium (arrow).
593
Ortiz, et al.
Figure 5. Arrow shows multiple large ventricular septal defects through the apex of the left ventricle.
unique since these combinations of injuries in nonfatal chest trauma have not been reported previously. Ventricular septal defects following nonpenetrating chest trauma can occur either acutely from direct mechanical injury or delayed from a microvascular disruption causing liquefaction necrosis and ischemic dissolution of septal tissue followed by a true defect.5 The mechanical injury may involve a sudden increase in intracardiac pressure caused by compression of the heart between the vertebral bodies and the sternum. If the trauma occurs during late diastole or isovolumetric systole when the heart has maximum volume and the valves are closed, the compression can result in an increase in intracardiac pressure above the threshold of cardiac septal wall integrity and rupture can occur acutely.6,7 Apical muscular VSDs are most common,8 and occasionally valvular injury may occur.9 The ischemic dissolution type rupture occurs when the myocardium is damaged resulting in localized inflammation and ultimately necrosis and rupture. This probably involves the microvasculature in the septal nutrient vessels10 and there may be delayed onset from hours to weeks after trauma occurs. This mechanism is consistent with the clinical findings in our case. The murmur was discovered 14 hours after the injury, not on admission. The compression forces must have been low enough to not acutely rupture the septa, papillary muscles, or heart valves but widespread enough to damage the microvasculature in both the ventricular and atrial septa. Why the atrial septum is not involved in all cases is not known but may reflect
594
the functional anatomy of the atrioventricular valves. Blood naturally flows forward during the cardiac cycle and if the valves remain intact and closed during the traumatic compression of the chamber nearest to the sternum, the right ventricle, the atrium should not be overfilled. In this particular case neither the papillary muscle nor the valves were damaged suggesting the atrial septal injury occurred from the kinetic energy transfer by the same compression forces that damaged the ventricular septum. Another variable that may be operative in the force distribution in this case is the lack of rib fractures. The thoracic wall may decrease the force of impact to the heart in cases of chest trauma in which skeletal rib fractures occur possibly because of the dissipation of kinetic energy. It is also possible that he simply could have had a previously undiagnosed septal defect or one that healed but was a point of unnatural weakness, but this is unlikely considering the normal chamber sizes and no history. References 1. Pretre R, Chilcott M: Blunt trauma to the heart and great vessels. N Engl J Med 1997;336:626–632. 2. Olsovsky MR, Topaz O, DiSciascio G, et al: Acute traumatic ventricular septal rupture. Am Heart J 1996;131:1039–1041. 3. Parmley LF, Manion WC, Mattingly TW: Nonpenetrating traumatic injury of the heart. Circulation 1958;18:371– 396. 4. Menaker J, Tesoriero RB, Hyder M, et al: Traumatic atrial septal defect and papillary muscle rupture requiring mitral valve replacement after blunt injury. J Trauma 2009;67:1126. 5. Liguori AE, Maertins BA, Richardson R: VSD following blunt cardiac trauma: MRI findings. Emerg Radiol 2013;20:459–463. 6. Rollins MD, Koehler RP, Stevens MH, et al: Traumatic ventricular septal defect: Case report and review of the English literature since 1970. J Trauma 2005;58:175–180. 7. Blasco PB, Comas JG, Munoz RDA: Spontaneous improvement of a haemodynamically significant ventricular septal defect produced by blunt chest trauma in a child. Cardiol Young 2009;19:109–110. 8. Ozay B, Ozer N, Ketenci B, et al: Unsuspected location of a ventricular septal defect after blunt chest trauma. Thorac Cardiovasc Surg 2008;56:110–111. du F, Gurlertop Y, Arslan S, et al: Ventricular sep€ ndog 9. Gu tal rupture and mitral regurgitation caused by trauma. Echocardiography 2007;24:174–175. 10. Ryan L, Skinner DL, Rodseth RN: Ventricular septal defect following blunt chest trauma. J Emerg Trauma Shock 2012;5:184–187.
Echocardiography
CASE REPORTS Section Editor: Brian D. Hoit, M.D.
Blunt Chest Trauma Resulting in Both Atrial and Ventricular Septal Defects Yahaira Ortiz, M.D.,* Adam J. Waldman, M.D.,† Jeff N. Bott, M.D.,† Steve J. Carlan, M.D.,‡ and Mario Madruga, M.D.* *Department of Internal Medicine, Orlando Regional Healthcare, Orlando, Florida; †The Orlando Health Heart Institute, Orlando Regional Healthcare, Orlando, Florida; and ‡Academic Center, Orlando Regional Healthcare, Orlando, Florida
Cardiac septal defects are known complications to blunt chest trauma. The incidence of a traumatic isolated atrial septal defect is unknown and the concurrent occurrence of nonlethal ventricular and atrial septal defects has not been reported. A healthy male sustained violent blunt chest trauma resulting in traumatic cardiac septal disruption in the atrium and ventricle. The defects were detected by echocardiography within 14 hours of the accident. The extent of damage was confirmed at the time of surgical repair. The patient recovered uneventfully. The diagnosis and management of concurrent ASD and VSD is similar to single septal injury. (Echocardiography 2015;32:592–594) Key words: blunt chest trauma, ventricular septal defect, atrial septal defect
Cardiac septal disruption is a known complication of violent blunt chest trauma.1 Traumatic ventricular septal defects (VSD) are reported in 5.5% of cases of severe blunt chest trauma2,3 and atrial septal defects (ASD) are less common.4 To date no reports of nonlethal traumatic concurrent VSDs and ASDs have been reported. We describe a case of a combined traumatic ASD and VSD discovered by transthroacic echocardiography within 14 hours of the injury and confirmed at the time of surgical repair. A 20-year-old previously healthy male presented after a single car crash into a tree. He was an unrestrained driver and no air bag was deployed. On arrival he was awake with a Glasgow Coma Scale of 15. His initial blood pressure was 88/47 mmHg and heart rate was 82 beats/min. His initial physical examination was unrevealing. He did have an abrasion over his forehead and left side of his chest, and a minor laceration on his left lower extremity. No murmurs were appreciated. Abdominal examination showed no liver enlargement, normal bowel sounds, no tenderness or guarding. Pulses were palpable, symmetric, and normal. Computed tomography (CT) (SOMATOM Sensation 64, Siemens, Forchheim, Germany) of the head and entire spine was normal except for bilateral pars fracture at L5. CT of chest, abdomen, and pelvis Address for correspondence and reprint requests: S. J. Carlan, M.D., 1401 Lucerne Terrace, 2nd floor, Orlando, FL 32806. Fax: 321-481-0182; E-mail: [email protected]
592
showed small left-sided pneumothorax, pulmonary contusions, mediastinal hematoma, and small splenic laceration. Initial electrocardiogram (MAC 5500, GE Healthcare, Bangalore, India) demonstrated incomplete right bundle branch block with ST depression in inferior leads and lateral leads and ST elevations in anteroseptal leads. His cardiac markers were elevated CK-MB 23.7 ng/mL (normal: 0.1–4), troponin I 7.63 ng/ mL (normal: 0–0.05). Within 2 hours he became tachypneic and hypoxic requiring endotracheal intubation. Follow-up chest x-ray showed progression of bilateral pulmonary contusions. At this point he was transferred to the intensive care unit for further care. Fourteen hours after admission a new harsh holosystolic murmur 4/6 was noted over the left lower sternal border with a thrill. Emergent transthoracic echocardiogram (Philips iE33 xMatrix, Philips, Uster, Switzerland) followed by transesophageal echocardiograms (Philips iE33 xMatrix) were performed which revealed a secundum-type atrial septal defect (Figs. 1 and 2) and a ventriculoseptal defect (Fig. 3) toward the apical portion of the septum with left to right shunt, septal dyskinesia and an ejection fraction of 55%. On the second day he was extubated and he remained hemodynamically stable. He had sinus tachycardia requiring an esmolol drip to control the heart rate. During the days that followed he underwent extensive cardiac evaluation by cardiology, interventional pediatric cardiology, and cardiothoracic surgeon
Blunt Chest Trauma and Cardiac Septal Defects
Figure 1. Two-dimensional transesophageal echocardiogram, bicaval view. The left ventricle (LA) is the left atrium and the arrow shows complete disruption of the interatrial septum.
to determine the approach and appropriate timing for surgical intervention. A repeat echocardiograph showed slight progression of the VSD. Right and left heart catheterization confirmed left-to-right shunt with pulmonary-to-systemic flow ratio of 1.6 and normal coronaries. On day 6, he was taken to the operating room. The septum secundum which was completely avulsed and shredded was repaired with autologous pericardium (Fig. 4). The lower two-thirds of the ventricular septum was shredded with multiple defects (Fig. 5). It was repaired with a bovine pericardial patch. He was extubated within a few hours after surgery and successfully recovered. He was discharged home 7 days after surgery. Two months after discharge patient reported doing well. A year later, transthoracic echocardi-
Figure 2. Transesophageal echocardiogram, color Doppler of the interatrial septal disruption. Arrow shows the turbulence from the left-to-right shunting across the defect.
Figure 3. Transesophageal echocardiogram, apical fourchamber view. Image shows the LV (left ventricle) and the apical ventricular septal defects at the arrows.
ography showed a confirmed repair and no evidence of residual shunting. Discussion: This case is unique for several reasons. First, this combination of cardiac injuries in a survivor is unreported. A detailed search of the published literature discovered no cases of posttraumatic ASD and VSD in the same patient secondary to blunt chest trauma. Second, the characteristics of the forces applied to the heart in our case may have been
Figure 4. Completed repair of atrial septal defect utilizing autogenous pericardium (arrow).
593
Ortiz, et al.
Figure 5. Arrow shows multiple large ventricular septal defects through the apex of the left ventricle.
unique since these combinations of injuries in nonfatal chest trauma have not been reported previously. Ventricular septal defects following nonpenetrating chest trauma can occur either acutely from direct mechanical injury or delayed from a microvascular disruption causing liquefaction necrosis and ischemic dissolution of septal tissue followed by a true defect.5 The mechanical injury may involve a sudden increase in intracardiac pressure caused by compression of the heart between the vertebral bodies and the sternum. If the trauma occurs during late diastole or isovolumetric systole when the heart has maximum volume and the valves are closed, the compression can result in an increase in intracardiac pressure above the threshold of cardiac septal wall integrity and rupture can occur acutely.6,7 Apical muscular VSDs are most common,8 and occasionally valvular injury may occur.9 The ischemic dissolution type rupture occurs when the myocardium is damaged resulting in localized inflammation and ultimately necrosis and rupture. This probably involves the microvasculature in the septal nutrient vessels10 and there may be delayed onset from hours to weeks after trauma occurs. This mechanism is consistent with the clinical findings in our case. The murmur was discovered 14 hours after the injury, not on admission. The compression forces must have been low enough to not acutely rupture the septa, papillary muscles, or heart valves but widespread enough to damage the microvasculature in both the ventricular and atrial septa. Why the atrial septum is not involved in all cases is not known but may reflect
594
the functional anatomy of the atrioventricular valves. Blood naturally flows forward during the cardiac cycle and if the valves remain intact and closed during the traumatic compression of the chamber nearest to the sternum, the right ventricle, the atrium should not be overfilled. In this particular case neither the papillary muscle nor the valves were damaged suggesting the atrial septal injury occurred from the kinetic energy transfer by the same compression forces that damaged the ventricular septum. Another variable that may be operative in the force distribution in this case is the lack of rib fractures. The thoracic wall may decrease the force of impact to the heart in cases of chest trauma in which skeletal rib fractures occur possibly because of the dissipation of kinetic energy. It is also possible that he simply could have had a previously undiagnosed septal defect or one that healed but was a point of unnatural weakness, but this is unlikely considering the normal chamber sizes and no history. References 1. Pretre R, Chilcott M: Blunt trauma to the heart and great vessels. N Engl J Med 1997;336:626–632. 2. Olsovsky MR, Topaz O, DiSciascio G, et al: Acute traumatic ventricular septal rupture. Am Heart J 1996;131:1039–1041. 3. Parmley LF, Manion WC, Mattingly TW: Nonpenetrating traumatic injury of the heart. Circulation 1958;18:371– 396. 4. Menaker J, Tesoriero RB, Hyder M, et al: Traumatic atrial septal defect and papillary muscle rupture requiring mitral valve replacement after blunt injury. J Trauma 2009;67:1126. 5. Liguori AE, Maertins BA, Richardson R: VSD following blunt cardiac trauma: MRI findings. Emerg Radiol 2013;20:459–463. 6. Rollins MD, Koehler RP, Stevens MH, et al: Traumatic ventricular septal defect: Case report and review of the English literature since 1970. J Trauma 2005;58:175–180. 7. Blasco PB, Comas JG, Munoz RDA: Spontaneous improvement of a haemodynamically significant ventricular septal defect produced by blunt chest trauma in a child. Cardiol Young 2009;19:109–110. 8. Ozay B, Ozer N, Ketenci B, et al: Unsuspected location of a ventricular septal defect after blunt chest trauma. Thorac Cardiovasc Surg 2008;56:110–111. du F, Gurlertop Y, Arslan S, et al: Ventricular sep€ ndog 9. Gu tal rupture and mitral regurgitation caused by trauma. Echocardiography 2007;24:174–175. 10. Ryan L, Skinner DL, Rodseth RN: Ventricular septal defect following blunt chest trauma. J Emerg Trauma Shock 2012;5:184–187.
