Ann Thorac Surg 2008;86:1371-1373. doi:10.1016/j.athoracsur.2008.04.007
© 2008 The Society of Thoracic Surgeons
Case Reports
Simultaneous Rupture of the Mitral and Tricuspid Valves With Left Ventricular Rupture Caused by Blunt Trauma
Jae-Sung Choi, MD, PhD,
Eung-Joong Kim, MD, PhD*
Department of Thoracic and Cardiovascular Surgery, Dongguk University International Hospital, Goyang, Korea
Accepted for publication April 3, 2008.
* Address correspondence to Dr Kim, Department of Thoracic and Cardiovascular Surgery, Dongguk University International Hospital, 814, Siksa-Dong, Ilsandong-Gu, Goyang City, Gyeonggi-Do, 410-773, Korea (Email: kimej{at}duih.org).
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Abstract
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To date, we believe that only 8 patients with simultaneous rupture of the mitral and tricuspid valves caused by blunt chest trauma have been reported. The correct diagnosis of this condition during the initial assessment is difficult and often delayed. Surgical experience with this condition has been quite limited. We present a unique case of atrioventricular valve rupture, combined with left ventricular rupture and a brief review of the relevant literature.
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Introduction
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Cardiac valve injury is an uncommon clinical entity, the recognition of which is difficult at the time of initial evaluation in cases of blunt chest trauma [1, 2]. Furthermore, cases involving simultaneous rupture of the mitral and tricuspid valves are exceptionally rare. Post-traumatic valve insufficiency, which differs from chronic valve insufficiency, must be promptly corrected to avert acute clinical deterioration. However, the limited surgical experience with rupture of cardiac valves makes it difficult to establish optimum operative strategies according to the extent of the injury, the involved valves, and the interval from trauma to surgery.
A 17-year-old man was referred to our institution with the diagnosis of diffuse axonal injury caused by a high-speed motor vehicle accident. He was in a coma with a Glasgow Coma Scale score of 6. His brain computed tomographic scan showed multiple small hemorrhagic areas in the right frontal lobe. The chest roentgenogram showed no definite abnormal findings. Although the cardiac enzymes were elevated, the electrocardiogram showed no ST-segment elevation changes, and no cardiac murmurs were audible.
As soon as the patient was transferred to the neurologic intensive care unit, he began to rapidly deteriorate. The hypoxia worsened and he was placed on mechanical ventilation. Hypotension and oliguria persisted, despite resuscitative efforts with inotropic support and aggressive volume challenge. A transthoracic echocardiography (TTE) was performed, which demonstrated a large hemopericardium (Fig 1A). The status of the valves could not be examined due to collapse of both ventricles. Prompt drainage of 150 mL of intrapericardial blood was performed by pericardiocentesis for cardiac resuscitation. Based on computed tomographic angiography, the aorta was intact. Subsequent pulmonary arteriography showed a faint pericardial staining with dye.
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Fig 1. (A) Transthoracic echocardiogram demonstrating a large hemopericardium (PE) and ventricular collapse. (B, C) A transesophageal echocardiogram revealed near-complete detachment of the anterolateral papillary muscle (ALPM) of the mitral valve (MV). (D) A transesophageal echocardiogram revealed a flail TV. (Ao = aorta; flail TV = flail tricuspid valve; LA = left atrium; LV = left ventricle; RA = right atrium; RV = right ventricle.)
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The patient was taken directly to the operating room with the impression of cardiac rupture. A 2-cm long rupture of the lateral wall of the left ventricle was noted; the left ventricle rupture was closed with three interrupted mattress sutures buttressed with Teflon felt pledgets (Bard Inc, Tempe, AZ). The patient was weaned from cardiopulmonary bypass without difficulty.
On postoperative day 1, a harsh systolic murmur was noted and the TTE was repeated. The TTE revealed a partial transection of the anterolateral papillary muscle (PM) of the mitral valve (MV) and a flail tricuspid valve (TV), causing severe mitral and tricuspid regurgitation. However, the patient's neurologic condition did not allow immediate reoperation.
The hemodynamic aberrations were reversed by medical therapy. The conditions of coma and disseminated intravascular coagulation gradually improved. A brain computed tomography was performed on postoperative day 3, which showed no evidence of further intracranial hemorrhage. The patient was weaned from mechanical ventilation on postoperative day 4. The patient gradually became more dyspneic, along with cardiomegaly and a bilateral pleural effusion.
Before reintubation was required, repeat surgery was performed and a transesophageal echocardiography was obtained (Figs 1B–1D) on postoperative day 10. Surgical inspection revealed a partial detachment of the anterolateral PM and complete transection of the anterior PM of the TV. Because of the possibility of failure with simple reattachment of the anterolateral PM to the friable ventricular wall, the MV was replaced with a 29-mm mechanical valve (St. Jude Medical Inc, St. Paul, MN). The ruptured anterior PM of the TV was reattached to the moderator band. A leaflet repair and the commissuroplasty were added to treat a septal leaflet tear and the worn-out leaflet tissue around the posteroseptal commissure. The patient was extubated the next day, and his postoperative course was uncomplicated. Postoperative TTE showed trivial tricuspid regurgitation with adequate functioning of the prosthetic MV. He was in good condition without any cardiac dysfunction at the 13-month follow-up.
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Comment
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Few cases of simultaneous rupture of the MV and TV caused by blunt chest trauma have been reported [3–5]. The present case is unique in that the left ventricle free wall rupture was combined with rupture of the atrioventricular valves.
Papillary muscle rupture is the most common cause of traumatic mitral regurgitation, followed by rupture of the chordae tendinea and leaflet tears [5]. In traumatic injury of the TV, chordal rupture occurs most frequently, followed by anterior PM rupture and leaflet tears [6]. Papillary muscle rupture has been purported to occur due to ventricular compression between the sternum and the spine during the period of isovolumic contraction when the cardiac valves are closed [6].
The differential diagnosis of this condition is difficult and tends to be delayed due to the combined thoracic injuries, inaudible murmur of mitral regurgitation caused by the rapid equilibration of the left atrial and ventricular pressures, and similar laboratory findings with myocardial contusions. In our case, the atrioventricular valve rupture was missed at the first diagnosis due to the cardiac tamponade and the resultant ventricular collapse.
The patient was able to tolerate the acute severe mitral regurgitation for 10 days until the second operation. This seems to imply that acute mitral regurgitation developed in circumstances other than coronary disease is more tolerable [7].
Because the patient with traumatic valve injury often has hemodynamic instability, insufficient visualization of the friable endocardium, and necrotic PM, the valve repair is neither easy nor safe. Especially for MV, some authors have recommended that valve replacement should be done for all cases of acute valvular disruption [2]. In our case, unlike most similar reports, the TV was reconstructed instead of being replaced. A TTE performed at the 13-month follow-up showed a trivial tricuspid regurgitation with well-functioning TV. Considering that the right heart is a low-pressure system and has a thick and prominent landmark (ie, the septomarginal trabecula extending from the septum to the base of the anterior PM), the ruptured anterior PM could be correctly and securely placed back to its own position and the reconstructed TV is expected to hold to its shape even in the setting of focal endocardial ischemia and myocardial contusion.
In conclusion, a high index of suspicion is important for the early diagnosis of traumatic valve injury. Even when cardiac valve injury is equivocal, one should not hesitate to perform transesophageal echocardiography. If the transesophageal echocardiography can not be achieved, serial TTEs should be performed. Although the experience of valve reconstruction in the setting of multiple blunt trauma is very limited, specific attention should be given to the possibility of valvular reconstruction, especially for the TV.
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References
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- Chirillo F, Totis O, Cavarzerani A, et al. Usefulness of transthoracic and transesophageal echocardiography in recognition and management of cardiovascular injuries after blunt chest trauma Heart 1996;75:301-306.[Abstract/Free Full Text]
- McDonald ML, Orszulak TA, Bannon MP, Zietlow SP. Mitral valve injury after blunt chest trauma Ann Thorac Surg 1996;61:1024-1029.[Abstract/Free Full Text]
- Pellegrini RV, Copeland CE, DiMarco RF, et al. Blunt rupture of both atrioventricular valves Ann Thorac Surg 1986;42:471-472.[Abstract]
- Bailey PL, Peragallo R, Karwande SV, Lapunzina P. Mitral and tricuspid valve rupture after moderate blunt chest trauma Ann Thorac Surg 2000;69:616-618.[Abstract/Free Full Text]
- Varahan SL, Farah GM, Caldeira CC, Hoit BD, Askari AT. The Double jeopardy of blunt chest trauma: a case report and review Echocardiography 2006;23:235-239.[Medline]
- Dounis G, Matsakas E, Poularas J, Papakonstantinou K, Kalogeromitros A, Karabinis A. Traumatic tricuspid insufficiency: case report with a review of the literature Eur J Emerg Med 2002;9:258-261.[Medline]
- Pizzarello R, Gulotta SJ. Cardiology acute severe mitral regurgitation Postgrad Med 1976;60:215-221.[Medline]
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Abstract
Introduction
