Ann Thorac Surg 2006;81:1111-1112
© 2006 The Society of Thoracic Surgeons
Case report
Subacute Tricuspid Valve Rupture After Traumatic Cardiac and Pulmonary Contusions
Alexander Kulik, MD
a
,
Manal Al-Saigh, MD
a
,
Jean-Denis Yelle, MD
b
,
Fraser D. Rubens, MD, MS
a
,
*
a Division of Cardiac Surgery, University of Ottawa Heart Institute, Ottawa, Ontario, Canada
b Department of Surgery, University of Ottawa, Ottawa, Ontario, Canada
Accepted for publication December 21, 2004.
* Address correspondence to Dr Rubens, Room H3403, University of Ottawa Heart Institute, 40 Ruskin St, Ottawa, Ontario, K1Y 4W7 Canada (Email: frubens{at}ottawaheart.ca).
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Abstract
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Tricuspid valve rupture is a rare complication after blunt chest trauma. We report the unusual presentation of a patient that suffered traumatic cardiac and pulmonary contusions, contributing to the rupture of the posterior papillary muscle of the tricuspid valve 24 hours after presentation. We believe that this is the first reported case of subacute tricuspid valve rupture after a normal echocardiogram at admission after blunt chest trauma.
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Introduction
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With an increase in the number of survivors of high speed motor vehicle accidents, blunt cardiac trauma has become an increasingly important health problem [1]. Although cardiac contusions occur in as many as 20% to 35% of patients after blunt chest trauma [2], tricuspid valve (TV) rupture is a rare complication. Valvular rupture may occur acutely from a sudden increase in cardiac pressure at the time of impact, or alternatively, it may be delayed resulting from disruption of contused papillary muscle [3]. The following case illustrates the development of subacute TV rupture 24 hours after traumatic cardiac and pulmonary contusions, despite a normal echocardiogram at initial presentation.
A 58-year-old previously healthy man presented to the hospital after a motor vehicle accident. At the scene of the crash, paramedics found the patient belted in the driver's seat after his vehicle had been hit by a truck traveling at a high speed. In the emergency room the patient was noted to have stable vital signs and a Glasgow Coma Scale of 14, but he was complaining of chest and back discomfort. Although the cardiovascular examination was normal, a new right bundle branch block was noted on electrocardiogram. Initial blood work suggested cardiac contusion, with creatinine kinase 829 U/L and troponin-T 0.42 µg/L. His other injuries included bilateral pulmonary contusions, numerous bilateral rib fractures, multiple thoracic spinous process fractures, and a splenic laceration, as demonstrated by computed tomography. A transthoracic echocardiography performed at the time of admission was normal, with normal right and left ventricular function, a normal TV, and no tricuspid regurgitation (TR).
Twenty-four hours after admission, the patient's condition deteriorated with acute respiratory distress, cyanosis, and marked swelling of his face and neck. After endotracheal intubation and transfer to the intensive care unit, a repeat thoracic computed tomographic scan was performed to rule out superior vena cava injury or pulmonary embolus. However, no new findings were demonstrated. Transesophageal echocardiography at that time illustrated severe tricuspid regurgitation, with a flail posterior leaflet of the TV, moderate right ventricular (RV) dysfunction, and pulmonary hypertension (mean pulmonary artery pressure greater than 40 mm Hg). Swan-Ganz catheterization revealed a cardiac index of 2.3 L/min/m2, a mean pulmonary pressure of 39 mm Hg, and a calculated pulmonary vascular resistance of 391 dynes · sec · cm-5. In order to manage the pulmonary hypertension and RV dysfunction, intravenous milrinone was administered. Intravenous amiodarone was also required to control supraventricular tachycardia. In light of the new onset of pulmonary hypertension, the flail TV was treated conservatively. After several days of ventilatory and inotropic support, the patient's hemodynamics slowly improved. The patient was extubated and transferred out of the intensive care unit 12 days after his acute deterioration. Continued clinical improvement allowed discharge to a rehabilitation center 25 days after the date of admission.
Five months later, the patient underwent elective surgical repair of his flail tricuspid valve. Although asymptomatic, he continued to have severe tricuspid regurgitation and was developing progressive RV dilatation. Surgery was performed through a median sternotomy with aortic and bi-caval cannulation. The right atrium was opened transversely and the tricuspid valve was inspected. The posterior leaflet was noted to be flail, and there was significant enlargement of the annulus involving the anterior leaflet. A small 3-mm piece of papillary muscle was still attached to the posterior leaflet. The chordae from the posterior leaflet were entangled in the chordae of the lateral aspect of the septal leaflet. The posterior leaflet was completely excised and repair of the tricuspid valve was performed with posterior annulus plication (bicuspidization) and insertion of a 29-mm Duran annuloplasty band (Medtronic Inc, Minneapolis, MN). Pathologic examination demonstrated chordal rupture secondary to infarcted papillary muscle. After an uncomplicated postoperative course, the patient was discharged home 8 days after surgery. One month later, the patient was doing well with increasing exercise tolerance. A transthoracic echocardiography showed no residual tricuspid regurgitation, normal RV function, and normal RV dimensions.
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Comment
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Although tricuspid valve rupture is a rare complication after blunt chest trauma, even more rare is traumatic rupture of the posterior leaflet, with only five cases having been described [4, 5]. Because of the location of the RV directly behind the sternum, the TV is vulnerable in blunt chest trauma. Acute valvular insufficiency appears to be the result of a sudden increase in cardiac pressure after compression of a full ventricle during isovolumetric contraction, leading to chordal or papillary muscle rupture [3]. Alternatively, delayed valvular rupture may result after papillary muscle contusion, with hemorrhage, inflammation, and late necrosis, ultimately causing disruption [3].
Pulmonary contusion is the most common injury identified in blunt chest trauma [6]. Segmental lung damage and intra-alveolar hemorrhage accumulate 24 to 48 hours after the initial injury, causing impaired gas exchange, increased pulmonary vascular resistance, reduced lung compliance, and reduced pulmonary flow [6]. Pulmonary vascular resistance and arterial pressures reach a peak within 2 days after pulmonary contusion, and can result in acute respiratory or ventricular failure [7]. With the current patient, bilateral pulmonary contusions and rising pulmonary vascular resistance likely contributed to overwhelming stress on the damaged TV papillary muscle, culminating in subacute valvular rupture and sudden tricuspid regurgitation.
We believe that this is the first case describing tricuspid valve rupture during hospitalization after chest trauma in which there was a normal echocardiogram at admission. This case highlights the importance of transesophageal echocardiography in the rapid diagnosis of a deteriorating patient after blunt cardiac trauma. Transesophageal echocardiography is safe, rapid, and provides high quality images of the heart and aorta, making it the diagnostic study of choice for assessing traumatic myocardial or valve injury [2]. Therefore, regardless of the initial echocardiogram, an appreciation that cardiac injuries can evolve with delayed muscular necrosis and rupture is essential in the management of victims of blunt chest trauma.
The timing of surgical intervention after acute valve rupture is a subject of debate. Although early surgery is indicated as a rule for mitral valve papillary rupture, damage to the TV is associated with less hemodynamic consequences, and early surgery is usually not necessary as a lifesaving procedure. Postponing surgery in the acute setting for this patient provided time for the contusion-induced pulmonary hypertension to resolve, improving the likelihood of a successful and durable repair. Valve repair is also technically easier in the delayed setting because mild fibrosis around the lesion allows for a more secure suture placement. However, a prolonged delay greater than a few months is contraindicated, as it could lead to progressive ventricular dysfunction and dilatation, as well as fibrosis and atrophy of the valvular apparatus, decreasing the possibility of valve repair [8].
In conclusion, this case report highlights an unusual presentation of subacute tricuspid regurgitation after blunt chest trauma, despite a normal initial echocardiogram. A high index of suspicion and early use of transesophageal echocardiography led to the diagnosis. With initial conservative management and delayed surgery, successful valve repair and excellent results were achieved.
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References
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Abstract
Introduction
