Tricuspid Valve Avulsion after Blunt Chest Trauma

Abstract

Blunt cardiac trauma causing tricuspid regurgitation is rare and is most often associated with traffic accidents. Falling from a height can also cause such injuries, resulting in hemodynamic compromise and arrhythmias. The signs of traumatic tricuspid regurgitation can appear early or be delayed, depending upon the severity of injury. We present the case of a 68-year-old woman who fell from a height onto rocks during a hike. She sustained blunt cardiac injury with complete tricuspid valve avulsion, and underwent successful repair. In addition, we review the relevant medical literature.

Tricuspid valve injury can occur secondary to various events, including blunt cardiac trauma. The manifestation of this condition after blunt cardiac trauma can vary, depending upon the structural damage to the tricuspid apparatus. We present the case of a patient who had severe tricuspid regurgitation due to tricuspid valve avulsion after blunt cardiac trauma, and we review the relevant medical literature.

Case Report

In June 2010, a 68-year-old woman with an active lifestyle was hiking in the woods. She fell approximately 8 to 10 meters onto rocks and sustained multiple injuries, chiefly blunt injury to the chest. She presented at the hospital with chest pain, moderate shortness of breath, and New York Heart Association functional class III symptoms. She was conscious, alert, and hemodynamically stable. She had giant V waves in her neck upon jugular venous pulse examination, an S₃, and a grade 3/6 pansystolic murmur of tricuspid regurgitation. An electrocardiogram showed sinus rhythm with frequent progressive ventricular arrhythmias and episodes of ventricular tachycardia. Chest radiography showed an increased cardiothoracic ratio. Results of laboratory tests were normal except for an elevated troponin level. Transthoracic echocardiography (TTE) revealed severe tricuspid regurgitation, a dilated right atrium, and normal left ventricular (LV) functions and dimensions. The regurgitation was secondary to a completely disrupted and avulsed tricuspid valve apparatus. A ruptured papillary muscle floated freely in the right atrium. A computed tomographic scan was performed to rule out other injuries. Coronary angiography revealed normal coronary arteries. The patient was referred for tricuspid valve repair or replacement.

Anesthesia was induced uneventfully. Transesophageal echocardiography (TEE) showed a completely avulsed tricuspid valve with resultant severe tricuspid regurgitation (Fig. 1). A free-floating, avulsed tricuspid valve and its papillary muscle were seen in the right atrium, with common right atrioventricular continuity. The septal leaflet was partially tethered. A median sternotomy was followed by full heparinization and central aortic and bicaval cannulation. There was no hemopericardium or myocardial contusion. After aortic cross-clamping and adequate myocardial protection, caval tapes were affixed and the right atrium was opened. The completely avulsed anterior and posterior leaflets of the tricuspid valve were prolapsing in the right atrium, with papillary muscle necrosis (Fig. 2). Further intraventricular examination revealed a very small stump of papillary muscle that remained attached to the right ventricular endocardium. The valvular anatomy was unsuitable for repair, so replacement with a bioprosthesis was performed. The right atrium was closed, and the patient was weaned from cardiopulmonary bypass. Her postoperative course was uneventful. On the 7th postoperative day, TTE showed satisfactory ventricular function with no paravalvular leaks, and she was discharged from the hospital on an 8-week course of anticoagulative therapy. Upon examination 6 months and 1 year postoperatively, she remained well.

Fig. 1 Transesophageal echocardiograms show A) the ruptured tricuspid valve with severe tricuspid regurgitation and B) the avulsed tricuspid valve and papillary muscles.

RA = right atrium; RV = right ventricle

Fig. 2 A) Intraoperative photograph shows completely avulsed papillary muscles and a free-floating anterior leaflet. B) Photograph of excised specimen shows avulsion of the tricuspid valve apparatus, with papillary muscle necrosis.

Discussion

Blunt cardiac trauma encompasses a spectrum of myocardial lesions that result from nonpenetrating chest trauma. The Centers for Disease Control and Prevention's estimate of the incidence is 30,000 cases per year in the United States.¹ Autopsy studies indicate that the aortic valve is most commonly involved, followed by the mitral valve and the tricuspid valve.² Tricuspid valve injury can often go unnoticed until its reported incidental discovery during an investigation of other trauma.³ The condition was first described by Williams in 1829.⁴ Its reported incidence has increased because of traffic accidents and advances in diagnostic echocardiography.⁵ Modes of injury can vary from a simple fall to a kick in the chest or even automotive airbag deployment.⁶ Injuries related to blunt cardiac trauma can be benign, such as myocardial contusion, or fatal, such as chamber rupture. Ventricular septal defect has been reported.⁷ Pericardial rupture with cardiac herniation is rare but has a high mortality rate.⁸

Clinical manifestations are related to the extent of tricuspid valve injury. These vary from the rapid onset of heart failure to slow but progressive clinical deterioration.^9,10 A delayed presentation of tricuspid regurgitation after trauma can lead to delays in treatment.^11,12 In a series of 13 cases of blunt traumatic tricuspid insufficiency reported by van Son and colleagues,¹³ the median duration between trauma and operation was 17 years (range, 1 mo–37 yr).

The mechanism of tricuspid valve injury is debated. The best postulated theory is extensive tricuspid “blowout” injury secondary to severe and sudden impact during end-diastole.¹⁴ The right ventricle is vulnerable to injury because of anteroposterior compression from the adjacent sternum. This vulnerability is compounded by increased hydrostatic pressure in the right ventricle during diastole. If damage is severe, symptomatic clinical deterioration and hemodynamic compromise can result.¹⁵ Our patient's case is unusual because the acute compression of the thoracic cavity was produced during the fall, but without the concomitant strong deceleration force typical of motor vehicle accidents.

A high degree of suspicion and the early use of TTE and TEE are important in the diagnosis of tricuspid valve injury. In our patient, TEE helped to diagnose the avulsion of the tricuspid leaflets and consequent atrioventricular continuity. Early valve repair is the preferred treatment; however, the extensive damage in our patient required replacement.