Traumatic avulsion of the tricuspid valve: an unusual cardiac complication of an equine accident

Background

Blunt cardiac injury (BCI) has no clear definition and is a difficult diagnosis to confirm, resulting in wide variations of estimates of its incidence, with some approaching one million cases per year in the USA.1 It comprises a wide spectrum of myocardial lesions that result from non-penetrating chest trauma.2 A range of 70%–80% of those with significant BCI have multiple other injuries which may distract from the cardiac lesion, with many dying at the scene of the accident.3 Resultant tricuspid insufficiency from blunt force chest trauma is rare, accounting for 2% of lesions in an autopsy study and <1% in a series of transoesophageal echocardiograms (TOE) performed in the emergency department.3 4 Clinical manifestations are related to the degree of injury to the tricuspid valve apparatus and range from acute right heart failure to a more common slow but progressive clinical deterioration over months to more than 20 years before presentation.2 5

Case presentation

A man in his 20s presented with progressive dyspnoea on exertion and increasing precordial chest pain. He was otherwise fit and healthy without any significant medical history. He had no family history of heart disease, never smoked, took no medications and worked as a stablehand with horses.

At the time of presentation, his vitals were stable, he was apyrexic and all initial investigations were normal. This encompassed a normal ECG, normal physical examination and normal laboratory tests including cardiac troponin I (cTnI).

On thorough questioning, it was discovered that the patient had suffered a work-place accident at the stables, where he had been kicked directly in the chest by a stallion. Apart from initial pain and shortness of breath he experienced no other symptoms. A chest X-ray performed at the time of injury revealed no pneumothorax, no rib fractures and no widening of the mediastinum. His blood results were normal, and he was discharged from the emergency department with pain relief.

Following his second presentation, 3 months since the time of injury, he was referred to the cardiothoracic surgery department and went on to have an echocardiogram and cardiac MRI which demonstrated isolated, primary, severe tricuspid regurgitation with markedly increased right ventricular volumes. However, on physical examination he had no signs of right heart failure (no distended neck veins or positive hepatojugular reflex) and despite a holosystolic murmur usually being present in the left parasternal region, no murmur could be appreciated.

On the basis of these results, along with his worsening symptoms, tricuspid valve surgery was recommended.

Investigations

Transthoracic echocardiography (figure 1) revealed moderate to severe tricuspid regurgitation with a moderately dilated and volume overloaded right ventricle with preserved systolic function. Tricuspid annulus size was not reported. The left heart was normal. Cardiac MRI confirmed markedly increased indexed right ventricular volumes with preserved systolic function secondary to isolated, primary, severe tricuspid regurgitation, without any evidence of a congenital shunt.

Differential diagnosis

Mild tricuspid regurgitation is common, occurring in 65%–85% of the population, and can be considered a normal variant in the presence of a normal valve apparatus.6 However, moderate to severe tricuspid regurgitation is usually pathological.6 Primary tricuspid regurgitation accounts for only 8%–10% of cases and is caused by an abnormality of the valve itself, either a congenital defect or an acquired lesion from infective endocarditis, rheumatic fever, trauma or other rarer causes.6 Secondary tricuspid regurgitation results from right heart enlargement causing annular dilation, usually as a result of left heart disease.6

Secondary tricuspid regurgitation was unlikely in this case due to normal left heart function and only moderate right heart dilation. There was no history to suggest previous infection, and no risk factors present for infective endocarditis. Given his history of substantial direct blunt injury to the chest, primary tricuspid regurgitation secondary to trauma was considered to be the most likely diagnosis.

Treatment

Following a diagnosis of isolated severe tricuspid regurgitation, he proceeded to surgery via median sternotomy. Standard cardiopulmonary bypass was established via ascending aortic and bi-caval cannulation. The ascending aorta was cross-clamped, and cardioplegic arrest was achieved. The right atrium was opened, and the tricuspid valve was carefully inspected. A large defect of the tricuspid valve was identified with disruption of the anterior leaflet at the annulus (figure 2). The subvalvar apparatus remained intact. The defect was initially repaired with a pericardial patch (figure 3). As the preoperative echo did not reveal any other pathology, it was thought that this repair would suffice; however, the intraoperative TOE demonstrated residual central incompetence due to annular dilatation. The annulus was then repaired using a combination of a 34 mm annuloplasty ring and the clover-leaf technique. This technique is especially useful to correct complex post-traumatic tricuspid lesions and involves stitching together the middle point of the free edges of the tricuspid leaflet, producing a clover-shaped valve.7

Outcome and follow-up

He had an uncomplicated postoperative course and was discharged home on postoperative day 6. Follow-up echo showed a satisfactory tricuspid valve repair with a mean gradient of 2.5 mm Hg with mild residual tricuspid regurgitation. He remains under the care of cardiology for yearly review.