Traumatic tricuspid insufficiency with a ventricular septal defect in a child: a case report

Traumatic tricuspid insufficiency is very rare. In this report we describe an interesting case of a 13-year-old boy who suffered chest trauma from a horse kick. Echocardiography demonstrated a remarkable tricuspid regurgitation with ventricular septal defect. Once assessing the diagnosis, an emergency open heart surgery was necessary to repair the injuries with good results.


Introduction
Blunt chest trauma leads to a wide range of lesions, relatively minor parietal injuries to potentially fatal cardiac lesions, making diagnosis and management difficult. The tricuspid valve is rarely involved [1], the interventricular septum defect is mostly encountered during penetrating trauma. We report a case of severe tricuspid insufficiency associated with an apical muscular Ventricular Septal Defect (VSD) in a thirteen year old patient following a horse kick. Management strategies are discussed and our treatment approach is presented.

Discussion
Valvular lesions following blunt thoracic injury are uncommon.
Tricuspid insufficiency is thought to be a rare complication of blunt, non-penetrating chest trauma. The incidence of blunt chest wall trauma and reported traumatic tricuspid regurgitation has been increasing during the last decade [1]. However, the diagnosis is difficult because this pathology slowly progress and its presentation can be atypical or asymptomatic, so its incidence rates may be underestimated. The most common mechanism of acute or subacute tricuspid regurgitation is an anteroposterior compression of the chest with a sudden increase in the right ventricular pressure during the end diastolic phase, when the main pulmonary vessels are compressed.
This generates a marked traction on both valvu¬lar and subvalvular apparatus. VSD is a particularly uncommon result [2,3]. Its severity, presentation and course are variable, with presenting signs often masked by concomitant injuries, [4] and the presentation of the murmur is often delayed. The pathogenesis of VSD following blunt chest trauma is unclear but is thought to be caused by either early mechanical rupture or delayed inflammatory rupture.
Mechanical septal rupture has been proposed to occur as the heart is compressed during late diastole, after atrial contraction, when the ventricles are filled and the valves closed. This may occur as a result of direct cardiac impact or when the heart is compressed between the sternum and the spine [5]. It has also been suggested that a healed congenital VSD with a weakened ventricular septum may re-open with significant blunt trauma to the chest [4]. Delayed inflammatory rupture is thought to occur when cardiac injury causes localised edema with disruption of microvascular flow, leading to infarction, septal liquefaction, and perforation. Small asymptomatic traumatic VSDs may be managed conservatively as they often close spontaneously [6]. Surgical repair is indicated if the defect is large, if the pulmonary to systemic blood flow ratio exceeds 2/1, or if there is evidence of cardiac failure [5]. However, a persisting small lesion with chronic left to right shunting may with time result in right ventricular failure. Cases of blunt chest trauma resulting in a combined lesion of traumatic VSD and tricuspid insufficiency, as in our patient, were also reported by others [7]. Signs of heart failure with elevated pulmonary pressure and a significant left-to-right shunt dominated the clinical picture in most patients.
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Conclusion
This case reminds us that physicians in the emergency department should be aware of this potential complication following nonpenetrating chest trauma. Early operation should be emphasized to achieve good functional results and preserve the right ventricular function.

Competing interests
The authors declare no competing interests.