Tricuspid valve chordal rupture due to airbag injury and review of pathophysiological mechanisms

Abstract

Blunt trauma to the chest is associated with significant morbidity and mortality. The latter is usually due to an aortic transection, whereas the former is related to myocardial contusion, cardiac valve injury, coronary artery disruption and intracardiac shunts due to the formation of septal defects. The main mechanisms causing these injuries are due to the sudden deceleration force and compression within the chest cavity. Moreover, there is also the sudden increase in intravascular pressure due to a mechanical compression effect and a hormonal adrenergic surge during the event. We report a case of a tricuspid valve injury caused by the deployment of the airbag during a high-speed impact car accident and the subsequent damage to the tricuspid valve chordal mechanism. The patient's management and the pathophysiological mechanisms involved in the injury are reviewed.

INTRODUCTION

Blunt cardiac trauma (BCT) has been estimated in around 0.25% of patients discharged from hospital after any form of injury [1]. In patients who survive a BCT incident, injury to the mitral valve seems to be the commonest, followed by aortic, tricuspid and pulmonary valves respectively. Isolated injury to the tricuspid valve causing tricuspid regurgitation (TR) is rare, and the pathological findings causing TR include chordal rupture, anterior papillary muscle rupture and anterior leaflet tear.

CASE REPORT

A 58-year old man was involved in a high-velocity (90 km/h) head-on-impact motorcar accident. He sustained significant injuries including splenic rupture, multiple long-bones and pelvic fractures along with sternal and multiple rib fractures despite the deployment of the airbag. The sudden inflation of the airbag must have had a significant impact on the sternum and the retrosternal structures to cause the sternal fracture. The patient underwent urgent splenectomy and treatment of long-bone fractures. Post-laparotomy, the patient had elevated central venous pressure with a large ‘v’ wave. The echocardiogram showed a significant TR with impaired right ventricular (RV) function and the patient was referred for potential tricuspid repair. In view of the significant RV-dysfunction and other risks, including that of heparinization in polytrauma patients, it was decided to manage the patient conservatively in the first instance. The patient remained stable and a repeat echocardiogram showed slowly improving RV function but a persistent significant TR. He was managed conservatively and was discharged home after 58 days.

He remained asymptomatic from a cardiac point of view. He was electively admitted for tricuspid valve repair 9 months after his initial injury. Intraoperatively, the chordal attachment to the anterior leaflet was found to be ruptured near the antero-septal commissure (Fig. 1). A tricuspid repair was performed using a 34 mm MC3 Edwards annuloplasty ring (Edwards Life Sciences LLC, Irvine, CA, USA) and chordal re-attachment with neo-chordae using pledgetted CV5 Gore-Tex suture (WL Gore & Associates Inc., Flagstaff, AZ, USA). The native chordae were not re-attached to the papillary muscle as they were too flimsy. Postoperatively, an echocardiogram showed minimal TR. He made an uneventful recovery and was discharged on the 4th postoperative day. He continued to make good progress 2 years after surgery.

Figure 1:

Intraoperative finding of anterior leaflet chordal rupture.

DISCUSSION

Cardiovascular injuries are the second leading cause of death following trauma. Injuries can be either penetrating or blunt. The latter can lead to myocardial contusion, cardiac valve injury, coronary artery disruption, cardiac laceration and intracardiac shunts due to the formation of septal defects.

The heart is ‘trapped’ within the chest cavity by the anteriorly positioned sternum and the vertebral column and ribs posteriorly. The chest wall does have a certain degree of compliance, and due to its visco-elastic properties, it can withstand considerable deformation [2].

The decelerating force leads to a change in the antero-posterior diameter of up to 50% [3], which is compounded at impact by the deployment of the airbag. The latter prevents the forward expansion of the anterior chest wall. As the heart is relatively unfixed, it retains the potential for high inertia, which is transmitted to the cardiac muscle and structures causing distortion to the cardiac chambers by shear stress. The right ventricle (RV) is in a disadvantageous position, being right behind the sternum, hence receiving the full impact of the airbag on the anterior chest wall. Moreover, its usual low pressure system ill-prepares the RV for this significant change in pressure. This is worsened if there is an associated abdominal compression by the seat belt. The latter forces the blood within the venous system into the right side of the heart, i.e. an increase in the intravascular hydrostatic pressure. The combined end-result of all these forces leads to an acute elevation of right intra-ventricular pressure, which has been shown by Perlroth et al. [4] to injure the tricuspid valve apparatus. Valve rupture is more likely if these sudden acute changes occur during the iso-volumetric phase of systole when the intraventricular pressure is low and the valve is closed, as this represents the timing of the maximal transvalvular gradient.

The rupture of the chordal apparatus is explained by the rush of blood towards the closed valve during the initial phase of deceleration (antegrade wave). The latter is caused by the initial anterior displacement of the heart, leading to blood acceleration towards the valve, and if the valve is closed, producing a significant extension-tensile tug on the chordal apparatus. This is quickly followed by the posterior displacement of the heart, creating a ‘reverse haemodynamic wave’ and a sudden increase in intracardiac pressure. Some of the above theories have been proven in an experimental laboratory using mathematical modelling principles [5].

The timing of intervention in the injured heart valve depends on the patient's clinical condition. In the case described above, the life-threatening injuries were dealt with at the outset and the cardiac intervention was delayed. Repair of the valve is preferable if possible. Long-term outcome is usually very good. If the patient is haemodynamically unstable due to the severe TR, then optimization of the medical therapy including the use of diuretics as well as the RV assist device to support the contused RV or extracorporeal membrane oxygenation could be considered.

Conflict of interest: none declared.