Abstract | March 15, 2023

A Rare Accident Resulting in a Traumatic Ventral Septal Defect

Victor Camba D.O, M.Ed, M.S

Victor Camba, DO, Internal Medicine, PGY2, MRHC, Corinth, MS; Carlos Pfeiffer, DO, Internal Medicine, PGY1, MRHC, Corinth, MS; Andrea Sparkman, BS,Medical Student, OMS3, MRHC, Corinth, MS; Talhah Siraj, MS, Cardiology, PGY4, MRHC, Corinth, MS; Paul Volansky, DO, Associate Program Director, Cardiology, MRHC, Corinth, MS

Learning Objectives

  1. Upon completion of this lecture, learners should be better prepared to diagnose a VSD.

Traumatic ventricular septal defect (VSD) secondary to blunt chest injury is a rare occurrence. Etiology of traumatic VSD has previously been investigated and has been narrowed down to two unique mechanisms. One mechanism is a posttraumatic myocardial infarction leading to weakened septal tissue resulting in decreased wall integrity and elasticity after the traumatic impact. Another possible pathogenesis is the compression of the spine against the sternum during blunt impact. This causes an increase in pressure on the septal wall resulting in an acute rupture. Most case reports with traumatic VSDs present acutely in addition to other traumatic injuries. In this case there is an unusual subacute presentation.

A 74 year old man presented to an outpatient clinic with complaints of progressive dyspnea. He was no longer able to ambulate due to the severity of the dyspnea. History revealed a strike to the chest by a horse two weeks ago. On physical exam, a holosystolic murmur was auscultated both anteriorly and posteriorly. Oxygen saturation on room air was 98% at rest, but 81% with exertion. An outpatient EKG showed sinus tachycardia with premature ventricular contractions but otherwise normal. An outpatient echocardiogram showed VSD in the area of the septal thinning with a serpiginous course starting in the apical region and terminating in the mid segment of the VSD. The left ventricular ejection fraction appeared to be normal, possibly hyperdynamic. The right ventricle size and function appear to be normal. A severe tricuspid regurgitation was noted. Patient was placed on the cardiology service and underwent coronary angiography with right heart catheterization. This revealed non-obstructive coronary artery disease with no prior infarction. Cardiothoracic surgery was consulted and recommended a percutaneous repair. The VSD was determined to be a result of the acute traumatic injury to the chest. This case demonstrates the potential for a delayed onset of symptoms. Due to the lack of extracardiac manifestations, no urgent treatment was sought. This led to the unique subacute presentation of an isolated traumatic VSD.

 

References

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