ABC | Volume 111, Nº2, August 2018

Case Report Transcatheter Closure of a Traumatic VSD with an ASD Occluder Rui Alexandre Pontes dos Santos, 1 Henrique Guedes, 1 Leonor Marques, 1 Carolina Lourenço, 1 João Carlos Silva, 2 Paula Pinto 1 Centro Hospitalar do Tâmega e Sousa, 1 Penafiel - Portugal Centro Hospitalar de São João, 2 Porto - Portugal Mailing Addres: Rui Alexandre Pontes dos Santos • Avenida do Hospital Padre Américo, 210, Guilhufe. 4564-007, Penafiel – Portugal E-mail: rui.pontes.santos@gmail.com Manuscript received December 19, 2016, revised manuscript September 08, 2017, accepted November 09, 2017 Keywords Heart Septal Defects, Ventricular / complications; Myocardial Contusions; Hemolysis; Heart Septal Defects, Ventricular / surgery. DOI: 10.5935/abc.20180122 Introduction Traumatic ventricular septal defects (VSD) are exceptionally rare. They can be a consequence of either blunt or penetrating trauma. It is believed that most patients die before reaching the hospital, which makes this condition even more challenging. Percutaneous closure of traumatic VSD has been presented as an alternative to open conventional surgery. 1 Transcatheter intervention may have some benefits. The objective of this case report is to present a situation where the defect was closed using an Amplatzer septal occluder. Case Report A 23-year-old man was admitted in the emergency department after a frontal car collision. He had suffered severe blunt trauma, which included cervical subcutaneous emphysema, bilateral pulmonary contusion, left hemothorax, pneumomediastinum and complex fractures of both femurs. He was in hemorrhagic shock and was immediately taken to the operatory room. After external fixation of both femurs and reaching hemodynamic stability, he was transferred to the Intensive Care Unit. The following morning the presence of a loud holosystolic murmur was noted. The 12‑lead electrocardiogram showed only sinus tachycardia. A transthoracic and later a transesophageal echocardiogram (TEE) were performed and both demonstrated a large muscular ventricular septal defect, located in the mid anteroseptal segment with signs of dissection through the basal septum (Figure 1). It measured 19 mm on the left ventricular (LV) side and 7 mm on the right ventricular (RV) side. The peak left to right shunt gradient was estimated in 84 mmHg and the Qp/Qs ratio was estimated in 1.8/1.0. Cardiac catheterization showed limited hemodynamic repercussion (systolic pulmonary artery pressure of 35 mmHg and a Qp/Qs ratio of 1.9/1.0) and the patient remained clinically stable, so a conservative strategy was decided at that time to allow the edges to heal and create a more delimited defect. He was released after recovering from orthopedic surgery. Threemonths later the patient was reevaluated and remained asymptomatic. He repeated cardiac catheterization, which showed a Qp/Qs ratio of 2.95/1.0. Because the shunt increased significantly, it was decided to close the defect percutaneously. Theprocedurewas doneunder general anesthesia and guided by transesophageal echocardiography. Cardiac catheterization was performed using the right femoral artery (6‑Fr sheath) and vein (7-Fr sheath) and unfractionated heparin was administered. Angiogram of the LV confirmed a VSD with an oblique entry from the LV into the right ventricular outflow tract. The VSD was crossed using a retrograde arterial approach with a floppy guidewire, which was advanced into the pulmonary artery. The guidewire then snared and brought out the femoral venous sheath. This created an arteriovenous loop to allow the delivery of the closure device. A NuMed sizing balloon catheter was subsequently utilized to measure the defect, but it was not possible to maintain it steady. Therefore, the echocardiographic calculations were used to choose the device size. An 8-mm Amplatzer septal occluder was first selected and loaded into the sheath. The device was advanced across the VSD, but prolapsed back to the RV when it was being released. After this failed attempt, a slightly different approach was used. The VSD was crossed once more using the guidewire, this time in the opposite direction into the right subclavian artery. Once again, it was snared to make an arteriovenous loop, but on this occasion pulled out through the femoral arterial sheath. For this second attempt, it was decided to employ a 10-mm Amplatzer septal occluder. The device was advanced through the venous sheath and this time was successfully placed (Figure 2). LV angiogram after the procedure revealed a mild residual shunt and the Qp/Qs ratio reduced to 1.53/1.0. A transesophageal echocardiography was repeated a month after the procedure, which showed the device well adapted to the defect. Nevertheless, a residual shunt remained in the superior border of the device with a peak gradient estimated in 90 mmHg (Figure 2). Another complication of this procedure was the appearance of transient self-limited hemolysis. Initial blood analysis showed a LDH value > 2000 UI/L and haptoglobin < 6 mg/dL. The condition remained stable and resolved without the need of blood transfusions. The patient continued to be asymptomatic and has returned to his previous professional life. Discussion There are a few possible mechanisms that explain the development of traumatic VSDs. In this case, cardiac contusion after compression between the sternum and the spine or due to high intrathoracic pressures at impact seems to be the most probable explanation. 1 223