Transcatheter device closure of a traumatic ventricular septal defect
A previously well 7-year-old boy was hit and run over by a truck. He presented to the local emergency department with evidence of head, chest, and abdominal injury. Clinical examination also revealed a harsh pansystolic murmur at the left sternal border. Echocardiography showed an 8-mm muscular VSD near the apex, which was initially thought to be a congenital defect []. The patient was hemodynamically stable and did not require inotropic support. Electrocardiogram showed normal sinus rhythm. Cardiac enzymes were not assayed on presentation.\nCT of head showed base of skull fracture. The CT chest and abdomen showed lung contusions at both bases and liver laceration []. Over the course of the next 24 hours, he developed progressive tachycardia, hypotension with hepatomegaly and elevated central venous pressure. He had also developed a right-sided pleural effusion. He underwent emergency laparotomy to exclude persistent hemorrhage from the liver laceration. A moderate volume of old blood was found and this was not able to explain the degree of hypotension. Repeat echocardiography documented ragged walls around the muscular VSD near the apex and significant left heart dilatation and right ventricular strain.\nThe patient was clinically in severe heart failure, which was very difficult to manage medically. In the context of multiple organ injuries, coagulopathy, hemodynamic instability, and technical difficulty in closing the VSD surgically, a decision was taken to close the defect percutaneously. In order to achieve the maximal coverage of the lacerated ventricular septum and in the context of his relatively small weight (23 kg), a 25-mm cribriform Amplatzer PFO device (St Jude Medical, Plymouth, MN USA) was selected. This was placed after forming an arterio-venous guidewire loop through a 7-Fr delivery system [Figures and ]. There were no complications. Post-procedure echocardiogram showed the presence of only a small residual VSD, which was anticipated due to the unusual morphology and ragged edges of the traumatic VSD [Figures and ].\nDespite apparent successful device placement, the patient required high-dose infusion of adrenaline to maintain adequate blood pressure. He also developed acute renal dysfunction and required continuous veno-venous hemofiltration. He had bilateral chest drains inserted for pleural effusions. His hypotension progressively worsened over the next 2 days. In spite of the multiple inotropes, the heart function was moderately reduced. He was already being treated with broad-spectrum antibiotics, adrenaline, vasopressin, and corticosteroids for inotrope-resistant shock. At this juncture, extracorporeal membrane oxygenation (ECMO) was considered as an alternative means of supporting the patient, despite the increased risk involved in view of liver laceration and lung contusion. The role of ECMO support provision in the post-trauma patient was discussed with international centers and it was decided that ECMO would be provided if further deterioration occurred, despite the risk of hemorrhage with systemic anticoagulation.\nHis clinical condition improved progressively with the inotropes stopped at day 5. His recovery over the next 2 weeks was complicated by episodes of pulmonary hemorrhage, bronchial occlusion with casts in left main bronchus, and critical illness myopathy. He was discharged from our intensive care unit after 20 days. At discharge, his heart function had returned to normal. The occluder device was in a good position. There remained a small residual VSD of 5 mm size, with a highly restrictive left-to-right shunt. There were no obvious signs of neurological damage except for the evidence of resolving myopathy.\nAfter 6 months of his first device closure, he underwent elective closure of his residual VSD with a duct occluder device (Amplatzer ADOII 6 mm, St Judes Medical, Plymouth, MN, USA) for persistent mild left ventricular dilatation. Following the second procedure, he had no residual shunt with complete resolution of left ventricular dilatation (Figures and ).