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Cardiac Intensive Care Unit, Royal Children’s Hospital, Melbourne, Vic, AustraliaDepartment of Cardiology, Royal Children’s Hospital, Melbourne, Vic, Australia
Cardiac Intensive Care Unit, Royal Children’s Hospital, Melbourne, Vic, AustraliaDepartment of Paediatrics, University of Melbourne, Melbourne, Vic, AustraliaMurdoch Children’s Research Institute, Melbourne, Vic, Australia
Corresponding author at: Royal Children’s Hospital, 50 Flemington Road, Parkville, Vic 3052, Australia
Affiliations
Department of Cardiac Surgery, Royal Children’s Hospital, Melbourne, Vic, AustraliaDepartment of Paediatrics, University of Melbourne, Melbourne, Vic, AustraliaMurdoch Children’s Research Institute, Melbourne, Vic, AustraliaMelbourne Centre for Cardiovascular Genomics and Regenerative Medicine, Melbourne, Vic, Australia
A 12-year-old boy had a blunt chest trauma in a motor vehicle accident. He arrested
on arrival to the hospital and underwent clamshell thoracotomy for bilateral haemothorax.
He required direct cardiac massage and massive transfusion for chest wall bleeding
and pulmonary haemorrhage. Computerised tomography revealed a large apical ventricular
septal defect (VSD) (Figure 1A). He developed cardiogenic shock with blood pressure 65/50 mmHg, central venous
pressure 15 mmHg and lactate of 24 mmol/L, despite adrenaline/noradrenaline at 1.5
mcg/kg/min and vasopressin at 0.06 units/kg/hr. He was emergently cannulated for central
extracorporeal membrane oxygenation (ECMO) and epicardial echocardiography confirmed
a large VSD (Figure 1B). He was transferred to theatre and ECMO was switched to cardiopulmonary bypass.
Emergent VSD closure was performed with cardioplegic arrest via right ventriculotomy
(Figure 1C). A pericardial patch was oversized and secured on the left ventricular (LV) side
with four sutures and a running suture (Figure 1D), so that the patch could reliably seal the hole in the ruptured septum with fragile
edges. The ventriculotomy was then closed between two felt strips (Figure 1E). Postoperatively, there were no myocardial contractions, despite normal sinus rhythm,
likely due to tachyphylaxis because of high preoperative catecholamine doses. Thus,
the LV was drained with apical venting to prevent pulmonary congestion. The patient
remained on ECMO support for 14 days. He also developed rhabdomyolysis with a creatine
kinase of 71,000 units/L and myoglobin of 59 mg/L, contributing to acute renal failure.
His cardiac function normalised after one month. He temporarily required a tracheostomy
and haemodialysis, but recovered with normal respiratory and renal function and without
any neurological sequelae.
Figure 1Post-traumatic ventricular septal defect (VSD) and the technique of VSD repair.