Although transcatheter closure of perimembranous ventricular septal defect is emerging as an accepted, viable alternative, conduction disturbances still remain a major concern. Although steroid treatment has shown encouraging results with complete recovery, efficacy of prophylactic use of steroids is still speculative. We aim to study the mid-term outcome of perimembranous ventricular septal defect closure in children who received prophylactic oral steroids.

A prospective study was designed and antegrade device closure was attempted in eligible children who met the following inclusion criteria: age 3–18 years and weight >10 kg, defect diameter ⩽12 mm, and symptomatic, haemodynamic changes or history of infective endocarditis. Prophylactic steroid protocol consisted of 2 weeks oral prednisolone (1 mg/kg/day) initiated immediately after the procedure, and in the event of bradyarrhythmia it was escalated to 2 mg/kg. Patients were regularly followed-up at 1, 6, and 12 months and then annually. Patients with post-procedure heart block underwent Holter monitoring after a minimum of 1 year interval.

Between May, 2007 and August, 2012, successful device closure was accomplished in 290/297 patients. Mean age and weight were 9±3.12 years and 21±8.27 kg, respectively. The defect measured 5±1.38 mm on echocardiography. Mean fluoroscopy time was 12.98±8.64 minutes. Eight patients with major complications included one each with device embolisation, haemolysis, severe aortic regurgitation, and five with bradyarrhythmias, including complete atrioventricular block in three, Mobitz II in one, and bifascicular block in one. Patients with complete atrioventricular block responded to high-dose steroid and temporary pacemaker. Minor complications included post-procedure heart block (n=22) and blood loss (n=2). At 18.23±13.15 months follow-up, 8/27 (five major, 22 minor) with arrhythmia had persistent post-procedure heart block of no clinical consequences.

In our patient population, transcatheter device closure of the perimembranous ventricular septal defect with prophylactic oral steroid resulted in excellent closure rate and acceptably low incidence of conduction disturbances at mid-term follow-up.

To determine risk factors for Serratia marcescens infection or colonization, and to identify the source of the pathogen and factors facilitating its persistence in a neonatal intensive-care unit (NICU) during an outbreak.

Retrospective case-control study; review of NICU infection control policies, soap use, and hand-washing practices among healthcare workers (HCWs); and selected environmental cultures.

A university-affiliated tertiary-care hospital NICU.

All NICU infants with at least one positive culture for S marcescens during August 1994 to October 1995. Infants who did not develop S marcescens infection or colonization were selected randomly as controls.

Thirty-two patients met the case definition. On multivariate analysis, independent risk factors for S marcescens infection or colonization were having very low birth weight (<1,500 g), a patent ductus arteriosus, a mother with chorioamnionitis, or exposure to a single HCW. During January to July 1995, NICU HCWs carried their own bottles of 1% chlorxylenol soap, which often were left standing inverted in the NICU sink and work areas. Cultures of 16 (31%) of 52 samples of soap and 1 (8%) of 13 sinks yielded S marcescens. The 16 samples of soap all came from opened 4-oz bottles carried by HCWs. DNA banding patterns of case infant, HCW soap bottle, and sink isolates were identical.

Extrinsically contaminated soap contributed to an outbreak of S marcescens infection. Very-low-birth-weight infants with multiple invasive procedures and exposures to certain HCWs were at greatest risk of S marcescens infection or colonization.