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Gastric outlet obstruction with prostaglandin E1 infusion in congenital diaphragmatic hernia

Prostaglandin E1 (PGE1) is used globally in neonatal medicine to maintain patency of the ductus arteriosus in ductdependent congenital heart disease. Due to its nonselective pulmonary vasodilator effect and its role in offloading the pressure on the right ventricle via the ductus arteriosus, PGE1 has been increasingly used in the management of neonatal pulmonary hypertension, especially in those patients with congenital diaphragmatic hernia (CDH). 2 Gastric outlet obstruction (GOO) has been described as a side effect of PGE1 in populations with congenital heart disease, most commonly secondary to hypertrophic pyloric stenosis (HPS) or antral foveolar hyperplasia (AFH). To describe our experience with the use of PGE1 in the CDH population and occurrence of GOO, we conducted a singlecentre retrospective study of all neonates with CDH admitted to The Royal Children’s Hospital neonatal intensive care unit (NICU) during the years 2010–2021. In the study period, 119 neonates were admitted to our NICU. Seventy neonates (58.8%) were exposed to PGE1. Of these neonates, 6/70 (8.6%) developed GOO. None of the 49 patients who did not receive PGE1 developed GOO. In statistical analysis, no differences were observed between the demographic data in the two groups (GOO vs no GOO) (table 1). In addition, there were no statistical differences in duration of treatment with inotropes, need for inhaled nitric oxide (iNO) or incidence of death. However, there were significantly more hours of mechanical ventilation (p=0.04, coefficient 0.001, 95% CI 0.00002 to 0.002), days of inpatient stay (p=0.002, coefficient 0.002, 95% CI 0.0009 to 0.004) and duration of PGE1 therapy (p=0.009, coefficient 0.002, 95% CI 0.0005 to 0.003) in the GOO group (table 1). Patients with GOO presented with abdominal distension, large gastric aspirates and nonbilious vomiting when they received at least 15 mL/kg/day of feeds following surgical repair of their diaphragm. In four neonates, GOO occurred due to AFH and no surgical intervention was needed. A nasojejunal tube was placed in 3/4, with subsequent successful introduction of enteral feeds. One neonate with AFH had a prolonged course of critical illness acuity where enteral feeding was contraindicated. Successful transition to gastric feeding occurred over 4 weeks in two neonates with AFH following discontinuation of PGE1. Two patients died from respiratory failure prior to the resolution of GOO. The two remaining neonates had a successful pyloromyotomy for HPS. Our results show that neonates with CDH who are exposed to prolonged infusions of PGE1 may be at increased risk of developing GOO and support previous descriptions of a temporal relationship between exposure to PGE1 and development of GOO. 5 It is important to distinguish between AFH and HPS as the cause for GOO, in order to direct the most appropriate treatment pathway. Nasojejunal feeding and discontinuation of PGE1 therapy is an effective intervention where feed intolerance is due to AFH, while HPS will need surgical treatment. The risk of GOO appears higher in patients requiring a longer duration of PGE1 infusion, mechanical ventilation and hospitalisation. Andrea Togo , David Stewart, Amanda Moody, Sebastian King, Ruth K Armstrong Department of Neonatal Medicine, The Royal Children’s Hospital Melbourne, Parkville, Victoria, Australia Paediatric Surgery, The Royal Children’s Hospital, Parkville, Victoria, Australia Murdoch Children’s Research Institute, Parkville, Victoria, Australia