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Gastric outlet obstruction after long-term prostaglandin administration mimicking hypertrophic pyloric stenosis
M Lacher1, K Schneider, R Dalla Pozza
1Kinderchirurgische Klinik im Dr. von Haunerschen Kinderspital, Ludwig-Maximilians-Universität München, Munich, Germany. Martin.Lacher@med.uni-muenchen.de
Insights
Prostaglandin E1 (PGE1) therapy in neonates can cause gastric outlet obstruction, mimicking pyloric stenosis. Symptoms resolve after discontinuing PGE1 and cardiac surgery.
Area of Science:
- Neonatal cardiology
- Pediatric gastroenterology
- Pharmacology
Background:
- Prostaglandin E1 (PGE1) is crucial for neonates with cyanotic congenital heart disease requiring ductal patency.
- Common PGE1 side effects include respiratory, cardiovascular, and neurological issues, but gastrointestinal effects are less understood.
Observation:
- A case report details an infant experiencing feeding difficulties and projectile vomiting at one month of age.
- Sonography revealed progressive antropyloric channel elongation causing gastric outlet obstruction, without pyloric wall thickening.
Findings:
- The infant's symptoms resolved within three days of cardiac surgery and cessation of PGE1 therapy, with normal feeding and weight gain.
- The observed sonographic findings of gastric outlet obstruction can be mistaken for hypertrophic pyloric stenosis.
Implications:
- This case highlights a rare gastrointestinal side effect of long-term PGE1 administration in neonates.
- Accurate diagnosis is crucial to differentiate PGE1-induced gastric outlet obstruction from hypertrophic pyloric stenosis, avoiding unnecessary surgical intervention.
Abstract:
Prostaglandin E1 (PGE1) is widely used in neonates with cyanotic congenital heart disease who depend on the patency of the ductus arteriosus for oxygenation. Side effects of prostaglandin therapy are common and include respiratory depression, generalized flushing, and cardiovascular and neurological effects. Little is known about the complex effects on the gastrointestinal tract. We report on an infant with gastric outlet obstruction after long-term prostaglandin administration. At the age of 1 month, feeding problems developed with projectile vomiting. Ultrasonography showed progressive elongation of the antropyloric channel without wall thickening, which was causing gastric outlet obstruction. Three days after cardiac surgery and cessation of prostaglandin therapy, the infant fed normally and rapidly gained weight. The clinical signs in such patients can mimic hypertrophic pyloric stenosis. Therefore, the sonographic findings should not be confused with pyloric wall thickening to avoid a false diagnosis and unnecessary surgery. The symptoms diminish with cessation of the prostaglandin therapy after a corrective cardiac operation.
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