Abstract

Sir, We report a case of prenatally diagnosed congenital diaphragmatic hernia (CDH) presenting with massive ascites and pleural effusion caused by intrauterine perforation of an incarcerated stomach through a small diaphragmatic defect. A 25-year-old woman, gravida 0, para 0, underwent a prenatal US scan at 31 weeks of gestational age (GA). Left-side CDH was detected in the fetus. Pleural effusion and polyhydramnios were observed at 32 weeks’ GA. Aspiration of the fetal pleural effusion revealed that it contained numerous squamous cells and neutrophils, indicating the presence of gastrointestinal perforation. Fetal MRI at 34 weeks’ GA demonstrated herniation of the stomach and intestine through a small defect in the diaphragm, as well as massive ascites and pleural effusion (Fig. 1). The liver was not herniated. The ascites and pleural effusion had the same intensity as the gastric contents and the amniotic fluid, but not as the meconium. These findings strongly suggested gastric perforation due to incarceration, resulting in massive pleural effusion and ascites, rather than intestinal perforation resulting in meconium peritonitis or pleuritis. At 35 weeks’ GA, the fetus showed hydrops with marked polyhydramnios. The female baby was subsequently delivered by Caesarian section at 36 weeks’ GA with a birth weight of 3,246 g. The baby was intubated immediately and highfrequency oscillatory ventilation and nitric oxide therapy were initiated. Radiographs showed marked generalised oedema, mediastinal shift to the right and gastric air in the left thoracic cavity. No intestinal gas or calcification was seen. Respiratory parameters improved soon after left thoracic drainage of 450 ml non-bilious pleural effusion, which also contained hair. The baby underwent CDH repair at 1 day of age. The poorly perfused stomach and small intestines were herniated through a slit-like diaphragmatic defect of 1.5 cm in length. After reduction of the hernia, a pinhole perforation was found in the stomach just proximal to the pylorus and repaired by direct closure. The stomach and intestines were viable. The small diaphragmatic defect was closed primarily. The baby recovered promptly from respiratory failure as well as from pleuritis and peritonitis. There have been only a few case reports of neonatal CDH presenting with gastric [1, 2] or intestinal [3–5] perforation. Most cases were discovered after birth as pneumothorax, meconium thorax or meconium peritonitis [2–5]. In our case, fetal MRI and aspiration of the pleural effusion were greatly helpful in prenatal diagnosis. There was one similar case of CDH presenting with gastrointestinal perforation with massive ascites and pleural effusion, which was observed on prenatal US [1]. Our case highlights the importance of fetal MRI in the diagnosis of intrauterine gastric perforation in CDH; MRI was greatly informative, demonstrating incarceration of the stomach and intestine through a small defect clearly as well H. Komuro : C. Gotoh Department of Pediatric Surgery, Faculty of Medicine, University of Tsukuba, Tsukuba, Ibaraki 305-8575, Japan

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