A case ofintrauterine gastric perforation in congenital diaphragmatic hernia.
A case ofintrauterine gastric perforation in congenital diaphragmatic hernia.
复制标题
先天性膈疝并发宫内胃穿孔1例。
DOI：
10.1007/s00247-012-2435-x
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发表时间：
2012
影响因子：
2.3
通讯作者：
Gotoh C
中科院分区：
文献类型：
--
作者：
Komuro H;Gotoh C
先生，我们报告一例产前诊断的先天性隔膜疝气(CDH)，表现为大量腹水和胸腔积液，其原因是宫内穿孔嵌顿的胃经小的横隔膜缺损处。一名25岁的女性，妊娠0，第0段，在妊娠31周时接受了产前超声扫描。胎儿左侧CDH阳性。胎龄32周时观察胸腔积液和羊水过多。胎儿胸腔积液抽吸发现含有大量鳞状细胞和中性粒细胞，表明存在胃肠道穿孔。胎龄34周的胎儿核磁共振显示，横隔膜上有一个小的缺陷，胃肠突出，并有大量的腹水和胸腔积液(图1)。肝脏没有突出。腹水和胸腔积液的密度与胃内容物和羊水的密度相同，但与胎粪的密度不同。这些发现强烈提示胃穿孔是由于嵌顿引起的，导致大量胸腔积液和腹水，而不是肠穿孔导致胎粪腹膜炎或胸膜炎。胎龄35周时，胎儿出现积水，羊水过多。女婴于胎龄36周剖宫产，出生体重3246 g，立即插管，开始高频振荡呼吸机及一氧化氮治疗。X线片显示明显的全身性水肿，纵隔向右移位，左侧胸腔有胃气。未见肠道气体或钙化。左胸引流450毫升非胆源性胸腔积液后呼吸参数很快改善，其中也含有毛发。婴儿出生后1天接受CDH修补术。胃和小肠的低血流通过1.5厘米长的裂隙状横隔膜缺损处突出。疝修复术后，在幽门近端的胃部发现一个针孔穿孔，直接缝合修补。胃和肠道都是活的。小的横隔膜缺损均一期闭合。婴儿很快从呼吸衰竭、胸膜炎和腹膜炎中恢复过来。仅有几例新生儿CDH表现为胃[1，2]或肠[3-5]穿孔。大多数病例在出生后被发现为气胸、胎粪胸或胎粪腹膜炎[2-5]。在我们的病例中，胎儿MRI和胸腔积液抽吸对产前诊断有很大帮助。有一例类似的CDH表现为胃肠道穿孔伴大量腹水和胸腔积液，这是产前超声观察到的[1]。我们的病例强调了胎儿mri在诊断cdh宫内胃穿孔中的重要性；mri提供了大量的信息，也清楚地显示了胃和肠通过一个小的缺陷嵌顿。
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