Severe abdominal distention at birth is usually a serious life-threatening condition. When diagnosed in the uterine cavity before delivery the problem of soft-tissue dystocia arises (8). The etiology of an enlarged fetal abdomen in the third trimester of gestational development is usually one of the following conditions: enterogenous tumor, teratoma, polycystic kidney, neuroblastoma, Wilms's tumor, polycystic disease or large neoplasm of the liver, hydrometrocolpos, ovarian tumor, generalized edema from hemolytic disease or maternal diabetes, absence of abdominal muscles, massive hydronephrosis, or ascites (7). Ascites is the rarest etiology of a distended abdomen in the neonatal period. It is interesting to note that approximately 200 ml of fluid must be present in the peritoneal cavity before ascites becomes evident clinically. As early as 1894 Fordyce (2) published a review of fetal and neonatal ascites. Among 63 cases he collected from the literature, 17 had urinary tract abnormalities accompanied by ascites. The majority of the other cases were the result of intrauterine infectious peritonitis. Lord (5) reviewed the literature from 1903 to 1952 and found that during this period 28 additional cases of ascites were recorded, 18 of which had associated urinary outlet obstruction. The following groups of underlying abnormalities have been implicated in the pathogenesis of ascites in the neonatal period: 1. Ascites secondary to hemolytic disease 2. Peritonitis from generalized sepsis (syphilis), perforation of a hollow viscus from atresia, meconium peritonitis or other congenital abnormalities, peritonitis following ruptured ovarian cyst 3. Chylous ascites-thoracic duct obstruction 4. Portohepatic abnormalities resulting in obstruction to the venous flow, such as congenital cirrhosis of the liver, cystic disease of the liver, hypoplasia, or thrombosis of the portal vein 5. Congenital anomalies resulting in obstruction at the urinary outlet (urine ascites). The most widely accepted hypothesis of the origin of the ascitic fluid in the last group of patients has been transudation of urine from the urinary tract into the peritoneal cavity. Evidence to support this assumption has been gained by the intravenous injection of phenolsulfonphthalein (P.S.P.) and indigo carmine dyes or radioactive 131I hippuric acid (5). Following the injection, simultaneous measurements in the urine and ascitic fluid have demonstrated in some cases a rapid appearance of such tracers in the ascitic fluid. Since no direct communication from the urinary tract to the peritoneal cavity has been shown to be present, it has always been assumed that the presence of these substances in the ascitic fluid is consistent with transudation of the urine from the urinary tract. In several reported cases an open communication from the bladder to the peritoneal cavity has been proposed (1).
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