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Fetal meconium peritonitis after maternal hepatitis A
McDuffie and Bader
Volume 180, Number 4 Am J Obstet Gynecol
Fetal meconium peritonitis after maternal hepatitis A Robert S. McDuffie, Jr, MD,a and Ted Bader, MDb Denver, Colorado Hepatitis A virus has rarely been implicated in congenital infections. After maternal hepatitis A at 13 weeks’ gestation, ultrasonographic examinations revealed fetal ascites (20 weeks) and meconium peritonitis (33 weeks). After delivery, a perforated distal ileum was resected. Elevated levels of hepatitis A immunoglobulin G persisted in the infant 6 months after delivery. (Am J Obstet Gynecol 1999;180:1031-2.)
Key words: Hepatitis A, intrauterine infection, meconium peritonitis, congenital malformation, pregnancy Although some viruses such as rubella cause congenital infection and malformations, most texts have not associated maternal hepatitis A with either congenital infection or malformation. We report a case of maternal hepatitis A infection in the late first trimester, after which ascites and meconium peritonitis developed in the fetus. Case report A 35-year-old Hispanic woman, para 1-0-0-1, was referred at 13 weeks of gestation with malaise, pruritus, dark urine, and scleral icterus. Laboratory evaluation revealed abnormal liver function test results and an elevated level of hepatitis A immunoglobulin M. The disease resolved over the next few weeks with conservative management. From the Departments of Obstetrics and Gynecologya and Gastroenterology,b Kaiser Permanente. Received for publication April 16, 1998; revised August 26, 1998; accepted September 15, 1998. Reprint requests: Robert S. McDuffie, Jr, MD, Kaiser Permanente, Department of Obstetrics and Gynecology, 2045 Franklin St, Denver, CO 80205. Copyright © 1999 by Mosby, Inc. 0002-9378/99 $8.00 + 0 6/1/94477
At 20 weeks of gestation, fetal ascites was noted. Amniocentesis revealed a 46,XX female karyotype, and an amniotic fluid culture for cytomegalovirus was negative. Fetal paracentesis was negative for hepatitis A by polymerase chain reaction (kindly performed by Dr Jack Stapleton, University of Iowa, Iowa City, Iowa). Abdominal calcifications were seen at 31 weeks of gestation (Fig 1). Cystic fibrosis screening was negative. By 33 weeks of gestation, there were findings consistent with meconium peritonitis, including abdominal calcifications and differential fluid levels in the ascites. At 35 weeks fetal surveillance revealed a nonreactive nonstress test and a poor biophysical profile, and labor was induced. After vaginal delivery of a 2390-g female infant with Apgar scores of 1 at 1 minute and 6 at 5 minutes, neonatal paracentesis revealed meconium. At surgical exploration, a perforation of the distal ileum was found, and bowel resection was performed. Since cord blood was not obtained to determine the level of hepatitis A immunoglobulin M, the persistence of hepatitis A immunoglobulin G in the infant was followed up. At the ages of 3 and 6 months elevated levels of hepatitis A immunoglobuliln G were found in the infant. By 1031
April 1999 Am J Obstet Gynecol
Fig 1. Transverse view of fetal abdomen demonstrating ascites and a peritoneal calcification at level of stomach.
6 months the infant weighed 14 lb 3 oz and was feeding without difficulty. Comment We believe this case demonstrates intrauterine infection with hepatitis A followed by the development of meconium peritonitis. The time course of late-firsttrimester maternal infection followed by fetal ultrasonographic abnormalities at 20 weeks of pregnancy supports
1032
this. In addition, we found serologic evidence of intrauterine infection, because hepatitis A immunoglobulin G was found at age 6 months. Catabolism of passively acquired antibody would be expected by age 3-4 months. We acknowledge that the presence of hepatitis A immunoglobulin M in cord blood would provide more compelling evidence of intrauterine infection. One other case with a nearly identical time course and presentation has been reported.1 In this case acute hepatitis A infection was documented in the mother at 20 weeks of gestation and in the fetus at 27 weeks of gestation by cordocentesis and at delivery by cord blood. Fetal ascites developed at 27 weeks and meconium peritonitis at 34 weeks. After delivery, a perforated distal ileum was resected. The similarity of findings in the 2 cases is striking. Whether the virus directly affects the bowel or induces damage through immune mechanisms is uncertain. Bowel perforation may appear early in gestation as ascites and later as meconium peritonitis. On the basis of these cases, we suggest serial ultrasonographic examinations after maternal hepatitis A for detection of fetal ascites and meconium peritonitis. A coordinated approach by obstetricians, pediatricians, and neonatal surgeons may lead to improved outcome when meconium peritonitis exists. REFERENCE
1. Leikin E, Lysikiewicz A, Garry D, Tejani N. Intrauterine transmission of hepatitis A virus. Obstet Gynecol 1996;88:690-1.
Volume 180, Number 4 Am J Obstet Gynecol
Fetal meconium peritonitis after maternal hepatitis A Robert S. McDuffie, Jr, MD,a and Ted Bader, MDb Denver, Colorado Hepatitis A virus has rarely been implicated in congenital infections. After maternal hepatitis A at 13 weeks’ gestation, ultrasonographic examinations revealed fetal ascites (20 weeks) and meconium peritonitis (33 weeks). After delivery, a perforated distal ileum was resected. Elevated levels of hepatitis A immunoglobulin G persisted in the infant 6 months after delivery. (Am J Obstet Gynecol 1999;180:1031-2.)
Key words: Hepatitis A, intrauterine infection, meconium peritonitis, congenital malformation, pregnancy Although some viruses such as rubella cause congenital infection and malformations, most texts have not associated maternal hepatitis A with either congenital infection or malformation. We report a case of maternal hepatitis A infection in the late first trimester, after which ascites and meconium peritonitis developed in the fetus. Case report A 35-year-old Hispanic woman, para 1-0-0-1, was referred at 13 weeks of gestation with malaise, pruritus, dark urine, and scleral icterus. Laboratory evaluation revealed abnormal liver function test results and an elevated level of hepatitis A immunoglobulin M. The disease resolved over the next few weeks with conservative management. From the Departments of Obstetrics and Gynecologya and Gastroenterology,b Kaiser Permanente. Received for publication April 16, 1998; revised August 26, 1998; accepted September 15, 1998. Reprint requests: Robert S. McDuffie, Jr, MD, Kaiser Permanente, Department of Obstetrics and Gynecology, 2045 Franklin St, Denver, CO 80205. Copyright © 1999 by Mosby, Inc. 0002-9378/99 $8.00 + 0 6/1/94477
At 20 weeks of gestation, fetal ascites was noted. Amniocentesis revealed a 46,XX female karyotype, and an amniotic fluid culture for cytomegalovirus was negative. Fetal paracentesis was negative for hepatitis A by polymerase chain reaction (kindly performed by Dr Jack Stapleton, University of Iowa, Iowa City, Iowa). Abdominal calcifications were seen at 31 weeks of gestation (Fig 1). Cystic fibrosis screening was negative. By 33 weeks of gestation, there were findings consistent with meconium peritonitis, including abdominal calcifications and differential fluid levels in the ascites. At 35 weeks fetal surveillance revealed a nonreactive nonstress test and a poor biophysical profile, and labor was induced. After vaginal delivery of a 2390-g female infant with Apgar scores of 1 at 1 minute and 6 at 5 minutes, neonatal paracentesis revealed meconium. At surgical exploration, a perforation of the distal ileum was found, and bowel resection was performed. Since cord blood was not obtained to determine the level of hepatitis A immunoglobulin M, the persistence of hepatitis A immunoglobulin G in the infant was followed up. At the ages of 3 and 6 months elevated levels of hepatitis A immunoglobuliln G were found in the infant. By 1031
April 1999 Am J Obstet Gynecol
Fig 1. Transverse view of fetal abdomen demonstrating ascites and a peritoneal calcification at level of stomach.
6 months the infant weighed 14 lb 3 oz and was feeding without difficulty. Comment We believe this case demonstrates intrauterine infection with hepatitis A followed by the development of meconium peritonitis. The time course of late-firsttrimester maternal infection followed by fetal ultrasonographic abnormalities at 20 weeks of pregnancy supports
1032
this. In addition, we found serologic evidence of intrauterine infection, because hepatitis A immunoglobulin G was found at age 6 months. Catabolism of passively acquired antibody would be expected by age 3-4 months. We acknowledge that the presence of hepatitis A immunoglobulin M in cord blood would provide more compelling evidence of intrauterine infection. One other case with a nearly identical time course and presentation has been reported.1 In this case acute hepatitis A infection was documented in the mother at 20 weeks of gestation and in the fetus at 27 weeks of gestation by cordocentesis and at delivery by cord blood. Fetal ascites developed at 27 weeks and meconium peritonitis at 34 weeks. After delivery, a perforated distal ileum was resected. The similarity of findings in the 2 cases is striking. Whether the virus directly affects the bowel or induces damage through immune mechanisms is uncertain. Bowel perforation may appear early in gestation as ascites and later as meconium peritonitis. On the basis of these cases, we suggest serial ultrasonographic examinations after maternal hepatitis A for detection of fetal ascites and meconium peritonitis. A coordinated approach by obstetricians, pediatricians, and neonatal surgeons may lead to improved outcome when meconium peritonitis exists. REFERENCE
1. Leikin E, Lysikiewicz A, Garry D, Tejani N. Intrauterine transmission of hepatitis A virus. Obstet Gynecol 1996;88:690-1.