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Meconium Peritonitis

Maria Moes, M.D.

Calcifications are seen throughout the abdomen in this 17 week fetus with meconium peritonitis
Meconium peritonitis in a fetus of 23 weeks gestational age. Numerous calcifications (arrows) are seen adjacent to the liver and anterior abdominal wall

Meconium peritonitis in a fetus at 29 weeks gestation. Dilatation of the small bowel and dense calcification is seen within the abdomen

Findings:

Punctate and linear calcifications are seen throughout the abdomen in this second trimester pregnancy.

Discussion:

Meconium peritonitis (MP) should be considered as a diagnostic possibility when hyperechogenic areas are seen within the fetal abdomen during the second and third trimesters of pregnancy. Neonatal studies suggest a prevalence of 1 in 35,000 live births. The etiology of MP is thought to be the result of a sterile chemical reaction resulting from bowel perforation in utero. A secondary inflammatory response results in the production of fluid (ascites), fibrosis, calcification and sometimes cyst formation. The end result of the process varies leading to four descriptive categories of meconium peritonitis: fibroadhesive, cystic, generalized and healed. Eighty-six percent of fetuses with meconium peritonitis have intra-abdominal calcifications. Experimental research in animals indicates that it takes at least 8 days after meconium has escaped into the peritoneal cavity before calcifications are detected. The most common causes of meconium peritonitis are ischemic lesions of the small bowel associated with mechanical obstruction (atresia, volvulus, intussusception, congenital bands, Meckel diverticulum and internal hernia). These likely account for 50% of the cases of meconium peritonitis. Meconium peritonitis may also be caused by viral infections (cytomegalovirus, or parvovirus B19). Meconium ileus accounts for less than 25% of cases of meconium peritonitis.


The sonographic findings vary depending on several factors: the etiology, the time interval since perforation and the degree of inflammatory response. It may be seen as early as 13 weeks gestation. In the typical case, diffuse hyperechoic punctate echoes with or without acoustic shadowing may be seen in the abdominal cavity, on the hepatic surface and in the scrotal sac. In addition, depending upon the etiology, ascites, polyhydramnios or fetal bowel distention may be present. Polyhydramnios, reported in approximately 50% of patients, may be caused by by peristaltic deficiency associated with decreased swallowing activity. If the inflammatory response remains localized a meconium pseudocyst may occur. This appears sonographically as a cystic heterogeneous mass with an irregular, calcified wall.
The prognosis depends upon the etiology. Bowel perforations may heal and the ascites and bowel dilatation may resolve, leaving only peritoneal calcifications as the only sonographic sign of meconium peritonitis. While cystic fibrosis is universally seen in cases of meconium ileus, it is seen in only 7-40% of cases of meconium peritonitis.

Meconium pseudocyst (arrow) in a second trimester fetus with meconium peritonitis.


In the absence of an intra-abdominal mass such as a meconium pseudocyst, the major differential diagnostic possibilities for bright echoes within the abdomen is “hyperechogenic bowel”. In this condition, the bowel appears as bright as bone. This is often normal, particularly in the third trimester, but has been described to be associated with cystic fibrosis and chromosomal abnormalities. It should be remembered that the use of high frequency transducers will cause the fetal bowel wall to be hyperechogenic and simulate this appearance.

References:

Hill LM Ultrasound of the fetal gastrointestinal tract. In: Ultrasonography in Obstetrics and Gynecology. Ed. Peter W. Callen, 4th Ed. W. B Saunders and Co., Philadelphia, 2000

Scioscia AL, Pretorius DH, Budorick NE et al. Second-trimester echogenic bowel and chromosomal abnormalities. Am J Obstet Gynecol 167:889-894, 1992

Park RW, Grand RJ. Gastrointestinal manifestation of cystic fibrosis: A review. Gastroenterology 1981;81:1143-1161.

Payne RM, Nielsen AM. Meconium peritonitis. Am Surg 1983;28:224-231.

Finkel LI, Slovis SL. Meconium peritonitis, intraperitoneal calcifications and cystic fibrosis. Pediatr Radiol 1982;12:92-93.

Rypens FE, Avni EF, Ababsena MM, Donner C et al. Areas of increased echogenicity in the fetal abdomen: Diagnosis and significance Radiographics 15:1329-1344, 1995

Ohmichi M, Kanai H, Kanzaki T et al. Meconium peritonitis: Changes in Fetal C-reactive protein and CA 125 levels in relation to stage of disease. J Ultrasound Med 16:289-292, 1997

Williams J, Nathan RO, Worthen JNJ. Sonographic demonstration of the progression of meconium peritonitis. Obstet Gynecol 64:822, 1984

Foster MA, Nyberg DA, Mahony BS, Mack LA et al. Meconium peritonitis: Prenatal sonographic findings and their clinical significance. Radiology 165:661-665, 1987

Dirkes K, Crombleholme TM, Craigo SD, Latchaw LA, Jacir NN, Harris BH, D’Alton ME. The natural history of meconium peritonitis diagnosed in-utero. J Pediat Surg 1995;30:979-982.

Pan EY, Chen LY, Zang JZ, Wang ZZ. Radiographic diagnosis of meconium peritonitis. A report of 200 cases including six fetal cases. Pediatr Radiol 1983; 13:199-205.

Patole S, Whitehall J, Almonte R, Stalewski H, Lee-Tannock A, Murphy A. Meconium thorax: A case report and review of the literature. Am J Perinatol 1998;15:53-56.

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Peter W. Callen, M.D.
Professor of Radiology, Obstetrics, Gynecology and Reproductive Science
University of California Medical Center, San Francisco, California