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Calcifications are seen throughout the abdomen in this
17 week fetus with meconium peritonitis
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Meconium peritonitis in a fetus
of 23 weeks gestational age. Numerous calcifications (arrows) are seen
adjacent to the liver and anterior abdominal wall
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Meconium peritonitis in a fetus at 29 weeks gestation. Dilatation of the small bowel and dense calcification is seen within the abdomen |
Punctate and linear calcifications are seen throughout the abdomen in this second trimester pregnancy.
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.
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Meconium pseudocyst (arrow) in a second trimester
fetus with meconium peritonitis.
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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.
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