Meconium Peritonitis

Fetal meconium peritonitis (MP) is a sterile chemical peritonitis resulting from extrusion of bowel content into the abdominal cavity through a bowel perforation. The perforation may represent a common end result of various bowel pathologies (i.e. complex MP), or an isolated event (i.e. simple MP).

Meconium peritonitis is a rare entity. The reported incidence is 1 in 30,000 live births (1).

P78.0-Perinatal intestinal perforation

Meconium peritonitis may result from various obstructive pathologies including: bowel atresia (1–6), meconium ileus (3,7), intestinal volvulus (1,2,8), internal hernia (9), Hirschsprung’s disease, enteric duplication, Meckel’s diverticulum (2), perforated appendix (10), intrauterine intussusception (11) cloacal anomaly (12,13) and fallopian tube torsion (14). Meconium peritonitis may also occur in fetuses with cystic fibrosis (CF) as a result of viscous meconium resulting in meconium ileus and subsequently perforation (15).

Meconium peritonitis has also been described in fetal cytomegalovirus (CMV) (16) and parvovirus B19 (17,18) infections. Rubella infection has also been suggested as the reason for MP in one case series (19) but this was not confirmed by a recent review of the literature of congenital rubella syndrome (20).  

An underlying etiology for MP cannot be detected in about 50% of cases (1,21,22). Vascular insufficiency and decreased mesenteric blood flow has been suggested as a causative mechanism in these cases (21). In-utero cocaine exposure has been associated with MP due to vascular disruption (23).  

Sterile meconium within the peritoneal cavity results in a dose-dependent pro-inflammatory response by peritoneal macrophages with increased macrophage TNF-α production and procoagulant activity (24). An exudative process contributes to the development of ascites (25). Fibrous adhesions are then formed to in an attempt to encapsulate the perforated bowel. When these focal events sufficiently seal the perforation, the intestinal mucosa is restored. If not, the lesion is confined by a thick walled pseudocyst (26,27). Eventually, foreign body granulomas and calcifications appear within the fibrous reaction (16,25,28). Interleukin 6 and interleukin 8  have been found to play a role in the inflammatory response associated with MP (29).  

This cascade of events may lead to one of three forms of meconium peritonitis; fibro-adhesive, cystic or generalized (26,27).

In contrast to simple MP, which occurs with no additional anomalies, complex MP is the end result of various obstructive bowel pathologies (see Pathogenesis and Etiology section), and each should be considered the primary anomaly, and managed accordingly. 

The following entities may be associated with MP:   

• Cystic fibrosis (CF) causes meconium ileus (MI). It can initially present as echogenic bowel that may evolve into MP. MI, however, is not pathognomonic for CF. Fetuses with isolated echogenic bowel have around 7% rate of CF (30). In newborns with perforated MI the rate of CF is 39% (7), and the rate of perforated MI among CF positive newborns is 40%-50% (31–33).
• Feng et al. found an increased incidence of intrahepatic cholestasis of pregnancy (ICP) among pregnant patients whose fetuses had MP (38.7%). In that study, lower rates of ICP were observed among mothers whose newborns who required surgical treatment compared to the non-surgical group (34). 
• An association between severe maternal liver disease during pregnancy and fetal MP was described in a small number of case reports (35–39). 
• Biliary atresia: In the neonatal literature, 2-3% of newborns with biliary atresia have been found to have MP. It has been suggested that an inflammatory reaction and secondary fibrosis of the extrahepatic biliary system are the pathogenic mechanisms (40). This suggests that some cases of biliary atresia are not an early developmental malformation, but late sequelae of MP (41).    

Meconium peritonitis appears as disseminated intra-abdominal calcifications (IAC) anywhere within the peritoneal cavity. This includes; the abdominal wall, liver and spleen surfaces, sub-phrenic space, paracolic gutters, and scrotum (1,42–45). Thoracic calcifications have been described in a case of asymptomatic diaphragmatic hernia (46,47). The gestational week at initial diagnosis varies widely from 15 weeks to term (2,22,48,49). 

When IAC are isolated, and no additional findings suggestive of bowel or extra-abdominal anomalies appear throughout pregnancy, the diagnosis is termed simple meconium peritonitis (42).    

The term complex meconium peritonitis is used when typical additional findings are present (30). These include cystic meconium peritonitis (CMP), meconium pseudocysts (MPC), ascites, dilated bowel loops, echogenic bowel, polyhydramnios and fetal hydrops.

Cystic meconium peritonitis (CMP)  results from a local inflammatory response aimed to confine the leakage (1,42). On ultrasound abdominal cysts containing thick fibrous walls covered by calcium plaques are seen. They may have irregular contours. CMP's have been described with either small bowel or colon perforations, and may be identified in both the second and third trimesters (3). Acording to a few pediatric case reports (31,32), a meconium pseudocyst is a distinct surgical entity with a typical "eggshell calcifications" appearence on abdominal US and X-ray, and a luminal continity with the proximal bowel. On histologic examination, The pseudocyst wall has a muscle layer continuous with the intestine (31). From the prenatal US point of view, this distinction is not readily feasable, nor it will change prenatal counseling (See VISUOG chapter on Meconium Pseudocysts).

Fetal ascites develops when the focal inflamatory reaction is not sufficient to wall-off the leakage. Since calcifications evolve over time, late-appearing ascites may be the only fetal finding in cases diagnosed postnatally to have isolated calcifications on X-ray or CT scans (50) or in newborns eventually diagnosed with colonic atresia (5). If ascites lasts long enough in the fetus, MPC's and or IAC'S appear. On the contrary, ascites may resolve spontaneously over time (22,51). In a series of 51 fetuses with isolated ascites, 17.6% was due to MP, and was significantly more common among fetuses in which ascites appeared after 24 gestational weeks (32% vs. 4%) (52). Achiron et al. described a case in which fetal ascites was diagnosed at 12 weeks, and two weeks later evolved into scattered IAC's and intra-hepatic hyperechogenic foci (53). Fetal anemia may occur from hemorrhagic ascites (54).

The combination of scattered abdominal calcifications, ascites and abdominal cysts with an echogenic lining are highly suggestive of cystic meconium peritonitis.

Bowel loop dilation represents bowel obstruction and can have different appearances at different sites:

Bowel atresia may be isolated or involve multiple sites. In more proximal jejunal obstruction, fewer loops will become dilated compared with more distal ones (55). Also, the more proximal the obstruction, the less complex is the bowel content (simple fluid- in proximal / echogenic content with debris- in distal) (56). Polyhydramnios may also be present in proximal lesions. (See VISUOG chapter on Jejunal-Ileal atresia.)

Duodenal atresia has traditionally diagnosed when the "Double bubble sign" is present. Perforation of the dilated segment leads to complex MP. This scenario may occur as late as the third trimester in cases with a normal mid-trimester US scan (6).  (See VISUOG chapter on Duodenal Atresia)

Fetal volvulus is a potentially life-threatening emergency in which the bowel loops are twisted around the mesenteric artery, resulting in mechanical bowel obstruction and ischemia, which may lead to bowel necrosis (54). The "whirlpool" or "coffee bean" signs are highly suggestive of intestinal volvulus (57) but have been reported in fewer than half of cases (58). Rarely, fetal volvulus may result from perforated atretic bowel distal to the twisting site without ascites or MPC formation (22).

Secondary mechanical bowel obstruction may also occour secondary to adhesions formation as part of the initial inflamatory responce to the leaked meconium.

Although polyhydramnios is frequently associated with bowel obstruction, it is more commonly seen in proximal bowel obstructions, and absent in cases of distal obstruction. Polyhydramnios was found only in half of MP fetuses in a small series of 17 cases (22). 

The added value of MRI has not been extensively studied. Typically, meconium appears distinctly bright on T1-weighted MR images, and it is first identifiable at around 18 weeks in the small bowel and colon (55,56). In jejunal atresia, bowel content produced in the ileum can continue to migrate to the colon, which remains normal in size. In distal ileal atresia, no bowel content migrates to the colon, resulting in a micro-colorectum appearance (45,59). Meconium ascites has a high signal intensity on T1 weighted MRI and low signal intensity on T2 weighted MRI (45). In addition, MPC's have been described on MRI as loculated collections with intense signal on T2 weighted MRI (59).    

The differential diagnosis for MP varies according to presenting US findings and the underlying pathology.

Intra-hepatic calcifications should be differentiated from peritoneal ones scattered on the liver surface in MP. Isolated Intra-hepatic foci usually carry good prognosis (33), and serial scans usually show stability or regression of the findings (34,35). Localized vascular event may be the cause of these findings (36). Hepatic hemangioma should also be considered in these cases (37). (See VISUOG chapter on Intra-hepatic calcifications).

Fetal cholelithiasis may also appear as either hyperechogenic intrahepatic findings or mildlly echogenic sludge filling the gallbladder (38). (See VISUOG chapter on Fetal Cholelithiasis).

Scattered calcifications should be differentiated from an echogenic mass suggesting an abdominal tumor such as hepatoblastoma or mesenteric cystic lymphangioma (37,39,40).

Fetal echogenic bowel is a brighter then normal appearence of the bowel wall, and should be distinguished from scattered echogenic spots. Of note, echogenic bowel may represent an early stage of a GI pathology (such as meconium ileus) that may later progress MP. (See VISUOG chapter on Echogenic Bowel).

Abdominal cysts may originate from various anatomic origins, including; gastrointestinal, ovarian, mesenteric, biliary, urogenital tracts, adrenal, splenic and hepatic (41,42). Efforts should be made to characterize the anatomic location, sonographic chrecteristics, additional findings and evolution of the findings. (See VISUOG chapters on Abdominal Cysts).

Fetal cholelithiasis may also appear as either hyperechogenic intrahepatic finding or mildly echogenic sludge filling the gallbladder (38). (See VISUOG chapter on Fetal Cholelithiasis.)

Scattered calcifications should be differentiated from an echogenic mass suggesting an abdominal tumor such as hepatoblastoma or mesenteric cystic lymphangioma (37,39,40).

Ultrasound findings in MP may evolve during pregnancy, and some findings may appear only late (6). In addition, initial findings suggestive of a perforation may also resolve over time. In a small series by Saleh et al. (n=14), the initial US findings of complex MP subsequently disappeared during gestation and the outcome was normal in five fetuses (43).

Follow up scans, including also measurements of the peak systolic velocity in the middle cerebral artery (PSV-MCA), are important to exclude anemia from hemorrhagic ascites (44).

In Simple MP, the postnatal outcome is uneventful and surgical intervention is not required (30,45). These cases represent a self-sealed leakage (30) in an otherwise normal GI tract. Postnatally, these children may have scattered abdominal calcifications (IAC) on X-ray without symptoms of GI obstruction (1). 

Complex MP is less benign. Zangheri et al. found that when IAC were associated with either ascites, cystic meconium peritonitis or bowel dilation, surgical intervention was required in 52% of newborns. When two of the above findings were additionally present, surgical intervention was needed in 80% of newborns, and when all three US features were present, 100% of neonates required surgery (45). Shyu et al. found that persistent ascites, pseudocyst or dilated bowel loops are most sensitive (92%) to predict postnatal surgery (22). Feng et al. found 61% of neonates needed surgery in a series of MP, and the predictors of surgical treatment were polyhydramnios, persistent ascites and maternal ICP (46).

In the past, reported mortality rates in neonatal meconium ileus were approximately 60% (47). Newer publications report mortality rates that range from around 6% (2,45,48) to 20% (3,44). Findings such as fetal hydrops and an elevated diaphragm raise the risk for poor prognosis (44).

Feng et al. found that early gestational age at birth, persistence of peritoneal fluid and polyhydramnios were independently associated with neonatal death or severe neonatal complications either poor outcome (46)

Accurate prenatal diagnosis and serial US scans enables prompt early postnatal intervention that may improve neonatal outcome.  

When diagnosing simple MP, the work-up should focus on genetic tests to rule out CF and test for an infective etiology. Although CMV and parvovirus B19 are the most common viruses described in the literature, it is a common practice to perform the TORCH work-up (Toxoplasmosis, Other (syphilis, parvovirus B19), Rubella, Cytomegalovirus, and Herpes).

Follow up US exams should be performed to rule out late-appearing findings. When subsequent scans are normal (as expected in most cases), parents should be reassured, since the vast majority of newborns have no clinical sequelae.

Complex MP requires more detailed management. In addition to CF and an infective etiology, the underlying bowel anomaly becomes the primary concern and should dictate the management. For example, fetal volvulus, which usually has non-specific US findings (58), can become a life-threatening condition due to significant bowel necrosis leading to MP (1). Such cases should be managed at a tertiary center, by a multidisciplinary team including a perinatologist, neonataologist and a pediatric surgeon. Parental counseling and decision making should take into consideration also the gestational age at diagnosis and local laws of pregnancy termination.

A detailed anatomic survey including echocardiography should be performed, since bowel anomalies may be part of a wide range of conditions, such as trisomy 21 with duodenal atresia (37) or heterotaxy syndromes with bowel malrotation and atresia (49,50). Diagnosing such conditions may considerably influence counseling, and make the MP merely a sonographic sign of a more significant underlying problem.

Parents should be offered genetic counseling and consider amniocentesis for karyotype/ microarray and viral PCR. The option of more extensive genetic testing, including cystic fibrosis testing or screening should be discussed with the parents in specific cases.

Some have suggested that cases with severe fetal ascites may benefit from aspiration of the ascites, but this therapy should be considered experimental. Theoretical benefits of aspiration may include: decreasing the inflammatory response, improving mesenteric blood flow, and preventing long-term fetal lung compression (22). Shyu et al. reported a series of 17 fetuses with MP, of which four fetuses underwent at least one US guided MP aspiration. The outcome was favorable in two, but the remaining two died after delivery (22).  Elevated total bilirubin levels in the aspirates confirm the diagnosis of MP. In a single case report, intra-abdominal administration of urinary trypsin inhibitor (UTI) to a fetus with severe meconium ascites and polyhydramnios, was able to ameliorate the ascites and abdominal distention, probably by controlling the meconium induced inflammation (51). This procedure should be considered experimental.

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