P*, Tiwari N**, Goel A***, Chauhan AR****.
First Year Resident, **Assistant Professor, *** Second Year resident
**** Additional Professor. Department of Obstetrics and Gynecology,
Seth G S Medical College and KEM Hospital, Mumbai, India.)
peritonitis is a nonbacterial, chemical inflammation of the
peritoneum caused by escape of meconium into the peritoneal cavity,
either in fetal life, at the time of delivery, or very shortly after
delivery. This escape of meconium is due to a breach somewhere in the
intestine and may be associated with bowel obstruction due to
imperforate lumen, congenital bands, or other anomalies. We report a
case of antenatally diagnosed meconium peritonitis without
obstruction, with no definite etiology found, which resolved
spontaneously; the neonate remained asymptomatic in the postnatal
peritonitis, a noninfectious
chemical peritonitis due to perforation of small intestine and
leakage of meconium into the fetal peritoneal cavity,[1,2]
seen in about 1 in 35,000 live births in the USA.
Its prevalence in the Indian scenario is unknown. Earlier
such cases were incidentally diagnosed during X- ray pelvimetry for
suspected fetal macrosomia and congenital malformations.
peritonitis may occur without any underlying cause, or the cause may
be innocuous and intervention may not be required. The common bowel
disorders leading to meconium peritonitis in utero are those
resulting in bowel perforation due to obstruction and ischemia such
as small bowel atresia, congenital bands, volvulus and meconium
ileus, of which intestinal
atresia appears to be the most common cause.
fibrosis may be a possible etiological factor in 7.7 – 40 % of
should be counseled regarding this possibility and ideally
such newborns must be screened.
23 year old primigravida, married for 1 year, presented to us with 5
months’ amenorrhea and vomiting. Routine antenatal investigations
were normal, blood group was O positive; liver function test (SGOT
and SGPT) were elevated. Ultrasonography (USG)
showed a single live fetus of 23 weeks’ gestational age and
an anterior placenta. There was evidence of moderate fetal ascites
with septations and echogenic foci (calcifications) over intestinal
loops. There were no cerebral or hepatic calcifications. A diagnosis
of meconium peritonitis was made and the
were counseled about possible need of operative intervention in
postnatal period. In light of these findings, TORCH titers
were done which were negative. Pregnancy was supervised and serial
done in the late second and third trimester showed persistence of the
multiple calcified foci over the intestinal loops with ascites
as seen in the first scan. Calcific densities also developed over
liver and stomach. Bowel loops were not dilated. Fetal kidney,
bladder and heart were normal. No obvious perforation was identified.
was induced at 37 weeks’ gestation. She delivered a female child of
with normal Apgar score. The
admitted in neonatal intensive
for observation. The
abdomen was soft and she passed meconium spontaneously within a
few hours of birth. She was given breastfeed, which was well
tolerated. USG of the neonatal abdomen revealed a normal scan.
of the abdomen confirmed intra-abdominal calcification consistent
with meconium peritonitis. The
was also evaluated for the possibility of cystic fibrosis;
immunoreactive trypsinogen test was found to be negative. The mother
and the baby were discharged on day 14 after delivery and the
asymptomatic at 6 weeks postpartum.
showing calcification of meconium peritonitis.
peritonitis is a sterile chemical peritonitis in which an intense
inflammation results in calcification along the surface of bowel or
peritoneum. Diagnosis of meconium peritonitis is rare before 20
weeks’ because peristalsis rarely commences before this time.
Prenatal sonographic diagnosis of meconium peritonitis is extremely
useful in postnatal management plan. Bilateral hydroceles, swollen
vulvae, fetal ascites,
polyhydramnios, intra-abdominal mass, bowel dilatation, snow storm
appearance, highly echogenic linear or clumped foci which represent
calcification may be seen. Fetal ascites tends to be echogenic.
Therefore, such USG
findings should be an indication for invasive procedures for fetal
blood testing and parental testing for cystic fibrosis.
peritonitis is associated with a 20-30% incidence of prematurity and
a 10-20% incidence of polyhydramnios. Pregnancy should be allowed to
continue till term depending upon fetal growth and progression of any
associated complication. Rarely, dystocia secondary to massive
or abdominal distension with meconium has been reported, for which
cesarean section may be required. With
the advent of prenatal diagnosis the outcome for this condition has
improved, with survival rates up to 90%.[6,7]
is high in cases where perforation persists postnatally.
shows that when only calcifications are present, the outcome is
favorable. Once an antenatal diagnosis of complicated meconium
peritonitis is reached, the mother should be referred to a tertiary
for delivery where close monitoring and facilities for urgent
perinatal intervention are available if needed.[8,9]
The pediatrician should be vigilant to look for early signs of bowel
obstruction in the neonate.
of the important factors for improving outcome in such cases is
anticipatory recognition of complications. Early recognition and
treatment of acid base imbalance, superimposed bacterial peritonitis,
and septic shock can prevent death. The timing of delivery should
therefore be discussed with pediatrician and pediatric surgeon.
Surgery performed within 24 hours in newborns with bowel obstruction
may also improve their outcome. However, asymptomatic infants may
develop bowel obstruction secondary to adhesions later in childhood
which may need an urgent surgical intervention.
conclusion, the infant in our case was asymptomatic and had an
uneventful postnatal period. Probably the site of perforation got
sealed spontaneously without any sequele, indicating a self- limiting
process. Such favorable outcome has been described by some
Jain P, Tiwari N, Goel A, Chauhan AR. Spontaneous Resolution Of Meconium Peritonitis.
Y, Sato Y, Kakui K, Tatsumi K, Fujiwara H, Konishi I. Prenatal
treatment of meconium peritonitis with urinary trypsin
Obstet Gynecol 2011;
G, Guarino A, Terrin G, et al. Neonatal
onset intestinal failure: an Italian multicenter study. J
Pediatr 2008; 153:
MA, Nyberg D, Mahony B, et al. Meconium peritonitis: prenatal
sonographic findings and their clinical
significance. Radiology 1987;
SH, Kima SC, Kima DY. Experience with meconium peritonitis. J
Pediatr Surg 2007;
E, Rodriguez D, Vela A, Cabre S, Lailla JM. Meconium pseudocyst
secondary to ileum volvulus perforation without peritoneal
calcification: a case report. Journal
C, Changa S, Chaoa A, Wanga T, Tsenga L, Changa Y. Meconium
Peritonitis In Utero—the Value of Prenatal Diagnosis in
Determining Neonatal Outcome. Taiwanese Journal of Obstetrics and
H, Urushihara N, Fukumoto K, Sugiyama A, Fukuzawa H, Watanabe K, et
Primary anastomosis for meconium peritonitis: first choice of
Pediatr Surg 2011;
G, Codrich D, Zennaro F, Dell'oste C, Maso G, D'Ottavio G, Schleef
J. Prenatal detection of the cystic form of meconium peritonitis: no
issues for delayed postnatal surgery. Pediatr Surg Int. 2008
S, Mayer C, Skarsgard ED.
Can we select fetuses with intra-abdominal calcification for
delivery in neonatal surgical centres? J
Pediatr Surg 2013;48(5):946-50.
S, Mizrahi S, Sujov P. Meconium peritonitis, a benign course in a
premature infant. Am J Perinatol 1990;7:31-2.
P, Dabral A, Arora R, Minocha B. Meconium Peritonitis – Two case
reports. J Obstet Gynaecol
India 2009; 59 (5): 475-476.
JPGO 2015. Volume 2 No.6. Available from: http://www.jpgo.org/2015/06/spontaneous-resolution-of-meconium.html