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Case Reports
 
Foetal Meconium Peritonitis : Early Diagnosis, Improved Outcome
Shilpa S Abhyankar*, YS Nandanwar**, Umesh Athavale***
 
Foetal meconium peritonitis is a rare condition in which foetal meconium escapes into peritoneal cavity through a perforation of the gut leading to inflammation. The bacterial colonisation starts after birth and hence an early diagnosis is seen as a decisive factor for prognosis of the neonates. The mortality rate is 50% in cases about diagnosed at birth. We report a case of foetal meconium peritonitis diagnosed antenataly and successfully treated with surgical intervention.
 
Introduction

Foetal meconium peritonitis is uncommon with an incidence of 1 in 35,000 live births.1 In foetal meconium peritonitis, the meconium escapes into peritoneal cavity through a perforation of the gut causing inflammatory reaction.
 
Case Report
A 26 year old, Mrs VP, primigravida presented with polyhydramnios at term. Fundal height was more than the weeks of gestation. Foetal parts were not felt and foetal heart sounds were faintly audible. Her complete blood count, glucose tolerance test and other routine investigations were normal. In view of polyhydramnios, a level II malformation scan was advised. Ultrasonography done showed foetal ascites with peritoneal calcifications, echogenic bowel and distended stomach suggestive of meconium peritonitis and polyhydramnios (Figs. 1 and 2). There were no other non-gastrointestinal anomalies noted. Paediatric surgery opinion was taken and the couple was explained the guarded prognosis. No perinatal intervention was done and patient delivered at 36 weeks. Patient went into spontaneous labour at 36 weeks. A controlled artificial rupture of membranes revealed 2 litres of amniotic fluid. Labour was augmented with oxytocics. Patient delivered a 3 kilogram female child with apgar of 9/10. At birth the child had abdominal distension and baby was transferred to the Paediatric surgical unit immediately. Meconium peritonitis with ileal perforation was confirmed on exploratory laparotomy. An ileal colostomy was performed. The baby recovered well with closure of ileal colostomy at 4 months. Long term follow up of the child showed normal milestones.
Fig. 1 : Ascites and echogenic bowel seen.
 
Discussion
Meconium peritonitis was first reported by Morgagni in 1761. Foetal meconium peritonitis is a sterile chemical inflammatory process due to escape of meconium into the peritoneal cavity via a gut perforation. Many intrauterine perforation occur proximal to an intestinal obstruction either intrinsic as in meconium ileus, intestinal atresia or stenosis or extrinsic as in volvulus or when there are peritoneal bands or adhesions.2 Occasionally intrauterine peritonitis occurs without perforation and these are sometimes in the area of developmental thinning of the intestinal wall. Other hypothesis has been of vascular occlusion and general hypoxia of the foetus.3 Meconium ileus accounts for majority of patients with meconium ileus and about 25% may be idiopathic. Viral infections such as parvovirus B 19,4 rubella5 and cytomegalovirus has been implicated. Meconium peritonitis secondary to meconium ileus is associated with cystic fibrosis among the Caucasian population but is rare among Asians. Antenatal radiological findings of intestinal obstruction, calcification, cyst formation or ascites have been associated with meconium peritonitis. The calcifications appear as linear or clumped foci and are plaque like in the abdomen, pelvis and the scrotum.1 In the new born with meconium peritonitis there is abdominal distension, bile stained vomiting and failure to pass meconium. Sometimes severe distension may cause dyspnoea. After birth the perforation may seal itself maintaining peritoneal sterility, but if not, bacterial peritonitis supervenes. The bacterial colonization of the meconium starts after birth and hence an early diagnosis is seen to be a decisive factor for the prognosis of these neonates. Survival rates of 90% have been reported in several series of antenatally diagnosed meconium peritonitis while Tibboel et al have reported 55% mortality in a literature review of 1084 patients, comprising mainly those diagnosed at birth. All neonates diagnosed antenatally may not require surgical management. The indication for operation are signs of intestinal obstruction or perforation. In a study by Dirkes only 22% foetuses with prenatal diagnosis developed complications and required surgery while in some other reports requirement for surgical intervention was upto 80%. In a study by Boix-Ochoa, mortality was three times more in patients operated after 24 hours of life. The availability of neonatal intensive care units and total parenteral nutrition results in improved survival. After the antenatal diagnosis of meconium peritonitis is made on ultrasound examination, the parents should be counselled and offered amniocentesis and DNA testing to rule out cystic fibrosis. The gestational age at diagnosis has no effect on the final outcome of the disease.10 Parents should therefore be informed that pregnancy can go upto term. Serial ultrasonography are necessary to assess the disease progression and foetal well being and growth. Delivery at term can be conducted vaginally unless there is an obstetric indication for caesarean section. Delivery should be in a tertiary centre where neonatal intensive care and paediatric surgical services are available.  
Fig. 2 : Peritoneal calcifications are present.
 
Acknowledgement
We would like to thank the Dean of Seth GS Medical College and KEM Hospital Dr. Nilima Kshirsagar for her kind support.
 
References
1. Foster MA, Nyberg DA, Mahoney BS, et al. Meconium peritonitis : prenatal sonographic findings and their clinical significance. Radiology 1987; 165 : 661-65.
2. Newborn Surgery. Editor Puri, Publisher : Butterworth Heinemann. Oxford J Boix - Ochao Meconium Peritonitis 1996; 328-33.
3. Rickham PP. Peritonitis of neonatal period. Arch Dis Child 30,23
4. Zerbini M, Gentilomi GA, Gallinella G, et al. Intrauterine parvovirus B 19 infection and meconium peritonitis. Prenat Diagn 1998; 18 (6) : 599-606.
5. Radner M, Vergesslich KA, Weninger M, et al. Meconium peritonitis : a new finding in Rubella syndrome. J Clin Ultrasound 1993; 21 (5) : 346-49.
6. Pletcher BA, Williams MK, Mulivor RA, et al. Intrauterine Cytomegalovirus infection presenting as fetal meconium peritonitis. Obstet Gynaecol 1991; 78 (5 pt2) : 903-5
7. MeDuffie RA, Bader T. Fetal meconium peritonitis after maternal hepatitis A. Am J Obstet Gynaecol 1999; 180 (4) : 1031-32.
8. Boix-Ochao U. Pathlogia quirurgica del meconio. Med Esp 1992; 81 : 30-51.
9. Tibboel D, Molenaar JC. Meconium Peritonitis - a retrospective prognostic analysis of 68 patients. Z kinderchir 1984; 39 (1) : 25-28.
10. Dirkes K, Crombleholme TM, Craigo SD, et al. The natural history of meconium peritonitis diagnosed in utero. J Paediatr Surg 1995; 30 (7) : 979-82.
11. Moslinger D, Chalubinski K, Radner M, et al. Meconium Peritonitis : intrauterine follow up postnatal outcome. Wien Klin Wochenschr 1995; 107 (4) : 141-45.
12. Wang YJ, Chen HC, Chi CS. Meconium peritonitis in neonates. Chang Hua I Hsueh Tsa Chih 1994; 53 (1) : 49-53.
 

ANGIOPLASTERS AND THROMBOLYSERS

Thrombolysis arrived as a routine treatment for patients with acute myocardial infarction just before primary angioplasty, but there are now enthusiasts arguing that primary angioplasty should become the first line treatment.

This week - perhaps because both protagonists are cardiologists - there is no such problem. If you were to read either piece alone you would, I suggest, be convinced. Reading them together, you will probably be grateful that it's somebody else's decision on whether to make primary angioplasty available to all.

Of 100 patients with infarcts about a quarter are not eligible for thrombolysis. Of those treated, a third to a half will have normal blood flow restored, but this would have happened in 10% anyway. Some patients are thus exposed to the hazards of thrombolysis but for no benefit. In contrast, argues Smith, angioplasty can be offered to everybody, needn't be done on those who spontaneously reperfuse, and can achieve normal blood flow in 90-97% of those treated.

But, argues Channer, you must be careful in extrapolating from the results of trials done in selective patients, mostly in the United States, to the real world and most other countries. A large Dutch trial in which patients were transferred from district general hospitals to regional centres found no improvement in all cause mortality. Even in the United States, registry data show less benefit than was expected from trials. The problem is the inevitable delay that occurs with angioplasy.

Perhaps the answer is yet another strategy - possibly home thrombolysis followed by rescue angioplasty. We also need some evidence on costs and benefits and on what it would be like to live in a world full of angioplasters.

Richard Smith, BMJ, 2004; 328 : 1255, 1257..