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[Meconium peritonitis: diagnosis, etiology and treatment]
P Govaert1, R van Hecke, P Vanhaesebrouck
1Neonatale Intensieve Zorgen, Universitair Ziekenhuis UZG, Gent-België.
Insights
Meconium peritonitis, a fetal intestinal perforation complication, presents with varied causes and requires surgical intervention. Most infants survive without long-term gastrointestinal issues, though neonatal mortality remains a concern.
Area of Science:
- Neonatology
- Pediatric Surgery
- Gastroenterology
Background:
- Meconium peritonitis is a sterile inflammatory peritoneal reaction resulting from fetal intestinal perforation.
- This study examines twelve perinatal patients to detail the clinical presentation, diagnostic imaging, management, and outcomes of meconium peritonitis.
Observation:
- The majority of cases presented as the fibro-adhesive type of meconium peritonitis.
- Identified causes included cystic fibrosis, organic obstruction, fetal appendicitis, and ischemic necrosis of the ileum.
- A rare case of spontaneous healing in an idiopathic perforation in a preterm infant was observed.
Findings:
- Neonatal mortality was 18%.
- Surgical interventions included primary enteric anastomosis, Bishop-Koop anastomosis, and intestinal stoma creation.
- Seven out of ten survivors, excluding those with cystic fibrosis, experienced no late gastrointestinal sequelae.
Implications:
- Early diagnosis and appropriate surgical management are crucial for improving outcomes in neonates with meconium peritonitis.
- Understanding the diverse etiologies aids in targeted prevention and treatment strategies.
- The study highlights the potential for good long-term gastrointestinal function in survivors.
Abstract:
Fetal intestinal perforation causes a sterile inflammatory reaction of the peritoneum called meconium peritonitis. Twelve patients studied in the perinatal period serve to describe the classical fetal and neonatal signs and symptoms, the iconographical findings, treatment and prognosis. All but one infant, with a meconium pseudocyst, presented with the fibro-adhesive variety. Two were caused by cystic fibrosis, two by organic obstruction, one by fetal appendicitis and another two by ischemic necrosis of part of the ileum. In one of the latter two, the probable mechanism was feto-fetal embolisation following the in utero death of a co-twin. One idiopathic perforation, diagnosed in a preterm infant, healed spontaneously. The neonatal mortality rate was 18%. Primary enteric anastomosis was feasible in 3, Bishop-Koop anastomosis in 2 and an intestinal stoma in two others. Apart from the two survivors with cystic fibrosis, seven have no late gastro-intestinal sequelae.