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Meconium-related ileus in extremely low-birthweight neonates: etiological considerations from histology and radiology
Akio Kubota1, Jun Shiraishi, Hisayoshi Kawahara
1Department of Pediatric Surgery, Osaka Medical Center and Research Institute for Maternal and Child Health, Osaka, Japan. kubota@mch.pref.osaka.jp
Insights
Meconium-related ileus in extremely low-birthweight neonates is not caused by immature ganglia. Obstruction results from excessive water absorption in the fetal bowel before birth, leading to inspissated meconium.
Area of Science:
- Neonatal Surgery
- Pediatric Gastroenterology
- Fetal Development
Background:
- Neonatal intestinal perforation mortality has risen, particularly in extremely low-birthweight (ELBW) neonates.
- The pathogenesis of meconium-related ileus remains unclear, distinguishing it from NEC and FIP.
- Increasing survival rates of ELBW neonates contribute to a higher incidence of intestinal perforation.
Purpose of the Study:
- To investigate the pathogenesis of meconium-related ileus in ELBW neonates.
- To determine if morphological immaturity of ganglia contributes to meconium-related ileus.
- To elucidate the cause of obstruction in meconium-related ileus.
Main Methods:
- Histological review of 13 ELBW neonates with meconium-related ileus and 16 age-matched controls.
- Radiological review of 33 cases of meconium-related ileus diagnosed via contrast enema.
- Comparison of ganglion cell nucleus size between cases and controls.
Main Results:
- No significant difference in ganglion cell nucleus size between neonates with meconium-related ileus and controls.
- Contrast enema revealed microcolon, gradual ileal caliber changes, and meconium filling defects in all meconium-related ileus cases.
- Locations of caliber changes and filling defects were not identical.
Conclusions:
- Morphological immaturity of ganglia is unlikely to be the cause of meconium-related ileus.
- Inspissated meconium is a consequence, not the cause, of obstruction.
- Excessive water absorption in hypoperistaltic fetal bowel is implicated, though the mechanism of hypoperistalsis is unknown.
Background:
A nationwide survey on neonatal surgery conducted by the Japanese Society of Pediatric Surgeons has demonstrated that the mortality of neonatal intestinal perforation has risen over the past 15 years. The incidence of intestinal perforation in extremely low-birthweight (ELBW) neonates has been increasing as more ELBW neonates survive and as the live-birth rate of ELBW has increased. In contrast to necrotizing enterocolitis (NEC) and focal intestinal perforation (FIP), the pathogenesis of meconium-related ileus, defined as functional bowel obstruction characterized by delayed meconium excretion and microcolon, remains unclarified.
Methods:
The histology of 13 ELBW neonates with intestinal perforation secondary to meconium-related ileus was reviewed, and the radiology of 33 cases of meconium-related ileus diagnosed on contrast enema was reviewed. Specimens obtained from 16 ELBW neonates without gastrointestinal disease served as age-matched controls for histological assessment.
Results:
The size of the ganglion cell nucleus in meconium-related ileus and in control subjects was 47.3 ± 22.0 µm(2) and 37.8 ± 11.6 µm(2), respectively, which was not significantly different. In all cases of meconium-related ileus, contrast enema demonstrated a microcolon or small-sized colon, with a gradual caliber change in the ileum and filling defects due to meconium in the ileum or colon, showing not-identical locations of caliber changes and filling defects.
Conclusion:
Morphological immaturity of ganglia was not suggested to be the pathogenesis of meconium-related ileus. Impaction of inspissated meconium is not the cause of obstruction, but the result of excessive water absorption in the hypoperistaltic bowel before birth, although the underlying mechanism responsible for the fetal hypoperistalsis remains unclear.
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