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EPIDEMIOLOGY

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Intestinal obstruction is a common condition in the neonatal period. Although precise data are not available, it is estimated to occur in approximately 1 in 2000 live births.1 Esophageal obstruction generally presents with respiratory symptoms and is not discussed here. Intestinal obstruction is frequently complete, as in intestinal atresia, or incomplete, as in duodenal stenosis. While the majority of obstructions are mechanical, others are functional, such as Hirschprung disease or meconium ileus. The ileus associated with septic or metabolic conditions may mimic intestinal obstruction and must be distinguished from obstruction, as it does not require operative intervention.

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Associated conditions include genetic abnormalities or associated malformations. Trisomy 21 and duodenal atresia are associated2; meconium ileus is associated with cystic fibrosis (CF) and familial forms of Hirschprung disease. Imperforate anus is associated with esophageal atresia and renal or musculoskeletal anomalies, as in the VACTERL (vertebral, anal, cardiac, tracheoesophageal, renal, and limb) association.

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PATHOPHYSIOLOGY

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The symptoms of intestinal obstruction may be catastrophic (eg, malrotation with midgut volvulus with ischemia or infarction) or relatively benign (eg, atresia of the duodenum or small intestine). The bowel proximal to the obstruction becomes dilated, presumably due to the effect of peristalsis against the obstruction, and the degree of dilation is considered to be related to the duration of the obstruction. The secretions of the intestine proximal to the obstruction accumulate in the dilated proximal bowel and result in vomiting or polyhydramnios. The vomitus is bilious in the majority of instances but will be nonbilious if the obstruction is proximal to the ampulla of Vater. If the vomiting is prolonged, the infant will become volume depleted and have electrolyte abnormalities.

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Abdominal distension develops as the obstruction continues and is more prominent the more distal the obstruction is. Proximal obstructions (pyloric, duodenal, high jejunal) will have little or no distension. Distal obstructions, such as imperforate anus, Hirschprung disease, or distal ileal obstruction, will develop significant abdominal distension. Malrotation with volvulus will have no distension early in the process but once the bowel has become ischemic may have significant distension and abdominal tenderness. Abdominal tenderness and erythema are not associated with intestinal obstruction unless it is complicated by ischemia or perforation.

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Failure to pass meconium or delayed passage may be associated with intestinal obstruction. Ninety-five percent of term infants will pass meconium during the first 24 hours of life.3 Of infants with Hirschprung disease, 60% to 95% will pass meconium after 24 hours following birth.4 Newborn boys with apparent imperforate anus are usually observed for up to 24 hours to identify passage of meconium through small openings on the perineum. The appearance of meconium or of white “pearls” on the perineum will identify a fistulous opening that can be probed to identify a low imperforate anus that is covered by an epithelial membrane as opposed to a high imperforate anus that ...

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