99% of healthy full-term infants pass their first stool or meconium within 24 hours of birth and all healthy term neonates should do so by 48 hours.
With preterm infants the length of time can extend up to 9 days.
Neonatal intestinal obstruction occurs in 1/1500 live births. Etiologies are from intrinsic developmental defects, abnormalities of peristalsis or abnormal intestinal contents, or from insults in utero after the formation of normal bowel. Failure to recognize neonatal bowel obstruction can result in aspiration of vomit, sepsis, mid-gut infarction or enterocolitis.
Differential Diagnosis for failure to pass meconium:
- Disorders of the small intestine
- Duodenal atresia
- Jejunoileal atresia
- Malrotation and volvulus
- Meconium ileus
- Disorders of the large intestine
- Meconium plug syndrome
- Anorectal malformation
- Hirschsprung's disease
- Small left colon syndrome
- Other causes
- Narcotics
- Electrolyte abnormalities; hypermagnesemia, hypokalemia, hypercalcemia
- Hypothyroidism
- Sepsis
- Congestive heart failure
It is a transient form of distal colon or rectal obstruction caused by inspissated and dehydrated meconium, the etiology for which is unknown.
Diagnosis is made through barium enema revealing the outline of meconium plug. Barium enema can also be therapeutic along with rectal stimulation in inducing passage of the meconium.
Generally, infants with meconium plug syndrome have normal bowel function after passing the meconium plug.
Anorectal malformation: The incidence of anorectal malformation is 1/4000 live births, including anal stenosis, imperforate anus, and fistula.
Malformations are caused by a defect in embryonal development where the urorectal septum, lateral mesoderm and ectodermal structures combine to form the normal rectum and lower urinary tract.
70% of infants with anorectal malformation have associated anomalies. The mnemonic VACTERL is used to describe the combination of vertebral defects, anal atresia, cardiac defects, tracheoesophageal fistula, renal defects and radial limb hypoplasia.
Anal stenosis accounts for 20% of anorectal anomalies and treatment is with dilatation.
The mortality rate for patients with anorectal malformation is directly related to associated anomalies.
Malrotation and volvulus: Malrotation of the midgut is caused by a failure of normal bowel rotation. The mid-gut does not complete its normal 290° counterclockwise rotation during embryologic development, resulting in abnormal placement and fixation of the small bowel. This can cause obstruction and sometimes infarction of the small and large bowel, known as volvulus. Volvulus usually occurs within the first week of life.
Upright abdominal films reveal the classic double bubble sign, showing air in the stomach and proximal duodenum.
Treatment is with the Ladd's procedure involving counterclockwise reduction of the volvulus, release of adhesive bands (Ladd's bands) to mobilize the duodenum, and appendectomy. Recurrence of mid-gut volvulus after the Ladd's procedure can occur in up to 10% of cases.
Meconium ileus: This disorder is differentiated from meconium plug syndrome by location of the stool. In meconium ileus, the thick, tenacious bowel is most commonly found in the ileum but occasionally occurs in the jejunum or proximal colon.
90%-95% of patients with meconium ileus have cystic fibrosis. But, only 15% of cystic fibrosis patients will have meconium ileus as neonates. Associated anomalies such as volvulus, jejunoileal atresia, or bowel perforation occur in over half of infants with meconium ileus.
Duodenal atresia: The etiology of duodenal atresia is from failure to recanalize the lumen after the solid phase of intestinal development. This occurs between the 4th and 5th week of gestation. 40% of the patients with duodenal atresia have Down Syndrome. Diagnosis can be made in utero if polyhydramnios is present. Plain films can reveal the double bubble sign and an upper GI series might be necessary to distinguish between malrotation and duodenal atresia. Treatment is with duodenoduodenostomy.
Hirchsprung's disease: Hirchsprung's disease, or congenital aganglionic megacolon, is a motor disorder of the colon that causes a functional intestinal obstruction. It occurs in 1/5000 infants with a male to female predominance of 4:1. The pathogenesis of the disease is failure of migration of the neural crest cells that form the colonic ganglion cells. Without parasympathetic innervation, the colon cannot relax or undergo peristalsis, resulting in a functional obstruction.
The aganglionic segment is limited to the rectosigmoid in the majority of patients. 10% have full colonic involvement and in 10% more, there is lack of ganglion cells into the small bowel.
Diagnosis of Hirchsprung's disease can be made with barium enema, revealing a transition zone between the constricted aganglionic segment and the proximal, normally dilated segment.
Confirmation of the diagnosis is made with rectal suction biopsy.
The treatment of Hirchsprung's disease is through surgical resection of the aganglionic bowel.
The major complications of the disease, even after surgical resection, are bowel obstruction and enterocolitis.
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