Vomiting

Vomiting or, more often, regurgitation is a relatively frequent symptom during the neonatal period. In the 1st few hours after birth, infants may vomit mucus, occasionally blood streaked. This vomiting rarely persists after the 1st few feedings; it may be due to irritation of the gastric mucosa by material swallowed during delivery. If vomiting is protracted, gastric lavage with physiologic saline solution may relieve it.

When vomiting occurs shortly after birth and is persistent, the possibilities of intestinal obstruction, metabolic disorders, and increased intracranial pressure must be considered. A history of maternal polyhydramnios suggests upper gastrointestinal (esophageal, duodenal, ileal) atresia. Bile-stained emesis suggests intestinal obstruction beyond the duodenum but may also be idiopathic. Abdominal radiographs (kidney-ureter-bladder [KUB] and cross-table lateral views) should be performed in neonates with persistent emesis and in all infants with bile-stained emesis to detect air-fluid levels, distended bowel loops, characteristic patterns of obstruction (double bubble: duodenal atresia), and pneumoperitoneum (intestinal perforation). A contrast swallow roentgenogram with small bowel follow-through is indicated in the presence of bilious emesis.

Obstructive lesions of the digestive tract are the most frequent gastrointestinal anomalies (Chapters 311, 321, 322, and 324). Vomiting (and drooling) from esophageal obstruction occurs with the 1st feeding. The diagnosis of esophageal atresia can be suspected if unusual drooling from the mouth is observed and if resistance is encountered during an attempt to pass a catheter into the stomach. The diagnosis should be made before the infant has trouble with oral feedings and aspiration pneumonia develops. Infantile achalasia (cardiospasm), a rare cause of vomiting in newborn infants, is demonstrable radiographically as obstruction at the cardiac end of the esophagus without organic stenosis. Regurgitation of feedings because of continuous relaxation of the esophageal-gastric sphincter, or chalasia, is a cause of vomiting. Keeping the infant in a semi-upright position, thickening the feeding, or administering prokinetic drugs can control it.

Vomiting due to obstruction of the small intestine usually begins on the 1st day of life and is frequent, persistent, usually nonprojectile, copious, and, unless the obstruction is above the ampulla of Vater, bile-stained; it is associated with abdominal distention, visible deep peristaltic waves, and reduction or absence of bowel movements. Malrotation with obstruction from midgut volvulus is an acute emergency that must be not only considered but also urgently evaluated by an upper gastrointestinal contrast radiographic series. Radiographs of the abdomen show the distribution of air in the intestine, which may point to the anatomic location of an obstruction; malrotation can be identified only by contrast studies. Normally, air can be demonstrated by radiographs in the jejunum by 15-60 min, in the ileum by 2-3 hr, and in the colon by 3 hr after birth. Absence of rectal gas at 24 hr is abnormal. Persistent vomiting may occur with congenital diaphragmatic hernia. The vomiting associated with pyloric stenosis may begin any time after birth but does not assume its characteristic pattern before the 2nd-3rd wk. Vomiting with obstipation is a common early sign of Hirschsprung disease. Vomiting may occur with many other disturbances that do not obstruct the digestive tract, such as milk allergy, adrenal hyperplasia of the salt-losing variety, galactosemia, hyperammonemias, organic acidemias, increased intracranial pressure, septicemia, meningitis, and urinary tract infection. In many infants, it is simply regurgitation from overfeeding or from failure to permit the infant to eructate swallowed air. (See Chapter 315 for a discussion of gastric emptying and gastroesophageal reflux.)

Diarrhea

See Chapters 332 and 333.

Constipation

More than 90% of full-term newborn infants pass meconium within the 1st 24 hr. The possibility of intestinal obstruction should be considered in any infant who does not pass meconium by 24-36 hr. Intestinal atresia, stricture, or stenosis; Hirschsprung disease; milk bolus obstruction; meconium ileus; or meconium plugs may manifest as constipation or, more often, obstipation. About 20% of very low birthweight (VLBW) infants do not pass meconium within the 1st 24 hr. Constipation not present from birth but appearing during the 1st mo of life may be a sign of short-segment congenital aganglionic megacolon, hypothyroidism, strictures after necrotizing enterocolitis (NEC), or anal stenosis. It must be kept in mind that infrequent bowel movements do not necessarily mean constipation. A breast-fed infant usually has frequent bowel movements, whereas a formula-fed infant may have 1-2 movements a day or every other day.

Meconium Plugs

Lower colonic or anorectal plugs (Fig. 96-1) with a lower than normal water content may cause intestinal obstruction. Rarely, a firm mass of meconium may form elsewhere in the intestine and cause intrauterine intestinal obstruction and meconium peritonitis unrelated to cystic fibrosis (CF). Anorectal plugs may also cause mucosal ulceration and intestinal perforation. Meconium plugs are associated with small left colon syndrome in infants of diabetic mothers and with CF, rectal aganglionosis, maternal opiate use, and magnesium sulfate therapy for preeclampsia. The plug may be evacuated by glycerin suppository or rectal irrigation with isotonic saline. Enemas with the iodinated contrast medium Gastrografin usually induce passage of the plug, presumably because the high osmolarity (1,900 mOsm/L) of the solution draws fluid rapidly into the intestinal lumen and loosens inspissated material. Such rapid loss of fluid into the bowel may result in acute dehydration and shock, so it is advisable to dilute the contrast material with an equal amount of water, correct any existing dehydration, and provide intravenous fluids during and for several hours after the procedure. After removal of a meconium plug, the infant should be observed closely for the possible presence of congenital aganglionic megacolon.

Figure 96-1 This plug of meconium and mucus (scale in cm) caused bowel obstruction in a premature infant. A radiograph showed marked gaseous distention and multiple fluid levels at 30 hr of age. Dramatic improvement occurred when the plug was passed after an enema.

(From: The abnormal fetus. In Beischer NA, Mackay EV, Colditz PB, editors: Obstetrics and the newborn, ed 3, Philadelphia, 1997, WB Saunders.)

Meconium Peritonitis

Perforation of the intestine may occur in utero or shortly after birth. Frequently, the intestinal perforation seals naturally with relatively little meconium leakage into the peritoneal cavity. In some cases, with long-standing perforation, meconium peritonitis is more pronounced. Perforations occur most often as a complication of meconium ileus in infants with CF but are occasionally due to a meconium plug or in utero intestinal obstruction of another cause. Cases at the most severe end of the spectrum may be diagnosed on prenatal ultrasonography with fetal ascites, polyhydramnios, bowel dilatation, intra-abdominal calcifications, and hydrops fetalis. At the other end are cases in which an intestinal perforation may seal spontaneously with only a minor meconium leak, so the event may never be detected except when meconium becomes calcified and is later discovered on radiographs of the abdomen. Alternatively, the clinical picture may be dominated by the signs of intestinal obstruction (as in meconium ileus) or chemical peritonitis. Characteristic clinical findings include abdominal distention, vomiting, and absence of stools. Treatment consists primarily of elimination of the intestinal obstruction and drainage of the peritoneal cavity.