Demographics

The child’s age is a major determinant of the diagnostic possibilities ( Table 12.5 ). Affected neonates present with congenital disorders and, in particular, structural abnormalities of the gastrointestinal tract or severe metabolic diseases. Sepsis is also an important neonatal consideration. Older infants with vomiting may have less severe structural or metabolic disorders, or they may have common acquired disorders such as gastroenteritis, mild systemic infections, gastroesophageal reflux, or allergies. Some metabolic disorders first manifest in older infants when dietary changes expose them to provocative foods for the first time; gastroenteritis and other infections are important considerations in these relatively immunocompromised younger patients.

Toddlers frequently experience gastroenteritis, because they are repeatedly exposed to organisms to which they have no immunity; this age group also presents with acquired obstructive gastrointestinal disorders, such as intussusception or volvulus or with vomiting caused by ingested poisons. Throughout childhood and adolescence, a wide variety of acquired disorders become symptomatic, and some subtle congenital malformations may also first become evident at these older ages. Metabolic disorders continue to be an important but infrequent cause of recurrent vomiting throughout childhood. In adolescents, pregnancy, drug ingestion, chronic marijuana use, and eating disorders are added to the diagnostic considerations.

Characteristics of Vomiting

The contents ( Table 12.6 ) and forcefulness (see Table 12.1 ) of the vomitus narrow the diagnostic possibilities. Hematemesis and bilious vomiting, in particular, are approached in a manner very different from that of vomiting without these characteristics, and they represent more serious underlying disorders.

Abdominal Examination

Simple observation of operative scars may suggest the possibility of obstruction from intestinal adhesions, and visible distention may represent ascites caused by liver disease or intraluminal distention caused by intestinal obstruction or ileus. The order of the examination is important because auscultation performed after stimulation of intestinal motility by palpation may artifactually change the auscultatory findings. An important distinction in the vomiting child is whether bowel sounds are increased, as in gastroenteritis or in bowel obstructions, or absent, as in ileus caused by peritonitis or in pseudoobstruction. Increased bowel sounds resulting from luminal obstruction are often characterized by intermittent “rushes” of high-pitched sounds that are coordinated with episodes of colicky pain.

Abdominal pain and tenderness associated with vomiting often represent disorders necessitating further imaging and/or surgery. Vague periumbilical pain is quite nonspecific, but the localized, very sharp pain signifying inflammation of the peritoneum requires immediate attention. Initial luminal obstruction may progress to later ileus as peritonitis intervenes. Localization of nonperiumbilical pain or tenderness helps a great deal in determining the diseased intraabdominal organ (see Tables 12.8 and 12.9 ).

Abdominal pain often represents luminal obstruction, ischemia, or perforation (surgical disease), but nonsurgical diseases must also be considered. These disorders include nonobstructive inflammatory diseases (infectious gastroenteritis, pancreatitis), metabolic crises (e.g., adrenal crisis), and poisonings (e.g., lead, narcotics, insecticides).

Rectal Examination

A rectal examination may be helpful in the vomiting child as the presence and consistency of rectal stool may be determined. Simple fecal impaction may theoretically contribute to vomiting in young children, whereas liquid stools may suggest gastroenteritis. Pelvic masses and tenderness identified rectally may represent appendicitis, ovarian torsion, or pelvic inflammatory disease. The stool should always be tested for blood and should be considered for testing for pH, reducing substances, fat, leukocytes, and infectious organisms, depending on the situation.

General Approach

Cardinal symptoms or signs accompanying the vomiting direct the differential diagnosis. Abdominal pain, which frequently accompanies vomiting, can suggest both the type of disorder (e.g., luminal obstruction, inflammation, ischemia, or peritonitis) and the organ involved (see Table 12.8 ). Hematemesis leads to the considerations indicated in Tables 12.13 and 12.14 . Symptoms referable to nongastrointestinal organ systems direct attention to those systems. For example, accompanying neurologic symptoms may direct attention to central nervous system disorders, metabolic disease, poisonings, or psychobehavioral disease.

Esophageal Obstruction

Esophageal lesions produce welling up or drooling of oropharyngeal secretions or esophageal contents rather than actual vomiting; the material is, of course, undigested. Respiratory symptoms from aspiration may be prominent.

Esophageal atresia.

Infants with esophageal atresia present at birth with a prenatal history of polyhydramnios and intolerance of initial feeding. The esophageal atresia is accompanied by a distal tracheoesophageal fistula in 85% of cases, by a proximal fistula in a small percentage, and by no fistula in the remainder ( Fig. 12.1 ). Esophageal atresia is associated with other anomalies in 15-50% of patients; cardiac, anorectal, and genitourinary defects are most common. Ten percent of all esophageal atresia patients and 25% of those without a fistula have the VATER or VACTERL (vertebral, anorectal, cardiac, tracheoesophageal, renal, radial, limb) association. Others may have Fanconi anemia, where esophageal atresia may provide an early sign for making the diagnosis. As many as 33% of affected infants are premature. Diagnosis can usually be made by plain films after passage of an opaque rubber catheter, which coils in the upper pouch ( Fig. 12.2 ). Treatment is surgical.

Various types of tracheoesophageal fistulas (TEF) with relative frequency (%).

Tracheoesophageal fistula. Coiled radiopaque nasogastric tube in blind upper pouch.

Esophageal strictures.

Esophageal strictures are acquired lesions that may be caused by reflux esophagitis, but more commonly result from caustic ingestions (acid, alkali) or other causes ( Fig. 12.3 ). The strictures are best demonstrated with contrast radiography; endoscopic biopsies may be important for diagnosis of the etiology. Gastroesophageal reflux disease (GERD) may be treated pharmacologically, but may also require a fundoplication; endoscopic dilation of the stricture is performed repeatedly with balloons or bougies until the strictured site remains patent.

Esophageal stricture. Radiograph of a peptic esophageal stricture (arrow) before and after treatment with dilations.

Pyloric Stenosis

Pyloric stenosis manifests with nonbilious projectile vomiting beginning at 2-3 weeks of age and increasing during the next month or so, usually in a firstborn male child. The vomitus may contain some blood, and propulsive gastric waves can be seen on the abdominal wall. Dehydration, poor weight gain, metabolic alkalosis, and mild jaundice are sometimes evident. A palpable “olive” in the epigastrium (felt best during or after feeding) represents the hypertrophied pyloric muscle.

Gastric distention is seen on the plain film, and a contrast study shows the “string sign” of contrast passing through the narrowed pyloric channel. Ultrasound diagnosis is less invasive ( Fig. 12.4 ). Eosinophilia, eosinophilic infiltration of endoscopic antral biopsy specimens, and an excellent response to treatment with a casein hydrolysate or elemental “hypoallergenic” formula are suggestive of an allergic or idiopathic eosinophilic gastroenteropathy and not pyloric stenosis. In older children, gastric outlet obstruction may result from ulceration, chronic granulomatous disease, foreign bodies, and bezoars. Bezoars may be caused by hair, vegetable matter, milk curds, or medications. Long-acting formulated oral medications may also become bezoars in the distal intestine and cause obstruction.

Pyloric stenosis. Cross-sectional (left) and transverse (right) sonograms of hypertrophic pyloric stenosis, showing increased thickness and length of pyloric muscle. pc, pyloric channel.

Intestinal Obstruction

Rushes of bowel sounds associated with cramping and colic often indicate intestinal obstruction. Vomiting is a cardinal sign of intestinal obstruction, being more prominent in high small bowel obstruction than in low small bowel or colon obstruction. With high obstructions, vomiting is not feculent, the onset is often acute, and crampy pain may occur at frequent intervals; abdominal distention is minimal. With low obstructions, in contrast, the vomiting may be feculent and less acute in onset, the interval between cramping is longer, and distention is more notable. Identification of the site of obstruction is aided by the plain film and by other radiographic studies (see Table 12.12 ).

Obstructions may be categorized by type and site. Intraluminal lesions (e.g., tumors; intussusceptions; or extrinsic material such as feces, foreign bodies, bezoars, and gallstones) can be differentiated from bowel wall lesions (strictures, stenoses, atresias) and from extraluminal lesions (adhesions, congenital bands, tumors, volvulus). Radiographic studies are useful, beginning with the plain film and progressing to ultrasonography or CT. Fluoroscopy with contrast material such as barium or diatrizoate (Gastrografin, Hypaque, water-soluble contrast) is very helpful in identifying both the site and the type of obstruction, but the decision to introduce contrast into an intestine that may perforate or be operated on must be made with surgical and radiologic consultation. Often the decision to operate can be made without certain identification of the lesion, and contrast studies are unnecessary.

Infantile bilious vomiting is an important symptom of intestinal obstruction, which often signals a congenital gastrointestinal anomaly, particularly intestinal obstruction below the ampulla of Vater. Surgical consultation is needed early in these infants because they often require emergency therapy ( Table 12.15 ).

TABLE 12.15

Causes of Gastrointestinal Obstruction

Esophagus
Congenital	Esophageal atresia (with or without fistula) Isolated esophageal stenosis Duplication Vascular ring
Acquired	Caustic agent esophageal stricture Peptic stricture Chagas disease Collagen vascular disease
Stomach
Congenital	Antral webs
Acquired	Pyloric atresia * Bezoars/foreign body Pyloric stenosis Pyloric stricture (ulcer) Crohn disease Eosinophilic gastroenteropathy Prostaglandin-induced pyloric stenosis Chronic granulomatous disease
Small Intestine
Congenital	Duodenal atresia Annular pancreas Malrotation/volvulus Malrotation/Ladd bands Ileal atresia, stenosis Duplications Meconium ileus Inguinal hernia Gastroschisis
Acquired	Postsurgical adhesions or strictures Crohn disease (stricture) Intussusception Duodenal hematoma (abuse, trauma) Meconium ileus equivalent
Colon
Congenital	Meconium plug Hirschsprung disease Colonic atresia, stenosis Imperforate rectum/anus Rectal stenosis Malrotation/volvulus Small left colon syndrome (IDM)
Acquired	Ulcerative colitis (toxic megacolon) † Crohn disease (stricture) Chagas disease Stricture post-NEC

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