Vomiting
Amanda Muir
Chris A. Liacouras
INTRODUCTION
Vomiting is the expulsion of stomach contents through the mouth. In children, vomiting is one of the most common presenting symptoms of upper gastrointestinal disease. The degree of emesis can vary from forceful, projectile vomiting to effortless regurgitation, to unseen rumination.
DIFFERENTIAL DIAGNOSIS LIST
Infectious Causes
Sepsis
Meningitis
Urinary tract infection
Parasitic infection—giardiasis, ascariasis
Helicobacter pylori gastritis
Otitis media
Gastroenteritis—viral, bacterial
Food-borne illnesses—Salmonella and Shigella
Hepatitis A, B, or C
Bordetella pertussis infection
Pneumonia
Sinusitis
Streptococcal pharyngitis
Toxic Causes
Drugs—aspirin, ipecac, theophylline, digoxin, opiates, anticonvulsants, barbiturates
Metals—iron, lead
Caustic ingestions
Alcohol
Neoplastic Causes
Intracranial mass lesions
Traumatic Causes
Duodenal hematoma
Pancreatic trauma
Congenital, Anatomic, or Vascular Causes
Esophageal stricture, web, ring, or atresia
Hypertrophic pyloric stenosis
Gastric web or duplication
Duodenal atresia
Malrotation
Intestinal duplication
Hirschsprung disease
Imperforate anus
Superior mesenteric artery syndrome
Metabolic or Genetic Causes
Galactosemia
Hereditary fructose intolerance
Other inborn errors of metabolism—amino acid or organic acid disorders, urea cycle defects, fatty acid oxidation disorders
Diabetes
Adrenal insufficiency
Inflammatory Causes
Cholecystitis or cholelithiasis
Eosinophilic enteritis
Milk-/soy-protein allergy
Inflammatory bowel disease
Appendicitis
Necrotizing enterocolitis
Peritonitis
Celiac disease
Peptic ulcer
Pancreatitis
Gastrointestinal Causes
Gastroesophageal reflux disease (GERD)
Eosinophilic esophagitis (EE)
Achalasia
Pseudo-obstruction
Obstruction—intussusception, volvulus, incarcerated hernia
Foreign body
Gastric and intestinal bezoars
Psychosocial Causes
Rumination
Bulimia
Psychogenic vomiting
Overfeeding
Functional Causes
“Cyclic vomiting” syndrome
Gastroparesis
Miscellaneous Causes
Pregnancy
Central nervous system disorders—hydrocephalus, pseudotumor cerebri, migraine, motion sickness, seizure
Renal disorders—ureteropelvic junction obstruction, obstructive uropathy, nephrolithiasis, glomerulonephritis, renal tubular acidosis
DIFFERENTIAL DIAGNOSIS DISCUSSION
H. pylori Infection
In older children and adults, H. pylori (a gram-negative, urease-producing bacterium) is the major cause of gastric and duodenal ulcers. Although the infection rate increases with age, infection with H. pylori is usually acquired during childhood. The overall rates of H. pylori infection in the United States are declining, but worldwide it remains a ubiquitous pathogen in developing nations. Furthermore, depending on socioeconomic status, rates of infection during childhood can vary from >60% in lower income homes to > 15% in higher income homes.
H. pylori appears to promote disease via several mechanisms: production of urease and ammonia, adhesion to the gastric mucosa, and proteolysis of gastric mucus. All of these mechanisms result in disruption of the gastric epithelium.
Clinical Features
Complaints commonly center around epigastric abdominal pain, vomiting, heartburn, and regurgitation. Hematemesis can also occur.
Evaluation
Currently, upper endoscopy with biopsy is the gold standard for the diagnosis of H. pylori infection. Serum antibodies to H. pylori can be detected; however, this test carries a poor specificity because previously infected individuals may remain serum antibody positive, despite lacking clinical evidence of gastritis. Stool H. pylori antigen testing and the urea breath test may supplant the need for upper endoscopy.
Treatment
Many treatment strategies are reported in the literature, but no single therapy is 100% effective in the eradication of H. pylori. Currently, the recommended treatment consists of a combination of a drug to suppress acid production (e.g., omeprazole), clarithromycin, and either metronidazole or amoxicillin. In the past, the treatment of choice was a combination of bismuth subsalicylate and antibiotics (amoxicillin and metronidazole).
Gastroesophageal Reflux Disease
Etiology
Gastroesophageal reflux is the movement of stomach contents into the esophagus, past the lower esophageal sphincter. It is commonly caused by a delay in gastric emptying or transient relaxation of the lower esophageal sphincter.
Clinical Features
Many newborns manifest inconsequential regurgitation after meals; this condition typically resolves by 3 to 6 months of age. In the usual presentation of GE reflux, frequent small mouthfuls of stomach contents are regurgitated in an effortless manner. No active emesis is observed. This phenomenon is frequently referred to as “spitting” or “wet burps.” Newborns with more severe reflux may also exhibit arching episodes (Sandifer syndrome) and irritability associated with feeding. Symptoms in older children include heartburn, chest or epigastric pain, dysphagia, water brash (a sour taste in mouth), or globus (the sensation that something is stuck in the throat).
In more pathologic cases, GERD is associated with more severe symptoms, such as weight loss, recurrent wheezing or coughing, recurrent pneumonia from aspiration, or apparent life-threatening episodes. Many times, concomitant esophagitis (manifested as irritability in infants) can occur. In many cases, no obvious spitting is seen, but studies clearly document gastroesophageal reflux.
Recently, an increasing number of children with symptoms of GERD were identified with EE. The presentation of EE is often very similar to GERD; however, these patients fail to respond adequately to antireflux medications. The disease is caused by food allergy and characterized by a severe isolated histologic esophageal eosinophilia despite aggressive acid suppression therapy.
Complications associated with GERD include hematemesis, aspiration, and failure to thrive.
Evaluation
GERD is primarily a clinical diagnosis, but several diagnostic tests can aid in the evaluation:
Contrast studies (upper gastrointestinal series) provide information regarding the upper intestinal anatomy.
Upper endoscopy is useful in assessing the degree of reflux and the presence of complications (e.g., esophagitis) and for reaching a definitive diagnosis in children.
Radiographic nuclear scintiscans (milk scans) provide information regarding gastric emptying and possible aspiration.
24-hour pH probe is useful when attempting to correlate acid reflux with atypical symptoms such as cough, hoarseness, or bronchospasm. An impedance probe can be used along with the pH probe to detect nonacid reflux.
Treatment
Conservative treatment includes improved positioning (upright and prone with head elevated 45°) after eating and while sleeping; feeding infants thickened food; and eliminating spicy foods and foods containing caffeine and peppermint.
The mainstay of medical treatment consists of gastric acid suppression and the use of intestinal prokinetic agents (e.g., metoclopramide, erythromycin). Acid-blocking medications (e.g., ranitidine, famotidine) are effective for preventing heartburn and for healing esophagitis. Proton pump inhibitors (PPIs) can be used for children with refractory disease. Antacids can be substituted; however, large doses must be given and the duration of action is short.
Eosinophilic Esophagitis
Etiology
EE is an allergic (autoimmune) esophageal disorder based on a clinicopathologic diagnosis that includes the presence of a large number of tissue eosinophils isolated from the esophagus.
Clinical Features
In children, EE presents with symptoms similar to those seen with GERD. These symptoms include vomiting, regurgitation, epigastric pain, poor feeding, and failure to thrive. Older children commonly manifest symptoms of heartburn, water brash, nausea, and dysphagia. It is not uncommon for adolescents to complain of difficulty in swallowing solid foods or have intermittent food impactions.
Evaluation
Upper endoscopy with biopsy is required to make the diagnosis. More than 15 esophageal eosinophils must be present per high power microscopic field. GERD must be ruled out.
Currently, there are no other useful noninvasive tests that can be performed.
HINT: Because patients with GERD can also manifest esophageal eosinophils, patients suspected of having EE should be treated with a PPI prior to performing upper endoscopy.