Acute viral gastroenteritis is the most common cause of vomiting and diarrhea in children and continues to cause approximately 800,000 deaths globally each year in children <5 years old.¹

Transmission of GI infections can be reduced by attention to good hand hygiene. Hand washing can reduce the incidence of diarrheal disease by approximately 30% in both high- and low-income countries.² The provision of alcohol-based hand sanitizer and educational materials can reduce GI illnesses in child care centers,³ and a multifactorial intervention including hand sanitizer and surface disinfection similarly reduces illness due to enteric pathogens in elementary school students.⁴

Rotavirus accounts for a large majority of severe cases and contributes significantly to hospitalizations in developed countries. Two live oral rotavirus vaccines, marketed as RotaTeq^® and Rotarix^®, are currently licensed for use in the United States and numerous other countries. These vaccines are recommended by the World Health Organization for immunization of children worldwide. They have been introduced into the immunization programs of >50 countries. Routine rotavirus vaccination, which began in the United States in 2006, has resulted in an approximately 80% reduction in rotavirus-related hospitalizations and ED visits for rotavirus among immunized children.^5,6 Although a prospective postlicensure study of more than 200,000 doses identified an increase in the rate of intussusception after vaccination (attributable risk ~5.3 per 100,000 infants vaccinated); this increased risk must be weighed against the benefits of preventing rotavirus-associated illness.⁷

Although the clinical diagnosis of gastroenteritis requires the presence of diarrhea, many infants present with isolated vomiting. This chapter focuses on one of the most frequent and important causes of vomiting and diarrhea in children, gastroenteritis, and will also review other important causes of these symptoms.

Vomiting is the forceful act of expelling gastric contents through the mouth. It is controlled by the vomiting center in the reticular formation of the medulla and the chemoreceptor trigger zone underlying the floor of the fourth ventricle. Trigger areas that excite the CNS vomiting centers are found in the pharynx, cardiac vessels, peritoneum, bile ducts, and stomach. Vomiting results when the stomach relaxes, the gastric pylorus constricts, and the contractions of surrounding muscles cause expulsion of the gastric contents. Acute vomiting is usually caused by a self-limited viral illness. Nonetheless, serious diagnoses that need to be considered include infections, metabolic abnormalities, neurologic processes, acute surgical/GI diseases, or other major organ system dysfunction. The differential diagnosis of vomiting is age specific (Table 128-1). Bilious or bloody vomitus, hematochezia, or significant abdominal pain should trigger concerns of a disease process other than simple viral gastroenteritis or a potential complication of viral gastroenteritis (Tables 128-2 and 128-3).

Bilious vomiting suggests an obstructive lesion distal to the ampulla of Vater and portends a surgical emergency. From one third to half of newborns with bilious vomiting have a surgical lesion, often malrotation with volvulus or Hirschsprung’s disease.^8,9 For further discussion, see chapter 130, “Acute Abdominal Pain in Infants and Children.” For discussion of hematemesis, see chapter 131, “Gastrointestinal Bleeding in Infants and Children.”

Diagnostically, it is important to consider children with isolated vomiting separately from those who present with vomiting and diarrhea. The differential diagnosis of vomiting is vast and age specific (Table 128-1). Gastroesophageal reflux, intussusception, pyloric stenosis, and malrotation are discussed briefly below and more fully in chapter 130.

GASTROESOPHAGEAL REFLUX

Gastroesophageal reflux is the spontaneous regurgitation of gastric contents into the esophagus. Reflux is physiologic in young infants and usually resolves by the end of the first year of life. It is considered pathologic only in the small subset that experiences complications. The typical infant with uncomplicated gastroesophageal reflux effortlessly brings up small amounts of milk after feeding but continues to grow well. Symptoms may begin as early as the first week of life and often resolve around the time of solid food introduction and the assumption of the sitting position. In infants with significant vomiting, pathologic conditions should be considered. Complications that can occur include esophagitis, failure to thrive/weight loss, respiratory disease, refractory asthma, recurrent pneumonia, apnea, and acute life-threatening events. In most infants, the diagnosis can be made based on clinical findings. The gold standard diagnostic test is continuous esophageal pH monitoring to detect the presence of gastric acid in the distal esophagus. Semi-supine positioning (e.g., infant carrier or car seat) may exacerbate gastroesophageal reflux and should be avoided, especially after feeding.¹⁰ Although severe cases may require a histamine-2 receptor antagonist or a proton pump inhibitor, the overuse of medications in the “happy spitter” should be avoided.¹¹

INTUSSUSCEPTION

Intussusception occurs when one segment of bowel invaginates into a more distal segment. It is the leading cause of acute intestinal obstruction in infants and occurs most commonly between 3 and 12 months of age. The most common location is ileocolic, and the lead point usually is a hypertrophied Peyer patch. However, in children >2 years of age, a specific pathologic lead point should be considered. The primary manifestation is colicky abdominal pain followed by the onset of vomiting. The “classic” triad of colicky abdominal pain, vomiting, and bloody stools is present in only 20% of cases. For further discussion of intussusception, see chapter 130.

PYLORIC STENOSIS

Pyloric stenosis results from pyloric muscle hypertrophy that obstructs gastric outflow. The incidence is 1 in 250 live births, and >80% of cases occur in males¹²; other risk factors include white race, first born birth order, and a positive family history. Over 90% of cases are diagnosed by 10 weeks of life, with a sharp increase in the incidence after the second week of life, peaking at the fifth week and then steadily declining until the tenth week.¹² Children typically present with nonbilious projectile vomiting associated with weight loss and dehydration. Initially, the vomiting is mild and often mistaken for regurgitation. However, vomiting progresses and becomes more severe over several days. ED treatment includes the correction of fluid and electrolyte abnormalities. The pathognomonic electrolyte abnormalities are a hyponatremic, hypokalemic, and hypochloremic metabolic alkalosis. At present, the diagnosis is usually confirmed by US.

MALROTATION

Malrotation occurs when incomplete rotation of the gut in utero places the cecum in the right upper quadrant and fixes the dorsal mesentery on a narrow base instead of the broad fixation that usually extends from the ligament of Treitz to the ileocecal junction. These anomalies place the small bowel at risk for twisting on the narrow pedicle of mesentery, resulting in a volvulus that subsequently impairs blood flow to the bowel. Although malrotation can present at any age, roughly one third of patients present in the first month of life.¹² Symptoms may include bilious vomiting, pain, abdominal distention, and, ultimately, shock due to intestinal ischemia. Bilious emesis, particularly in a young infant, should immediately raise a concern for possible malrotation and volvulus. In some children, the volvulus can be intermittent, resulting in episodic vomiting and pain. Prompt diagnosis and surgical repair are needed to minimize the risk of bowel necrosis and death.

Diarrhea is loose or liquid stools and/or an increase in the frequency of evacuations with at least three stools in 24 hours. The child’s age and diet affect stool consistency and frequency. For example, in the first month of life, a change in stool consistency is more specific for diarrhea than absolute stool number. Breastfed infants typically have several poorly formed, yellow-green stools per day. Recognition of diarrhea in infants is important, because given their small size, they have limited fluid reserves and are at high risk for developing dehydration.

Most children with diarrhea have an acute viral infection, but diarrhea may be a presenting symptom of many conditions (Tables 128-4 and 128-5). Preexisting conditions may contribute to the clinical presentation or predispose the patient to an unusual cause of diarrhea, so it is important to inquire about previous GI surgery or chronic illnesses such as inflammatory bowel disease and immunodeficiency states. Bacterial and parasitic infections are more likely in institutionalized children and those returning from travel in low- and middle-income countries. Other causes of diarrhea include food allergies, antibiotic-associated diarrhea, and secondary lactase deficiency.

Acute onset of bloody diarrhea suggests a bacterial cause and a need to perform stool cultures. If there is a known outbreak of Escherichia coli O157:H7 or clinical features of hemolytic-uremic syndrome, obtain further testing to exclude renal failure, thrombocytopenia, and hemolytic anemia and provide early volume expansion.¹³ An infant with intermittent, crampy abdominal pain, vomiting, and bloody stools raises concern for intussusception, pseudomembranous colitis, parasitic infection, or inflammatory bowel disease.

Regardless of the cause of vomiting and diarrhea, the end result is fluid loss. Parental reports of dehydration, although highly sensitive, have a high false-positive rate. However, a history of normal fluid intake and normal urine output drastically reduces the likelihood of significant dehydration.¹⁴ Thus, for the majority of children, the physical examination remains crucial and should begin by assessing the child’s overall appearance, level of activity, responsiveness, respiratory pattern, and vital signs. Although the American Academy of Pediatrics, Centers for Disease Control and Prevention, World Health Organization, and European Society for Paediatric Gastroenterology, Hepatology, and Nutrition have developed treatment guidelines based on the degree of dehydration, no single variable in isolation is sufficiently accurate to determine the severity of dehydration.¹⁵ The percentage of body weight lost remains the gold standard measurement of dehydration, but it is infrequently available in the ED. Thus, physicians need to continue to rely on the presence of a combination of clinical findings as well as historical features to determine the degree of dehydration (see Table 129-2).

Three clinical signs have significant positive likelihood ratios for 5% dehydration: prolonged capillary refill time, abnormal skin turgor, and abnormal respiratory pattern.¹⁵ Well appearance, moist mucous membranes, and the absence of sunken eyes can help exclude dehydration.¹⁵

A validated dehydration score (Table 128-6) derived from several clinical studies^{16,17,18,19,20} correlates with length of stay and need for IV rehydration.²⁰

EPIDEMIOLOGY

Diarrheal diseases are the second leading cause of death worldwide in children. Rotavirus is the most common pathogen in areas without a vaccination program,²¹ and in areas with widespread rotavirus vaccination,²² norovirus is the most common pathogen.

PATHOPHYSIOLOGY

To cause diarrhea, an infectious agent must overcome numerous host defense factors, including gastric acidity, intestinal immunity, motility, mucus, and the resident microflora. The interaction between these factors and the infecting agent’s virulence mechanisms determines the subsequent clinical course (Table 128-5). No matter what the mechanism is, acute gastroenteritis is associated with fluid shifts and has the potential to cause dehydration, shock, and even death. The common final pathway results in fluid output exceeding the absorptive capacity of the GI tract. Fasting, which sometimes occurs with gastroenteritis, actually worsens the capacity of the bowel to absorb fluids. Continued feeding not only slows the progression of dehydration by increasing the volume of fluid available to the intravascular space, but the presence of nutrients in the bowel lumen also promotes mucosal recovery and improves fluid absorption.²³

CLINICAL FEATURES

Diarrhea associated with acute viral gastroenteritis typically lasts <7 days and not longer than 14 days, and it may be accompanied by vomiting or fever. Clinical features associated with the most important causes of bacterial gastroenteritis are listed in Table 128-7. Isolated vomiting should not be diagnosed as acute gastroenteritis. The differential diagnosis for isolated vomiting in the absence of diarrhea is broad.