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Approach to the infant or child with nausea and vomiting

Approach to the infant or child with nausea and vomiting
Author:
Carlo Di Lorenzo, MD
Section Editor:
B UK Li, MD
Deputy Editor:
Alison G Hoppin, MD
Literature review current through: Feb 2022. | This topic last updated: Jan 21, 2021.

INTRODUCTION — Nausea and vomiting are common sequelae of a multitude of disorders that can range from mild, self-limited illnesses to severe, life-threatening conditions. Vomiting and nausea may or may not occur together or may be perceived at the same level of intensity. As an example, vomiting can occur without preceding nausea in individuals with mass lesions in the brain or increased intracranial pressure (ICP). Furthermore, some medications may alleviate vomiting but not nausea or vice versa.

The symptoms of nausea and vomiting may be caused by many pathologic states involving several systems (including gastrointestinal, neurologic, renal, and psychiatric). Younger children may not be able to describe nausea, which may further complicate diagnosis. The best course of action should be dictated by the medical history, taking into consideration clinical features of specific disorders and their relative frequency among children in different age groups. The most important consideration during the initial encounter is recognition of serious conditions, such as intestinal obstruction and increased ICP, for which immediate intervention is required. (See 'Concerning signs' below.)

This topic review will provide an overview of the neurophysiology and differential diagnosis of nausea and vomiting in children, while suggesting a general approach to specific testing. Individual disorders are discussed in further detail in linked topic reviews. Several gastrointestinal disorders present with abdominal pain in addition to nausea and vomiting, and these are discussed below. However, evaluation of the child in whom abdominal pain is the primary presenting complaint is discussed separately. (See "Emergency evaluation of the child with acute abdominal pain" and "Chronic abdominal pain in children and adolescents: Approach to the evaluation".)

DEFINITIONS

Vomiting (emesis) refers to the forceful oral expulsion of gastric contents associated with contraction of the abdominal and chest wall musculature. Vomitus often has a slight yellow tinge, which is caused by reflux of small amounts of bile into the stomach. Vomitus is considered bilious if it has a green or bright yellow color, indicating larger amounts of bile in the stomach; bilious vomiting is often associated with intestinal obstruction, as described below.

Nausea generally refers to an unmistakable sensation of unpleasantness that may precede vomiting but may be present even in a child who does not vomit. It is often associated with autonomic changes such as salivation, increased heart and respiratory rates, and a reduction in gastric tone and mucosal blood flow [1].

The related terms regurgitation, anorexia, sitophobia, early satiety, retching, and rumination are defined in the table (table 1).

PHYSIOLOGY OF EMESIS

Neurophysiology — Vomiting may have a physiologic benefit since it provides a means to expel potential toxins. Nausea and vomiting may also induce a conditioned aversion to ingested toxins [2]. In disease states, however, vomiting pathways are activated inappropriately. The major pathways through which nausea and vomiting are induced are vagal afferents, the area postrema, the vestibular system, and the amygdala [1]. Five principal neurotransmitter receptors mediate vomiting: muscarinic (M1), dopamine (D2), histamine (H1), serotonin (5-hydroxytryptamine 3 [5-HT3]), and substance P (neurokinin 1 [NK1]). (See "Characteristics of antiemetic drugs".)

Vagal afferent pathway – Abdominal vagal afferents are involved in the emetic response. These pathways can be evoked by either mechanical or chemosensory sensations. Examples of sensations that trigger this pathway include overdistension, food poisoning, mucosal irritation, cytotoxic drugs, and radiation [2]. Vagal afferents are an important site of action of 5-HT3 receptor antagonists used as antiemetic drugs [1].

Area postrema – The area postrema has been referred to as the "chemoreceptor trigger zone." Anatomically, this region is located at the caudal extremity of the floor of the fourth ventricle. Because the area postrema represents a relatively permeable blood-brain barrier region, it is the place where many, but not all, systemic chemicals act to induce emesis [1]. The area postrema is an important site for M1, D2, 5-HT3, and NK1 receptors, each of which is a key mediator of vomiting.

Vestibular system – The vestibular system is involved in the emetic response to motion. This response is often exacerbated when vestibular input is in conflict with visual sensations [2]. Irritation or labyrinthine inflammation can produce vomiting. Others have suggested that overstimulation of the vestibular system is not a complete explanation for motion sickness and that circulating neuroactive compounds may be involved. H1 receptors in the vestibular nucleus have a role in this response.

Amygdala – The amygdala is involved in a variety of stress and emotional responses. Among other structures, it receives input from the olfactory bulb and olfactory cortex and sends impulses to the hypothalamus. Aberrant activation of the amygdala may lead to a sensation of nausea.

Somatomotor events — The act of vomiting represents a highly coordinated sequence of events. As noted above, vomiting describes the act of emptying out the stomach, characterized by cycles of retching followed by the forceful expulsion of gastric contents. The detailed sequence of events is as follows [1]:

The diaphragm descends and the intercostal muscles contract while the glottis is closed

The abdominal muscles contract and the gastric contents are forced into the upper gastric vault and lower esophagus

The abdominal muscle relaxes and the esophageal refluxate empties back into the gastric vault

Several cycles of retching, each more rhythmical and forceful in nature, occur, with shorter intervals in between

Abdominal contraction associated with elevation of diaphragms results in forceful expulsion of gastric contents

APPROACH TO MANAGEMENT — Patients with acute vomiting, typically for hours to a few days, most often present to an emergency department, whereas patients with chronic symptoms are more often initially evaluated in outpatient office settings. Emergency department clinicians should expeditiously exclude life-threatening disorders such as bowel obstruction, diabetic ketoacidosis, adrenal crisis, toxic ingestion, or increased intracranial pressure (ICP) (table 2).

In both urgent care and routine outpatient settings, the following three steps should generally be undertaken in patients with nausea and vomiting:

The etiology should be sought, taking into account the child's age and whether the nausea and vomiting are acute, chronic, or episodic.

The consequences or complications of nausea and vomiting (eg, fluid depletion, hypokalemia, and metabolic alkalosis) should be identified and corrected.

Targeted therapy should be provided when possible (eg, surgery for bowel obstruction or insulin for diabetic ketoacidosis). In other cases, the symptoms should be treated.

EVALUATION — A careful history and physical examination should be performed. In many cases, the cause of the nausea and vomiting can be determined from the history and physical examination and additional testing is not required. The urgency with which various diagnostic possibilities should be pursued depends upon a number of factors, including the duration of illness, overall clinical status of the patient (especially hydration, circulatory, and neurologic status), and associated findings.

Concerning signs — Warning signs that may indicate a serious cause of vomiting include (table 3):

Nonspecific symptoms:

Prolonged vomiting

Profound lethargy

Significant weight loss

Symptoms of gastrointestinal obstruction or disease:

Bilious vomiting

Projectile vomiting in an infant three to six weeks of age

Hematemesis

Hematochezia (rectal bleeding)

Marked abdominal distension and tenderness

Symptoms or signs suggesting neurologic or systemic disease

Bulging fontanelle in a neonate or young infant

Headache, positional triggers for vomiting or vomiting on awakening, and/or lack of nausea

Altered consciousness, seizures, or focal neurologic abnormalities

History of head trauma

Hypotension disproportionate to the apparent illness and/or hyponatremia and hyperkalemia

Patients should be referred to a pediatric gastroenterologist or other appropriate specialist (eg, pediatric surgeon, neurologist) when there are symptoms or physical findings that are of particular concern. Immediate pediatric surgical consultation is warranted if appendicitis, bowel obstruction, or bowel perforation are suspected.

History — The history should detail the onset and pattern of the vomiting or nausea (acute, chronic, or episodic) as well as associated symptoms, especially fever, abdominal pain, diarrhea, or headache (table 4). Recent exposures to contacts with similar symptoms should be explored as well as a history of ingestion, or opportunity for ingestion, of medications or toxic substances. Key information from the child's past medical history includes known or suspected congenital anomalies or diseases, developmental delay, and neurologic symptoms or disorders.

The following clinical features are especially important:

Nature of vomiting:

Bilious (green or bright yellow) vomiting suggests intestinal obstruction, especially in a neonate (eg, due to intestinal atresia or volvulus) [3]. (See 'Intestinal obstruction' below and 'Intussusception' below.)

Projectile (very forceful) vomiting in an infant three to six weeks of age suggests pyloric stenosis. (See 'Pyloric stenosis' below.)

Bloody vomiting (hematemesis) suggests bleeding from esophageal varices if severe. Hematemesis also may be caused by esophageal injury from recurrent vomiting (Mallory-Weiss tear) or by mucosal injury from erosive esophagitis, gastritis, or peptic ulcer. (See "Mallory-Weiss syndrome" and "Approach to upper gastrointestinal bleeding in children", section on 'Etiology'.)

Sporadic or periodic episodes of vomiting suggest inborn errors of metabolism (especially in a newborn or young infant), cyclic vomiting syndrome, or cannabis hyperemesis syndrome. (See 'Inborn errors of metabolism' below and 'Cyclic vomiting syndrome' below.)

Early morning nausea or vomiting suggests pregnancy, increased intracranial pressure (ICP), or cyclic vomiting syndrome. (See 'Intracranial hypertension' below.)

Prolonged vomiting (eg, >12 hours in a neonate, >24 hours in children younger than two years, and >48 hours in older children) suggests a cause that may require intervention, such as obstruction, metabolic disorder, or cyclic vomiting syndrome. In addition, patients with prolonged vomiting are at risk for developing dehydration and electrolyte abnormalities.

Headache, positional triggers for vomiting or vomiting on awakening, and/or lack of associated nausea suggest increased ICP. (See 'Intracranial hypertension' below.)

Associated symptoms:

Diarrhea (with or without fever) in a patient with acute onset of vomiting is consistent with viral gastroenteritis. This possibility is supported by a history of close contacts with vomiting and/or diarrhea and suggests gastroenteritis. However, more serious causes of these symptoms should be considered in patients with atypical features. These causes include infection (sepsis, infectious enteritis/colitis, appendicitis, or inflammatory bowel disease [IBD]) and Hirschsprung disease-associated enterocolitis (especially in neonates or infants with risk factors, such as trisomy 21). (See 'Gastroenteritis' below.)

Rectal bleeding (hematochezia) suggests intussusception (especially in infants and toddlers), infectious colitis, or IBD. (See 'Intussusception' below and 'Inflammatory bowel disease' below.)

Fever is associated with many causes of nausea and vomiting, including viral gastroenteritis, appendicitis, streptococcal pharyngitis, urinary tract infection, and, sometimes, IBD. (See 'Gastroenteritis' below and 'Appendicitis' below and 'Other infections' below and 'Inflammatory bowel disease' below.)

A history of chronic or recurrent infections raises the possibility of an immunodeficiency. Recurrent pneumonia in an infant also may be caused by a tracheoesophageal fistula. (See "Approach to the child with recurrent infections".)

Prominent headache associated with nausea can be consistent with either migraine or increased ICP. (See 'Migraine' below and 'Intracranial hypertension' below.)

Physical examination — The physical examination should include a detailed evaluation of the abdomen for signs of obstruction or focal tenderness, as well as a neurologic assessment (table 4).

Abdominal examination:

Signs suggestive of intestinal obstruction include marked abdominal distension, visible bowel loops, absent bowel sounds or increased high-pitched bowel sounds ("borborygmi"), severe abdominal pain, or vomitus that is bilious (green or yellow) or feculent (with the odor of feces). By contrast, milder abdominal distension and active bowel sounds with normal pitch are common in simple gastroenteritis. (See 'Intestinal obstruction' below and 'Intussusception' below.)

Focal abdominal tenderness in the right lower quadrant suggests appendicitis or Crohn disease. Focal tenderness in the right upper quadrant suggests gallbladder disease (cholelithiasis or cholecystitis) or pancreatitis. Tenderness in the costovertebral angle suggests pyelonephritis. Abdominal pain or tenderness in the epigastric area is nonspecific but is also consistent with esophagitis, gastritis, peptic ulcer disease, or pancreatitis. (See 'Appendicitis' below and 'Inflammatory bowel disease' below.)

Hepatomegaly, splenomegaly, or jaundice may be caused by hepatitis, viral infection, or metabolic disorders. (See 'Inborn errors of metabolism' below.)

Neurologic examination:

Altered consciousness, seizures, or focal neurologic abnormalities may be caused by toxic ingestion, diabetic ketoacidosis, central nervous system mass, or inborn error of metabolism.

Bulging fontanelle in a neonate or young infant suggests the possibility of hydrocephalus or meningitis.

Ataxia, dizziness, or nystagmus (eye twitching) suggest vestibular neuronitis or acute cerebellar ataxia. (See "Evaluation of dizziness and vertigo in children and adolescents" and "Acute cerebellar ataxia in children".)

Other findings:

Ambiguous genitalia and/or hyperkalemia suggest the possibility of adrenal crisis (usually due to congenital adrenal hyperplasia). (See 'Adrenal insufficiency' below.)

An unusual odor emanating from the patient, especially in infants and toddlers, should prompt an investigation for metabolic causes of vomiting. (See 'Inborn errors of metabolism' below and "Inborn errors of metabolism: Epidemiology, pathogenesis, and clinical features", section on 'Abnormal odors'.)

Enlarged parotid glands in an adolescent should raise suspicion for bulimia. (See 'Bulimia or psychogenic vomiting' below.)

Laboratory testing — For patients with vomiting that is severe, prolonged (eg, >12 hours in a neonate, >24 hours in children younger than two years, and >48 hours in older children), or unexplained, screening laboratory tests should include a complete blood count, electrolytes, glucose, blood urea nitrogen, amylase, lipase, liver aminotransferases, and urinalysis. For patients with fever, urinary symptoms, or diarrhea, the evaluation may include urine culture and stool studies for occult blood, bacterial pathogens, and parasites.

Additional laboratory testing and imaging should be tailored to the differential diagnosis of the symptoms, based upon the history and physical examination (table 5).

DIFFERENTIAL DIAGNOSIS OF VOMITING BY AGE GROUP — The differential diagnosis of vomiting varies with the age of the child (table 2). The following sections will summarize the clinical features of the relatively common disorders and the less common but serious disorders in various age groups. Many of these disorders occur in several age ranges but are discussed below within the age group in which they present most frequently.

Neonates and young infants — Uncomplicated gastroesophageal reflux (GER), characterized by effortless regurgitation, is common and inconsequential in otherwise healthy infants. By contrast, forceful and repeated vomiting in infants is not normal and should be taken seriously, particularly if there are other signs of illness (eg, fever, weight loss, or feeding refusal). Important causes of these symptoms include pyloric stenosis and intestinal obstruction (table 6).

Gastroesophageal reflux disease — Physiologic GER in newborns and infants is common and is characterized by effortless regurgitation in an otherwise healthy infant (a "happy spitter"). This symptom may be described as vomiting by parents. The symptom gradually improves in most infants during the first year of life and may be minimized by conservative antireflux measures [4]. (See "Gastroesophageal reflux in infants".)

A minority of infants who regurgitate have pathologic GER, termed GER disease (GERD). No specific clinical features definitively identify these infants, but they may have recurrent fussiness or irritability and feeding aversion. These symptoms are thought to result from pain caused by esophageal acid exposure. Bradycardia or cyanotic episodes also may occur, particularly in preterm or neurologically impaired infants. Poor weight gain despite an adequate intake of calories should prompt evaluation for causes of vomiting and weight loss other than GERD. (See "Gastroesophageal reflux in infants", section on 'Evaluation and management by presenting symptoms'.)

GERD also is an important consideration in older infants, children, and adolescents presenting with subacute or chronic nausea or vomiting. The assessment and management of this disorder are discussed in separate topic reviews. (See "Clinical manifestations and diagnosis of gastroesophageal reflux disease in children and adolescents" and "Management of gastroesophageal reflux disease in children and adolescents".)

Food protein-induced enteropathy — Allergy to dietary proteins (most commonly milk protein) typically manifests as colitis, presenting with bloody stools. However, in some infants, the dietary protein causes enteritis, with or without associated colitis, and affected infants may present with vomiting, diarrhea, and failure to thrive. These disorders may or may not be mediated by immunoglobulin E (IgE) and tend to have subacute or delayed onset. (See "Food protein-induced allergic proctocolitis of infancy".)

Food protein-induced enterocolitis syndrome — Food protein-induced enterocolitis syndrome (FPIES) is a gastrointestinal food hypersensitivity that manifests as profuse, repetitive vomiting, often with diarrhea, leading to dehydration and lethargy in the acute setting (typically within one to three hours of ingestion) or weight loss and failure to thrive in a chronic form. The disease usually begins in early infancy, within one to four weeks following introduction of cow's milk or soy protein. It is most commonly caused by cow's milk or soy protein, although other foods can be triggers; it is uncommon in breastfed infants. FPIES is a non-IgE-mediated reaction to food, similar to food protein-induced enteropathy but with more severe manifestations. (See "Food protein-induced enterocolitis syndrome (FPIES)".)

Pyloric stenosis — Infantile hypertrophic pyloric stenosis is a condition of hypertrophy of the pylorus, with elongation and thickening, eventually progressing to near-complete obstruction of the gastric outlet. It occurs in approximately 3 in 1000 live births, more commonly in males (4:1 to 6:1). Approximately 30 percent of cases occur in firstborn children. (See "Infantile hypertrophic pyloric stenosis".)

The classic presentation of infantile hypertrophic pyloric stenosis is the three- to six-week-old baby who develops immediate postprandial, nonbilious, often projectile vomiting and demands to be refed soon afterwards (a "hungry vomiter"). In the past, patients were classically described as being emaciated and dehydrated with a palpable "olive-like" mass at the lateral edge of the rectus abdominus muscle in the right upper quadrant of the abdomen. Laboratory evaluation classically showed a hypochloremic, metabolic alkalosis, resulting from the loss of large amounts of gastric hydrochloric acid, the severity of which depended upon the duration of symptoms prior to initial evaluation.

The typical presentation has changed over time. Infants are diagnosed earlier, tend to be better nourished, and generally present without significant electrolyte imbalances. The diagnosis is made by ultrasound examination of the abdomen [5]. (See "Infantile hypertrophic pyloric stenosis".)

Adrenal insufficiency — Infants presenting with symptoms similar to those of pyloric stenosis, but with hyponatremia, hyperkalemic acidosis, and/or disproportionate hypotension, should raise concern for adrenal crisis. This is a life-threatening condition and should be evaluated and treated urgently.

The most common cause of adrenal insufficiency in infants is congenital adrenal hyperplasia due to 21-hydroxylase deficiency. In the United States, 21-hydroxylase deficiency is part of the newborn screen in most states, so most such infants will be diagnosed prior to developing adrenal crisis. Adrenal crisis usually presents between the first and fourth week of life. Affected females will have ambiguous genitalia; males usually have no obvious genital abnormalities. (See "Clinical manifestations and diagnosis of adrenal insufficiency in children", section on 'Adrenal crisis'.)

Intestinal obstruction — There are multiple causes of intestinal obstruction in neonates and young infants [6]. Causes of intestinal obstruction that present during early infancy include:

Intestinal atresia (see "Intestinal atresia")

Hirschsprung disease (see "Congenital aganglionic megacolon (Hirschsprung disease)")

Pyloric stenosis (see 'Pyloric stenosis' above)

Malrotation with or without volvulus (see "Intestinal malrotation in children")

Intussusception (see 'Intussusception' below and "Intussusception in children")

Bilious (bile-stained) vomitus in a neonate should be treated as a life-threatening emergency because this is often a symptom of obstruction due to intestinal atresia or mid-gut volvulus [3], although bilious vomiting can be seen occasionally in infants without bowel obstruction. Vomiting that is not bile stained may be caused by proximal obstruction, such as pyloric stenosis, upper duodenal stenosis, gastric volvulus, or annular pancreas [7].

If intestinal obstruction is suspected, the specific diagnosis often can be suggested by the patient's history and with appropriate radiologic imaging, as outlined in this appropriateness criteria table for infants [8]. Plain radiographs of the abdomen generally provide a rapid assessment of possible bowel obstruction with relatively little radiation exposure. Abdominal ultrasound provides high sensitivity and specificity for detecting intussusception and pyloric stenosis. If a diagnosis is not established by ultrasound and proximal bowel obstruction is suspected, then an upper gastrointestinal contrast study usually is appropriate. If the abdominal radiograph or physical examination suggests distal bowel obstruction (as might be seen in Hirschsprung disease), then a contrast enema usually is appropriate. (See "Intussusception in children".)

Malrotation with volvulus — Malrotation is an anomaly of fetal intestinal development that occurs in approximately 1 in 6000 newborns. In this condition, the cecum is abnormally positioned in the right upper quadrant and is fixated to the right lateral abdominal wall by bands of peritoneum. These abnormalities predispose to intestinal volvulus, in which the intestine twists on its mesentery. This causes acute small bowel obstruction and ischemia, which usually presents with sudden onset of bilious vomiting and an acute abdomen. Volvulus occurs early in infancy in approximately one-half of infants with malrotation. Other infants with malrotation may remain asymptomatic or present later in childhood with volvulus. Affected infants also may present with signs of duodenal obstruction or with associated congenital anomalies such as intestinal atresias. (See "Intestinal malrotation in children".)

Hirschsprung disease — Most patients with Hirschsprung disease are diagnosed in the neonatal period. Patients present with symptoms of distal intestinal obstruction: bilious emesis, abdominal distension, and failure to pass stool. The diagnosis can be suggested by a delay in passage of the first meconium (greater than 48 hours of age). Affected children may also present initially with enterocolitis, a potentially life-threatening illness in which patients have a sepsis-like picture with fever, vomiting, diarrhea, and abdominal distension, which can progress to toxic megacolon. (See "Congenital aganglionic megacolon (Hirschsprung disease)".)

Inborn errors of metabolism — Inborn errors of metabolism are rare causes of vomiting in neonates and young infants. Nonetheless, recognition of these disorders is important because the institution of appropriate therapy can be life-saving. The clinical presentation varies with the type of metabolic disorder.

Organic acidemias and urea cycle disorders are characterized by recurrent episodes of vomiting and dehydration (see "Inborn errors of metabolism: Epidemiology, pathogenesis, and clinical features" and "Metabolic emergencies in suspected inborn errors of metabolism: Presentation, evaluation, and management"):

Organic acidemias – The typical presentation of organic acidemias in newborns is an acute, severe illness characterized by lethargy, poor feeding, vomiting, metabolic acidosis, and shock. (See "Organic acidemias: An overview and specific defects".)

Urea cycle disorders – Urea cycle disorders typically present during infancy or early childhood, with episodes of altered mental status with gastrointestinal symptoms and hyperammonemia, often triggered by catabolic stress (intercurrent illness or fasting) or increased protein load. (See "Urea cycle disorders: Clinical features and diagnosis".)

Disorders of carbohydrate intolerance are triggered by specific sugars in the diet; non-glucose reducing substances are usually present in the urine:

Galactosemia – Infants with classic galactosemia usually present in the first few days after birth and initiation of breast milk or cow's milk-based formula feedings. Typical symptoms include jaundice, vomiting, hepatomegaly, failure to thrive, poor feeding, and susceptibility to gram-negative infections; some develop lenticular cataracts. (See "Galactosemia: Clinical features and diagnosis".)

Hereditary fructose intolerance – Most cases of hereditary fructose intolerance present with recurrent hypoglycemia and vomiting at the age of weaning, when fructose or sucrose (a disaccharide that is hydrolyzed to glucose and fructose) typically is added to the infant diet. However, some infants may present earlier because many commercial formulas and medications contain sucrose.

Older infants and children — Gastroenteritis is by far the most common disorder presenting with vomiting in infants, children, and adolescents (table 2). GERD, gastroparesis, mechanical obstruction, anaphylaxis, Munchausen syndrome by proxy (factitious disorder by proxy), intracranial masses, peptic ulcer disease, cyclic vomiting, and diabetic ketoacidosis also may be diagnostic considerations. Adrenal crisis and anaphylaxis should be considered in children with disproportionate hypotension and/or predisposing factors.

Gastroenteritis — Gastroenteritis usually is viral in etiology, occurring in clusters, sudden in onset, and quick to resolve. Bacterial causes may be associated with more prolonged and severe illness. (See "Acute viral gastroenteritis in children in resource-rich countries: Clinical features and diagnosis" and "Clinical manifestations and diagnosis of rotavirus infection", section on 'Clinical manifestations'.)

Other infections — Pharyngitis (particularly streptococcal pharyngitis) and urinary tract infections frequently present with nausea and/or vomiting. (See "Group A streptococcal tonsillopharyngitis in children and adolescents: Clinical features and diagnosis", section on 'Clinical features' and "Urinary tract infections in infants and children older than one month: Clinical features and diagnosis", section on 'Clinical presentation'.)

Gastroparesis — Gastroparesis is the condition of impaired emptying of gastric contents into the duodenum in the absence of a mechanical obstruction; this may cause postprandial fullness and nausea as well as postprandial vomiting. In gastroparesis, the vomiting usually occurs many hours after ingestion of food, a characteristic that differentiates this entity from GER or rumination syndrome, in which the emesis occurs during or immediately after eating. (See "Gastroparesis: Etiology, clinical manifestations, and diagnosis".)

The following conditions may cause gastroparesis:

Viral illness (postviral gastroparesis)

Surgery with vagus nerve damage (eg, fundoplication)

Use of drugs such as opioids or anticholinergics

Metabolic disturbances such as hypokalemia, acidosis, or hypothyroidism

Eosinophilic gastroenteropathy

Neuromuscular disorders such as cerebral palsy, diabetes mellitus, pseudo-obstruction, and muscular dystrophy

Postviral gastroparesis is often found in children who have experienced an acute, short viral illness (often rotavirus gastroenteritis) and is associated with postprandial antral hypomotility. In most cases, the symptoms resolve spontaneously within 6 to 24 months [9].

Intussusception — Intussusception is the most common cause of intestinal obstruction in infants between 6 and 36 months of age. Patients with intussusception typically develop the sudden onset of intermittent, severe, crampy, progressive abdominal pain, accompanied by inconsolable crying and drawing up of the legs toward the abdomen. The episodes become more frequent and more severe over time. Vomiting may follow episodes of abdominal pain. Initially, emesis is nonbilious, but it may become bilious as the obstruction progresses. A sausage-shaped abdominal mass may be felt in the right side of the abdomen. As symptoms progress, increasing lethargy develops, which can be mistaken for meningoencephalitis. In up to 70 percent of cases, the stool contains gross or occult blood. (See "Intussusception in children".)

Intussusception also can occur in neonates and young infants. In infants, intussusception may present as lethargy with or without vomiting or rectal bleeding. In young infants, intussusception is more often caused by a pathologic lead point, such as Meckel diverticulum or a duplication cyst.

Anaphylaxis — Anaphylaxis, triggered by ingested items (typically foods or medications), tends to present with prominent gastrointestinal symptoms, including nausea, crampy or colicky abdominal pain, vomiting (sometimes large quantities of "stringy" mucus), and diarrhea. These immediate (IgE-mediated) anaphylactic reactions are rapid in onset, typically beginning within minutes to two hours from the time of ingestion.

During anaphylaxis, gastrointestinal symptoms usually are accompanied by various signs and symptoms involving the skin and mucosa tissue, respiratory tract, and/or cardiovascular system. These include pruritus, flushing, urticaria/angioedema, periorbital edema, conjunctival injection, rhinorrhea, nasal congestion, cough, wheezing, dyspnea, change of voice quality, sense of choking, tachycardia (or, less commonly, bradycardia), dizziness, hypotension, sense of impending doom, and cardiovascular collapse. The gastrointestinal symptoms are rarely the sole manifestations of a food-allergic reaction. In most cases, an allergic reaction to food can be readily distinguished from other causes of vomiting by the presence of concurrent anaphylactic symptoms and by the history. The diagnosis and treatment of anaphylaxis are reviewed separately. (See "Anaphylaxis: Emergency treatment" and "Clinical manifestations of food allergy: An overview" and "Food allergy in children: Prevalence, natural history, and monitoring for resolution".)

Adrenal crisis — Although it is uncommon, adrenal crisis should be considered in children of any age, particularly if they have risk factors (such as known adrenal insufficiency or history of glucocorticoid use) and/or present with disproportionate hypotension, hyponatremia, and/or hyperkalemic acidosis. (See "Clinical manifestations and diagnosis of adrenal insufficiency in children", section on 'Adrenal crisis'.)

Intracranial hypertension — Brain tumors and other intracranial masses can cause nausea, vomiting, or both by increasing the intracranial pressure (ICP) at the area postrema of the medulla. (See "Elevated intracranial pressure (ICP) in children: Clinical manifestations and diagnosis".)

Clinical characteristics suggesting increased ICP include emesis that is triggered by an abrupt change in body position, especially upon awakening, with little or no accompanying nausea. More importantly, neurogenic vomiting usually is associated with other neurologic symptoms such as headache or focal neurologic deficit, although these signs and symptoms may be subtle. (See "Overview of the clinical features and diagnosis of brain tumors in adults".)

Idiopathic intracranial hypertension (pseudotumor cerebri) refers to increased ICP with normal cerebrospinal fluid content, normal neuroimaging, absence of neurologic signs except cranial nerve VI palsy, and no known cause. It is usually associated with headache, and occasionally with nausea and vomiting. In the pediatric age range, it is most likely to affect adolescent girls who are obese. (See "Idiopathic intracranial hypertension (pseudotumor cerebri): Clinical features and diagnosis".)

Cyclic vomiting syndrome — Cyclic vomiting syndrome is a disorder characterized by repeated episodes of nausea and vomiting that last for hours to days separated by symptom-free periods of variable length. This on-off pattern of emesis is quite distinct from most other causes of vomiting. Intense vomiting and nausea are the cardinal symptoms and usually lead to significant deficits of fluids and electrolytes. Cyclic vomiting has been most often described in school-aged children but may affect other age groups. The etiology is unknown. An association between cyclic vomiting syndrome and migraine headaches has been most consistently described, suggesting that there may be a common pathophysiologic process. (See "Cyclic vomiting syndrome".)

Migraine — Migraine is characterized by periodic episodes of paroxysmal headache often accompanied by nausea, vomiting, abdominal pain, and relief with sleep. The disorder occurs at all ages, beginning before age 20 years in 50 percent of cases. The family history is positive in most patients. Migraine usually can be distinguished from other causes of vomiting by the periodic nature and associated characteristic headache with photophobia and phonophobia. (See "Pathophysiology, clinical features, and diagnosis of migraine in children".)

Eosinophilic esophagitis or gastroenteritis — Eosinophilic disease can affect multiple parts of the upper gastrointestinal tract, together or separately. In eosinophilic esophagitis, boys compared with girls are disproportionately affected. Toddlers tend to experience epigastric pain, nausea and vomiting, and feeding aversion. Adolescents tend to have symptoms of dysphagia and may present acutely to the emergency department with a food impaction [10]. In many cases, the disorder appears to be mediated by a delayed, cell-mediated hypersensitivity to foods. Many but not all patients have associated allergic disorders such as eczema and asthma. (See "Clinical manifestations and diagnosis of eosinophilic esophagitis".)

Eosinophilic gastroenteritis can present at any age with abdominal pain, nausea, diarrhea, malabsorption, hypoalbuminemia, and weight loss. In infants, it may present as outlet obstruction with postprandial projectile vomiting. In adolescents and adults, it can also present with nausea and vomiting or may mimic irritable bowel syndrome. Symptoms vary depending on the layer and site of involved gastrointestinal tract. Approximately one-half of patients have allergic disease, such as defined food sensitivities, asthma, eczema, or rhinitis. (See "Eosinophilic gastrointestinal diseases".)

Medical child abuse — Medical child abuse (also known as fabricated or induced illness by carers or Munchausen syndrome by proxy) consists of fabricating or inducing illness in a child in order to get attention. The patient may have a history of frequent recurrent illnesses without a clear etiology. As an example, ipecac poisoning can present with recurrent, unexplained vomiting and repeated hospitalizations and can be confirmed by urine toxicology [11,12]. (See "Medical child abuse (Munchausen syndrome by proxy)".)

The diagnosis should be considered if the following features are present:

The reported history varies from what is observed or does not make sense

The illness is unexplained, unusual, or prolonged and does not respond to treatment as expected

The symptoms seem to originate only in the presence of the suspected perpetrator

The problem resolves or improves when the child is separated from the suspected perpetrator

The problem recurs when the suspected perpetrator is told that the child is improving or is soon to be released from the hospital or treatment program

Family members (eg, siblings) have unexplained symptoms, illness, or death

The suspected perpetrator behaves in a manner that appears to be consistent with exaggeration, fabrication, or induction of physical, psychological, or behavioral problems in the child

The alleged perpetrator does not seem to be as worried by the child's illness as the health professionals who are caring for the child

Adolescents — In addition to the disorders affecting children listed above (see 'Older infants and children' above), some of the more common causes of nausea and vomiting in adolescents include gastroenteritis, functional disorders, appendicitis, inflammatory bowel disease (IBD), cannabis hyperemesis syndrome, pregnancy, and toxic ingestions (table 2).

Functional dyspepsia — Dyspepsia is defined by a persistent or recurrent pain or discomfort localized to the upper abdomen; it is often associated with postprandial nausea, vomiting, and early satiety. In most cases, dyspepsia appears to be functional in nature due to a disorder of upper gastrointestinal sensation and motility [13]. Patients with functional dyspepsia often report nausea, but persistent vomiting is uncommon. Dyspepsia may occasionally arise from an organic disease such as peptic ulcer (with or without underlying Helicobacter pylori infection), food allergy, or Crohn disease. The approach to the adolescent patient with dyspeptic symptoms and a more detailed discussion of functional dyspepsia are given separately. (See "Chronic abdominal pain in children and adolescents: Approach to the evaluation", section on 'Functional disorders' and "Approach to the adult with dyspepsia".)

Functional nausea and functional vomiting — These categories were added to the descriptions of functional gastrointestinal disorders in the 2016 Rome IV classification [14]. By definition, neither is caused by underlying gastrointestinal disease and the vomiting is not self-induced. Some patients have nausea alone, others have vomiting alone, and others have both symptoms; there may be associated autonomic symptoms such as pallor, sweating, or dizziness. These diagnostic categories are distinguished from functional dyspepsia by the absence of abdominal pain. They are more common in individuals with underlying anxiety or depression. Early morning nausea that improves throughout the day is a common temporal pattern [15].

The evaluation includes a focused history and physical examination to identify alarm symptoms suggesting a central nervous system disorder (eg, weight loss, neurologic symptoms, severe morning vomiting or headaches), exclusion of pregnancy where appropriate, assessment for psychological distress, and a family history of functional gastrointestinal disorders. The possibility of gastroparesis (eg, postviral) should be considered (see 'Gastroparesis' above). Similar to other functional gastrointestinal disorders, the most valuable intervention is an interdisciplinary approach addressing the psychosocial contributors, which may include reassurance, relaxation strategies, and/or cognitive behavioral therapy. Antiemetic medications are generally ineffective for functional nausea. Selected patients with refractory functional nausea after referral to a specialist may benefit from a trial of pharmacotherapy with cyproheptadine or antidepressants [15-17]. (See "Functional abdominal pain in children and adolescents: Management in primary care".)

Appendicitis — Appendicitis presents most frequently in the second decade of life and is the most common indication for emergent abdominal surgery in childhood. Early signs and symptoms of appendicitis are often subtle and may vary depending upon the location of the appendix. An inflamed anterior or pelvic appendix produces marked symptoms in the right lower quadrant, while a retrocecal appendix may not cause the same degree of local signs of peritonitis, because the inflammation is masked by the overlying bowel.

In many patients, initial features are nonspecific, including indigestion, flatulence, bowel irregularity, and, sometimes, just a sense of feeling unwell. These symptoms usually are followed by pain in the epigastrium or periumbilical region, which is visceral in character (ie, constant, not very severe in intensity, and poorly localizable). The symptoms eventually localize to the right lower quadrant once inflammation involves the overlying parietal peritoneum. Nausea and vomiting, if they occur, follow the onset of pain. The diagnosis of appendicitis is less likely in patients in whom nausea and emesis are the first signs of illness. (See "Acute appendicitis in children: Clinical manifestations and diagnosis".)

Inflammatory bowel disease — IBD (ulcerative colitis and Crohn disease) may present with complaints of nausea, but frank vomiting is rarely a primary presenting symptom. The disease should be considered if there are suggestive features in the history and clinical presentation, especially growth failure, anemia, abdominal pain, perianal disease, bloody diarrhea, or arthritis. (See "Clinical presentation and diagnosis of inflammatory bowel disease in children".)

Cannabis hyperemesis syndrome — Chronic use of cannabis in adolescents may trigger episodes of vomiting that resemble cyclic vomiting syndrome. Diagnostic criteria include onset after prolonged, excessive cannabis use; relief of vomiting episodes by cessation of cannabis use; and association with pathologic bathing behavior (prolonged hot baths or showers) [18]. (See "Cannabis use: Epidemiology, pharmacology, comorbidities, and adverse effects", section on 'Medical and systemic effects'.)

Pregnancy — Pediatricians should have a low threshold for suspecting pregnancy in adolescents. Adolescents may or may not have considered the possibility of pregnancy or may present with vague complaints with suspected pregnancy as a "hidden agenda." (See "Pregnancy in adolescents", section on 'Diagnosis of pregnancy'.)

Bulimia or psychogenic vomiting — Bulimia nervosa should be considered in a patient with concerns about body weight and shape. Psychogenic vomiting is more likely in a patient with an anxiety disorder or may coincide with particularly stressful situations. (See "Eating disorders: Overview of epidemiology, clinical features, and diagnosis" and "Somatic symptom disorder: Epidemiology and clinical presentation" and "Somatic symptom disorder: Assessment and diagnosis".)

Rumination syndrome — Rumination syndrome, characterized by effortless regurgitation and/or re-swallowing of food, has previously been recognized as a disorder of emotionally deprived infants. More recently, it was recognized as a problem of older children and adolescents [19]. Some patient groups, such as adolescent girls, are at higher risk of rumination syndrome [14]. The severity of adolescent rumination syndrome varies, ranging from a benign disorder amenable to behavioral therapies to much more severe forms associated with substantial weight loss and inability to attend school [20]. (See "Eating disorders: Overview of epidemiology, clinical features, and diagnosis", section on 'Rumination disorder' and "Management of gastroesophageal reflux disease in children and adolescents", section on 'Rumination'.)

The characteristic of this condition is the presence of regurgitation and re-chewing or expulsion of food beginning soon after a meal, without nausea or retching [14]. The symptoms disappear hours after eating once the regurgitated material becomes acidic and do not occur during sleep. The clinical characteristics and diagnosis of rumination syndrome are discussed in more detail separately. (See "Rumination syndrome".)

TREATMENT — Treatment should be directed toward the underlying etiology. Electrolyte abnormalities, metabolic abnormalities, or nutritional deficiencies should be corrected. Cognitive-behavioral interventions are useful for vomiting associated with functional dyspepsia, adolescent rumination syndrome, and bulimia.

Antiemetics are useful for selected causes of persistent vomiting to avoid electrolyte abnormalities or nutritional sequelae. They typically are not recommended for vomiting of unknown etiology and are not appropriate for treatment of vomiting caused by anatomic abnormalities or surgical abdomen; they are also contraindicated in infants. Selection of antiemetics varies with the cause of the vomiting, as summarized in the table (table 7); more details are available in the linked topic reviews:

Gastroenteritis. (See "Oral rehydration therapy", section on 'Antiemetic therapy' and "Acute viral gastroenteritis in children in resource-rich countries: Management and prevention", section on 'Antiemetic agents'.)

Cyclic vomiting syndrome. (See "Cyclic vomiting syndrome", section on 'Management'.)

Motion sickness – The first-line approach for preventing motion sickness is to avoid environmental triggers, such as reading or viewing a screen while riding in a car. Drug therapy for motion sickness depends upon inhibition of activity in the vestibular nuclei, where labyrinthine and visual sensory cues are combined and synthesized. Drugs that reduce activity in the vestibular nuclei include antihistamines and anticholinergics [2]. (See "Motion sickness".)

Gastroparesis – The prokinetic agents erythromycin, metoclopramide, and domperidone have a role in the management of chronic intestinal pseudo-obstruction and gastroparesis (including postviral gastroparesis) [9]. The US Food and Drug Administration has issued a "boxed warning" about the potential for tardive dyskinesia associated with chronic or high-dose use of metoclopramide. Hence, this drug should be used only after a careful discussion with the patient and his or her caretakers about its possible risks and benefits. Drug selection and the potential adverse effects of these drugs are discussed separately. (See "Treatment of gastroparesis", section on 'Prokinetics' and "Chronic intestinal pseudo-obstruction: Management", section on 'Initial management'.)

Postoperative nausea and vomiting – During the last two decades, there have been considerable advances in the development of antiemetics. These include the emergence of 5-hydroxytryptamine 3 receptor (5-HT3) antagonists (ondansetron, granisetron), which have one primary site of antagonism and have helped in the treatment of postoperative nausea and vomiting as well as chemotherapy-associated emesis [2,21]. (See "Postoperative nausea and vomiting".)

Chemotherapy-induced nausea and vomiting – Tremendous strides have been made in development of antiemetics over the past two decades, especially 5-HT3 antagonists (ondansetron) and neurokinin 1 (NK1) antagonists (aprepitant). Factors that increase the incidence of vomiting include young age (toddler), female sex, agent emetogenicity (especially cisplatin), and higher rate of administration. 5-HT3 antagonists are generally effective in the acute phase (the first 24 hours), whereas NK1 antagonists are more effective in the delayed phase >24 hours.

Patients and families are increasingly turning to complementary and alternative medicine for a variety of complaints, particularly if the symptom is chronic or does not have a clear diagnostic explanation [22]. Applications of these techniques to the symptoms of nausea and vomiting have not been well studied, but there is some evidence for efficacy of some nutraceuticals, such as ginger and other herbal compounds for functional dyspepsia and other motility disorders [13,23,24]. Hypnotherapy is often helpful for treatment of anticipatory nausea and vomiting (eg, prior to chemotherapy) [25], whereas studies of hypnotherapy for functional dyspepsia are less conclusive [26-28]. The definitions and general approaches of other complementary and alternative techniques are discussed separately. (See "Complementary and alternative medicine in pediatrics".)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Nausea and vomiting".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

Basics topic (see "Patient education: Pyloric stenosis in babies (The Basics)")

Beyond the Basics topic (see "Patient education: Nausea and vomiting in infants and children (Beyond the Basics)")

SUMMARY — The symptoms of nausea and vomiting may be caused by a wide range of conditions affecting several different organ systems, with vastly different health implications. The immediate goal of the evaluation is to recognize serious conditions for which immediate intervention is required and then to identify a specific cause of the symptoms.

The causes of vomiting vary by age. Many of these disorders present in several age ranges but can be grouped into age ranges in which they present most frequently (table 2). (See 'Differential diagnosis of vomiting by age group' above.)

In many cases, the cause of the nausea and vomiting can be determined from the history and physical examination. The differential diagnosis is informed by the child's age and whether the nausea and vomiting are acute, chronic, or episodic. Certain clinical features may offer diagnostic clues that can further narrow the differential diagnosis (table 4). Laboratory testing should be performed to screen for causes of the symptom, guided by the history and physical examination (table 5). (See 'Evaluation' above.)

Concerning signs – The history and physical examination provide important clues to disorders requiring urgent intervention (table 3) (see 'Concerning signs' above and 'History' above and 'Physical examination' above):

Prolonged vomiting (eg, >12 hours in a neonate, >24 hours in children younger than two years, and >48 hours in older children) suggests a cause that may require urgent intervention. In addition, patients with prolonged vomiting are at risk for developing dehydration and electrolyte abnormalities.

Symptoms and signs suggestive of intestinal obstruction include marked abdominal distension, visible bowel loops, absent bowel sounds or increased high-pitched bowel sounds ("borborygmi"), severe abdominal pain, or vomitus that is bilious (green or yellow) or feculent (with the odor of feces). Bilious vomiting is a particularly important warning sign of possible intestinal obstruction in a neonate (eg, due to intestinal atresia or volvulus). (See 'Intestinal obstruction' above.)

The sudden onset of intermittent, severe, crampy, progressive abdominal pain in an infant or toddler suggests the possibility of intussusception, which is the most common cause of intestinal obstruction in infants between 6 and 36 months of age. (See 'Intussusception' above.)

Headache, positional triggers for vomiting, vomiting on awakening, and/or lack of nausea suggest the possibility of increased intracranial pressure (ICP). An adolescent female with early morning vomiting also should be evaluated for pregnancy. (See 'Intracranial hypertension' above.)

Altered consciousness, seizures, or focal neurologic abnormalities suggest the possibility of toxic ingestion or central nervous system mass (all ages), inborn error of metabolism (primarily infants and toddlers), or diabetic ketoacidosis (primarily children and adolescents). (See 'Intracranial hypertension' above and 'Inborn errors of metabolism' above.)

Recurrent episodes of vomiting and dehydration in an infant or young child suggest the possibility of an inborn error of metabolism, particularly organic acidemias and urea cycle disorders. Similar patterns are seen in cyclic vomiting syndrome, which is most common in school-aged children. Migraine also may present with sporadic or periodic vomiting but can usually be distinguished by the family history of migraine and associated headache. (See 'Inborn errors of metabolism' above and 'Cyclic vomiting syndrome' above and 'Migraine' above.)

Hypotension disproportionate to the apparent illness and/or hyperkalemia suggest the possibility of adrenal crisis. (See 'Adrenal crisis' above.)

REFERENCES

  1. Hornby PJ. Central neurocircuitry associated with emesis. Am J Med 2001; 111 Suppl 8A:106S.
  2. Li B U.K.. Nausea, vomiting and pyloric stenosis. In: Pediatric Gastrointestinal Disease, 5th Ed, Kleinman RE, Goulet OJ (Eds), BC Decker Inc, Ontario 2008. Vol 1, p.127.
  3. Mohinuddin S, Sakhuja P, Bermundo B, et al. Outcomes of full-term infants with bilious vomiting: observational study of a retrieved cohort. Arch Dis Child 2015; 100:14.
  4. Rosen R, Vandenplas Y, Singendonk M, et al. Pediatric Gastroesophageal Reflux Clinical Practice Guidelines: Joint Recommendations of the North American Society for Pediatric Gastroenterology, Hepatology, and Nutrition (NASPGHAN) and the European Society for Pediatric Gastroenterology, Hepatology, and Nutrition (ESPGHAN). J Pediatr Gastroenterol Nutr 2018.
  5. Niedzielski J, Kobielski A, Sokal J, Krakós M. Accuracy of sonographic criteria in the decision for surgical treatment in infantile hypertrophic pyloric stenosis. Arch Med Sci 2011; 7:508.
  6. McCollough M, Sharieff GQ. Abdominal surgical emergencies in infants and young children. Emerg Med Clin North Am 2003; 21:909.
  7. Cribbs RK, Gow KW, Wulkan ML. Gastric volvulus in infants and children. Pediatrics 2008; 122:e752.
  8. American College of Radiology, ACR appropriateness criteria for vomiting in infants (2014). https://acsearch.acr.org/docs/69445/Narrative/ (Accessed on April 17, 2017).
  9. Rodriguez L, Irani K, Jiang H, Goldstein AM. Clinical presentation, response to therapy, and outcome of gastroparesis in children. J Pediatr Gastroenterol Nutr 2012; 55:185.
  10. Aceves SS, Newbury RO, Dohil MA, et al. A symptom scoring tool for identifying pediatric patients with eosinophilic esophagitis and correlating symptoms with inflammation. Ann Allergy Asthma Immunol 2009; 103:401.
  11. McClung HJ, Murray R, Braden NJ, et al. Intentional ipecac poisoning in children. Am J Dis Child 1988; 142:637.
  12. Carter KE, Izsak E, Marlow J. Munchausen syndrome by proxy caused by ipecac poisoning. Pediatr Emerg Care 2006; 22:655.
  13. Perez ME, Youssef NN. Dyspepsia in childhood and adolescence: insights and treatment considerations. Curr Gastroenterol Rep 2007; 9:447.
  14. Hyams JS, Di Lorenzo C, Saps M, et al. Functional Disorders: Children and Adolescents. Gastroenterology 2016.
  15. Kovacic K, Miranda A, Chelimsky G, et al. Chronic idiopathic nausea of childhood. J Pediatr 2014; 164:1104.
  16. Kovacic K, Di Lorenzo C. Functional Nausea in Children. J Pediatr Gastroenterol Nutr 2016; 62:365.
  17. Madani S, Cortes O, Thomas R. Cyproheptadine Use in Children With Functional Gastrointestinal Disorders. J Pediatr Gastroenterol Nutr 2016; 62:409.
  18. Zhu JW, Gonsalves CL, Issenman RM, Kam AJ. Diagnosis and Acute Management of Adolescent Cannabinoid Hyperemesis Syndrome: A Systematic Review. J Adolesc Health 2021; 68:246.
  19. Chial HJ, Camilleri M, Williams DE, et al. Rumination syndrome in children and adolescents: diagnosis, treatment, and prognosis. Pediatrics 2003; 111:158.
  20. Alioto A, Di Lorenzo C. Long-term Follow-up of Adolescents Treated for Rumination Syndrome in an Inpatient Setting. J Pediatr Gastroenterol Nutr 2018; 66:21.
  21. Loewen PS. Anti-emetics in development. Expert Opin Investig Drugs 2002; 11:801.
  22. Vlieger AM, Blink M, Tromp E, Benninga MA. Use of complementary and alternative medicine by pediatric patients with functional and organic gastrointestinal diseases: results from a multicenter survey. Pediatrics 2008; 122:e446.
  23. Ghayur MN, Gilani AH. Pharmacological basis for the medicinal use of ginger in gastrointestinal disorders. Dig Dis Sci 2005; 50:1889.
  24. von Arnim U, Peitz U, Vinson B, et al. STW 5, a phytopharmacon for patients with functional dyspepsia: results of a multicenter, placebo-controlled double-blind study. Am J Gastroenterol 2007; 102:1268.
  25. Marchioro G, Azzarello G, Viviani F, et al. Hypnosis in the treatment of anticipatory nausea and vomiting in patients receiving cancer chemotherapy. Oncology 2000; 59:100.
  26. Soo S, Moayyedi P, Deeks J, et al. Psychological interventions for non-ulcer dyspepsia. Cochrane Database Syst Rev 2005; :CD002301.
  27. Calvert EL, Houghton LA, Cooper P, et al. Long-term improvement in functional dyspepsia using hypnotherapy. Gastroenterology 2002; 123:1778.
  28. Chiarioni G, Vantini I, De Iorio F, Benini L. Prokinetic effect of gut-oriented hypnosis on gastric emptying. Aliment Pharmacol Ther 2006; 23:1241.
Topic 5902 Version 40.0

References

1 : Central neurocircuitry associated with emesis.

2 : Central neurocircuitry associated with emesis.

3 : Outcomes of full-term infants with bilious vomiting: observational study of a retrieved cohort.

4 : Pediatric Gastroesophageal Reflux Clinical Practice Guidelines: Joint Recommendations of the North American Society for Pediatric Gastroenterology, Hepatology, and Nutrition (NASPGHAN) and the European Society for Pediatric Gastroenterology, Hepatology, and Nutrition (ESPGHAN).

5 : Accuracy of sonographic criteria in the decision for surgical treatment in infantile hypertrophic pyloric stenosis.

6 : Abdominal surgical emergencies in infants and young children.

7 : Gastric volvulus in infants and children.

8 : Gastric volvulus in infants and children.

9 : Clinical presentation, response to therapy, and outcome of gastroparesis in children.

10 : A symptom scoring tool for identifying pediatric patients with eosinophilic esophagitis and correlating symptoms with inflammation.

11 : Intentional ipecac poisoning in children.

12 : Munchausen syndrome by proxy caused by ipecac poisoning.

13 : Dyspepsia in childhood and adolescence: insights and treatment considerations.

14 : Functional Disorders: Children and Adolescents.

15 : Chronic idiopathic nausea of childhood.

16 : Functional Nausea in Children.

17 : Cyproheptadine Use in Children With Functional Gastrointestinal Disorders.

18 : Diagnosis and Acute Management of Adolescent Cannabinoid Hyperemesis Syndrome: A Systematic Review.

19 : Rumination syndrome in children and adolescents: diagnosis, treatment, and prognosis.

20 : Long-term Follow-up of Adolescents Treated for Rumination Syndrome in an Inpatient Setting.

21 : Anti-emetics in development.

22 : Use of complementary and alternative medicine by pediatric patients with functional and organic gastrointestinal diseases: results from a multicenter survey.

23 : Pharmacological basis for the medicinal use of ginger in gastrointestinal disorders.

24 : STW 5, a phytopharmacon for patients with functional dyspepsia: results of a multicenter, placebo-controlled double-blind study.

25 : Hypnosis in the treatment of anticipatory nausea and vomiting in patients receiving cancer chemotherapy.

26 : Psychological interventions for non-ulcer dyspepsia.

27 : Long-term improvement in functional dyspepsia using hypnotherapy.

28 : Prokinetic effect of gut-oriented hypnosis on gastric emptying.