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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

All topics are updated as new evidence becomes available and our peer review process is complete.

Literature review current through: Mar 2019. | This topic last updated: Apr 01, 2019.

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 nausea but not vomiting, 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].
Although there is no forceful expulsion of gastric contents with nausea, there may
be retrograde reflux of fluids from the duodenum to the gastric antrum.

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 [5-HT3]), and substance P (neurokinin 1).
(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 neurokinin 1 (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 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 is 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 dietary changes for food sensitivity). 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), and 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 mucosal injury from erosive esophagitis,
gastritis, or peptic ulcer. (See "Mallory-Weiss syndrome" and "Approach to
upper gastrointestinal bleeding in children", section on 'Etiology'.)

• Periodic episodes of vomiting suggest inborn errors of metabolism, especially in

a newborn or young infant, or cyclic vomiting 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; >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.

• Positional triggers for vomiting or vomiting on awakening, lack of associated

nausea, and/or headache suggests 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 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 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; >48 hours in older
children) or unexplained, screening laboratory tests should include a complete blood
count, electrolytes, glucose, blood urea nitrogen (BUN), 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, 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). Other conditions that may present with vomiting are sepsis,
excessive feeding volume, hydrocephalus, or inborn errors of metabolism.

Gastroesophageal reflux disease — Physiologic gastroesophageal reflux 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 gastroesophageal reflux, termed

gastroesophageal reflux 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 '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 — Intolerance 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. In
contrast to food allergy/anaphylaxis, these disorders are not 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, 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 (IHPS) 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 IHPS is the three- to six-week-old baby who develops
immediate postprandial, nonbilious, often projectile vomiting and demands to be re-fed
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 (CAH) 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 "Causes and clinical
manifestations of primary 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. 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 "Inborn errors of
metabolism: Metabolic emergencies"):

• 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, and postprandial vomiting. In gastroparesis, the
vomiting usually occurs many hours after ingestion of food, a characteristic that
differentiates this entity from gastroesophageal reflux 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 bradycardia less commonly),
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 is 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 "Causes and clinical
manifestations of primary 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 (CSF) content, normal neuroimaging, the 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, although many hypotheses have been proposed.
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 4:1. 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 gastroenteritis".)

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, appendicitis, inflammatory bowel disease (IBD),
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, and 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".)

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 her "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 [18]. 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 [19].
(See "Eating disorders: Overview of epidemiology, clinical features, and diagnosis",
section on 'Rumination disorder'.)

The characteristic of this condition is the presence of regurgitation and rechewing 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 "Gastroparesis: Etiology, clinical
manifestations, and diagnosis", section on 'Differential diagnosis'.)

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 'Treatment'.)

● 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 (FDA) 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
the caretakers about its possible risks and benefits. Drug selection and the potential
adverse effects of these drugs are discussed separately. (See "Chronic intestinal
pseudo-obstruction", section on 'Treatment' and "Treatment of gastroparesis",
section on 'Prokinetics'.)

● 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, and chemotherapy-associated
emesis [2,20]. (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 [21]. 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 [13,22,23]. Hypnotherapy is often helpful for treatment of
anticipatory nausea and vomiting (eg, prior to chemotherapy) [24], whereas studies of
hypnotherapy for functional dyspepsia are less conclusive [25-27]. 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, whether the nausea and vomiting is 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 provides 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; >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, lack of nausea, and/or vomiting on

awakening suggest the possibility of increased intracranial pressure. 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
(DKA, 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 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

suggests the possibility of adrenal crisis. (See 'Adrenal crisis' above.)

Use of UpToDate is subject to the Subscription and License Agreement.

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 Dise
ase, 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 infant
s (2014). https://acsearch.acr.org/docs/69445/Narrative/ (Accessed on April 17, 20
17).

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. Chial HJ, Camilleri M, Williams DE, et al. Rumination syndrome in children and
adolescents: diagnosis, treatment, and prognosis. Pediatrics 2003; 111:158.

19. 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.
20. Loewen PS. Anti-emetics in development. Expert Opin Investig Drugs 2002;
11:801.

21. 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.

22. Ghayur MN, Gilani AH. Pharmacological basis for the medicinal use of ginger in
gastrointestinal disorders. Dig Dis Sci 2005; 50:1889.

23. 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.

24. 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.

25. Soo S, Moayyedi P, Deeks J, et al. Psychological interventions for non-ulcer

dyspepsia. Cochrane Database Syst Rev 2005; :CD002301.

26. Calvert EL, Houghton LA, Cooper P, et al. Long-term improvement in functional
dyspepsia using hypnotherapy. Gastroenterology 2002; 123:1778.

27. 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 34.0

GRAPHICS

Definitions of terminology

Vomiting Forceful oral expulsion of gastric contents associated with contraction of the
abdominal, diaphragmatic, and chest wall musculature

Nausea The unpleasant sensation of the imminent need to vomit, usually referred to the
throat or epigastrium; a sensation that may or may not ultimately lead to the act
of vomiting

Regurgitation The act by which food is brought back into the mouth without the abdominal and
diaphragmatic muscular activity that characterizes vomiting

Anorexia Loss of desire to eat, that is, a true loss of appetite

Sitophobia Fear of eating because of subsequent or associated discomfort

Early satiety The feeling of being full after eating an unusually small quantity of food

Retching Spasmodic respiratory movements against a closed glottis with contractions of the
abdominal musculature without expulsion of any gastric contents, referred to as
"dry heaves"

Rumination Chewing and swallowing of regurgitated food that has come back into the mouth
through a voluntary increase in abdominal pressure within minutes of eating or
during eating

Reproduced with permission from: the American Gastroenterological Association. Gastroenterology 2001;
120:263.

Graphic 55952 Version 2.0

Common or critical causes of vomiting in the pediatric age range

Neonate Infancy Childhood Adolescence

Physiologic reflux or Physiologic reflux or Gastroenteritis* Gastroenteritis*
GERD* GERD*
Streptococcal Posttussive* (asthma,
Dietary protein Gastroenteritis* pharyngitis* infection, foreign body)
intolerance* or
Dietary protein Posttussive* Functional dyspepsia*
allergy (eg, milk
intolerance* or (asthma, infection,
protein-induced GERD*
allergy (eg, milk foreign body)
enteritis)
protein-induced Streptococcal pharyngitis
Functional
Pyloric stenosis enteritis)
dyspepsia* Pregnancy
Necrotizing Obstruction (eg,
GERD* Bulimia
enterocolitis intussusception,
malrotation, Peptic ulcer Drugs of abuse
Malrotation with
Hirschsprung disease, Suicide attempt
midgut volvulus Cyclic vomiting
pyloric stenosis)
Congenital atresias, Psychogenic Peptic ulcer
Inborn errors of
stenoses, webs Appendicitis
metabolism (eg, Increased
Gastroenteritis hereditary fructose intracranial
Psychogenic
intolerance, pressure (tumor,
Hirschsprung Gastroparesis
galactosemia, organic hydrocephalus,
disease
acidemias, urea cycle subdural hematoma Intracranial mass
Inborn errors of disorders) from child abuse)
metabolism (eg, Cyclic vomiting
Infant rumination Otitis media
organic acidemias, Eosinophilic
urea cycle Otitis media Urinary tract gastroenteritis/esophagitis
disorders, infection
Urinary tract infection Diabetic ketoacidosis
galactosemia,
Toxic ingestion
hereditary fructose Toxic ingestion Obstruction (eg,
intolerance) Diabetic malrotation,
Increased intracranial
ketoacidosis intussusception,
Feeding intolerance pressure (subdural
(may be associated hematoma from child Eosinophilic incarcerated hernia)
with cardiac, abuse, esophagitis Hepatobiliary disease
pulmonary, renal, or hydrocephalus) Obstruction (eg, Renal disease (renal
neuromotor malrotation,
Hepatobiliary disease insufficiency)
disorders) intussusception,
Renal disease Pancreatitis
Adrenal crisis incarcerated hernia)
(obstructive
Hepatobiliary Adolescent rumination
Hepatobiliary uropathy, renal
disease syndrome
disease insufficiency)
Renal disease (renal Adrenal crisis
Medical child abuse Pancreatitis
insufficiency) Medical child abuse
Adrenal crisis
Pancreatitis
Medical child abuse
Gastroparesis

Adrenal crisis

Medical child abuse

GERD: gastroesophageal reflux disease

*Common cause in this age group

Graphic 51919 Version 13.0

Concerning signs in an infant or child with nausea or vomiting

Increased possibility of an
Comments or diagnostic
underlying systemic or metabolic
considerations
disorder: Concerning signs

Nonspecific symptoms

Prolonged vomiting ◾ Concerns for fluid and electrolyte

◾ >12 hours in a neonate abnormalities
◾ >24 hours in children <2 years ◾ Increased possibility of underlying systemic
◾ >48 hours in older children or metabolic disorder

Profound lethargy ◾ Increased possibility of an underlying

systemic or metabolic disorder

Significant weight loss ◾ Increased possibility of an underlying

systemic or metabolic disorder

Symptoms of GI obstruction or disease

Bilious vomiting Intestinal obstruction, especially in a neonate

Projectile vomiting ◾ Pyloric stenosis in a young infant (3 to 6

weeks of age)
◾ Intestinal obstruction, cyclic vomiting
syndrome

Hematemesis ◾ Severe hematemesis suggests esophageal

varices.
◾ Milder hematemesis may be due to injury to
the esophagus (Mallory-Weiss tear) or
stomach (prolapse gastropathy), due
to recurrent vomiting.

Hematochezia Intussusception (especially in infants and

toddlers), infectious colitis, or IBD

Marked abdominal distension, peritoneal signs Intestinal obstruction or intra-abdominal process

(eg, appendicitis, obstruction)

Symptoms or signs suggesting neurologic or systemic disease

Bulging fontanelle (infant) Hydrocephalus or meningitis

Headache, positional triggers for vomiting or Increased intracranial pressure (eg, CNS mass,
vomiting on awakening, lack of nausea hydrocephalus, or pseudotumor cerebri)

Altered consciousness, seizures, or focal Toxic ingestion, diabetic ketoacidosis, CNS mass,
neurologic abnormalities or inborn error of metabolism

History or physical signs of trauma Intracranial or intra-abdominal injury (eg,

duodenal hematoma)

Hypotension disproportionate to apparent Adrenal crisis

illness, and/or hyponatremia with
hyperkalemia

GI: gastrointestinal; IBD: inflammatory bowel disease; CNS: central nervous system.

Courtesy of Dr. Carlo Di Lorenzo.

Graphic 100349 Version 3.0

Key elements of the history and physical examination in a pediatric
patient with nausea or vomiting

Symptoms Diagnostic considerations

History

Contacts with vomiting or ◾ Gastroenteritis

diarrhea

Acute onset of diarrhea ◾ Viral gastroenteritis (if typical features)

and fever ◾ Infection (sepsis, infectious enteritis/colitis, appendicitis, IBD)
◾ Hirschsprung-associated enterocolitis

Early morning vomiting ◾ Pregnancy (adolescent females), increased ICP, or cyclic vomiting
syndrome

Vomiting without nausea ◾ Increased ICP

Effortless vomiting ◾ Gastroesophageal reflux

◾ Rumination syndrome

Chronic or recurrent ◾ Immunodeficiency

infections ◾ Tracheoesophageal fistula (infant with recurrent pneumonia)

Periodic episodes of ◾ Cyclic vomiting syndrome

vomiting ◾ Inborn error of metabolism
◾ Migraine (usually with headache and family history)
◾ Porphyria, carcinoid, pheochromocytoma, familial dysautonomia

Vomiting triggered by specific foods

Vomiting begins within ◾ Food allergy (eg, anaphylaxis)

minutes to two hours of
ingesting the food,
usually with cutaneous or
respiratory symptoms

Subacute or chronic, with ◾ Food protein-induced enteropathy or FPIES

diarrhea

Triggered by introduction ◾ Galactosemia

of lactose

Triggered by introduction ◾ Hereditary fructose intolerance

of fructose or sucrose

Undigested food in ◾ Achalasia

vomitus

Heartburn ◾ Esophagitis (peptic or eosinophilic)

Physical examination

Marked abdominal ◾ Intestinal obstruction

distension; visible bowel
loops; bilious vomitus
(green or yellow); absent
bowel sounds or increased
high-pitched bowel sounds
("borborygmi"); or
feculent (with the odor of
feces)

Focal tenderness ◾ RLQ: Appendicitis or Crohn disease

◾ RUQ: Gallbladder disease, pancreatitis
 ◾ Costovertebral angle: Pyelonephritis
◾ Epigastric: Pancreatitis, peptic ulcer disease/gastritis

Hepatomegaly, ◾ Hepatitis, viral infection (eg, EBV), metabolic disorders

splenomegaly, jaundice

Ataxia, dizziness, ◾ Vestibular neuronitis or acute cerebellar ataxia

nystagmus

Papilledema ◾ Increased ICP

Ambiguous genitalia ◾ Congenital adrenal hyperplasia with vomiting due to adrenal crisis

Unusual odor ◾ Inborn error of metabolism

Enlarged parotid glands ◾ Bulimia

IBD: inflammatory bowel disease; ICP: intracranial pressure; FPIES: food protein-induced enterocolitis
syndrome; RLQ: right lower quadrant; RUQ: right upper quadrant; EBV: Epstein-Barr virus.

Courtesy of Dr. Carlo Di Lorenzo.

Graphic 100350 Version 4.0

Clinical utility of various diagnostic studies in the diagnosis of vomiting
in a child

Name of study Utility

Complete blood count Anemia and iron deficiency may be associated with obstruction, IBD,
gastritis, and ulcer disease.

Elevated white blood cell count is associated with bacterial infections and
sepsis.

Electrolytes, Electrolyte abnormalities are associated with pyloric stenosis, adrenal

BUN/Creatinine insufficiency, and metabolic diseases.

Elevated BUN/Creatinine are seen in renal disease.

Liver function tests Elevated AST, ALT, total bilirubin, and GGT are seen in liver and gallbladder
disease.

Amylase, lipase Elevated in pancreatitis.

Plasma ammonia, urine If an inborn error of metabolism is suspected. Ammonia is elevated in urea
reducing substances cycle disorders and organic acidemias. Non-glucose reducing substances are
usually present in the urine in galactosemia or hereditary fructose
intolerance.

Plain radiograph of the If intestinal obstruction is suspected.

abdomen

Upper gastrointestinal If an anatomic abnormality of upper GI tract is suspected (eg, neonate with
series bilious vomiting).

CT of the head If increased intracranial pressure is suspected (rule out mass).

Abdominal ultrasound If pyloric stenosis or intussusception are suspected; also useful

for evaluation of liver, gallbladder, kidneys, and pancreas.

Radionucleotide gastric If gastroparesis is suspected.

emptying study

Endoscopy If peptic disease, eosinophilic esophagitis, IBD, or other causes of intestinal

inflammation are suspected.

IBD: inflammatory bowel disease; BUN: blood urea nitrogen; AST: aspartate aminotransferase; ALT: alanine
aminotransferase; GGT: gamma-glutamyl transpeptidase; GI: gastrointestinal; CT: computerized
tomography.

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Differential diagnosis of vomiting in infants

Gastrointestinal obstruction Infectious

Pyloric stenosis Sepsis

Malrotation with volvulus Meningitis

Intussusception (may be intermittent) Urinary tract infection

Intestinal duplication, stenosis, or atresia Pneumonia

Hirschsprung disease Otitis media

Antral/duodenal web Hepatitis

Foreign body Metabolic/endocrine

Incarcerated hernia
Galactosemia

Other gastrointestinal causes Hereditary fructose intolerance

Physiological gastroesophageal reflux or GERD Urea cycle defects

Food protein-induced (eg, anaphylaxis, food protein- Amino and organic acidemias
induced enteropathy, or FPIES)
Fatty acid oxidation disorders
Gastroenteritis
Metabolic acidosis
Peptic ulcer disease
Congenital adrenal
Eosinophilic esophagitis/gastroenteritis hyperplasia/adrenal crisis

Gastroparesis Renal
Pancreatitis
Obstructive uropathy

Neurologic Renal insufficiency

Hydrocephalus Toxic
Subdural hematoma
Lead
Intracranial hemorrhage
Iron
Mass lesion
Vitamin A or D

Medications (ipecac, digoxin,

theophylline, etc)

Other toxins

Cardiac
Heart failure

GERD: gastroesophageal reflux disease; FPIES: food protein-induced enterocolitis syndrome.

Modified with permission from: Rudolph CD, Mazur LJ, Liptak GS, et al. Guidelines for evaluation and
treatment of gastroesophageal reflux in infants and children: recommendations of the North American
Society for Pediatric Gastroenterology and Nutrition. J Pediatr Gastroenterol Nutr 2001; 32:S1. Copyright ©
2001 Lippincott Williams & Wilkins.

Graphic 61133 Version 11.0

Antinausea, antiemetic, and related medications used for children

Drug class and Mechanism of

Indications Side effects
drug action

Antihistamines Minimal antiemetic

activity

Diphenhydramine Vestibular suppression, Motion sickness Sedation, anti-ACh

anti-ACh effect, and H 1 effects*
Hydroxyzine
antagonist
Dimenhydrinate

Meclizine

Phenothiazines Mild-moderate
antiemetic activity

Promethazine D 2 antagonist at CTZ Chemotherapy-induced Anti-ACh effects,*

and H 1 antagonist vomiting extrapyramidal
reactions
Prochlorperazine D 2 antagonist at CTZ

Chlorpromazine

Substituted Moderate antiemetic

benzamides activity

Metoclopramide D 2 antagonist at CTZ GERD, gastroparesis, Irritability and

and 5-HT 4 agonist in chemotherapy-induced extrapyramidal
gut vomiting reactions

Trimethobenzamide D 2 antagonist at CTZ

Cisapride 5-HT 4 agonist, ACh GERD, gastroparesis Diarrhea, abdominal

release in gut pain, headache, QT
prolongation

Benzimidazole Moderate antiemetic

derivatives activity

Domperidone D 2 antagonist in gut Gastroparesis, Headaches. This drug is

chemotherapy-induced not available in United
vomiting States.

5-HT 3 receptor High antiemetic

antagonists activity

Ondansetron 5-HT 3 antagonist at Chemotherapy- and Headache

CTZ and ↓ vagal postoperative-induced
Granisetron
afferents from gut vomiting, cyclic
Tropisetron vomiting.
Ondansetron as also
been used in the
Tachykinin receptor High antiemetic treatment of acute
antagonists activity gastroenteritis.
Aprepitant NK 1 antagonist on Chemotherapy-induced Fatigue, dizziness,
emesis program vomiting, effecting on diarrhea
delayed phase

Anticholinergics Minimal-mild
antiemetic activity

Scopolamine Vestibular suppression, Motion sickness Sedation, anti-ACh

anti-ACh effects*

Butyrophenones Moderate antiemetic

activity
 Droperidol D 2 antagonist at CTZ; Chemotherapy- and Hypotension, sedation,
anxiolytic action and postoperative-induced extrapyramidal effects
sedation vomiting

Benzodiazepines Minimal antiemetic

activity

Lorazepam Enhanced central Adjunctive therapy Sedation, respiratory

GABA-ergic induction of (sedation) for depression
Diazepam
anxiolysis, sedation, chemotherapy-induced
and amnesia vomiting and cyclic
Antimigraine- vomiting
abortive triptans

Sumatriptan 5-HT 1B1D agonist; Abortive approach for Transient burning

induces cerebral migraine, abdominal sensation in chest and
vasoconstriction, migraine, cyclic neck
relaxes gastric fundus vomiting;
subcutaneous, PO, and
nasal forms

Zolmitriptan PO, nasal forms

Frovatriptan PO, longer half-life

Other - NSAIDS

Ketorolac Cyclooxygenase Abortive approach for Gastrointestinal

inhibitor of migraine, cyclic bleeding
prostaglandin synthesis vomiting

Antimigraine -
prophylactic
medication

Cyproheptadine H 1 antagonist and Prevention of migraine, Sedation, anti-ACh

5-HT 2 antagonist abdominal migraine, effects,* weight gain
cyclic vomiting due to appetite
stimulation

Pizotyline 5-HT 2 antagonist Not available in United

States

Propranolol β 1 , β 2 adrenergic Prevention of Hypotension,

antagonist abdominal migraine, bradycardia,
cyclic vomiting fatigability; monitor
pulse

Amitriptyline 5-HT 2 antagonist, ↑ Prevention of migraine, Sedation, anti-ACh

synaptic norepinephrine abdominal migraine, effects,* QT
cyclic vomiting prolongation

Phenobarbital GABA A inhibition; Prevention of cyclic Sedation, cognitive

results in ↑ chloride ion vomiting learning difficulties
current

Corticosteroids

Dexamethasone Unknown Adjunctive therapy for Adrenal suppression

chemotherapy- and
postoperative-induced
vomiting

Cannabinoids

Dronabinol Acts on CB1R receptors Chemotherapy-induced Disorientation, vertigo,

on vagus vomiting hallucinations
Nabilone
 ACh: acetylcholine; CB1R: cannabinoid receptor 1; CTZ: chemoreceptor trigger zone; D: dopamine; GERD:
gastroesophageal reflux disease; H: histamine; 5-HT: 5-hydroxytryptamine (serotonin); GABA: gamma
aminobutyric acid; NK: neurokinin; QT: Q-T interval; NSAID: nonsteroidal antiinflammatory drug.
* Anticholinergic effects include blurred vision, dry mouth, hypotension, palpitations, urinary retention.

From B U K. Li, "Vomiting and pyloric stenosis." In Walker's Pediatric Gastrointestinal Disease, 5th Edition.
Kleinman RE, Sanderson IR, Goulet O, Sherman PM, Mieli-Vergani G, and Shneider BL, Eds. B.C. Decker Inc.
Hamilton, Ontario, 2008. Used with permission from People's Medical Publishing House—USA (PMPH-USA),
Shelton, CT.

Graphic 100351 Version 3.0

Contributor Disclosures
Carlo Di Lorenzo, MD Nothing to disclose B UK Li, MD Consultant/Advisory Boards: Takeda
Pharmaceuticals [Antiemetics (Potential drug in early development)]. Alison G Hoppin,
MD Nothing to disclose

Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found,
these are addressed by vetting through a multi-level review process, and through requirements for
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