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Approach To The Infant or Child With Nausea and Vomiting - UpToDate

This document provides an overview of the approach to evaluating and managing nausea and vomiting in infants and children. It defines key terms, describes the physiology and causes of vomiting, and outlines the clinical approach. The clinical approach involves identifying concerning signs that require urgent treatment, determining the etiology based on factors like age and chronicity, treating any complications, and providing supportive care and targeted treatment when possible.
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0% found this document useful (0 votes)
173 views47 pages

Approach To The Infant or Child With Nausea and Vomiting - UpToDate

This document provides an overview of the approach to evaluating and managing nausea and vomiting in infants and children. It defines key terms, describes the physiology and causes of vomiting, and outlines the clinical approach. The clinical approach involves identifying concerning signs that require urgent treatment, determining the etiology based on factors like age and chronicity, treating any complications, and providing supportive care and targeted treatment when possible.
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PDF, TXT or read online on Scribd
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23/2/24, 16:31 Approach to the infant or child with nausea and vomiting - UpToDate

Official reprint from UpToDate®


www.uptodate.com © 2024 UpToDate, Inc. and/or its affiliates. All Rights Reserved.

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: Jan 2024.


This topic last updated: Feb 01, 2023.

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. The symptoms may be
caused by many pathologic states involving several systems (including gastrointestinal,
neurologic, endocrine, renal, and psychiatric). Younger children may not be able to describe
nausea, which may further complicate diagnosis. The diagnostic process is guided by the
medical history and clinical features of specific disorders and their relative frequency among
children in different age groups.

Vomiting and nausea may occur together or separately and may not 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 the accompanying nausea.

This topic review will provide an overview of the causes of nausea and vomiting and a
general approach to diagnosis and management. Individual disorders are discussed in
further detail in linked topic reviews. These include several gastrointestinal disorders that
present with both abdominal pain and nausea or vomiting. 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".)

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DEFINITIONS

● Vomiting (emesis) refers to the forceful oral expulsion of gastric contents associated
with coordinated 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.
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• 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 diaphragm results in forceful


expulsion of gastric contents

CLINICAL APPROACH

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

● Identify concerning signs and symptoms that suggest a serious cause of vomiting that
requires urgent treatment ( table 2). For example, emergency department clinicians
should expeditiously exclude life-threatening disorders such as bowel obstruction,
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diabetic ketoacidosis, adrenal crisis, toxic ingestion, or increased intracranial pressure


(ICP). (See 'Concerning signs' below.)

● Determine the etiology if possible. The differential diagnosis is determined, in part, by


the child's age and whether the nausea and vomiting are acute, chronic, or episodic.

● Treat as appropriate for the cause and severity of vomiting:

• Identify and correct the consequences or complications of nausea and vomiting (eg,
fluid depletion, hypokalemia, and metabolic alkalosis)

• Provide targeted therapy when possible, such as nonoperative reduction for


intussusception, surgery for bowel obstruction or appendicitis, or insulin for diabetic
ketoacidosis

• Provide supportive care and treatment to relieve symptoms (see 'Treatment' below)

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 of pursuing a diagnostic evaluation depends
on 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 2):

● Nonspecific:

• Prolonged vomiting
• Profound lethargy
• Significant weight loss

● Gastrointestinal obstruction or disease:

• Bilious vomiting
• Projectile vomiting in a young infant <12 weeks of age
• Hematemesis
• Hematochezia (rectal bleeding)
• Marked abdominal distension and tenderness

● Neurologic or systemic disease:

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• 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 an appropriate specialist (eg, pediatric gastroenterologist,


pediatric surgeon, neurologist) depending on the suspected cause. As an example,
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), associated symptoms, recent exposures to contacts with similar
symptoms, and the possibility of ingestion of medications or toxic substances.

The following clinical features are especially important ( table 3):

● 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) nonbilious vomiting in an infant <12 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'.)

• Acute, recent onset of vomiting, especially with diarrhea and/or fever, suggests an
infectious gastroenteritis. (See 'Gastroenteritis' below.)

• Onset after infectious illness suggests postinfectious gastroparesis.

• Recurrent 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.)

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• 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.

• Lack of associated nausea and positional triggers for vomiting suggest increased
ICP (especially with headache). (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, inflammatory bowel disease (IBD), and Hirschsprung disease-
associated enterocolitis (especially in neonates or infants with predisposition, 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.)

● Medical history – Underlying disorders may provide clues to the cause of vomiting:

• Congenital anomalies or diseases – Consider anatomic, motility, or immunologic


causes of vomiting

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• Developmental delay – Raises the possibility of undiagnosed metabolic disorder or


syndrome
• Neurologic symptoms or disorders – Consider central nervous system lesions or
dysmotility

Physical examination — The physical examination should include ( table 3):

● 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

• Atypical ("ambiguous") genitalia in an infant and/or hyperkalemia suggest the


possibility of adrenal insufficiency (usually due to congenital adrenal hyperplasia).

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(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' 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:

● Complete blood count


● Electrolytes, glucose, blood urea nitrogen
● Alanine aminotransferase, aspartate aminotransferase
● Amylase, lipase
● Urinalysis

Additional laboratory testing and imaging should be tailored to the differential diagnosis of
the symptoms, based on the history and physical examination ( table 4). For patients with
fever, urinary symptoms, or diarrhea, the evaluation may include urine culture and stool
studies for occult blood, bacterial pathogens, and parasites.

DISORDERS PRIMARILY SEEN IN NEONATES AND YOUNG INFANTS

Gastroesophageal reflux (GER) is common and inconsequential in otherwise healthy infants.


The symptom may be described as vomiting by parents/caregivers but is physiologic and
gradually improves in most infants during the first year of life [4]. (See "Gastroesophageal
reflux in 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 ( table 5):

Pyloric stenosis — Pyloric stenosis is the most common cause of obstruction in infants. It
typically presents with immediate postprandial vomiting in infants <12 weeks of age (usually
between three and six weeks) and is more common in males. It is a condition of hypertrophy
of the pylorus, with elongation and thickening, eventually progressing to near-complete
obstruction of the gastric outlet. (See "Infantile hypertrophic pyloric stenosis".)

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The vomiting is nonbilious and forceful or may become more forceful over time, with
associated weight loss. A minority of infants develop electrolyte imbalances, particularly
hypochloremia, due to loss of gastric hydrochloric acid. An "olive-like" mass is often palpable
at the lateral edge of the rectus abdominis muscle in the right upper quadrant of the
abdomen. Infants who present very early or those who are premature tend to have more
subtle signs and symptoms at presentation. The diagnosis is generally made by abdominal
ultrasound, and surgical treatment is curative.

Intestinal obstruction — 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 midgut volvulus [3]. Bilious vomiting occasionally occurs in infants without bowel
obstruction. Vomiting that is not bilious may be caused by proximal obstruction, most
commonly pyloric stenosis (see 'Pyloric stenosis' above) and, rarely, upper duodenal stenosis,
gastric volvulus, or annular pancreas [5].

● Causes – Causes of intestinal obstruction that present during early infancy include [6]:

• Intestinal atresia – Intestinal atresia typically presents with vomiting (usually


bilious) beginning in the first two days of life. Many patients fail to pass meconium,
depending on the level of obstruction. (See "Intestinal atresia".)

• Intestinal volvulus – Intestinal volvulus presents with sudden onset of vomiting


(usually bilious) with an acute abdomen. It is usually associated with underlying
malrotation, an anomaly of fetal intestinal development in which 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, causing acute
small bowel obstruction and ischemia. Infants with malrotation also may present
with signs of duodenal obstruction (due to Ladd bands that cross the duodenum) or
with associated congenital anomalies such as intestinal atresia or stenosis. (See
"Intestinal malrotation in children".)

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 acute or chronic symptoms. (See 'Malrotation' below.)

• Hirschsprung disease – Most patients with Hirschsprung disease are diagnosed in


the neonatal period, presenting 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). The disorder can also present initially with enterocolitis, a potentially life-
threatening illness in which patients have a sepsis-like picture with fever, vomiting,

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diarrhea, and abdominal distension, which can progress to toxic megacolon. (See
"Congenital aganglionic megacolon (Hirschsprung disease)".)

• Intussusception – Occasionally, intussusception presents in young infants,


although it is most common between 6 and 36 months of age. (See 'Intussusception'
below and "Intussusception in children".)

● Imaging – 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 [7]. In general:

• Conventional abdominal radiograph – Appropriate for suspected bowel obstruction;


it provides a rapid assessment of obstruction with relatively little radiation exposure.

• Abdominal ultrasound – The procedure of choice for detecting pyloric stenosis and
intussusception.

• Upper gastrointestinal contrast study – Usually appropriate if a diagnosis is not


established by ultrasound and proximal bowel obstruction is suspected.

• Contrast enema – Usually appropriate if the abdominal radiograph or physical


examination suggests distal bowel obstruction (as might be seen in Hirschsprung
disease). A contrast enema may be used for diagnostic and therapeutic purposes for
intussusception.

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 prompt initiation of appropriate therapy can be lifesaving and prevent long-term
complications. The clinical presentation varies with the type of metabolic disorder. (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".)

● 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
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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 or fructose. (See "Causes of
hypoglycemia in infants and children", section on 'Hereditary fructose intolerance'.)

Immunologic reactions to food — Immunologic reactions to food that present with


vomiting in infancy include:

● Food protein-induced enterocolitis syndrome (FPIES) – FPIES is an uncommon


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-immunoglobulin E (IgE)-mediated reaction to food, similar to food
protein-induced enteropathy but with more severe manifestations. (See "Food protein-
induced enterocolitis syndrome (FPIES)".)

The term "food protein-induced enteropathy" has been used to describe an


immunologic reaction to dietary proteins that causes a diffuse enteritis and presents
with subacute onset of vomiting, diarrhea, and poor weight gain, sometimes with
bloody stools. This is an older diagnostic term based on findings of flattened intestinal
villi, and the disorder likely overlaps with the more current diagnostic category chronic
FPIES, which is based on clinical description only (without biopsy). (See "Food protein-
induced enterocolitis syndrome (FPIES)", section on 'Allergic food protein-induced
proctocolitis and enteropathy'.)

● IgE-mediated food allergy – IgE-mediated food allergies can present any time after a
dietary protein is introduced. They generally occur shortly after ingestion of the
allergen (usually within minutes). Vomiting is a very common manifestation, often in
conjunction with other symptoms such as diarrhea, urticaria, or wheezing. In young
infants, a common trigger is cow's milk protein. This is most common in infants fed a
cow's milk-based formula or complementary food (eg, yogurt) but occasionally occurs
in exclusively breastfed infants. (See "Milk allergy: Clinical features and diagnosis" and
'Food allergy' below.)
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A more common immunologic reaction to food in infants is isolated allergic proctocolitis,


which presents with bloody stools, usually without vomiting in an otherwise healthy infant.
(See "Food protein-induced allergic proctocolitis of infancy".)

Adrenal insufficiency — Neonates 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. Adrenal crisis occasionally presents in older
individuals with risk factors for adrenal insufficiency. (See 'Adrenal crisis' below.)

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 (but not all) affected infants will be diagnosed
prior to developing adrenal crisis. Adrenal crisis usually presents between the first and fourth
week of life. Affected females have atypical genitalia; males usually have no obvious genital
abnormalities. (See "Clinical manifestations and diagnosis of adrenal insufficiency in
children", section on 'Adrenal crisis'.)

DISORDERS SEEN IN MANY AGE GROUPS

Important causes of vomiting in older infants, children, and adolescents are listed in the
table and outlined below ( table 6):

Infectious causes

Gastroenteritis — Gastroenteritis is by far the most common cause of vomiting in infants,


children, and adolescents and is usually caused by a virus. The vomiting is sudden in onset,
quick to resolve, and often associated with diarrhea. Ill contacts or clusters of cases are
common. Bacterial causes of gastroenteritis may be associated with more prolonged and
severe illness. (See "Acute viral gastroenteritis in children in resource-abundant countries:
Clinical features and diagnosis" and "Clinical manifestations and diagnosis of rotavirus
infection", section on 'Clinical manifestations'.)

Other infections — Pharyngitis (particularly streptococcal pharyngitis), otitis media, and


urinary tract infections are often associated with nausea and/or vomiting, particularly in
young children. (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'.)

Gastrointestinal obstruction

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Intussusception — Intussusception is the most common cause of intestinal obstruction in


children between 6 and 36 months of age but occasionally occurs in younger infants or older
children. In some cases, especially those presenting outside of the typical age range, there is
an associated pathologic lead point, such as a Meckel diverticulum, duplication cyst, or
polyp.

Patients with intussusception typically present with 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. In infants, intussusception may present as lethargy with
or without vomiting or rectal bleeding. (See "Intussusception in children".)

Malrotation — Intestinal malrotation is a congenital anomaly that can present with


symptoms at any age or remain asymptomatic. Among those who develop symptoms,
approximately one-third present during infancy, typically with acute intestinal obstruction
and bilious vomiting due to midgut volvulus [8]. (See 'Intestinal obstruction' above.)

Among those who develop symptoms during childhood or adolescence (approximately 20


percent), the presentation varies from acute obstruction to subacute onset with intermittent
abdominal pain, usually but not always with vomiting, which may or may not be bilious.

The clinical presentation, diagnosis, and management of intestinal malrotation are discussed
separately. (See "Intestinal malrotation in children".)

Other gastrointestinal causes

Gastroesophageal reflux disease — Gastroesophageal reflux disease (GERD) is an


important consideration in 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".)

In infants, most regurgitation is physiologic and inconsequential. A minority of infants who


regurgitate have 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. Reflux may be associated
with bradycardia or cyanotic episodes, particularly in preterm or neurologically impaired
infants. Poor weight gain despite an adequate intake of calories should prompt evaluation
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for causes of vomiting and weight loss other than GERD. (See "Gastroesophageal reflux in
infants", section on 'Evaluation and management by presenting symptoms'.)

Gastroparesis — Postinfectious gastroparesis is a relatively common cause of vomiting in


children. It is a consequence of an acute viral illness (often rotavirus gastroenteritis) that
results in chronic postprandial antral hypomotility. Typical symptoms are postprandial
fullness and nausea as well as postprandial vomiting. 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. In
most cases, the symptoms resolve spontaneously within 6 to 24 months [9]. (See
"Gastroparesis: Etiology, clinical manifestations, and diagnosis".)

Uncommon causes of gastroparesis in children are:

● 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

Appendicitis — Appendicitis presents most frequently in the second decade of life and is
the most common indication for emergency abdominal surgery in childhood.

Typical symptoms are:

● Early symptoms – Often subtle and nonspecific, including indigestion, flatulence, bowel
irregularity, and malaise.

● Pain – Subsequently, pain develops in the epigastrium or periumbilical region, which is


visceral in character (ie, constant, not very severe in intensity, and poorly localizable).
The location of the pain may vary depending on 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. The pain
eventually localizes to the right lower quadrant once inflammation involves the
overlying parietal peritoneum.

● Nausea and vomiting – If nausea and vomiting occur, they 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".)

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Eosinophilic esophagitis or gastroenteritis — Eosinophilic disease can affect multiple


parts of the upper gastrointestinal tract, together or separately.

● Eosinophilic esophagitis is much more common in males than in females. Toddlers tend
to experience epigastric pain, nausea and vomiting, and feeding aversion. Adolescents
tend to have symptoms of dysphagia and may present with an acute 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 (EoE)".)

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

Inflammatory bowel disease — inflammatory bowel disease (IBD; ulcerative colitis and
Crohn disease) may present with complaints of nausea, but frank vomiting is rarely a primary
presenting symptom. These diseases should be considered if there are suggestive chronic
features in the history and clinical presentation, especially growth failure, diarrhea (with or
without blood), abdominal pain, perianal disease, anemia, or arthritis. (See "Clinical
presentation and diagnosis of inflammatory bowel disease in children".)

Functional gastrointestinal disorders

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 [11]. Patients with functional
dyspepsia often report nausea or postprandial distress, but persistent vomiting is
uncommon.

Functional dyspepsia must be distinguished from dyspepsia caused by 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".)

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Functional nausea and functional vomiting — These categories were added to the
descriptions of functional gastrointestinal disorders in the 2016 Rome IV classification [12].
By definition, these disorders are not otherwise explained and the vomiting is not self-
induced; they are distinguished from functional dyspepsia by the absence of abdominal pain.
They occur in approximately 1 percent of school-aged children and adolescents [13,14].

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. They are more common in individuals with underlying anxiety or depression.
Patients often report early morning nausea that improves throughout the day [15].

The diagnosis requires excluding other causes of the symptoms, usually with a focused
history and physical examination, considering especially pregnancy, postviral gastroparesis
(see 'Gastroparesis' above), and intracranial hypertension (suggested by weight loss,
neurologic symptoms, severe morning vomiting or headaches) (see 'Intracranial
hypertension' below). Endoscopy is sometimes appropriate but not required to make the
diagnosis [12]. In addition, the diagnosis is supported by the presence of risk factors for
functional gastrointestinal disorders, including psychological distress or a family history of
functional gastrointestinal disorders.

Similar to other functional gastrointestinal disorders, the most valuable intervention for
functional nausea and vomiting 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".)

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 pattern of episodic 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. A notable feature
is compulsive hot water bathing during an episode; this behavior is also seen in cannabis
hyperemesis syndrome.

Cyclic vomiting has been most often described in school-aged children but may affect other
age groups. The etiology is unknown, but many patients have a personal or family history of
migraine headaches, suggesting that there may be a common pathophysiologic process.
(See "Cyclic vomiting syndrome".)

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Cannabis hyperemesis syndrome — Chronic use of cannabis in adolescents may trigger


episodes of vomiting that resemble cyclic vomiting syndrome. Diagnostic criteria include
[18]:

● Onset after prolonged, excessive cannabis use


● Relief of vomiting episodes by sustained cessation of cannabis use

The syndrome is also associated with pathologic bathing behavior (prolonged hot baths or
showers), which supports the diagnosis. However, these behaviors are also found in cyclic
vomiting syndrome. (See "Cannabis use and disorder: Epidemiology, pharmacology,
comorbidities, and adverse effects", section on 'Medical and systemic effects'.)

Rumination syndrome — Rumination syndrome is characterized by effortless


regurgitation and rechewing or expulsion of food beginning soon after a meal, without
nausea or retching [12]. The symptoms disappear hours after eating, once the regurgitated
material becomes acidic, and do not occur during sleep. (See "Rumination syndrome".)

Rumination syndrome has been described in infants with sensory and emotional deprivation
[19]. The disorder occurs more commonly in older children and is especially prevalent in
adolescent girls [12,20]. 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 [21]. (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'.)

Endocrine/metabolic

Diabetic ketoacidosis — Approximately 30 percent of children with type 1 diabetes first


present with signs and symptoms of diabetic ketoacidosis. Most present with anorexia,
nausea, vomiting, abdominal pain, and polyuria, sometimes with neurologic symptoms. The
onset can be insidious so that the diagnosis is not recognized until laboratory testing is
performed. The symptoms may be harder to appreciate in infants and very young children
who are not toilet trained, leading to delayed diagnosis and more severe ketoacidosis. (See
"Diabetic ketoacidosis in children: Clinical features and diagnosis".)

Adrenal crisis — Adrenal crisis is uncommon but should be considered as a cause of


unexplained vomiting in children of any age with:

● Risk factors for adrenal insufficiency – Known adrenal insufficiency, history of


glucocorticoid use
● Suspicious symptoms and signs – Disproportionate hypotension, hyponatremia, and/or
hyperkalemic acidosis and hyperpigmentation

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Adrenal crisis is a medical emergency requiring immediate treatment with intravenous fluids
and stress doses of glucocorticoids. Clinical features and management of adrenal crisis are
summarized in the table ( table 7) and discussed in more detail in a separate topic review.
(See "Clinical manifestations and diagnosis of adrenal insufficiency in children", section on
'Adrenal crisis'.)

Neurologic

Intracranial hypertension — Brain tumors and other intracranial masses can cause
vomiting 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 have obesity. (See "Idiopathic intracranial hypertension
(pseudotumor cerebri): Clinical features and diagnosis".)

Migraine — Migraine is characterized by periodic episodes of paroxysmal headache, often


accompanied by nausea, vomiting, and abdominal pain and often with vertigo, relieved by
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".)

Miscellaneous

Posttussive — Posttussive emesis is a common consequence of vigorous or paroxysmal


coughing. It is a classic symptom of pertussis infection but also can occur with vigorous
coughing from any cause, including asthma or an airway foreign body [22,23]. It may also
occur in children with developmental disabilities who may have abnormal swallowing and
may choke and cough when oral and nasal secretions accumulate in the hypopharynx. The
cough is then often followed by vomiting. (See "Pertussis infection in infants and children:

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Clinical features and diagnosis" and "Airway foreign bodies in children" and "Approach to
chronic cough in children".)

Food allergy — Anaphylaxis is an IgE-mediated hypersensitivity reaction. When triggered


by ingested substances (typically foods or medications), it tends to present with prominent
gastrointestinal symptoms, including nausea, crampy or colicky abdominal pain, vomiting
(sometimes large quantities of "stringy" mucus), and diarrhea. The symptoms' reactions are
rapid in onset, typically beginning within minutes to two hours from the time of ingestion.

Gastrointestinal symptoms are rarely the sole manifestations of a food-allergic reaction.


Concurrent anaphylactic symptoms may 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.

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".)

Pregnancy — Pediatricians should have a low threshold for suspecting pregnancy in


adolescents. Adolescents may present with complaints of menstrual irregularity, abdominal
pain, or other symptoms. These complaints may represent a "hidden agenda," or the
adolescent may not have considered the possibility of pregnancy. (See "Pregnancy in
adolescents", section on 'Diagnosis of pregnancy'.)

Bulimia — Bulimia nervosa is characterized by episodes of binge eating, with inappropriate


compensatory behavior to prevent weight gain (typically vomiting). The vomiting is typically
self-induced, but some patients can trigger vomiting at will. This diagnosis should be
considered in a patient with excessive concerns about body weight and shape. Most but not
all cases are in females, with onset during adolescence or young adulthood. (See "Eating
disorders: Overview of epidemiology, clinical features, and diagnosis", section on 'Bulimia
nervosa'.)

Toxic ingestions — Toxic ingestions often present with vomiting and/or altered mental
status, especially in a younger child with acute onset of symptoms. Particular considerations
for a young child include lead toxicity and any medications or household cleaning agents
that the child may have had access to. Common ingestions in adolescents are alcohol and
recreational drugs. (See "Approach to the child with occult toxic exposure".)

Medical child abuse — Medical child abuse consists of a caregiver fabricating or inducing
illness in a child in order to get attention. The patient may have a history of frequent
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recurrent illnesses without a clear etiology. As an example, ipecac poisoning can present with
recurrent, unexplained vomiting and repeated hospitalizations; the diagnosis can be
confirmed by urine toxicology [24,25]. (See "Medical child abuse (Munchausen syndrome by
proxy)".)

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

● Reported history varies from what is observed or does not make sense
● Illness is unexplained, unusual, or prolonged and does not respond to treatment as
expected
● Symptoms seem to originate only in the presence of the suspected perpetrator
● Problem resolves or improves when the child is separated from the suspected
perpetrator
● 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
● 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
● Alleged perpetrator does not seem to be as worried by the child's illness as the health
professionals who are caring for the child

Diagnostic differences between children and adolescents — There are a few notable
differences in the diagnostic profile between children and adolescents:

● Pregnancy and acute intermittent porphyria can present with vomiting in postpubertal
adolescents. Migraines, bulimia, and cannabis hyperemesis syndrome also occur more
frequently in adolescents than in children.

● In contrast, intussusception, renal hydronephrosis, and medical child abuse occur more
commonly during childhood.

TREATMENT

Treatment of nausea and vomiting depends on the underlying etiology:

● Targeted treatment – Provide targeted therapy if appropriate for the cause, such as
nonoperative reduction for intussusception, surgery for bowel obstruction or
appendicitis, or insulin for diabetic ketoacidosis.

● Supportive care – Correct any electrolyte abnormalities, metabolic abnormalities, or


nutritional deficiencies. Offer referral for cognitive-behavioral interventions for

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vomiting associated with functional dyspepsia, adolescent rumination syndrome, and


bulimia.

● Antiemetics – Antiemetics are useful for selected causes of persistent vomiting to


avoid electrolyte abnormalities or nutritional sequelae. They are not generally
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 8); 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-abundant 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 on 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 postinfectious 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 [2,26]. (See "Postoperative nausea and vomiting".)
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• 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.

● Complementary and alternative medicine – Patients and families/caregivers 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 [27]. 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 [11,28,29]. Hypnotherapy is often helpful for treatment of
anticipatory nausea and vomiting (eg, prior to chemotherapy) [30] and has been found
beneficial in children with functional nausea [31]. The definitions and general
approaches of other complementary and alternative techniques are discussed
separately. (See "Complementary and integrative health 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.)

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● 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

● Goals – Nausea and vomiting may be caused by a wide range of conditions affecting
several different organ systems, with vastly different health implications. The goals of
the evaluation are to quickly identify serious conditions for which immediate
intervention is required and then to identify a specific cause of the symptoms to guide
management. (See 'Clinical approach' above.)

● Causes – The causes of vomiting vary by age at presentation:

• Disorders primarily seen in neonates and young infants ( table 5) (see 'Disorders
primarily seen in neonates and young infants' above)

• Disorders in older infants, children, and adolescents ( table 6) (see 'Disorders seen
in many age groups' above)

● Evaluation – 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. The
diagnostic evaluation includes:

• A focused history and physical examination ( table 3) (see 'History' above and
'Physical examination' above)

• Laboratory testing, guided by the history and physical examination ( table 4) (see
'Laboratory testing' above)

● Concerning signs – The following symptoms and signs provide important clues to
disorders requiring urgent intervention ( table 2) (see 'Concerning signs' above and
'History' above and 'Physical examination' above):

• Prolonged vomiting – 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.

• Obstruction – Symptoms and signs suggestive of intestinal obstruction include


marked abdominal distension, visible bowel loops, absent bowel sounds or

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increased high-pitched bowel sounds ("borborygmi"), severe abdominal pain, or


vomitus that is bilious (green or yellow) or feculent (with the odor of feces).

- In a neonate, 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.)

- In an infant or toddler, the sudden onset of intermittent, severe, crampy,


progressive abdominal pain 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.)

• Neurologic symptoms – Headache, positional triggers for vomiting, vomiting upon


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.)

• Hypotension – Hypotension disproportionate to the apparent illness and/or


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

• Recurrent episodes – 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.)

● Treatment – Treatment of nausea and vomiting depends on the underlying etiology


and involves targeted treatment for certain disorders, supportive care, and,
occasionally, antiemetics ( table 8) (for selected patients). (See 'Treatment' above.)

Use of UpToDate is subject to the Terms of Use.

REFERENCES

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16. Kovacic K, Di Lorenzo C. Functional Nausea in Children. J Pediatr Gastroenterol Nutr


2016; 62:365.
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Adolescent Cannabinoid Hyperemesis Syndrome: A Systematic Review. J Adolesc Health
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19. Zeevenhooven J, Koppen IJ, Benninga MA. The New Rome IV Criteria for Functional
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20. Chial HJ, Camilleri M, Williams DE, et al. Rumination syndrome in children and
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22. Kang L, Cui X, Fu J, et al. Clinical characteristics of 967 children with pertussis: a single-
center analysis over an 8-year period in Beijing, China. Eur J Clin Microbiol Infect Dis
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23. Turbyville J, Gada S, Payne K, et al. Posttussive emesis as a symptom of asthma in
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24. McClung HJ, Murray R, Braden NJ, et al. Intentional ipecac poisoning in children. Am J Dis
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27. Vlieger AM, Blink M, Tromp E, Benninga MA. Use of complementary and alternative
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28. Ghayur MN, Gilani AH. Pharmacological basis for the medicinal use of ginger in
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29. von Arnim U, Peitz U, Vinson B, et al. STW 5, a phytopharmacon for patients with
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30. 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.
31. Browne PD, de Bruijn CMA, Speksnijder EM, et al. Skills or Pills: Randomized Trial
Comparing Hypnotherapy to Medical Treatment in Children With Functional Nausea. Clin

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Gastroenterol Hepatol 2022; 20:1847.


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GRAPHICS

Terminology related to nausea and vomiting

Anorexia Loss of desire to eat, ie, a true loss of appetite

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

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 abdomina
and diaphragmatic muscular activity that characterizes vomiting

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 Regurgitation of food into the mouth through a voluntary increase in


abdominal pressure within minutes of eating or during eating. The
regurgitated food is then chewed and reswallowed or spit out.

Sitophobia Fear of eating because of subsequent or associated discomfort

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

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

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Concerning signs in an infant or child with nausea or vomiting

Concerning signs Comments or diagnostic considerations

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 or
>48 hours in older children 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 gastrointestinal obstruction or disease

Bilious vomiting Intestinal obstruction, especially in a neonate

Projectile vomiting Pyloric stenosis in a young infant (<12 weeks o


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)

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 idiopathic intracranial
hypertension)

Altered consciousness, seizures, or focal Toxic ingestion, diabetic ketoacidosis, CNS


neurologic abnormalities mass, or inborn error of metabolism

History or physical signs of trauma Subdural hematoma or intra-abdominal injury


(eg, duodenal hematoma)

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Hypotension disproportionate to apparent Adrenal crisis


illness and/or hyponatremia with hyperkalemia

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

Courtesy of Carlo Di Lorenzo, MD.

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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 Gastroesophageal reflux


vomiting/regurgitation 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)
Cannabis hyperemesis syndrome
Porphyria, carcinoid, pheochromocytoma, familial dysautonomia

Vomiting triggered by specific foods

Vomiting begins within Food allergy (eg, anaphylaxis)


minutes to 2 hours of
ingesting the food,
usually with cutaneous
or respiratory
symptoms

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


with diarrhea

Triggered by Galactosemia
introduction of lactose

Triggered by Hereditary fructose intolerance


introduction of
fructose or sucrose

Undigested food in Can be seen with vomiting from any cause that occurs immediately
vomitus after eating

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Achalasia*
Other esophageal obstructions (eg, foreign body in the esophagus)

Heartburn Esophagitis (peptic or eosinophilic)

Physical examination

One or more of these Intestinal obstruction


findings:
Marked abdominal
distension
Visible bowel loops
Vomitus bilious
(green or yellow) or
feculent (with the
odor of feces)
Bowel sounds either
absent, or increased
and high-pitched

Focal tenderness RLQ – Appendicitis or Crohn disease


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

Hepatomegaly, Viral hepatitis, viral infection (eg, EBV), metabolic disorders


splenomegaly, jaundice

Ataxia, dizziness, Vestibular neuronitis or acute cerebellar ataxia


nystagmus

Papilledema Increased ICP

Atypical genitalia Congenital adrenal hyperplasia with vomiting due to adrenal crisis
(infants)

Unusual odor Inborn error of metabolism

Enlarged parotid glands Bulimia (adolescents)

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.

* Typical symptoms of achalasia include gradual onset of recurrent nonforceful regurgitation of bland
undigested food or saliva, sometimes with a sensation of retrosternal fullness after a meal.

Courtesy of Carlo Di Lorenzo, MD.

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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,


appendicitis, and sepsis.

Electrolytes, BUN, creatinine Electrolyte abnormalities are associated with pyloric stenosis, adrenal
insufficiency, and metabolic diseases.

Elevated BUN and creatinine are seen in kidney disease.

Hepatic aminotransferases Elevated AST, ALT, total bilirubin, and GGTP 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


reducing substances urea 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 (including upright
view)

Upper gastrointestinal series If an anatomic abnormality of the upper gastrointestinal tract is


suspected (eg, neonate with bilious vomiting).

Head imaging (CT or MRI) 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; GGTP: gamma-glutamyl transpeptidase; CT: computed tomography; MRI:
magnetic resonance imaging.

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Differential diagnosis of vomiting or reflux in neonates and young infants

Disorder Typical clinical features in neonates and young infants

Gastrointestinal obstruction

Pyloric stenosis * Forceful vomiting, typically nonbilious, and beginning at 3 to 6 weeks o


age.

Malrotation with Sudden onset of bilious vomiting and an acute abdomen, starting at
volvulus * any age.

Intussusception * (may be Sudden onset of intermittent colicky abdominal pain, sometimes with
intermittent) vomiting and maroon-colored hematochezia. Most common between 6
and 36 months of age but may present in neonates. May have Dance
sign (retraction of the right iliac fossa).

Intestinal atresia, Bilious vomiting (if lesion distal to ampulla of Vater) and gastric or
stenosis, or duplication * abdominal distension, usually presenting within hours or days of birth.

Antral or duodenal web * Range of presentation, depending on severity of obstruction. In


neonates, presents with vomiting (usually bilious) and gastric
distension. Older children may present with foreign body retention.

Hirschsprung disease * Abdominal distension, often with failure to pass meconium within the
first 48 hours of life and sometimes with bilious emesis. A minority of
patients present with Hirschsprung-associated enterocolitis, with an
acute presentation including fever, vomiting, diarrhea, and septic
shock. Increased risk in infants with Down syndrome.

Foreign body More common in infants 6 to 36 months. Wide range of presentations,


including asymptomatic, choking, vomiting, feeding refusal, or delayed
symptoms of esophageal perforation.

Incarcerated hernia Irritability, sometimes with abdominal distension and vomiting; firm
inguinal mass.

Other gastrointestinal causes

Uncomplicated Infant with regurgitation but otherwise healthy ("happy spitter").


gastroesophageal reflux *

Infant rumination Chewing and re-swallowing of regurgitated food within minutes of


syndrome eating or during eating; may be associated with emotional and sensory
deprivation. Onset is typically between 3 and 8 months.

GERD with esophagitis Infant with frequent regurgitation and concerning symptoms (poor
weight gain, feeding refusal, or marked irritability). These symptoms
are nonspecific and are more commonly due to causes other than
GERD.

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Food protein-induced (eg, Anaphylaxis – Vomiting and diarrhea, beginning within minutes to 2
anaphylaxis, food protein- hours after ingestion of triggering food, often accompanied by
induced enteropathy urticaria, angioedema, and other anaphylactic symptoms.
[chronic FPIES], or acute
Acute FPIES – Severe vomiting, diarrhea, and lethargy within 2 hours of
FPIES)
ingesting an offending protein. Typically presents in early infancy,
approximately 1 to 4 weeks after introduction of cow's milk, soy, or
solid foods.

Gastroenteritis Acute onset in otherwise healthy infant, often with diarrhea. May have
contacts with similar symptoms.

Peptic ulcer disease, Rare in infants but may be associated with use of NSAIDs.
gastritis

Eosinophilic esophagitis Uncommon in infants. Feeding aversion, weight loss, sometimes with
hypoalbuminemia; often associated with atopic disorders such eczema
or asthma.

Eosinophilic Uncommon in infants. Weight loss or poor weight gain, vomiting, and
gastroenteritis hypalbuminemia.

Gastroparesis Uncommon in infants. May be postviral, due to metabolic disturbance,


or associated with disorders with neuromuscular dysfunction or
pseudo-obstruction.

Central nervous system

Hydrocephalus Signs of increased intracranial pressure: bulging fontanelle (in younger


infants), papilledema, emesis that is triggered by an abrupt change in
Subdural hematoma
body position, neurologic deficit.
Intracranial hemorrhage

Mass lesion

Infection

Sepsis Refer to UpToDate content on these disorders for clinical presentation


and diagnosis.
Meningitis

Urinary tract infection

Pneumonia

Otitis media

Hepatitis Elevated liver enzymes. Many causes and clinical presentations, ranging
from asymptomatic to acute liver failure.

Metabolic/endocrinologic disorders

Galactosemia * Vomiting, jaundice, hepatomegaly, and poor weight gain, typically


developing within the first few days after birth (if feeds are with breast
milk or any cow's milk-based formula).

Hereditary fructose Recurrent hypoglycemia and vomiting after feeds with fructose or
intolerance sucrose (eg, fruits or infant formula containing these sugars).

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Urea cycle defects * Frequent vomiting and poor appetite, often developing within a few
days after birth. Plasma ammonia elevated for age, sometimes with
respiratory alkalosis.

Amino and organic Wide range of presentations; may include associated hypoglycemia or
acidemias * liver disease. Many of these disorders are included in newborn
screening. Refer to UpToDate content on inborn errors of metabolism.
Fatty acid oxidation
disorders *

Congenital adrenal May have atypical genitalia, diarrhea, hypovolemia, hyponatremia,


hyperplasia with adrenal hyperkalemia, hypoglycemia, and hypotension. Often but not always
crisis * detected by newborn screening.

Kidneys

Obstructive uropathy Hydronephrosis or oligohydramnios on prenatal ultrasound;


overdistended bladder, failure to thrive, urosepsis.

Kidney function Edema, reduced urine output, hypertension; elevated creatinine and
impairment BUN.

Cardiac

Heart failure Presentation varies but may include poor feeding, respiratory distress,
cyanosis, shock, acidosis, and congestive heart failure. For some types
of congenital heart disease, presents during the first few weeks of life
as the ductus arteriosus closes.

This table describes important considerations in the differential diagnosis of vomiting in neonates and
young infants. For more details and the range of clinical presentations, refer to UpToDate content on
the individual disorders.

BUN: blood urea nitrogen; FPIES: food protein-induced enterocolitis syndrome; GERD:
gastroesophageal reflux disease; NSAIDs: nonsteroidal antiinflammatory drugs.

* Disorders that typically present in the neonatal period.

Adapted 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.

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Common or critical causes of vomiting in older infants, children, or


adolescents

Disorder Typical clinical features

Infectious

Gastroenteritis* Sudden onset, usually with diarrhea and ill contacts. Most common
cause of vomiting in all age groups.

Pharyngitis* Sore throat, pharyngeal erythema. Vomiting is common with


streptococcal pharyngitis.

Otitis media* Ear pain, fever, often with vomiting. May include labyrinthitis, which
tends to cause vertigo or ataxia.

Urinary tract infections Urinary symptoms, fever. Vomiting is common, particularly in infants.

Gastrointestinal obstruction

Intussusception Intermittent, crampy abdominal pain and vomiting; may have lethargy,
bloody stools, or palpable right lower quadrant mass. Most common
between 6 and 36 months of age.

Malrotation Can present at any age and with variable symptoms:


Acute onset – Symptoms of intestinal obstruction due to midgut
volvulus, including bilious vomiting (especially in infants).
Subacute or recurrent onset – Abdominal pain, usually with
vomiting, which may or may not be bilious.

Other intestinal Incarcerated inguinal hernia, superior mesenteric artery syndrome,


obstructions duodenal hematoma (post-trauma).

Other gastrointestinal causes

GERD* Vomiting is typically small volume, postprandial, and not forceful.

Peptic ulcer disease, Helicobacter pylori or chronic NSAID use may be implicated in both
gastritis* disorders.

Gastroparesis* Vomiting tends to occur several hours after eating. May be


postinfectious or related to underlying neuromuscular disorders or
metabolic disturbances.

Appendicitis* Abdominal pain and tenderness, migrating to the right lower quadrant

Celiac disease* Vomiting is more common in the younger child, along with growth
failure.

Eosinophilic esophagitis Epigastric pain, nausea and vomiting, and feeding aversion; older
or gastroenteritis patients may present with dysphagia or food impaction.

Inflammatory bowel Most common after 6 years of age but can present in any age group.
disease Gastrointestinal symptoms often include diarrhea, hematochezia, and,
occasionally, vomiting.

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Pancreatitis Epigastric, left upper quadrant pain radiating to back. Suggested by


elevated lipase, with or without elevated bilirubin or liver
transaminases. Uncommon in infants. May be viral induced or genetic
(if recurrent) or associated with biliary obstruction (eg, biliary stones).

Functional gastrointestinal disorders

Functional dyspepsia* Persistent or recurrent pain in upper abdomen; often associated with
postprandial nausea, vomiting, and early satiety.

Functional nausea and Nausea and/or vomiting without associated abdominal pain and with
vomiting* no underlying gastrointestinal cause. More common in individuals with
underlying anxiety or depression.

Cyclic vomiting syndrome Recurrent episodes of nausea and intense vomiting lasting hours to
days, separated by symptom-free periods.

Cannabis hyperemesis Episodes of vomiting that resemble cyclic vomiting syndrome, often
syndrome with repetitive hot water bathing behavior. Associated with prolonged,
excessive cannabis use in adolescents and young adults.

Rumination syndrome Painless chewing and re-swallowing of regurgitated food within


minutes of eating or during eating.

Endocrine/metabolic

Diabetic ketoacidosis* Polydipsia, polyuria, fatigue, sometimes with nocturia or enuresis.


Nausea, vomiting, and acute weight loss are common. May present
with vaginal or cutaneous candidiasis, especially in infants.

Adrenal crisis Signs may include hyponatremia, hyperkalemia, hypoglycemia, and


hypotension. Consider in infants with atypical genitalia or any child with
known adrenal insufficiency or pituitary hormone deficiencies.

Neurologic

Increased intracranial Causes include intracranial tumor, subdural hematoma from head
pressure (eg, mass, trauma, or hydrocephalus. Vomiting tends to occur in the morning and
hemorrhage) with associated headaches.

Migraine Episodic headache, nausea, vomiting, and abdominal pain, often with
vertigo, relieved by sleep. Family history of migraines is common.

Miscellaneous

Posttussive* Causes include coughing related to asthma, infection, or foreign body.

Food allergy (anaphylaxis) Vomiting, abdominal pain, and diarrhea, usually with urticaria,
angioedema, and/or respiratory and cardiovascular symptoms. Onset
within minutes to hours after ingesting an allergen.

Acute hydronephrosis Can present with abdominal pain and vomiting (Dietl crisis) that may
mimic a cyclic vomiting syndrome episode.

Pregnancy Consider in any adolescent female presenting with nausea or vomiting


especially with complaints of menstrual irregularity.

Bulimia nervosa Consider in a patient with concerns about body weight and shape. Mos

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cases are in adolescent females.

Toxic ingestion Refer to UpToDate content on the child with occult toxic exposure.

Medical child abuse (eg, May present with frequent recurrent illnesses without a clear etiology;
poisoning, head trauma) often requiring hospitalization. For details, refer to UpToDate content
on medical child abuse.

This table highlights common or critical causes of nausea and vomiting in infants (beyond the
neonatal period), children, and adolescents. For details on clinical presentation and evaluation, refer
to the relevant UpToDate content.

GERD: gastroesophageal reflux disease; NSAID: nonsteroidal antiinflammatory drug.

* Relatively common causes.

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Rapid overview: Adrenal crisis in children and adolescents

Signs and symptoms that may indicate adrenal crisis:

Vomiting and diarrhea, sometimes with severe abdominal pain or unexplained fever, weight loss,
and anorexia.

Serum electrolyte abnormalities:

Hyponatremia with or without hyperkalemia.

Metabolic acidosis.

Hypoglycemia (especially in young children).

Hypotension or shock, particularly if disproportionate to apparent underlying illness.

Consider the diagnosis in:

Neonates with atypical genitalia and/or electrolyte abnormalities, lethargy, hypoglycemia,


hypotension or shock, or failure to thrive. These may be presenting features of CAH due to 21-
hydroxylase deficiency* or (very rarely) other causes of adrenal insufficiency.

In the United States, 21-hydroxylase deficiency is part of the newborn screen in all states, so
most affected infants will be diagnosed prior to presentation with adrenal crisis. Adrenal crisis
usually presents between 10 and 20 days of life. Affected females usually have atypical
genitalia (varying severity). Males usually do not have genital abnormalities.

The presentation of adrenal crisis in an infant may mimic that of pyloric stenosis. However,
infants with pyloric stenosis typically have hypokalemic alkalosis rather than the hyperkalemic
acidosis that is typical of adrenal crisis.

Any patient with known disorders of adrenal insufficiency (eg, CAH), especially if exposed to
stress (illness).

Patients on chronic treatment with corticosteroids, especially if exposed to stress or during a


tapering of the corticosteroid dose.

Patients with other autoimmune endocrine deficiencies, such as type 1 diabetes mellitus,
hypothyroidism, or gonadal failure.

Critically ill patients with septic shock, who are unresponsive to fluid resuscitation and
inotropic medications (in this case, adrenal crisis can be caused by bilateral adrenal hemorrhage)

Other patients presenting with the above signs, especially those with hyperpigmentation or
vitiligo.

Evaluation:

If adrenal crisis is suspected, then patients should be treated empirically with stress doses of
glucocorticoids, as outlined below.

For patients without a preexisting diagnosis of adrenal insufficiency, draw baseline blood
samples prior to the administration of glucocorticoids for subsequent testing for electrolytes,
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glucose, cortisol and other adrenal steroids (17-hydroxyprogesterone if CAH is suspected)*,


ACTH, and plasma renin activity. Treatment with glucocorticoids can be initiated presumptively
once blood samples are drawn. If the blood samples cannot be rapidly obtained and the patient
is acutely ill, proceed immediately to treatment.

Treatment:

Shock – Give a bolus of normal saline (0.9%), 20 mL/kg IV over 1 hour. If shock is persistent,
repeat up to a total of 60 mL/kg within 2 hours.

Hypoglycemia – Give an initial bolus of 0.5 to 1 g/kg of dextrose IV (maximum single dose 25 g).
The glucose bolus is infused slowly, at 2 to 3 mL per minute.

For all age groups, this can be given as 25% dextrose solution (D25W), 2 to 4 mL/kg. (D25W is
250 mg dextrose/mL.)

An alternative for infants and children up to 12 years of age is to use 10% dextrose solution
(D10W), 5 to 10 mL/kg. (D10W is 100 mg dextrose/mL.)

Stress glucocorticoids – Administer hydrocortisone (Solu-Cortef) as a bolus, using a dose of 50


to 100 mg/m 2 IV. ¶ Δ If body surface area is not available, age-based dosing may be used as
follows:

Infants and toddlers 0 to 3 years old – 25 mg IV.

Children 3 to 12 years – 50 mg IV.

Children and adolescents 12 years and older – 100 mg IV.

Continue glucocorticoids at the same dose given as a constant rate or as 4 divided doses over the
following 24 hours. The subsequent dose and duration depend on the patient's clinical status.

Electrolytes – If hyperkalemia is present, perform EKG to evaluate:

EKG changes consistent with hyperkalemia – Initially a tall, peaked T wave with shortened QT
interval, followed by progressive lengthening of the PR interval and QRS duration.

Hyperkalemia typically improves promptly with fluids and hydrocortisone therapy alone.
Rarely, severe and symptomatic hyperkalemia requires emergency therapy (ie, IV calcium
infusion followed by IV insulin and glucose infusion; refer to UpToDate topic on the
management of hyperkalemia in children).

Monitor and treat other electrolyte abnormalities and fluid balance.

CAH: congenital adrenal hyperplasia; ACTH: adrenocorticotropic hormone (corticotropin); IV:


intravenous; EKG: electrocardiogram; BSA: body surface area; IM: intramuscularly.

* Refer to UpToDate content on classic CAH due to 21-hydroxylase deficiency.

¶ Dosing based on BSA is preferred if the patient's BSA is known or if the BSA can be promptly
calculated based on measured height and weight. A BSA calculator is available in the UpToDate
program.

Δ Hydrocortisone also may be given IM if IV access is not readily available.

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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 H1 effects*
Hydroxyzine
antagonist
Dimenhydrinate

Meclizine

Antipsychotics Mild to moderate


antiemetic activity

Promethazine D2 antagonist at CTZ Chemotherapy-induced Anti-ACh effects*,


and H1 antagonist vomiting. extrapyramidal
reactions, QTc
Prochlorperazine D2 antagonist at CTZ
prolongation
Chlorpromazine

Olanzapine D2 antagonist at CTZ, 5-


HT6 antagonist

Substituted Moderate
benzamides antiemetic activity

Metoclopramide D2 antagonist at CTZ GERD; gastroparesis; Irritability and


and 5-HT4 agonist in chemotherapy-induced extrapyramidal
gut vomiting. reactions

Trimethobenzamide D2 antagonist at CTZ

Cisapride 5-HT4 agonist, ACh GERD; gastroparesis. Diarrhea, abdominal


release in gut pain, headache, QT
prolongation

Benzimidazole Moderate
derivatives antiemetic activity

Domperidone D2 antagonist in gut Gastroparesis; Headaches; not


chemotherapy-induced available in the United
vomiting. States

Motilin agonist

Erythromycin Motilin agonist and ACh Gastroparesis (eg, Nausea, diarrhea


release postinfectious).

5-HT3 receptor High antiemetic


antagonists activity

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Ondansetron 5-HT3 antagonist at CTZ Chemotherapy- and Headache, constipation


and decreases vagal postoperative-induced
afferents from gut vomiting; cyclic
Granisetron vomiting syndrome.

Ondansetron has also


been used in the
Tropisetron treatment of acute
gastroenteritis.

Ondansetron comes in
Dolasetron PO, IM, and IV
formulations. All others
are IV formulations
Palonosetron only. Palonosetron has
a longer half-life (40
hours).

Tachykinin receptor High antiemetic


antagonists activity

Aprepitant NK1 antagonist, acts on Chemotherapy-induced Fatigue, dizziness,


emetic program vomiting (effect is on diarrhea
delayed phase, >24
hours); cyclic vomiting
syndrome.

Anticholinergics Minimal to mild


antiemetic activity

Scopolamine Vestibular suppression, Motion sickness. Sedation, anti-ACh


anti-ACh effects*

Butyrophenones Moderate
antiemetic activity

Droperidol D2 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 signaling; (sedation) for depression
induces anxiolysis, chemotherapy-induced
sedation, and amnesia vomiting and cyclic
Diazepam vomiting syndrome ¶ .
Diazepam may be
given rectally.

Antimigraine-
abortive triptans

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Sumatriptan 5-HT1B1D agonist; Abortive approach for Transient burning


induces cerebral migraine, abdominal sensation in chest and
vasoconstriction, migraine, cyclic neck
relaxes gastric fundus vomiting syndrome ¶ .
Subcutaneous, PO,
nasal and rectal
formulations.

Zolmitriptan PO, ODT, and nasal


formulations.

Frovatriptan PO formulation; longer


half-life (26 hours).

Rizatriptan ODT formulation.

Other – NSAIDs

Ketorolac Cyclooxygenase Abortive approach for Gastrointestinal


inhibitor of migraine, cyclic bleeding
prostaglandin synthesis vomiting syndrome ¶ .

Antimigraine –
prophylactic
medication

Cyproheptadine H1 antagonist and 5- Prevention of migraine, Sedation, anti-ACh


HT2 antagonist abdominal migraine, effects*, weight gain
cyclic vomiting due to appetite
syndrome. stimulation

Pizotifen, pizotyline 5-HT2 antagonist Not available in the


United States

Propranolol β1, β2 adrenergic Prevention of Hypotension,


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

Amitriptyline, 5-HT2 antagonist, Prevention of migraine, Sedation, anti-ACh


nortriptyline increases synaptic abdominal migraine, effects*, QTc
norepinephrine cyclic vomiting prolongation
syndrome ¶ .

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

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ACh: acetylcholine; H: histamine; D: dopamine; CTZ: chemoreceptor trigger zone; 5-HT: 5-


hydroxytryptamine (serotonin); GERD: gastroesophageal reflux disease; PO: orally; IM:
intramuscularly; IV: intravenously; NK: neurokinin; GABA: gamma aminobutyric acid; ODT: orally
dissolving tablet; NSAID: nonsteroidal antiinflammatory drug; CB1R: cannabinoid receptor 1.

* Anticholinergic effects include blurred vision, dry mouth, hypotension, palpitations, and urinary
retention.

¶ Pharmacotherapy for cyclic vomiting syndrome may be preventive, supportive, or abortive,


depending on the patient's characteristics. For detailed guidance, refer to UpToDate content and
tables on cyclic vomiting syndrome.

Adapted 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.

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