DOI:10.1542/pir.

19-10-337
1998;19;337 Pediatr. Rev.
Karen F. Murray and Dennis L. Christie
Vomiting
http://pedsinreview.aappublications.org/cgi/content/full/19/10/337
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Definition
Vomiting is a generally unpleasant
activity that results in the expulsion
of stomach contents through the
mouth. It is a physical act that has
clearly associated gastrointestinal
motor activity. Nausea, on the other
hand, although frequently accompa-
nying vomiting, is not universally
associated with it and does not have
an obvious physical mechanism. It
is an uncomfortable feeling known
to be relieved by vomiting.
Physiology
The ability to vomit presumably
conveys a survival advantage by
enabling the expulsion of toxins
from the stomach. Vomiting occurs
after stimulation of either the vomit-
ing center (VC), a central control
center in the medulla near the re-
spiratory center, or the chemorecep-
tor trigger zone (CTZ) in the area
postrema on the floor of the fourth
ventricle (Fig. 1). These coordina-
tion centers can be stimulated
through multiple pathways. Vomit-
ing resulting from psychological
stress occurs via pathways traveling
through the cerebral cortex and lim-
bic system to the VC. Anticipatory
vomiting may be mediated through
this mechanism. Vomiting related
to motion occurs when the VC is
stimulated through the vestibular
or vestibulocerebellar system from
the labyrinth of the inner ear. Chem-
ical signals from the bloodstream
and cerebrospinal fluid are detected
by the CTZ. This mechanism has
been the target of many antiemetic
medications. The vagal and visceral
nerves are the fourth pathway for
stimulation of vomiting via gastro-
intestinal irritation, distention, and
delayed gastric emptying.
Once the vomiting centers are
stimulated, the cascade of motor
events leading to the act of vomiting
is the same. Nonperistaltic contrac-
tions in the small intestine increase,
the gallbladder contracts, and some
of the duodenal contents regurgitate
into the stomach. This is followed
by a large retrograde
peristaltic wave that
pushes small bowel
contents and pancre-
atobiliary secretions
into the stomach and
suppresses gastric
activity. Meanwhile,
the inspiratory
muscles contract
against a closed
glottis, resulting in
esophageal dilatation.
As the abdominal
muscles contract,
the stomach con-
tents are forced
into the distal
esophagus. Relax-
ation of the abdom-
inal muscles allows
the esophageal con-
tents to re-enter the
stomach. The cycles
of retching quicken
until the esophagus
no longer empties
between cycles, and the contents
finally are extruded. The gastroin-
testinal motor events of vomiting
are mediated through vagal and
sympathetic efferents from the
VC, as are the autonomic events
associated with the act of vomiting,
namely, increased salivation,
increased respiratory and heart
rates, and pupillary dilatation.
Pathogenesis
True vomiting can be divided into
two broad categories: nonbilious
and bilious. Bilious vomiting occurs
when bile is purged along with the
gastric contents. Although some
small intestinal reflux into the stom-
ach is common with all vomiting,
in nonbilious vomiting, antegrade
intestinal flow is preserved, and
the majority of the bile drains into
the more distal portions of the intes-
tine. If an obstruction is present,
nonbilious vomiting implies that
the obstruction is proximal to the
ampulla of Vater. Conditions leading
to bilious vomiting involve either
a disorder of motility or physical
blockage to this antegrade flow of
Pediatrics in Review Vol. 19 No. 10 October 1998 337
Vomiting
Karen F. Murray, MD* and Dennis L. Christie, MD*
IMPORTANT POINTS
1. Because the causes of vomiting are broad, proper diagnosis requires
a high index of suspicion and a thorough history and evaluation.
2. Bilious vomiting is an ominous sign that mandates immediate
evaluation.
3. Vomiting may be a symptom of a systemic disease that is not primar-
ily of the gastrointestinal tract.
4. The patient who has bloody emesis requires hemodynamic stabiliza-
tion before diagnostic studies are performed.
5. Psychological causes of vomiting can be serious and difficult to treat.
*Division of Gastroenterology, Childrens
Hospital and Regional Medical Center,
Seattle, WA.
ARTICLE
FIGURE 1. Central nervous system coordination of vomit-
ing: LS = limbic system, CTZ = chemoreceptor trigger
zone, VC = vomiting center, VIII = vestibular nerve, X =
vagus nerve.

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proximal intestinal contents distal
to the ligament of Treitz.
Gastroesophageal reflux (GER),
although not true vomiting, fre-
quently is included in discussions
of vomiting. In contrast to the
mechanism of true vomiting dis-
cussed previously, GER occurs as
a result of failed normal esophageal
function. Normally, the lower eso-
phageal sphincter (LES) relaxes
with swallowing and propagation
of esophageal peristalsis, allowing
a food bolus to enter the stomach.
Its basal contraction prevents food
from re-entering the esophagus from
the stomach. Transient relaxation of
the LES predisposes to GER and is
the major mechanism in infants who
have GER. The LES is aided by sur-
rounding structures, especially the
crural diaphragm, and disruption of
these structures, as with a hiatal her-
nia, contributes to the GER in some
patients. Nicotine, alcohol, caffeine,
and some medications can increase
relaxation of the LES, contributing
to GER in some individuals. GER
also is distinguished from true vom-
iting by its symptoms; the emesis of
GER is effortless and generally not
associated with retching or auto-
nomic symptoms.
Causes of Vomiting
Although the causes of vomiting in
children are many, a thorough his-
tory of the nature of the vomiting
and any associated signs or symp-
toms as well as a complete physical
examination generally helps narrow
the differential diagnosis (Table 1).
Targeted studies help identify the
cause of the illness.
NONBILIOUS
Infectious/inflammatory
Acute gastroenteritis is the most
common cause of vomiting in
children. It is usually associated
with diarrhea and abdominal pain,
and viruses are common etiologic
agents, although bacterial patho-
gens also must be considered.
The most common viral agent
in infants is rotavirus. Bacterial
pathogens include Salmonella,
Shigella, Campylobacter, and
Escherichia coli. Bacterial infec-
tions are associated more com-
monly with bloody diarrhea and
high fevers than are viral infections.
Enterohemorrhagic E coli 0157:H7
can cause hemorrhagic colitis and
may be complicated by the devel-
opment of hemolytic-uremic syn-
drome. Clostridium difficile is a
bacterial pathogen that frequently
is associated with the recent use
of antibiotics. It causes a pseudo-
membranous colitis, often with
bloody diarrhea and associated
with abdominal pain and vomiting.
Giardia lamblia is a protozoan
commonly associated with contami-
nated water and attendance at child
care centers. It may cause watery
diarrhea and vomiting.
Diagnosis is made with stool
bacterial cultures, rotazyme analysis
for rotavirus, detection of C difficile
toxin, and detection of ova and
parasites for G lamblia. Sepsis,
central nervous system infections,
urinary tract infections, and pneu-
monia all can present with or in-
volve vomiting, usually in addition
to other symptoms.
Labyrinthitis and pancreatitis
both cause vomiting. Dizziness
usually is associated with labyrin-
thitis and abdominal pain with
pancreatitis.
Inflammatory conditions of the
intestinal tract, such as inflammatory
bowel disease, also tend to involve
vomiting. In these conditions, the
vomiting frequently is related to
altered motility with abnormal or
dysfunctional swallowing, gastric
emptying, or peristalsis.
Metabolic/endocrinologic
Both inborn errors of metabolism
and endocrinologic disorders can
cause vomiting (Table 2). The
inborn errors of metabolism gener-
ally present in early infancy, and
the vomiting is associated with
symptoms of lethargy, hypo- or
hypertonia, seizures, or coma.
The constellation of symptoms is
similar to that seen in sepsis, neces-
sitating a high index of suspicion
in the evaluation of these patients.
The presence or absence of meta-
bolic acidosis, hypoglycemia, hyper-
ammonemia, or ketosis and a family
history that includes possible con-
sanguinity can help to determine
the diagnosis.
One endocrinologic condition
associated with vomiting is diabetes
mellitus. Vomiting can complicate
acute ketoacidosis or occur in
patients who have had long-stand-
ing diabetes and consequent gastro-
paresis. Slowed gastric motility
usually presents after diabetes
mellitus has been present for
approximately 10 years. Early
338 Pediatrics in Review Vol. 19 No. 10 October 1998
GASTROENTEROLOGY
Vomiting
TABLE 1. General Causes
of Vomiting
Nonbilious
Infectious/inflammatory
Metabolic/endocrinologic
Neurologic
Psychological
Obstructive lesion
Bilious
Distal obstructive lesion
TABLE 2. Selected
Inborn Errors of Metabolism
Associated With Vomiting
Carbohydrate Metabolism
Defects
Glycogen storage disease II
(Pompe disease)
Galactosemia
Hereditary fructose intolerance
Pyruvate carboxylase deficiency
Pyruvate dehydrogenase
complex deficiency
Amino Acid/Organic Acid
Metabolism Defects
Urea cycle defects
Phenylketonuria
Maple syrup urine disease
Propionic acidemia
Glutaric acidemia
Isovaleric acidemia
Tyrosinemia type I
Lysosomal Storage Diseases
Mucopolysaccharidoses
Mucolipidoses
Niemann-Pick disease
Wolman disease
Peroxisomal Disorders
Zellweger disease
Adrenal leukodystrophy
Fatty Acid Oxidation Disorders
Carnitine deficiency syndromes
MCAD, LCAD

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satiety and a sense of fullness
frequently precede the onset of
vomiting in diabetic gastroparesis.
Vomiting as a consequence of
food-related sensitivity always
should be considered. The variants
encountered most commonly in
pediatric patients are cow milk
and soy protein intolerance, type I
(IgE-mediated) food allergy, and
celiac disease. Cow milk protein
intolerance affects 2% to 7% of
infants, with approximately 20% of
these also sensitive to soy protein.
In addition to vomiting, the patients
usually have diarrhea that frequently
is guaiac-positive. Celiac disease
occurs only in children who eat
gluten-containing foods. Patients
typically suffer from wasting, irri-
tability, and diarrhea, but vomiting
also can occur.
Neurologic
Vomiting occurs in any neurologic
condition that involves increased
intracranial pressure (ICP) (Table 3).
Additionally, patients who have
seizures, autonomic disorders
(Riley-Day syndrome), and con-
ditions affecting the floor of the
fourth ventricle without increased
ICP frequently have their condition
worsened with vomiting.
Cyclic vomiting is a unique entity
that must be considered separately.
Onset occurs typically at early
school age, and it is characterized
by acute-onset periodic episodes of
nausea and vomiting interspersed
with conspicuous periods of well-
ness. Approximately 77% of patients
can identify precipitating events,
usually intense emotional states.
These patients have an increased
incidence of migraine headaches
and prevalence of epilepsy and irri-
table bowel syndrome. Because no
diagnostic test or specific clinical
identifying feature distinguishes
cyclic vomiting syndrome from
other potentially life-threatening con-
ditions, the diagnosis can be made
only after time has elapsed and
upon exclusion of other diagnoses.
Psychological
Behavioral or psychological causes
of vomiting can be problematic
in the pediatric age group. Some
children induce vomiting to seek
attention in environments in which
personal attention is lacking. The
extreme of this behavior is rumina-
tion. Rumination is a serious condi-
tion that occurs in infants when
there is a failure in reciprocal inter-
action between the infant and care-
giver. The purposes of rumination
are self-stimulation and satisfaction
of needs. Rumination also is seen in
older children, especially those who
are severely mentally retarded.
Classically, the infant (older than
3 months) learns to bring up gastric
contents into the mouth, frequently
by inserting a hand into the back of
the throat or simply through rhyth-
mic contractions of the pharynx,
tongue, and abdominal muscles. The
oral contents then are reswallowed,
although spillage does occur. Not
only do these patients suffer social
deprivation, but the chronic emesis
can lead to inanition and growth
failure. The failure to thrive does
not improve with traditional medical
intervention, but rather requires
sensitive and interactive nurturing.
A mother-substitute who is empathic
with and observant of both the par-
ents and infants needs is required
to help the parent establish more
nurturing skills. More formal psy-
chotherapeutic help frequently is
needed for the parents.
Bulimia, characterized by secre-
tive binge-eating episodes followed
by self-induced vomiting, is a cause
of vomiting especially among
teenagers.
Anatomic
The anatomic and, thus, the gener-
ally surgical causes of nonbilious
vomiting are those that affect the
intestinal tract proximal to the
point of bilious drainage (ampulla
of Vater), which is proximal to
the ligament of Treitz (Table 4).
Whereas congenital anomalies usu-
ally present in the newborn period,
acquired lesions can present at any
age. Any infant who exhibits persis-
tent nonbilious vomiting, with or
without feeding, in the immediate
newborn period must be suspected
of having an intestinal atresia or a
luminally obstructing lesion (pyloric
stenosis, luminal band, web) proxi-
mal to the point of bile drainage
(ampulla of Vater).
An easy and rapid test to eval-
uate possible esophageal atresia
is the ability to pass a nasogastric
tube easily into the stomach. After
the tube has been passed, it is
important to obtain a radiograph to
assure that the tube is in the stom-
ach and not coiled in an atretic
esophagus. Any resistance to pas-
sage of the tube is an indication
for evaluation by contrast radio-
graph for an obstruction. If an
obstruction is present, nasoesopha-
geal tube drainage is important to
prevent aspiration of pooled esopha-
geal secretions. Contrast studies are
the standard for the diagnosis of
these conditions (Figs 2-4).
Pediatrics in Review Vol. 19 No. 10 October 1998 339
GASTROENTEROLOGY
Vomiting
TABLE 3. Selected
Neurologic Conditions
Associated With Vomiting
Structural
Hydrocephalus
Congenital malformations
Intracranial hemorrhage
Intracranial mass lesions
Infectious
Congenital infections
Encephalitis and meningitis
Toxic
Kernicterus
Acidosis and other metabolic
byproducts
TABLE 4. Physical
Conditions of the
Gastrointestinal Tract That
Cause Nonbilious Vomiting
Structural
Foreign body
Esophageal/gastric atresia
Esophageal/gastric stenosis
Stricture
Duplication/diverticulum/
choledochal cyst
Pyloric stenosis
Annular pancreas
Web
Peptic disease
Disorders of Motility
Achalasia
Ileus
Scleroderma
Gastroparesis
Appendicitis
Pseudo-obstruction

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BILIOUS
Although not absolute, anatomic
conditions causing luminal obstruc-
tion distal to the ligament of Treitz
usually cause bilious vomiting. Bil-
ious vomiting is an ominous sign
that mandates immediate evaluation
(Table 5).
In the newborn period, intestinal
atresias and stenosis and malrotation
with or without volvulus need to be
ruled out immediately. In the older
child, malrotation with volvulus also
is a surgical emergency that is diag-
nosed relatively easily by gastroin-
testinal contrast study. After the
diagnosis has been established radio-
graphically, the gastrointestinal tract
should be decompressed with a naso-
gastric tube, food and drink withheld,
and the patient supported with intra-
venous fluids until definitive surgi-
cal intervention can be undertaken.
Vomiting of Blood
Bright red blood in emesis implies
active bleeding in the esophagus,
stomach, or proximal duodenum.
Coffee-ground color (darker oxi-
dized blood), on the other hand,
implies a recent history of bleeding.
Fortunately, gastrointestinal bleeding
is relatively rare in children. Chil-
dren who experience massive gas-
trointestinal bleeding frequently
have predisposing conditions, such
as esophageal varices from chronic
liver disease (Table 6). When such
bleeding is encountered, initial
therapy always is stabilization and
resuscitation of the patient. Minimal
bleeding that does not result in any
change in hemodynamics or hemat-
ocrit frequently can be treated with
histamine-2 blockers or antacids.
Larger hemorrhages, however,
require further intervention. The rate
and volume of bleeding should be
measured early, and if significant,
a nasogastric tube left in place for
340 Pediatrics in Review Vol. 19 No. 10 October 1998
GASTROENTEROLOGY
Vomiting
FIGURE 2. Barium study showing a dis-
tal esophageal stricture with proximal
esophageal dilatation.
FIGURE 3. Barium study showing a
coin partially obstructing the duodenum.
FIGURE 4A. Barium study illustrating a
malrotation with volvulus.
FIGURE 4B. Surgical photo of an
intestinal malrotation with volvulus.
TABLE 5. Conditions
That Can Cause Bilious
Vomiting in Children
Intestinal atresia and stenosis
Malrotation with or without
volvulus
Ileus from any cause
Intussusception
Intestinal duplication
Compressing or obstructing
mass lesion
Incarcerated inguinal hernia
Superior mesenteric artery
syndrome
Appendicitis
Peritoneal adhesions
Pseudo-obstruction
TABLE 6. Some Causes
of Upper Gastrointestinal
Bleeding
Esophagitis/gastritis
Peptic ulcer disease (gastric/
duodenal)
Mallory-Weiss tear
Bleeding varices
Dieulafoy lesion

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continuous monitoring and removal
of the gastric blood. After stabiliza-
tion, the patient should be trans-
ported to a facility where there are
endoscopists and surgeons skilled in
pediatric care and management of
gastrointestinal bleeding.
SUGGESTED READING
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ditions of the abdomen. Pediatr Ann. 1994;
4:192201
Cohen R. Metabolic and infectious disorders
associated with emesis in infants. Semin
Pediatr Surg. 1995;4:136146
Fleisher DR. Functional vomiting disorders
in infancy: innocent vomiting, nervous
vomiting, and infant rumination syndrome.
J Pediatr. 1994;125(suppl):S84S94
Fleisher DR. The cyclic vomiting syndrome
described. J Pediatr Gastroenterol Nutr.
1995;21(suppl):S1S5.
Forbes D. Differential diagnosis of cyclic
vomiting syndrome. J Pediatr Gastroen-
terol Nutr. 1995;21(suppl):S11S14
Gordon N. Recurrent vomiting in childhood,
especially of neurological origin. Dev Med
Child Neurol. 1994;36:463470
Johns DW. Disorders of the central and auto-
nomic nervous systems as a cause for
emesis in infants. Semin Pediatr Surg.
1995;4:152156
Keller VE. Management of nausea and vomit-
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Orenstein SR. Gastroesophageal reflux.
Pediatr Rev. 1992;13:174182
Sondheimer JM. Vomiting. In: Walker WA,
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Watkins JB, eds. Pediatric Gastrointestinal
Disease, Pathophysiology, Diagnosis,
Management. Vol. 1. St. Louis, Mo:
Mosby; 1996:195203
Pediatrics in Review Vol. 19 No. 10 October 1998 341
GASTROENTEROLOGY
Vomiting
PIR QUIZ
6. A newborn male spits up his first
feeding and develops bilious emesis
with subsequent feedings. On physical
examination, he appears ill, has a
scaphoid abdomen, and has absent
bowel sounds. A plain radiograph
reveals air in the proximal small
bowel but a paucity of air in the
distal digestive tract. Of the following,
the most likely cause for this infants
vomiting and clinical findings is:
A. Antral web.
B. Choledochal cyst.
C. Hirschsprung disease.
D. Tracheoesophageal fistula.
E. Volvulus.
7. A 13-month-old girl is referred
because of nonbilious vomiting,
failure to thrive, and chronic diar-
rhea. She had done well on a cow
milk formula until 6 months of
age, but difficulties developed
when solid foods were introduced.
Physical examination reveals a
wasted, irritable toddler who has a
protuberant abdomen and wasted
extremities. The most likely cause
for this childs vomiting and clinical
symptoms is:
A. Celiac disease.
B. Cow milk/soy protein allergy.
C. Hiatal hernia.
D. Intussusception.
E. Urinary tract infection.
8. A 6-year-old girl has had abdominal
pain and nonbilious vomiting for
8 hours. History reveals cough and
fever for the past 3 days. Findings
on physical examination include
temperature of 39C (102.2F);
tachypnea; toxic appearance; dif-
fuse, voluntary guarding; and quiet
bowel sounds. The examination
most likely to confirm the etiology
of the abdominal pain and fever in
this patient is a(n):
A. Abdominal radiograph.
B. Chest radiograph.
C. Complete blood count.
D. Rectal examination.
E. Upper gastrointestinal series.
9. A 7-year-old girl has been having
recurrent bouts of nonbilious
emesis for 18 months. The vomit-
ing episodes occur every 3 to
4 weeks, last 48 hours, and often
require intravenous fluids to pre-
vent dehydration. The patient is
otherwise well between vomiting
episodes. Results of evaluation,
including blood chemistries, com-
plete blood count, urinalysis, upper
endoscopy, abdominal computed
tomography, barium swallow, and
head magnetic resonance imaging,
have been normal. The most likely
cause for this childs vomiting is
A. Cyclic vomiting syndrome.
B. Glycogen storage disease II.
C. Hydrocephalus.
D. Peptic ulcer disease.
E. Recurrent intussusception.
10. A 12-year-old boy with alpha
1
-
antitrypsin deficiency presents
vomiting bright red blood. Physical
examination reveals an anxious,
diaphoretic child who is incon-
solable. He has a firm, enlarged
liver palpable 2 cm below the right
costal margin; splenomegaly; and
a prominent vascular pattern over
the abdomen. Of the following,
the most important first step in
management is to:
A. Order an acute abdominal
radiographic series.
B. Perform a tagged red cell
study.
C. Prepare for variceal sclero-
therapy.
D. Schedule for an upper endos-
copy.
E. Start fluid resuscitation.

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DOI:10.1542/pir.19-10-337
1998;19;337 Pediatr. Rev.
Karen F. Murray and Dennis L. Christie
Vomiting

& Services
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