Vomiting in Children: Reassurance, Red Flag, or Referral? Latha Chandran and Maribeth Chitkara P ediatr. Rev.

2008 :29 :l 83 - 192 DOI: I 0. 1 5 42lpir.29-6-183

The online version of this article, along with updated information and services, is located on the World Wide Web at: http:"ipeclsinrevier.v.aappublicati*ns.org/cgiici:ttentiftrll'/29/6i I8-l

Pediatrics in Review is the official joumal of the American Academy of Pediatrics. A monthly publication, it has been published continuously since 1979. Pediatrics in Review is owned, published, and trademarked by the American Academy of Pediatrics, l4l Northwest Point Boulevard, Elk Grove Village, lllinois, 60007. Copyright O 2008 by the American Academy of Pediatrics. All rights reserved. Print ISSN: 0l9l-9601. Online ISSN: 1526-3347.

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Discuss

After completing this articit, reader! should be able to:

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the m*st coffm$n causes of vorniting in children af different age gro,up;.

uncierstand the physiolagy hehind the protess

Recogniee comrylon causes

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vomiting"

Author Disclosure
Drs Chandran and

of vamitinq based an the pattern and nature of er*esis. Be familiar with the basic Siagnostic evaluaticn *nd treatment strategies fsr different
car;ses

0f vamiting.

Chitkara have
disclosed no financial

relationships relevant

to this article.

This

commentary does contain a discussion

Case Study A l-rnonth-old boy who has had postprandial romiting for I weeh is admitted frow the ernergncy depal'trnent. He tpas bont at term with no complications and hod. regained his
binhweight by the second. weeh after birth, feeding on a milk protein Jbrtnwla. He has been 'vomiting cu.rd.led wilh intennittentlyfor rhe p&st week, nnd. on the day of admission was noted. by bis pediatrician to hape last 4 oz in weight ince his last chech-up. On pbysicwl exaruination, the irfant is sligbtly lethargic and. ltas a sunhenfontuuelle. Tbt rest of his physical exarnination f.nd.ings, includ.ing etalwation of'his abdomen, a.re nortnol. Abdominal whrasonograpby shows normal wid.th ond length of the piloral Howeuer, no fbod

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Fhysiology of Vomiting
Vomiting involves the forceful expulsion of the contents of the stomach and is a highlv cgordinated, reflexive process. It is a feature of many acute and chronic disorders,
including those causing incrcased intracranial pressure, metabolic diseases, and atratomic and mucosal GI abnormalities. Descent of the diaphragrn and constriction of the abdominal musculatlrre on relaxation of the gastric cardia force gastric contents back up the *vomiting center" in the central nen'ous esc'rphagus. The process is coordinated by the system. 'fhe vomiting center reccives scnsor)- input from dre vestibular nucleus (cranial nen'e WII), thc GI tract via vagal afferents (cranial nen'e X), and the bloodstream via the area postrema, aiso known as the chemoreceptor (or chemoreceptive) trigger zone. The stereotypic behaviors associated rvith emesis are a result of output from the vomiting center througir vagal, phrenic, and sympathetic nerves.

Types of Vcmiting

Vorniting can be classified according to its nature and causc as well as by the character of the vomirus. The nature of the vomiting may bc projcctilc or nonprojectile. Projectile vomiting refbrs to forceful vomiting and may indicate itrcreased intracranial pressure,
cspecially if

it occurs early in the morning. Projectile vornitirrg also is a classic fcature of

pyloric stenosis. Nonprojectile vomiting is seen more comnonly in gastroesophageal

reflux. These somervhat arbitrary descriptions are not definitive in establishing a diagnosis. -Ihe vomitus may be bilious, bloody, or Ernesis often is classified based on its qualir.v. nonbloodv and nonbilious. Emesis originating fiom the stomach usuallv is characterized as beir.rg clear or yellor,v and often contains re mrants of prcviousll, ingested foocl. Emesis that

'Editorial Board.
rAssistant Professor of Pediatrics and Emergency Medicine, Pediatric Hospitalist, State Universlty of New York at Stony Brook, Stony Brook, NY.

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is dark green is referrecl to as bilious because it indicates the prescnce of bile. Bilious r,omiting frequendy is

pathologic because it may be a sign of an underlf ing abdominal problem such as intestinal obstrrrction beyoncl the duoderral ampulla of lhter, rvhere the c<lmmon bile duct empties. 'fhe presencc of blood in the ernesis, also knolvn as hematemesis, indicates acute bleeding from the upper portion of the GI tract, as can occur with gastritis, Mallorv-lVeiss tears, or peptic ulcer
disease. Coffee ground-like material often is reprcsentatil'e of an old GI hernorrhage becausc blood darkens to a black or dark-brown color rvhen exposed to the acidity of

loops ancl air-fluid levels, rvhich strongly suggest borvel obstruction. Contrast imaging studies are more specific and can help pinpoint a precise diagnosis. Surgical and

neonatal consultations should be obtained urgently rvhen the diagnosis of txlwel obstruction is considered.
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the gastric secretions. The more nrassive or proximal the bleecling, the more likely it is to bc bright red.

Sifferential Iiagnosis A r.'ariery of organic and nonorganic

clisorders can be associated rvith vomiting. Organic callscs are those related to specific medical conditions. The primarv care practitioner needs to remember that vomiting does not localize the problem to the GI system in 1'oung infbnts but can be a nonspecific manifbstation of an underlying systemic illness such as a urinary tract infection, sepsis, or an inborn errcrr of rnetabolism. Nonorganic causes are much more clifficult to identiflz and often arc vierved as diagnoses of exclusion. Examples of nonorganic causes of vomiting are psychogenic vomiting, cyclic vomiting

svndrome, abdominal migraine, and bulimia. Table

iists the dillbrential diagnosis ofvomidng based on organ systems. Florvever, frorn a clinical perspective, it often is useful to consider causes from an age-related perspective.

Vomiting in lnfancy
Table 2 details the age-related differential diagnosis of vomiting in infants. Vomiting in the first felv days after birth may be a sign of serious pathology. Bilious emesis is suggestive of congenital obstmctive GI malfcrrrnations, such as duodenal/ejunal atresias, rnalrotation u'ith rnidgut vohulus, rncconium ileus or plugs, and Hirschsprung disease. Published reports ofneonates evaluated in neonatal intensive care units r,vith a principal diagnosis of bilious emesis revealed that 38% to 690/o had an intestinal obstmction. (l) Nonsurgical causes of bilious emesis include llecrotizirlg enterocolitis and gastroesophageal reflux (GER). When caring for a neonate lvho has prersistent bilious vomiting, the clinician should placc a nasogastric or orogastric catheter to decompress the stomach and prevent any aclditional vomiting or aspiration before initiating anl' dixgnostic or therapeutic ntaneuvers. Plain radiographs of the abdomen can demonstrate dilated trorvel
I84
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Intestinal atresias are surgical cmergencics and rypicall,v present r.vitl-rin a feu' hours after birth. Duodenal atresia is a cor-rgenital obstr-r-rction of the second portion of tht: duodenum that occurs in I per 5,000 to 10,000 live births and is associated r,vith trisomy 2l in approximately 25oA of cases. It is believed to be duc to a failure of recanalization of the bou'el during early gestation. Infants present with clinical features of thilure to tolerate feedings and bilious emcsis shonly after birth. Due to the proximal nature of the obstruction, abdominal distention usually is not present. Plain abdominal radiographs may 5lstu i<4ouble bubble" sign, lvhich represerlts air in " the stomach and proximal cluodenum (Fig. l). More distal ot'rstructions, such as jejunoileal atresias, typically present rvirh bilious vomiting along u'ith abdonrinal distention within the first 24 hours after birth. The cause of these atresias is believed to be a n'rscnteric vascular accident at somt: point during the course of gestation. The frequency ofdreir occurrence is approximately I per 3,000 live births. Anatomically, jejunoileal atresias can be classified into four q'pes: rnembranous) internrpted, apple-pecl, and multiple. Abdominal racliographv may shorv dilated loops of small bowel with air-fluid levels (Fig. 2). Urgent surgical correction is necessary for all ty'pes ofintestinal atresias.
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Understanding malrotation requires a revier.v of the organogenesis of the gut. During the third week of fetal development, the prirnitive gut is divided into three regions: the fcrregut, midgut, and hindgut, based on
vascular supply. The first stage of intestinal development

involvcs rapid growth of the rnidgut outside the abdominal cavity through a herniation of the umbilical orifice.

l)uring the second stage, the rnidgut returns to the abdominal cavitv, rotating 180 degrees and pushing the hindgut to the left. The last stage of intestinal developnent involves the retroperitonealization of portions of the right colon, lcft colon, duodenum, and intestinal mesentery, helping them serve as anchors for the borvel.
Disnrption of this process during the second or third
stage can rcsult in an aberrant return or anchoring

ofthe

midgut u'ithin the abdominal cavity.

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r. Differential Diagnosis of Vomiting by Systems

Neurologic
Endocrine

Gastrointestinal

r r r

r r r r Appendicitis r Celiac disease r Milldsoy protein allergy r lnflammatory bowel disease r Pancreatitis r Cholecystitis or cholelithiasis r lnfectious and noninfectious hepatitis r Peritonitis
r
Trauma: Duodenal hematoma

Esophagus: Stricture, web, ring, atresia, tracheoesophageal fistula, achalasia, foreign body Stomach: pyloric stenosis, web, duplication, peptic ulcer, gastroesophageal refl ux lntestine: duodenal atresia, malrotation, duplication, intussusception, volvulus, foreign body, bezoar, pseudo-obstruction, necrotizing enterocolitis Colon: Hirschsprung disease, imperforate anus, foreign body, bezoar Acute gastroenteritis Helr'cobacter pylori infection Parasitic infections: ascariasis, giardiasis

r r r
o

Tumor
Cyst Hematoma Cerebral edema

o
o

Diabetic ketoacidosis Adrenal insufficiency

Respiratory

r Hydroctphalus r Pseudotumor cerebri r Migraine headache c AMominal migraine r Seizure

e
Meningitis
Renal

r Pneumonia r Sinusitis r Pharyngitis

Miscellaneous

r
e

Sepsis syndromes Pregnancy

Rumination Bulimia
Psychogenic Cyclic vomiting syndrome

r
o

Obstructive uropathy: Ureteropelvic junction obstruction, hydronephrosis, nephrolithiasis

Renal insufFrciency

o o

Glomerulonephritis Urinary tract infection

Renal tubular acidosis

r r
o

Overfeeding

r r

Medications/vitamin/drug toxicity
Superior mesenteric artery syndrome Child abuse

Metabolic

r Galactosemia r Hereditary fructosemia r Amino acidopathy

o

r
o

Organic acidopathy
Urea cycle defects

r r

Fatty acid oxidation disorders

lactic adidosis
Lysosomal storage disorders Peroxisomal disorden

Although most infhnts who have intestinal malrota-

tion present rvithin the first rveek after birth due to the
accompanying volvulus, the malrotation itself cloes not cause an)r notable symptoms and may be undetected for vears. Bowel strangulation can occur at anv age and any time because affcctetl patierlts arc at incrcascd risk of vohulus due to a lack olproper mesenteric anchoring t<-r the retroperitoneum. The midgut tvvists in a clockwise direction around the superior mesenteric vessels, leading to obstruction of vascular supply to most of thc sn'rall and large intestine. Once bowel ischemia occurs, metabolic
aciclosis, unstable hemodynamics, and intestinal necrosis r.vith perforation may ensue if the condition is not diag-

malposition ol the superior mesenteric vessels. Timely surgical correction rvidr the Ladd procedure is critical. If bou'el ischemia is prolonged, lc.rss of bowel and resultant short gut slndrome nray occur.

V*miting in lnfancy Beyond the Neonatal

Perind
The differential diagnosis of vomiting in inihnts beyond dre neonatal period is more extensive. Common causes are aclrte gastroenteritis, GE\ and nutrient intolcrances such as rnilk or soy protein allergies. Metabolic diseases ar,d inborn errors of metabolism also shouicl be considered for infants lvho have persistent progressive vomiting. Acquired or mildcr intestinal obstructive lesions, such as infantile h,vpertrophic p1'loric stenosis (IHPS), also are possible and should be mled out lvhen clinically
indicated.

nosed and rapidly corrected surgically. A spiral configu-

mtion of the jejunum or demonstration of failure of contrast to pass beyond the second portion ofthe cluodenum on upper GI radiographic series is diagnostic
(Fig. 3). Abdominal ultrasonographv also may reveal
a

Common entities such as GER" dietary protein intol185

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Age-related Differential Diagnosis of Vomiting in Children Younger Thanl2 Months of Age

rabre 2.
Age Newborn Common Causes Type of Vomiting

Comment/Associated Features May occur at level of esophagus, duodenum, jejunum Strongly associated with cystic fi brosis; genetic testing
suggested

lntestinal atresia/webs
Meconium ileus

Bilious, depending on level of

lesion Bilious

Hirschsprung disease

Bilious or nonbilious

History of non-passage of stools in nursery suggestive; suction rectal biopsy may demonstrate lack of intestinal ganglion
ce

lls

Necrotizing enterocolitis lnborn errors of

Bilious or nonbilious Bilious or nonbilious Nonbilious

Bilious

Plain films of abdomen may reveal intestinal pneumatoses May have acidosis or
hypoglycemia

0 to 3 months

metabolism Pyloric stenosis

Hypochloremic metabolic
alkalosis

Malrotation with
midgut volvulus

Abdominal distention may be present; plain radiographs may show air-fluid levels and paucity of distal bowel gas; emergent surgical consultation
necessary

lnborn errors of
metabolism

Bilious or nonbilious

Milk/soy protein allergy

Bilious or nonbilious; may

have gross or occult blood

Gastroesophageal

Nonbilious; may have gross

reflux
Child abuse

or occult blood
Nonbilious

Newborn metabolic screen may be abnormal; acidosis or hypoglycemia may be present History of extreme fussiness may be present; fecal occult blood testing of stools may be positive Emesis usually within 30 minutes of feeding; symptoms worse in supine flat position Anterior fontanelle fullness may be present; central nervous system (CNS) imaging studies may reveal acute or subacute
bleeding

3 to 12
months

Gastroenteritis
lntussusception

Nonbilious initially; may progress to bilious

Bilious

Stool studies may help establish

offending pathogen
Abdomen distention may be present; plain radiographs may show air-fluid levels and paucity of distal bowel gas; stools may be grossly bloody with "currant jelly" appearance; emergent surgical consultation indicated; may be reduced by contrast enema Anterior fontanelle fullness may be present; CNS imaging studies may reveal acute or
subacute bleeding

Child abuse

Nonbilious

lntracranial mass lesion

Nonbilious

Anterior fontanelle fullness may

be present; CNS imaging

studies diagnostic
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Figure

I. 'Double bubble" sign on plain radiograph, which represents air in the stomach and proximal duodenum and indicates duodenal atresiaerance, and IHPS are discussed in greater detail in this

section. Intussusception is another important cause of vomiting in the young intbnt that is discussed in the next
section because it also rnav present beyoncl infancy. The managerrent of acute gastroenteritis is discussed in tl're scction on mallagcmerrt.
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GER is the most comlnon cause of recurrent nonbiiious

ernesis in infancy.

of contrast to pass beyond the second portion of the duodenum, which is characteristic of malrotation with midgut volvulus.
relaxations of the LES that are not precipitated bv a sr.vallorv, allorvir-rg gastric contcnts to move fi'eely back

It involves the retrogradc movement of

gastric contents into the esophagus as a result of an abnormally functioning lower esophageal sphinctcr
(LH,S). Under normal circumstances, the LES relarics after swallolving to allo*' passage of ingested food into the stomach. Patients who havc GER have transient

into the esophagus from an area of higher to lorver pressure. In young infants, such rela.xation often results from der,rlopmental immaurity of the LES, which may
impror,e over time . Infhnts who have CiER present u'ith recurrerlt postprandial regurgitation of ingested food or milk, rnost often within 30 minutes of a feeding. Affected children may appear irritable during or after feedings, and stcreotypic opisthotonic movements u'ith extension and stiffi:ning of arms and legs ancl cxtcnsiotr of the head (Sandifer syndrorne) occasionally may be obsen'ed. Infb.nts rvho have sevr: re GER calt have recurrent microaspi-

ration into their lungs, resulting in chronic whcezing, respiratory symptoms, and even failure to thrive.
sis

Infants rvho have the classic history of recurrent emebut who are thriving and have normal plrysical examination findings do not need specific treatment. Thick-

Figurc 2. Dilated loops of small bowel with air-fluid levels, indicative of jejunoileal atresia.

ening the fbrmula or human milk by adding cereai ma1' help reduce vomiting in such infants, but elevating the hcad in tl're supine positiotl has uo proven beneficial elI'ect. (2) Infants who are irritable during fbedings and those who have respiratory or gror'vth problems ma,v
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vomiting

neecl pharmacologic intenrention. Acid blockade with histamine, receptor antagonists or protoll-purnp inhibitors may help lessen the burning sensation caused by the gastric refluxant. Prokinetic agents such as metocloprarnide and er)'thromycin may help decrease the phy5isal process of GER by targeting the l,ES. A Cochrane meta-analysis revieu'ing seven randomized control trials showed that metoclopramide \vas superior to placebo in reducing daily symptoms of GER (2) Horvelcr, its use must be weighed against the potential adverse effects of extrapyrsplclal symptoms, headache. and drolvsiness. Recent studies have suggcsted that baclofen, a GABA receptor agonist, mav lessen the number of transient LES rclaxations via vagal-mediated

those lvho are firstborn, are alibcted approximately four times as often as females. fhe incidcnce is approximately 3 per 1,000 live births. The exact cause of pyloric stenosis -lhe relaxation mechanism remains unclear. ofthe pyloric smooth muscle depends on nonadrenergic noncholinergic inhibitory inncnation, mcdiated by vasoactive in-

testinal peptide and nitric oxide (NO). Deficiencies in neuropeptidergic innen'ation and NO have been implicated in cases of pyloric stenosis, but neither has been substantiated as etiologic. \'ery early exposure to erythromycin (within the firct 2 rveeks after birth) also has been associated with an eightfbld increased risk ofpvloric stenosis. (5) It is hypothesized that erythromycin inter-

mechanisms and, thus, improve the pathophvsiologic process associated rvith CIER (3) Additional inlcstigation into this agent's overall efficacy for the treatrnent of GER is necessary.
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Dietary protein intolerance is a non-irnrnunoglobulin E-n-rediatcd q?e of food hypersensitivity that typically presents in infants in the first postnatal year, shortlv after exposure to the ollbnding allergen. Commonly implicated proteins include corv milk protein, soy protein, and egg protein. Among the clinical symptoms are irritability,

acts rvith intestinal motilin rcceptors, causing strong gastric and pyloric contractions and subsequent pvloric muscle hypertrophy. Pl,loric stenosis usually is diagnosed by a rypical history and physical findings. Inspection of the abdomen shortly after an infant fbeding may reveal a peristaltic lvave because thc stomach muscles contract in an aftempt to pass ingested milk past the pyloms. A palpable *olive" in the mid-epigastric region represents thc hypertrophic pylolic muscle and strongly supports the diagnosis of

pyloric stenosis. Rcpeated episodes of vomiting of the gastric contents due to pyloric stenosis may result in
characteristic electrolyte abnormalities, although serum electrolyte values may be norrnal if the patient is diagnosed in the early stages. I'he classic electrolyte abr.rormality is a hlpochloremic hypokalemic metabolic alkalosis. Normal acid production in the stomach is accompanied by tl're release of bicarbonate ions into the blood as a result ofthe action of carbonic anhydlns.. Ilecause ofthe loss ofthe hydrogen ions, this bicarbonate is unbuffered, resulting iu an eusuing metabolic a.lkalosis. Under normal conditions, the excess bicarbonate is excreted in the urine. I{ou.'ever, affectecl infants also lose significant amounts of fluid in

feeding intolerance, recurrent vomiting and diarrhca, and in severe cases, failure to thrive. Occasionally, patients may present with Heine r syndrome , manifesting as pulmonary hemosiderosis (due to recurrent rnicrohemorrhages into the lungs), iron deficiency anemia, and failure to thrive. Examination of stools in patients who
have protein intoler'ance may reveal occult blood, with polymorphonuclear cells, lyrnphocytes, ancl eosinophils. Stool-reducing substances mav be positive due to carbo-

hydrate rnalabsorption. Intestinal biopsics nay reveal

flattened villi and colitis with infiltration of lyn'rphocytes, eosinophils, and mast cells. Treatmcnt of dietaqr protcin intolerancc involves removal of tire allergen from the diet. In the case of corv milk protein allergy, 80% of patients respond to hyclrcllyzed casein formula; the remaining 2Uo/o require

to the elcctroll.tes. The subsequent volume corltraction triggers a renal response ofenhanced proximal tribular reabsorption of bicarbonate and activation of
addition
mechanisms. In addition, the lack of chloride ion in the proximal tubule results in increased local production and reabsorption of dre renin-angiotensin-aldosterone bicarbonate, thus worsening the existing metabolic alka-

I.-amino acicl-based fcrrn-rulas or intravenous nutrition. (4) Once elimination has occurred, svmptoms usually
resolve in 3
days. The dietary protein intolerance q'pically subsicies by l8 to 24 months of age . (4)
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Infants rvho have pyloric stenosis typically present to meclical attention with persistent projectile nonbilious emesis between 2 and 6 rveeks of age. Males, especially
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potassium and hydrogen ions in exchangc of sodium. Lack of h)drogen ions results in enhanced excretion of potassium, leading to significant hypokalernia. When the diagnosis of py'loric stenosis is being consiclered, ultrasc.rnography of thc pyloric muscle cal-! conat Hospital For Sick Children on August 8, 2008

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Figure 4. Thickened and lengthened pyloric muscle that

characteristic of pyloric stenosis.

is

firm the clinical suspicion, rvith sensitivity

from
85%o

rates ranging

to 1007o. (6) Pvloric muscle thickness of4 mm or more and muscle length of 14 mm or mor are diagnostic of pvloric stcnosis (Fig. a). If ultrasonographic examination findings are normal, an upper GI radiographic series can be performed. The radiographic series has a slightlv highcr sensitivitv for pyloric stenosis (89% to 100%) and can aid in the cliagnosis of other
causcs

of age. Intussusception is the telescoping of one portion of the borvel into its distal segment. Most commonlv, the terminal ileum invaginates into the cecum, often as a result of lymphatic hypertrophy in the Peyer patches from a recent viral infection. A history of intermittent episodes of severe and crampv abdominal pain lvith biiious emesis is classic. Parents often repnn that their child is lethargic in betu.een episodes ofpain and may describe blood-tinged, *currant jelly" stoois. P\sical examination mav reveal intestinal obstmction with a salrsageshape mass palpable in the right lou'er quadrant. Rapid consultation with a peciiatric surgeon is rvarranted. Contrast or air enemas can be diagnostic, r,vith dre contrast outlining the lead portion of the intussusception. giving the wpical "coiled spring" appearance (Fig. 5). In addition, thc hydrostatic pressurc from the contrast erlema may reduce telescoping of the intestine. Surgical reduction of the intussusception is indicated when the contrast enema is not successftil.
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Cyclic vomiting syndron're (CVS) is characterizecl by stereoq'pic recurrent episodes of nausea and vorniting lvidrout an identifiable organic cause. It is an idiopathic
disorder that usually begins in early childhood; relatively little is knolvn about its pathogenesis or cause. The

antral web and other structural abnormalities. Surgical pvlorornyotomy is the definitive treatmellt of pyloric
stenosis and is being perforrned laparoscopically at many centers.

Vomiting in Older Children

Vorniting occurs most commonly in older childrcn in the
setting of an acute gastroenteritis accompanied by 6st.t and diarrhea. Vomiting also can be a nonspecific manifestation of a systemic illness, although much less commonly than in the young infant. Both viral and bacteriai meningitis can present vvith vomiting, usually accompanied b1, cornplaints of headache, fever, and neck stifTness. Elevation of intracranial pressure fuom entities such as a brain tumor or an intracranial hemorrhage also may prr:sent with a chief complaint of vomiting in association w'ith a severe, progressive headache. Vomiting in such pratients often occurs shortly after waking in the morning because of a gradual rise in intracranial pressure as the child sleeps in the supine position. Inaclvertcut toxic ingestions also should be considered, especially in toddlers.
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diaguosis is based on several characteristic fbatures: I) three or rlore episodes of recurrettt vomiting, 2) inIervals of normal health benveen episodes, 3) episodes that are stereotypic r.vith regard to synptom onset and duration, and 4) lack of laboratory or radiographic evidence to support an alternative diagnosis. Vomiting episodes are of rapid ouset and persist for hours to days, separated by s1'pplottt-fi'ee inten'als that can range from rveeks to years. 'l'reatment is supportive , fbcused on fluid manaiement in cases where dehydration and electrolyte

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Acquired bowel obstructions such as intussusception

may present in the older infhnt and young child, rvith the peak incidelrce occurring betrveen 3 rnonths and 3 years Figure 5. Contrast outlining the lead portion ofthe intussusception, giving the typical "coiled spring" appearance.
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imbalance occur. Amitriptvline and propranolol have been clescritred a^s effective for prophylactic therapy (antiemetics may be of benefit during an acute episode).

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Abdominal rnigraines involve episodic attacks olepigastric or periumbilical abdorninal pain and are believed to share pathophvsiologic mechanisms with CVS. Abdominal migraines are more comrnon in females than in males, r,r'ith a ratio of 3:2, and the orlset is primarily betrvcen 7 and 12 years. A familv l'ristory of migraine headaches may be prescnt. Episodes of abdominal pain are acute in onset and last for I hour or more . The pain is so intense that it intcrferes rvith thc perlbrmance of normal activities and is associated with anorexia, nausea, vomiting, headache, photophobia, and pallor. Much like those r.vho have CVS, patients have abdominal ",r'ho migraines report inten'als of cornpletely normal health betu'een dre episodes of pain. Diagnostic evaluation looking for alternative organic conditions yields negative results. The diagnosis of abdominal n"rigraine is supported by a favorable respol"lse to meclications used tbr treatlnent of migraine headaches. Patients should be adl'ised about trigger avoidance, specifically caffeinecontaining fbods, alterec-l sleep patterns, prolonged fhsting, emotional stress, and exposure to flickering lights.

Superior mesenteric artery (SMA) s1'ndrome, othenvise knorvn as Wilkie svndrome or cast syndrome, is a functional upper intestinal obstructive condition. Normally, the SMA fbrn.rs a 4S-degree angle, with the abdominal aorta at its origin and thc third portion of thc duoclenum crossing berrveen tl"le t\.{,o structures. When the angle betu.een the SMA and the aorta is narrorved to less than 25 degrees, the duodenum may become entrapped and compressed. This condition most comn-ronly is described in patients who have experienced rapid u'eight loss, imrnobilization in a body cast) or surgical correction of
spinal deformities. SMA syndrome typically presents rvith epigastric ab' dominal pain, early satiet,r,, nausea, and bilious vomiting. Patients experience lr.orsening pain in the supine position, lvhich may be relieved in the prone or knee-chest

position. Diagnosis usually is confirmed by upper GI

radiographic series (Fig. 6) or computed tomography scan (Fig. Z) *'idr failure of contrast to pass beyond the thircl portion of the duodenum. Conservative initial nlanagement of SMA svndrome focuses on gastric decompression, follorved by the cstablishment of adequate nutrition and proper positioning after rneals. Placernent of an enteral fceding tube distal to the obstruction or
parenteral nutrition may be needed in sevrre cases. Surgical cc.rrrection r,vith a duotlenojejunostomv is a last
res.)rt.

{}.tsrxt*atir.sn

Rumination is the repeated ancl painless regurgitation of ingested food into the mouth begimring soon after food intake. The food is re-cherved and su'allowed or spit out. Symptoms do not occur during sleep and do not respond to the standard treatment of GER. To quali!, for the diagnosis, symptoms must be present fc.rr longer than 8 weeks. Rumination is not associated r.r,ith retching and ofterr is vicu,ed as a behavioral entiqv, wpically seen in mentally retarded children, neonates cluring prolongcd hospitalization, and children and infbirts u,ho havc GER.

Rumination also has been described in cases of child neglect and in older children and adolescents rvho have
bulimia or are depressect. Mc;st commonly, rumination is seen among female adolescents or male infants. One third of affected individuals have underlying psychological disturbances. The management of rumination involves a multidisciplinary approach, with a primary focus on behavioral therapy and biofeedback. Occasionally, tricyclic antidepressants and nutritional support may be
llecessary.
190 Ptditirics irr Rcvitw r r "- -" --Dciwnloaded

Figure 6. Severely dilated stomach and proximal duodenum indicative of high obstruction consistent with superior mesenteric artery syndrome,

from http:/,ipedsirrrcviL-rv.aappublications.org at Hospital For Sick Children on August 8, 2008

vomiting

reccptor antagonists at the chemoreceptor trigger zone.

Such dmgs rarely are used in pediatric patients because

of

their extrapyramidal and sedative adverse effects. Antihistarnincs such as diphenhydramine, hydrox,vzir.re, ar-rei dimenhydrinate also may help alleviate nausea and vomiting but have a sedative effect that makes clinical reevaluation diflicult. A nen'er class of antiemetics is the SH-I3-receptor antagonists, ondansetron and granisetron. The 5HT3 blockac{e occurs both at the enteric level and at the chemoreceptor trigger zoIre. These drugs, unlike the phenothiazines and antihistamines, do

not have centra.l nen'ous system adverse effects, rnaking them more attractive options. The SHT3-recptor antagonists havc been approved for the management of chemotherapy-induccd nausea and vomiting and for
Figure 7, Computed tomography scan of the abdomen reveals dilated stomach and duodenum with air-fluid levels. The duodenum tapers abruptly (arrow) as it crosses the midline between the aorta and the superior mesenteric artery.

pregnancy-associated

and postoperative von'fting in

adults. For children, however, there is no substantive scientific evidence supporting their efficacy in treating acute gastroenteritis. Therefore, these agents have not been endorsed officially for routine use .

Seneral Principles in the Management of Vomiting

Therapy to alleviate vomiting should be directed at the specific cause, when possiblc. Clastrointestinal obstructions shcluld be corrected, as deemed appropriate by the pediatric surgery team. Management of nonsurgical causes of rromiting include steps to correct fluid and elcctrolvte imbalances that result lrcrm prolonged or excessive vomiting and to identi$ and treat the underlying disorder causing the symptom. Thc 2003 Centers for Disease Control and Prevention practice guidelines for the management of acute gastroenteritis in children, endorsed by the Americur Academy of Pediatrics, rec-

Conclusion
Vomiting
a

is a nonspecific symptom

that may accompany

rvide variery of GI and extraintestinal disorders. Serious extraintestinal causes of von-riting include brain tumor

and meningitis; congenital or acquired intestinal obstmctive s\,ndromes arc the most seriolrs intestinal
causes. Associated

fluid and electroll.te imbalances

ahva,vs

must be considereci rvhen assessing a child w'ho has a histo4' of r.omiting. Conditions such as mild GER may

r:mmend oral rehydration therap,v (ORT) in cases of mild-to-moderate dehydration frorn acute gastroenteritis. (7) Using an appropriatc glucose-electrolytc solution, 50 to 100 n"L/kg of fluid sl'rould be adrninistcred to the child over the course of 4 hours, along u'ith replacement of continuing losscs from stool and emesis. This is most effective w,hen the ORI is administered in small, 5-mL increments every I to 2 minutes. In cases of severe dehydration, ileus, or persistent vomiting despite adequate attempts at ORT, parenteral fluids must be
administered.

only necessitate reassurance, but svmptoms of bilious vomiting should prompt immediate rcferral to a pediatric surgeon. Results of the history and physical examination, keeping in rnind the nature of the vomiting and age of the child, may help the clinician determine the likely cause and the necd fbr emerg5cnt treatment.
1,.{{"lt*'iiLl*{ilJ{:i:i?. The authors rvould like to extheir gratitude to Dr Dvorah Balsam fbr the images

press

and thc descriptions of the findings.

Although the previously cited guidelines clo not recommend the routine use of antiemetic drugs in the
management of patients who have acute gastroenteritis, unique situations may warrant their use. If the cause of the vomiting is unclear, antiemetics are contraindicated. Phenothiazines such as prochlorperazine, prolnethazine,

fr.*j*itn{:{:'j
1 , Godbolc P, Stringe r MD. Bilious vomiting in the ncu'born: hos' often is it patlrologicl / Pe d Swrg. 2002;37:909-91I 2. Craig WR, Har-rlon-Dcarman A, Sinclair C, Taback S, N{offatt

M.

gastrr.r-ocscrphageal

and chlorpromazine are antiemetics that act as D2Downloaded from hfip:i,'pedsirrrcvierv.aappublicnrions.org

Metocloprarnide, thickcncci feedings, and positioning for rcflux irr childrcn undcr fwo yc;trs. Coclnane Databav Sy* Rrr. ?004;4:CD003502 3. l)i L,orenzo C. (iastroesophirgcal rcflux: not a time to "rclax." J Pe dintr. 2O0 6;149 :436 - 438
at Hospital For Sick

Chid;8iit8f ,t,ftil3i'A;'ZO0g

Vomiting in Children: Reassurance, Red Flag, or Referral?

Latha Chandran and Maribeth Chitkara P ediatr. Rev. 2008;29 ;183 -192 DOI: 1 0. I 5 42/pir.29 -6-183

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Scurkrck

Aill, he I,A, Burks ,{lV. Fotxl allergy in children.

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approach t<r

Haghighat M, l\afic SN{, Dchghani SlvI, Fallahi GH, Nejabat il{. C,vclic vomiting s-vndromc in childrcn: cxperience with l8l cascs fiorn southcrn lran. World f Gastroenterol. 2007'13

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Hulka F, Campbcll T), Crrmpbcll ]R, Harrison rMW. Flrolution ir-r thc recognition of infantile hlpertrophic py,loric stenosis. Perllatrics. 1997;'lO0:c9 Kapf'er SA, Rappold JF. lntestinal malrotation-not just the pediatric surgeon's problcm. J Aw Coll Surg. 2OO4;199:

thc nonbiliou.s vomiting nfant. Pediatrics. 1999;103:

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qJ

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Biank V, We rlin S. Supcrior mcscnteric artcry syndromc in childlcn: a 20 year experience. J Pediatr Gq.struenterol Nu*. 2006;42:

Rasquin A,

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Ouiz also ffvailabie snline at www.pedsinreview.org.

Match the clinical finding with the most likely condition.

Each answer may be used once, more

than once, or

not at all.

1. Flattened villi and colitis on biopsy. 2. Uncoordinated esophageal relaxation. 3. Hypochloremic hypokalemic metabolic alkalosis. 4. Recurrent microaspiration. 5, "Coiled spring" appearance on radiography. A. Abdominal migraine.
B. Gastroesophageal reflux.

C. lntussusception. D. Protein intolerance. E. foloric stenosis.

192 Fed'atlicsfl-q*"ilw;ad,i

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at Hospital For Sick children on August 8, 2008