Vomiting in Children

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

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

The online version of this article, along with updated information and services, islocated 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 monthlypublication, it has been published continuously since 1979. Pediatrics in Review is owned,published, and trademarked by the American Academy of Pediatrics, l4l Northwest PointBoulevard, Elk Grove Village, lllinois, 60007. Copyright O 2008 by the American Academy ofPediatrics. All rights reserved. Print ISSN: 0l9l-9601. Online ISSN: 1526-3347.

American Acaclemy of Pecliatric ,mDF]I)ICAI'ED'1'O ]'HI] H},AL]'H OF AI.,I. CHII.,DR}:.N- WJ

Downloaded from http:l.rpetlsinrevicrr.aappilbli0ati{rns.org at Hospital For Sick Children on August 8, 2008

Article

% # n&% * m& ffiffi &

wffiffi*Kffiffiffi ffiffi wffixxffiwwffix

Latha Chandran, MD,

MPH,- Maribeth Chitkara,

MDT

Author Disclosure

Drs Chandran and

Chitkara have

disclosed no financial

relationships relevant

to this article. This

commentary does

contain a discussion

of an unapprovedl

investigative use of a

commercial producti

device.

' .; , it :,' : , ,,. '' After completing this articit, reader! should be able to:

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

2. uncierstand the physiolagy hehind the protess *f vomiting"

3. Recogniee comrylon causes of vamitinq based an the pattern and nature of er*esis.

4. Be familiar with the basic Siagnostic evaluaticn *nd treatment strategies fsr different

car;ses 0f vamiting.

Case StudyA l-rnonth-old boy who has had postprandial romiting for I weeh is admitted frow the

ernerg€ncy 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. Tbtrest 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?nlvem.ent past the pylorus is obserped. An echogenic densiw in tlte prepyloric area is noted.. Anwppergastrointestinfl.l (GI) rndiographic series and. encloscopy ra'eal wn antral web, wbich is

excised nrgically.

Fhysiology of VomitingVomiting involves the forceful expulsion of the contents of the stomach and is a highlvcgordinated, 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 abdom-inal musculatlrre on relaxation of the gastric cardia force gastric contents back up the

esc'rphagus. The process is coordinated by the *vomiting center" in the central nen'oussystem. '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 VcmitingVorniting can be classified according to its nature and causc as well as by the character ofthe 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 ofpyloric stenosis. Nonprojectile vomiting is seen more comnonly in gastroesophageal

reflux. These somervhat arbitrary descriptions are not definitive in establishing a diagnosis.

Ernesis often is classified based on its qualir.v. -Ihe vomitus may be bilious, bloody, ornonbloodv 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.

Downloaded from htrp:tipedsinrer,icrv.aappribticariuns.org at Hospital For Sick Chidigiit8iiA,ftIiiS, Z00br83

var?1 ltl nq

is dark green is referrecl to as bilious because it indi-cates the prescnce of bile. Bilious r,omiting frequendy ispathologic because it may be a sign of an underlf ingabdominal problem such as intestinal obstrrrction be-yoncl the duoderral ampulla of lhter, rvhere the c<lm-

mon bile duct empties. 'fhe presencc of blood in theernesis, also knolvn as hematemesis, indicates acutebleeding from the upper portion of the GI tract, as can

occur with gastritis, Mallorv-lVeiss tears, or peptic ulcerdisease. Coffee ground-like material often is reprcsenta-til'e of an old GI hernorrhage becausc blood darkens to ablack or dark-brown color rvhen exposed to the acidity ofthe gastric secretions. The more nrassive or proximal thebleecling, the more likely it is to bc bright red.

Sifferential IiagnosisA r.'ariery of organic and nonorganic clisorders can be

associated rvith vomiting. Organic callscs are those re-lated to specific medical conditions. The primarv care

practitioner needs to remember that vomiting does notlocalize the problem to the GI system in 1'oung infbntsbut can be a nonspecific manifbstation of an underlyingsystemic illness such as a urinary tract infection, sepsis, oran 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 vomitingsvndrome, abdominal migraine, and bulimia. Table Iiists the dillbrential diagnosis ofvomidng based on organsystems. Florvever, frorn a clinical perspective, it often is

useful to consider causes from an age-related perspective.

Vomiting in lnfancyTable 2 details the age-related differential diagnosis ofvomiting in infants. Vomiting in the first felv days afterbirth may be a sign of serious pathology. Bilious emesis is

suggestive of congenital obstmctive GI malfcrrrnations,such as duodenal/ejunal atresias, rnalrotation u'ith rnid-gut vohulus, rncconium ileus or plugs, and Hirsch-sprung disease. Published reports ofneonates evaluatedin neonatal intensive care units r,vith a principal diagnosisof bilious emesis revealed that 38% to 690/o had an intes-

tinal obstmction. (l) Nonsurgical causes of bilious eme-

sis include llecrotizirlg enterocolitis and gastroesopha-geal reflux (GER).

When caring for a neonate lvho has prersistent biliousvomiting, the clinician should placc a nasogastric ororogastric catheter to decompress the stomach and pre-vent any aclditional vomiting or aspiration before initiat-ing anl' dixgnostic or therapeutic ntaneuvers. Plain radio-graphs of the abdomen can demonstrate dilated trorvel

loops ancl air-fluid levels, rvhich strongly suggest borvelobstruction. Contrast imaging studies are more specific

and can help pinpoint a precise diagnosis. Surgical andneonatal consultations should be obtained urgentlyrvhen the diagnosis of txlwel obstruction is considered.

1 rs I t:..", li r zal fi.1: r * y,i *tIntestinal atresias are surgical cmergencics and rypicall,vpresent r.vitl-rin a feu' hours after birth. Duodenal atresia isa cor-rgenital obstr-r-rction of the second portion of tht:duodenum that occurs in I per 5,000 to 10,000 livebirths and is associated r,vith trisomy 2l in approximately25oA of cases. It is believed to be duc to a failure ofrecanalization of the bou'el during early gestation. In-fants present with clinical features of thilure to toleratefeedings and bilious emcsis shonly after birth. Due to theproximal nature of the obstruction, abdominal disten-tion usually is not present. Plain abdominal radiographsmay 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 ab-

donrinal distention within the first 24 hours after birth.The cause of these atresias is believed to be a n'r€scntericvascular accident at somt: point during the course ofgestation. The frequency ofdreir occurrence is approxi-mately I per 3,000 live births. Anatomically, jejunoileal

atresias can be classified into four q'pes: rnembranous)internrpted, apple-pecl, and multiple. Abdominal racli-

ographv may shorv dilated loops of small bowel withair-fluid levels (Fig. 2). Urgent surgical correction is

necessary for all ty'pes ofintestinal atresias.

t\iri r,r. t., t,*, \h!:, i,,1,r;ri^,,, \r,,i.,.,'.,,17' t rt t'. \2 t(z tl n t I V u t Lt r r t I iULJa,4 t V'J 1 V U : \,43

Understanding malrotation requires a revier.v of theorganogenesis of the gut. During the third week of fetaldevelopment, the prirnitive gut is divided into threeregions: the fcrregut, midgut, and hindgut, based onvascular supply. The first stage of intestinal developmentinvolvcs rapid growth of the rnidgut outside the abdom-inal cavity through a herniation of the umbilical orifice.l)uring the second stage, the rnidgut returns to theabdominal cavitv, rotating 180 degrees and pushing thehindgut to the left. The last stage of intestinal develop-nent involves the retroperitonealization of portions ofthe right colon, lcft colon, duodenum, and intestinalmesentery, helping them serve as anchors for the borvel.Disnrption of this process during the second or thirdstage can rcsult in an aberrant return or anchoring ofthemidgut u'ithin the abdominal cavity.

I84 Pediatrit:r iri Rtvit:iv .., r:

Downloaded from htfp:1.;pedsinrevi*w.aappnblication-c.org at Hospital For Sick Children on August 8, 2008

!r$fiiting

rabrc r. Differential Diagnosis of Vomiting by Systems

Gastrointestinal Neurologic Endocrine

r Esophagus: Stricture, web, ring,atresia, tracheoesophagealfistula, achalasia, foreign body

r Stomach: pyloric stenosis, web,duplication, peptic ulcer,gastroesophageal refl ux

r lntestine: duodenal atresia,malrotation, duplication,intussusception, volvulus,foreign body, bezoar, pseudo-obstruction,necrotizing enterocolitis

r Colon: Hirschsprung disease,

imperforate anus, foreign body, bezoarr Acute gastroenteritisr Helr'cobacter pylori infectionr Parasitic infections: ascariasis, giardiasisr Appendicitisr Celiac diseaser Milldsoy protein allergyr lnflammatory bowel disease

r Pancreatitisr Cholecystitis or cholelithiasisr lnfectious and noninfectious hepatitisr Peritonitisr Trauma: Duodenal hematoma

r Tumorr Cystr Hematomao Cerebral edemar Hydroctphalusr Pseudotumor cerebrir Migraine headachec AMominal migrainer Seizuree Meningitis

Renal

r Obstructive uropathy: Ureteropelvicjunction obstruction,hydronephrosis, nephrolithiasis

r Renal insufFrciencyo Glomerulonephritis. Urinary tract infectiono Renal tubular acidosis

Metabolic

r Galactosemiar Hereditary fructosemiar Amino acidopathyo Organic acidopathy

r Urea cycle defectso Fatty acid oxidation disordersr lactic adidosis

o Lysosomal storage disorders

r Peroxisomal disorden

o Diabetic ketoacidosis

o Adrenal insufficiency

Respiratory

r Pneumoniar Sinusitisr Pharyngitis

Miscellaneous

r Sepsis syndromese Pregnancyr Rumination

o Bulimia

o Psychogenic

r Cyclic vomiting syndromer Overfeedingo Medications/vitamin/drug toxicityr Superior mesenteric artery

syndromer Child abuse

Although most infhnts who have intestinal malrota-tion present rvithin the first rveek after birth due to theaccompanying volvulus, the malrotation itself cloes notcause an)r notable symptoms and may be undetected forvears. Bowel strangulation can occur at anv age and anytime because affcctetl patierlts arc at incrcascd risk ofvohulus due to a lack olproper mesenteric anchoring t<-r

the retroperitoneum. The midgut tvvists in a clockwisedirection around the superior mesenteric vessels, leadingto obstruction of vascular supply to most of thc sn'rall andlarge intestine. Once bowel ischemia occurs, metabolicaciclosis, unstable hemodynamics, and intestinal necrosis

r.vith perforation may ensue if the condition is not diag-nosed and rapidly corrected surgically. A spiral configu-mtion of the jejunum or demonstration of failure ofcontrast to pass beyond the second portion ofthe cluo-denum on upper GI radiographic series is diagnostic(Fig. 3). Abdominal ultrasonographv also may reveal a

malposition ol the superior mesenteric vessels. Timelysurgical correction rvidr the Ladd procedure is critical. Ifbou'el ischemia is prolonged, lc.rss of bowel and resultantshort gut slndrome nray occur.

V*miting in lnfancy Beyond the NeonatalPerindThe differential diagnosis of vomiting in inihnts beyonddre neonatal period is more extensive. Common causes

are aclrte gastroenteritis, GE\ and nutrient intolcrancessuch as rnilk or soy protein allergies. Metabolic diseases

ar,d inborn errors of metabolism also shouicl be consid-

ered for infants lvho have persistent progressive vomit-ing. Acquired or mildcr intestinal obstructive lesions,such as infantile h,vpertrophic p1'loric stenosis (IHPS),also are possible and should be mled out lvhen clinicallyindicated.

Common entities such as GER" dietary protein intol-

Downloaded from http:i,ipeilsinrevicw.aappublications.org at Hospital For Sick ChikffSii'8ff X,ftij6fe, zOoS185

v*mrtrng

Common Causes

lntestinal atresia/webs

Meconium ileus

Hirschsprung disease

Necrotizingenterocolitis

lnborn errors ofmetabolism

Pyloric stenosis

Malrotation withmidgut volvulus

lnborn errors ofmetabolism

Milk/soy protein allergy

Gastroesophagealreflux

Child abuse

Gastroenteritis

lntussusception

Child abuse

lntracranial mass lesion

Type of Vomiting

Bilious, depending on level oflesion

Bilious

Bilious or nonbilious

Bilious or nonbilious

Bilious or nonbilious

Nonbilious

Bilious

Bilious or nonbilious

Bilious or nonbilious; mayhave gross or occult blood

Nonbilious; may have grossor occult blood

Nonbilious

Nonbilious initially; mayprogress to bilious

Bilious

Nonbilious

Nonbilious

rabre 2. Age-related Differential Diagnosis of Vomiting in ChildrenYounger Thanl2 Months of Age

Age

Newborn

0 to 3 months

3 to 12months

Comment/Associated Features

May occur at level of esophagus,duodenum, jejunum

Strongly associated with cysticfi brosis; genetic testingsuggested

History of non-passage of stoolsin nursery suggestive; suctionrectal biopsy may demonstratelack of intestinal ganglionce lls

Plain films of abdomen mayreveal intestinal pneumatoses

May have acidosis orhypoglycemia

Hypochloremic metabolicalkalosis

Abdominal distention may bepresent; plain radiographs mayshow air-fluid levels andpaucity of distal bowel gas;

emergent surgical consultationnecessary

Newborn metabolic screen maybe abnormal; acidosis orhypoglycemia may be present

History of extreme fussiness maybe present; fecal occult bloodtesting of stools may bepositive

Emesis usually within 30 minutesof feeding; symptoms worse insupine flat position

Anterior fontanelle fullness maybe present; central nervoussystem (CNS) imaging studiesmay reveal acute or subacutebleeding

Stool studies may help establishoffending pathogen

Abdomen distention may bepresent; plain radiographs mayshow air-fluid levels andpaucity of distal bowel gas;

stools may be grossly bloodywith "currant jelly"appearance; emergent surgicalconsultation indicated; may be

reduced by contrast enemaAnterior fontanelle fullness may

be present; CNS imagingstudies may reveal acute orsubacute bleeding

Anterior fontanelle fullness maybe present; CNS imagingstudies diagnostic

186 Pedratrirs in Rtvicir'"" "'"'""'Ddivn'lilaited frrini hitp:r:ipedsinrevi*rv.iiilppuhlications.org at Hospital For Sick Children on August 8, 2008

Figure I. 'Double bubble" sign on plain radiograph, whichrepresents air in the stomach and proximal duodenum andindicates duodenal atresia-

erance, and IHPS are discussed in greater detail in thissection. Intussusception is another important cause ofvomiting in the young intbnt that is discussed in the nextsection because it also rnav present beyoncl infancy. Themanagerrent of acute gastroenteritis is discussed in tl'rescction on mallagcmerrt.

{} ;: 1,"t: t: ;:t'::i St i :it i} t,t:. ;: l. t4 r: i i Z f t;GER is the most comlnon cause of recurrent nonbiiiousernesis in infancy. It involves the retrogradc movement ofgastric 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 intothe stomach. Patients who havc GER have transient

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

indicative of jejunoileal atresia.

vcmitinq

Figure 3, Failure of contrast to pass beyond the secondportion of the duodenum, which is characteristic of malrota-tion with midgut volvulus.

relaxations of the LES that are not precipitated bv a

sr.vallorv, allorvir-rg gastric contcnts to move fi'eely back

into the esophagus from an area of higher to lorverpressure. 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'ithrecurrerlt postprandial regurgitation of ingested food ormilk, rnost often within 30 minutes of a feeding. Affectedchildren may appear irritable during or after feedings,

and stcreotypic opisthotonic movements u'ith extensionand stiffi:ning of arms and legs ancl cxtcnsiotr of the head(Sandifer syndrorne) occasionally may be obsen'ed. In-fb.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.

Infants rvho have the classic history of recurrent eme-

sis but who are thriving and have normal plrysical exam-

ination findings do not need specific treatment. Thick-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

Downloaded from hup:tipedsinrcvicw.a*ppuhlications.org at Hospital For Sick Chil,iigli'8iiA,ftil$i8, Z60Ar87

vomiting

neecl pharmacologic intenrention. Acid blockade withhistamine, receptor antagonists or protoll-purnp inhibi-tors may help lessen the burning sensation caused by thegastric refluxant. Prokinetic agents such as metoclopra-rnide and er)'thromycin may help decrease the phy5isalprocess of GER by targeting the l,ES.

A Cochrane meta-analysis revieu'ing seven random-ized control trials showed that metoclopramide \vas su-

perior to placebo in reducing daily symptoms of GER(2) Horvelcr, its use must be weighed against the poten-tial adverse effects of extrapyrsplclal symptoms, head-ache. and drolvsiness. Recent studies have suggcsted thatbaclofen, a GABA receptor agonist, mav lessen the num-ber of transient LES rclaxations via vagal-mediatedmechanisms and, thus, improve the pathophvsiologicprocess associated rvith CIER (3) Additional inlcstiga-tion into this agent's overall efficacy for the treatrnent ofGER is necessary.

:i ,&,.-. t:-^r-:- 1*t.^1,..^^^^

Dietary protein intolerance is a non-irnrnunoglobulinE-n-rediatcd q?e of food hypersensitivity that typicallypresents in infants in the first postnatal year, shortlv afterexposure to the ollbnding allergen. Commonly impli-cated proteins include corv milk protein, soy protein, andegg protein. Among the clinical symptoms are irritability,feeding intolerance, recurrent vomiting and diarrhca,and in severe cases, failure to thrive. Occasionally, pa-

tients may present with Heine r syndrome , manifesting as

pulmonary hemosiderosis (due to recurrent rnicrohem-orrhages into the lungs), iron deficiency anemia, andfailure to thrive. Examination of stools in patients whohave protein intoler'ance may reveal occult blood, withpolymorphonuclear 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 re-

moval of tire allergen from the diet. In the case of corvmilk protein allergy, 80% of patients respond to hyclrcl-lyzed casein formula; the remaining 2Uo/o requireI.-amino acicl-based fcrrn-rulas or intravenous nutrition.(4) Once elimination has occurred, svmptoms usuallyresolve in 3 to l0 days. The dietary protein intoleranceq'pically subsicies by l8 to 24 months of age . (4)

j.r i3 n l, ;." L i y, ftr, r I ; t)1.j ; t :..: p.; 1;:' " : -l ir r .i i r

Infants rvho have pyloric stenosis typically present tomeclical attention with persistent projectile nonbiliousemesis between 2 and 6 rveeks of age. Males, especially

those lvho are firstborn, are alibcted approximately fourtimes as often as females. fhe incidcnce is approximately3 per 1,000 live births. The exact cause of pyloric stenosisremains unclear. -lhe relaxation mechanism ofthe pyloricsmooth muscle depends on nonadrenergic noncholin-ergic inhibitory inncnation, mcdiated by vasoactive in-testinal peptide and nitric oxide (NO). Deficiencies inneuropeptidergic innen'ation and NO have been impli-cated in cases of pyloric stenosis, but neither has beensubstantiated as etiologic. \'ery early exposure to eryth-romycin (within the firct 2 rveeks after birth) also has

been associated with an eightfbld increased risk ofpvloricstenosis. (5) It is hypothesized that erythromycin inter-acts rvith intestinal motilin rcceptors, causing stronggastric and pyloric contractions and subsequent pvloricmuscle hypertrophy.

Pl,loric stenosis usually is diagnosed by a rypical his-

tory and physical findings. Inspection of the abdomenshortly after an infant fbeding may reveal a peristalticlvave because thc stomach muscles contract in an aftemptto pass ingested milk past the pyloms. A palpable *olive"

in the mid-epigastric region represents thc hypertrophicpylolic muscle and strongly supports the diagnosis ofpyloric stenosis. Rcpeated episodes of vomiting of thegastric contents due to pyloric stenosis may result incharacteristic electrolyte abnormalities, although serumelectrolyte values may be norrnal if the patient is diag-nosed in the early stages.

I'he classic electrolyte abr.rormality is a hlpochloremichypokalemic metabolic alkalosis. Normal acid produc-tion in the stomach is accompanied by tl're release ofbicarbonate ions into the blood as a result ofthe action ofcarbonic anhydlns.. Ilecause ofthe loss ofthe hydrogenions, this bicarbonate is unbuffered, resulting iu an eu-

suing 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 inaddition to the elcctroll.tes. The subsequent volumecorltraction triggers a renal response ofenhanced proxi-mal tribular reabsorption of bicarbonate and activation ofdre renin-angiotensin-aldosterone mechanisms. In addi-tion, the lack of chloride ion in the proximal tubuleresults in increased local production and reabsorption ofbicarbonate, thus worsening the existing metabolic alka-

losis. Under the influence of high concentrations ofaldosterone, the distal rubule excretes large amounts ofpotassium and hydrogen ions in exchangc of sodium.Lack of h)drogen ions results in enhanced excretion ofpotassium, leading to significant hypokalernia.

When the diagnosis of py'loric stenosis is being con-siclered, ultrasc.rnography of thc pyloric muscle cal-! con-

r88 p*diarri$S*evlwdtdA iiom hiip:.ilpedsinrevi*rv.aappublie:ations.org at Hospital For Sick Children on August 8, 2008

Figure 4. Thickened and lengthened pyloric muscle that is

characteristic of pyloric stenosis.

firm the clinical suspicion, rvith sensitivity rates rangingfrom 85%o to 1007o. (6) Pvloric muscle thickness of4 mmor more and muscle length of 14 mm or mor€ are

diagnostic of pvloric stcnosis (Fig. a). If ultrasono-graphic examination findings are normal, an upper GIradiographic series can be performed. The radiographicseries has a slightlv highcr sensitivitv for pyloric stenosis

(89% to 100%) and can aid in the cliagnosis of othercauscs of progressive emesis in this a65c group, such as

antral web and other structural abnormalities. Surgicalpvlorornyotomy is the definitive treatmellt of pyloricstenosis and is being perforrned laparoscopically at manycenters.

Vomiting in Older ChildrenVorniting occurs most commonly in older childrcn in thesetting of an acute gastroenteritis accompanied by 6st.tand diarrhea. Vomiting also can be a nonspecific mani-festation of a systemic illness, although much less com-monly than in the young infant. Both viral and bacteriaimeningitis can present vvith vomiting, usually accompa-

nied b1, cornplaints of headache, fever, and neck stifTness.

Elevation of intracranial pressure fuom entities such as a

brain tumor or an intracranial hemorrhage also mayprr: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 morningbecause of a gradual rise in intracranial pressure as thechild sleeps in the supine position. Inaclvertcut toxicingestions also should be considered, especially in tod-dlers.

i. . . ; . . " , . . - *.-. .- r '.

-. *.1JJ1 .J1"lJ" -i: ;t: :1,i?

Acquired bowel obstructions such as intussusceptionmay present in the older infhnt and young child, rvith thepeak incidelrce occurring betrveen 3 rnonths and 3 years

vrnr iti ng

of age. Intussusception is the telescoping of one portionof the borvel into its distal segment. Most commonlv, theterminal ileum invaginates into the cecum, often as aresult of lymphatic hypertrophy in the Peyer patches

from a recent viral infection. A history of intermittentepisodes of severe and crampv abdominal pain lvith bii-ious emesis is classic. Parents often repnn that their childis lethargic in betu.een episodes ofpain and may describeblood-tinged, *currant jelly" stoois. P\sical examina-

tion mav reveal intestinal obstmction with a salrsage-

shape mass palpable in the right lou'er quadrant. Rapidconsultation with a peciiatric surgeon is rvarranted. Con-trast or air enemas can be diagnostic, r,vith dre contrast

outlining the lead portion of the intussusception. givingthe wpical "coiled spring" appearance (Fig. 5). In addi-tion, thc hydrostatic pressurc from the contrast erlemamay reduce telescoping of the intestine. Surgical reduc-

tion of the intussusception is indicated when the contrastenema is not successftil.

{'S t 1t r: \'l * r* tttrtg 9V * * r r:r*,tCyclic vomiting syndron're (CVS) is characterizecl bystereoq'pic recurrent episodes of nausea and vornitinglvidrout an identifiable organic cause. It is an idiopathicdisorder that usually begins in early childhood; relativelylittle is knolvn about its pathogenesis or cause. Thediaguosis is based on several characteristic fbatures:

I) three or rlore episodes of recurrettt vomiting, 2) in-Iervals 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 evi-dence to support an alternative diagnosis. Vomiting ep-

isodes are of rapid ouset and persist for hours to days,

separated by s1'pplottt-fi'ee inten'als that can range fromrveeks to years. 'l'reatment is supportive , fbcused on fluidmana€iement in cases where dehydration and electrolyte

Figure 5. Contrast outlining the lead portion ofthe intussus-ception, giving the typical "coiled spring" appearance.

Downloaded from hup:ipe<lsinrevicrv.aapptblicarir.rns.org at Hospital For Sick ChidlgiitSiili ffisi'g; 260S189

v0rnitinq

imbalance occur. Amitriptvline and propranolol have

been clescritred a^s effective for prophylactic therapy (an-tiemetics may be of benefit during an acute episode).

h* * * nzi *'*I ?'&', :1r ;:i rt r:

Abdominal rnigraines involve episodic attacks olepigas-tric or periumbilical abdorninal pain and are believed toshare pathophvsiologic mechanisms with CVS. Abdom-inal migraines are more comrnon in females than inmales, r,r'ith a ratio of 3:2, and the orlset is primarilybetrvcen 7 and 12 years. A familv l'ristory of migraineheadaches may be prescnt. Episodes of abdominal painare acute in onset and last for I hour or more . The pain isso intense that it intcrferes rvith thc perlbrmance ofnormal activities and is associated with anorexia, nausea,vomiting, headache, photophobia, and pallor. Much likethose r.vho have CVS, patients

",r'ho have abdominal

migraines report inten'als of cornpletely normal healthbetu'een dre episodes of pain. Diagnostic evaluationlooking for alternative organic conditions yields negativeresults. The diagnosis of abdominal n"rigraine is sup-

ported by a favorable respol"lse to meclications used tbrtreatlnent of migraine headaches. Patients should be

adl'ised about trigger avoidance, specifically caffeine-

containing fbods, alterec-l sleep patterns, prolonged fhst-

ing, emotional stress, and exposure to flickering lights.

{}.tsrxt*atir.sn

Rumination is the repeated ancl painless regurgitation ofingested food into the mouth begimring soon after foodintake. The food is re-cherved and su'allowed or spit out.Symptoms do not occur during sleep and do not respondto the standard treatment of GER. To quali!, for thediagnosis, symptoms must be present fc.rr longer than8 weeks. Rumination is not associated r.r,ith retching andofterr is vicu,ed as a behavioral entiqv, wpically seen inmentally retarded children, neonates cluring prolongcdhospitalization, and children and infbirts u,ho havc GER.Rumination also has been described in cases of childneglect and in older children and adolescents rvho have

bulimia or are depressect. Mc;st commonly, rumination is

seen among female adolescents or male infants. Onethird of affected individuals have underlying psycholog-ical disturbances. The management of rumination in-volves a multidisciplinary approach, with a primary focuson behavioral therapy and biofeedback. Occasionally,tricyclic antidepressants and nutritional support may be

llecessary.

| ,, , ( I

Superior mesenteric artery (SMA) s1'ndrome, othenviseknorvn as Wilkie svndrome or cast syndrome, is a func-tional upper intestinal obstructive condition. Normally,the SMA fbrn.rs a 4S-degree angle, with the abdominalaorta at its origin and thc third portion of thc duoclenumcrossing berrveen tl"le t\.{,o structures. When the angle

betu.een the SMA and the aorta is narrorved to less than25 degrees, the duodenum may become entrapped and

compressed. This condition most comn-ronly is describedin patients who have experienced rapid u'eight loss, im-rnobilization in a body cast) or surgical correction ofspinal 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 posi-

tion, lvhich may be relieved in the prone or knee-chestposition. Diagnosis usually is confirmed by upper GIradiographic series (Fig. 6) or computed tomographyscan (Fig. Z) *'idr failure of contrast to pass beyond thethircl portion of the duodenum. Conservative initialnlanagement of SMA svndrome focuses on gastric de-

compression, follorved by the cstablishment of adequate

nutrition and proper positioning after rneals. Placernentof an enteral fceding tube distal to the obstruction orparenteral nutrition may be needed in sevrre cases. Sur-gical cc.rrrection r,vith a duotlenojejunostomv is a lastres.)rt.

Figure 6. Severely dilated stomach and proximal duodenum

indicative of high obstruction consistent with superior mes-

enteric artery syndrome,

190 Ptditirics irr Rcvitw r r : :"- -" --Dciwnloaded from http:/,ipedsirrrcviL-rv.aappublications.org at Hospital For Sick Children on August 8, 2008

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 midlinebetween the aorta and the superior mesenteric artery.

Seneral Principles in the Management ofVomitingTherapy to alleviate vomiting should be directed at thespecific cause, when possiblc. Clastrointestinal obstruc-tions shcluld be corrected, as deemed appropriate by thepediatric surgery team. Management of nonsurgicalcauses of rromiting include steps to correct fluid andelcctrolvte imbalances that result lrcrm prolonged orexcessive vomiting and to identi$ and treat the underly-ing disorder causing the symptom. Thc 2003 Centers forDisease Control and Prevention practice guidelines forthe management of acute gastroenteritis in children,endorsed by the Americur Academy of Pediatrics, rec-

r:mmend oral rehydration therap,v (ORT) in cases ofmild-to-moderate dehydration frorn acute gastroenteri-tis. (7) Using an appropriatc glucose-electrolytc solu-tion, 50 to 100 n"L/kg of fluid sl'rould be adrninistcredto the child over the course of 4 hours, along u'ithreplacement of continuing losscs from stool and emesis.

This is most effective w,hen the ORI is administered insmall, 5-mL increments every I to 2 minutes. In cases ofsevere dehydration, ileus, or persistent vomiting despite

adequate attempts at ORT, parenteral fluids must be

administered.Although the previously cited guidelines clo not rec-

ommend the routine use of antiemetic drugs in themanagement of patients who have acute gastroenteritis,

unique situations may warrant their use. If the cause ofthe vomiting is unclear, antiemetics are contraindicated.Phenothiazines such as prochlorperazine, prolnethazine,and chlorpromazine are antiemetics that act as D2-

vomiting

reccptor antagonists at the chemoreceptor trigger zone.Such dmgs rarely are used in pediatric patients because oftheir extrapyramidal and sedative adverse effects. Antihis-tarnincs such as diphenhydramine, hydrox,vzir.re, ar-rei di-menhydrinate also may help alleviate nausea and vomit-ing but have a sedative effect that makes clinical re-

evaluation diflicult. A nen'er class of antiemetics is theSH-I3-receptor antagonists, ondansetron and granis-etron. The 5HT3 blockac{e occurs both at the entericlevel and at the chemoreceptor trigger zoIre. These

drugs, unlike the phenothiazines and antihistamines, donot have centra.l nen'ous system adverse effects, rnaking

them more attractive options. The SHT3-rec€ptor an-

tagonists havc been approved for the management ofchemotherapy-induccd nausea and vomiting and forpregnancy-associated and postoperative von'fting inadults. For children, however, there is no substantive

scientific evidence supporting their efficacy in treatingacute gastroenteritis. Therefore, these agents have notbeen endorsed officially for routine use .

ConclusionVomiting is a nonspecific symptom that may accompanya rvide variery of GI and extraintestinal disorders. Serious

extraintestinal causes of von-riting include brain tumorand meningitis; congenital or acquired intestinal ob-stmctive s\,ndromes arc the most seriolrs intestinalcauses. 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 mayonly necessitate reassurance, but svmptoms of biliousvomiting should prompt immediate rcferral to a pediatricsurgeon. Results of the history and physical examination,keeping in rnind the nature of the vomiting and age ofthe child, may help the clinician determine the likelycause and the necd fbr emerg5cnt treatment.

1,.{{"lt*'iiLl*{ilJ{:i:i?. The authors rvould like to ex-

press their gratitude to Dr Dvorah Balsam fbr the images

and thc descriptions of the findings.

fr.*j*itn{:{:'j1 , Godbolc P, Stringe r MD. Bilious vomiting in the ncu'born: hos'often is it patlrologicl / Pe d Swrg. 2002;37:909-91I2. Craig WR, Har-rlon-Dcarman A, Sinclair C, Taback S, N{offattM. Metocloprarnide, thickcncci feedings, and positioning forgastrr.r-ocscrphageal rcflux irr childrcn undcr fwo yc;trs. Coclnane

Databav Sy* Rrr. ?004;4:CD0035023. l)i L,orenzo C. (iastroesophirgcal rcflux: not a time to "rclax."

J Pe dintr. 2O0 6;149 :436 - 438

Downloaded from hfip:i,'pedsirrrcvierv.aappublicnrions.org 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 -192DOI: 1 0. I 5 42/pir.29 -6-183

*r::::f,,'.^i,:^Tl :i :::l?:;f : ffi

Updated Information& Services

Subspecialty Collections

Permissions & Licensing

Reprints

including high-resolution figures, can be found at:http:iiperlsinrevisu'.aappuhiications.ilrg,/cgiicrrntent firlll29I6I183

This article, along with others on similar topics, appears in thefollowing collection(s):Gastrointestinal Disordershttp:ir'pcdsirrre view.aappublications.orgr'cgii'collectiorrigastrointestinal disorders Neurologic Disordershttp :,llpcdsinrcvierv. aappuhlica iions. org,'cgiico ilectionr'ne uralogic_disorders

Information about reproducing this article in parts (flrgures,tables) or in its entirety can be found online at:htt;r:,','pedsinrevier.v.aappublicaiions.orgirnisciPennissions.shtml

Information about ordering reprints can be found online:littp:i..,pedsinr"eview.aappubl icati<lns.orylorisclrcprints. shtrrrl

Downloaded from http:/ipedsinrevi*rt'.aappublications.org at Hospital For Sick Children on August 8, 2008

vomrt'nq

4. Scurkrck Aill, he I,A, Burks ,{lV. Fotxl allergy in children.Iwrnunol Alletgy Clin North Aw. 200525:369-3885, Curpcr lVO, Griffin N{R, Arbogast P, Hickson GB, Girutam S, Ray

WA. \try carly exposure to e4throm''cin and infantile \peruophicp,r4oric stenosis. Arch Pediatr Adoltsc Mcd. 20O2;156l.647 - 65O

6. Mandcll GA, lVoliion Pf, Adkins H,S, et al. Cost-effective irnrgingapproach t<r thc nonbiliou.s vomiting nfant. Pediatrics. 1999;103:tt98-12027. King CK, Glass \ Bresee fS, Duggan C. Managing acute gastro-entcritis among children: oral lry'dration maintenancc and nutritionaldrcrapy. MMWR Morbid tVorta| Whly Rcp.2003152(RRI6):I-f 6

5 t t q :S r;9'r451 l'.';;;';1 qJ i rs 4Biank V, We rlin S. Supcrior mcscnteric artcry syndromc in childlcn:

a 20 year experience. J Pediatr Gq.struenterol Nu*. 2006;42:522,525

Haghighat M, l\afic SN{, Dchghani SlvI, Fallahi GH, Nejabat il{.C,vclic vomiting s-vndromc in childrcn: cxperience with l8lcascs fiorn southcrn lran. World f Gastroenterol. 2007'13r833*r836

Hulka F, Campbcll T), Crrmpbcll ]R, Harrison rMW. Flrolution ir-r

thc recognition of infantile hlpertrophic py,loric stenosis. Perll-

atrics. 1997;'lO0:c9Kapf'er SA, Rappold JF. lntestinal malrotation-not just the

pediatric surgeon's problcm. J Aw Coll Surg. 2OO4;199:628-635

Kimura ( baning-Baucke V. Bilious vomiting in the nervbom:rapid diagnosis of intcstinal obstmction. Aw Fom Pbysicinn.

200O:61:2791-2798Rasquin A, Dilorcnzo C, l-orbcs D, et al. Childhood firnctional

gastrointestinal disordcrs: child,/adolescent, Gnstroenterolagy.

2006,-1301527-1537

Ouiz also ffvailabie snline at www.pedsinreview.org.

Match the clinical finding with the most likely condition. Eachnot 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.

answer may be used once, more than once, or

192 Fed'atlicsfl-q*"ilw;ad,i iil ilipilipe<isinrevi,lr".aappublications.org at Hospital For Sick children on August 8, 2008