pediatrics in review-2008-vomiting in children

Vomiting in Children:Reassurance, Red Flag, or Referral?Latha Chandran, MD,

MPH,* Maribeth Chitkara,

MD†

Author Disclosure

Drs Chandran and

Chitkara have

disclosed no financial

relationships relevant

to this article. This

commentary does

contain a discussion

of an unapproved/

investigative use of a

commercial product/

device.

Objectives After completing this article, readers should be able to:

1. Discuss the most common causes of vomiting in children of different age groups.2. Understand the physiology behind the process of vomiting.3. Recognize common causes of vomiting based on the pattern and nature of emesis.4. Be familiar with the basic diagnostic evaluation and treatment strategies for different

causes of vomiting.

Case StudyA 1-month-old boy who has had postprandial vomiting for 1 week is admitted from theemergency department. He was born at term with no complications and had regained hisbirthweight by the second week after birth, feeding on a milk protein formula. He has beenvomiting curdled milk intermittently for the past week, and on the day of admission was notedby his pediatrician to have lost 4 oz in weight since his last check-up.

On physical examination, the infant is slightly lethargic and has a sunken fontanelle. Therest of his physical examination findings, including evaluation of his abdomen, are normal.Abdominal ultrasonography shows normal width and length of the pylorus. However, no foodmovement past the pylorus is observed. An echogenic density in the prepyloric area is noted. Anupper gastrointestinal (GI) radiographic series and endoscopy reveal an antral web, which isexcised surgically.

Physiology of VomitingVomiting involves the forceful expulsion of the contents of the stomach and is a highlycoordinated, reflexive process. It is a feature of many acute and chronic disorders,including those causing increased intracranial pressure, metabolic diseases, and anatomicand mucosal GI abnormalities. Descent of the diaphragm and constriction of the abdom-inal musculature on relaxation of the gastric cardia force gastric contents back up theesophagus. The process is coordinated by the “vomiting center” in the central nervoussystem. The vomiting center receives sensory input from the vestibular nucleus (cranialnerve VIII), the GI tract via vagal afferents (cranial nerve X), and the bloodstream via thearea postrema, also known as the chemoreceptor (or chemoreceptive) trigger zone. Thestereotypic behaviors associated with emesis are a result of output from the vomiting centerthrough vagal, phrenic, and sympathetic nerves.

Types of VomitingVomiting can be classified according to its nature and cause as well as by the character ofthe vomitus. The nature of the vomiting may be projectile or nonprojectile. Projectilevomiting refers to forceful vomiting and may indicate increased intracranial pressure,especially if it occurs early in the morning. Projectile vomiting also is a classic feature ofpyloric stenosis. Nonprojectile vomiting is seen more commonly in gastroesophagealreflux. These somewhat arbitrary descriptions are not definitive in establishing a diagnosis.

Emesis often is classified based on its quality. The vomitus may be bilious, bloody, ornonbloody and nonbilious. Emesis originating from the stomach usually is characterized asbeing clear or yellow and often contains remnants of previously ingested food. Emesis that

*Editorial Board.†Assistant Professor of Pediatrics and Emergency Medicine, Pediatric Hospitalist, State University of New York at Stony Brook,Stony Brook, NY.

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is dark green is referred to as bilious because it indi-cates the presence of bile. Bilious vomiting frequently ispathologic because it may be a sign of an underlyingabdominal problem such as intestinal obstruction be-yond the duodenal ampulla of Vater, where the com-mon bile duct empties. The presence of blood in theemesis, also known as hematemesis, indicates acutebleeding from the upper portion of the GI tract, as canoccur with gastritis, Mallory-Weiss tears, or peptic ulcerdisease. Coffee ground-like material often is representa-tive of an old GI hemorrhage because blood darkens to ablack or dark-brown color when exposed to the acidity ofthe gastric secretions. The more massive or proximal thebleeding, the more likely it is to be bright red.

Differential DiagnosisA variety of organic and nonorganic disorders can beassociated with vomiting. Organic causes are those re-lated to specific medical conditions. The primary carepractitioner needs to remember that vomiting does notlocalize the problem to the GI system in young infantsbut can be a nonspecific manifestation of an underlyingsystemic illness such as a urinary tract infection, sepsis, oran inborn error of metabolism. Nonorganic causes aremuch more difficult to identify and often are viewed asdiagnoses of exclusion. Examples of nonorganic causesof vomiting are psychogenic vomiting, cyclic vomitingsyndrome, abdominal migraine, and bulimia. Table 1lists the differential diagnosis of vomiting based on organsystems. However, from a clinical perspective, it often isuseful to consider causes from an age-related perspective.

Vomiting in InfancyTable 2 details the age-related differential diagnosis ofvomiting in infants. Vomiting in the first few days afterbirth may be a sign of serious pathology. Bilious emesis issuggestive of congenital obstructive GI malformations,such as duodenal/jejunal atresias, malrotation with mid-gut volvulus, meconium ileus or plugs, and Hirsch-sprung disease. Published reports of neonates evaluatedin neonatal intensive care units with a principal diagnosisof bilious emesis revealed that 38% to 69% had an intes-tinal obstruction. (1) Nonsurgical causes of bilious eme-sis include necrotizing enterocolitis and gastroesopha-geal reflux (GER).

When caring for a neonate who has persistent biliousvomiting, the clinician should place a nasogastric ororogastric catheter to decompress the stomach and pre-vent any additional vomiting or aspiration before initiat-ing any diagnostic or therapeutic maneuvers. Plain radio-graphs of the abdomen can demonstrate dilated bowel

loops and air-fluid levels, which strongly suggest bowelobstruction. Contrast imaging studies are more specificand can help pinpoint a precise diagnosis. Surgical andneonatal consultations should be obtained urgentlywhen the diagnosis of bowel obstruction is considered.

Intestinal AtresiasIntestinal atresias are surgical emergencies and typicallypresent within a few hours after birth. Duodenal atresia isa congenital obstruction of the second portion of theduodenum that occurs in 1 per 5,000 to 10,000 livebirths and is associated with trisomy 21 in approximately25% of cases. It is believed to be due to a failure ofrecanalization of the bowel during early gestation. In-fants present with clinical features of failure to toleratefeedings and bilious emesis shortly after birth. Due to theproximal nature of the obstruction, abdominal disten-tion usually is not present. Plain abdominal radiographsmay show a “double bubble” sign, which represents air inthe stomach and proximal duodenum (Fig. 1).

More distal obstructions, such as jejunoileal atresias,typically present with bilious vomiting along with ab-dominal distention within the first 24 hours after birth.The cause of these atresias is believed to be a mesentericvascular accident at some point during the course ofgestation. The frequency of their occurrence is approxi-mately 1 per 3,000 live births. Anatomically, jejunoilealatresias can be classified into four types: membranous,interrupted, apple-peel, and multiple. Abdominal radi-ography may show dilated loops of small bowel withair-fluid levels (Fig. 2). Urgent surgical correction isnecessary for all types of intestinal atresias.

Malrotation With Midgut VolvulusUnderstanding malrotation requires a review of theorganogenesis of the gut. During the third week of fetaldevelopment, the primitive gut is divided into threeregions: the foregut, midgut, and hindgut, based onvascular supply. The first stage of intestinal developmentinvolves rapid growth of the midgut outside the abdom-inal cavity through a herniation of the umbilical orifice.During the second stage, the midgut returns to theabdominal cavity, rotating 180 degrees and pushing thehindgut to the left. The last stage of intestinal develop-ment involves the retroperitonealization of portions ofthe right colon, left colon, duodenum, and intestinalmesentery, helping them serve as anchors for the bowel.Disruption of this process during the second or thirdstage can result in an aberrant return or anchoring of themidgut within the abdominal cavity.

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184 Pediatrics in Review Vol.29 No.6 June 2008



Although most infants who have intestinal malrota-tion present within the first week after birth due to theaccompanying volvulus, the malrotation itself does notcause any notable symptoms and may be undetected foryears. Bowel strangulation can occur at any age and anytime because affected patients are at increased risk ofvolvulus due to a lack of proper mesenteric anchoring tothe retroperitoneum. The midgut twists in a clockwisedirection around the superior mesenteric vessels, leadingto obstruction of vascular supply to most of the small andlarge intestine. Once bowel ischemia occurs, metabolicacidosis, unstable hemodynamics, and intestinal necrosiswith perforation may ensue if the condition is not diag-nosed and rapidly corrected surgically. A spiral configu-ration of the jejunum or demonstration of failure ofcontrast to pass beyond the second portion of the duo-denum on upper GI radiographic series is diagnostic(Fig. 3). Abdominal ultrasonography also may reveal a

malposition of the superior mesenteric vessels. Timelysurgical correction with the Ladd procedure is critical. Ifbowel ischemia is prolonged, loss of bowel and resultantshort gut syndrome may occur.

Vomiting in Infancy Beyond the NeonatalPeriodThe differential diagnosis of vomiting in infants beyondthe neonatal period is more extensive. Common causesare acute gastroenteritis, GER, and nutrient intolerancessuch as milk or soy protein allergies. Metabolic diseasesand inborn errors of metabolism also should be consid-ered for infants who have persistent progressive vomit-ing. Acquired or milder intestinal obstructive lesions,such as infantile hypertrophic pyloric stenosis (IHPS),also are possible and should be ruled out when clinicallyindicated.

Common entities such as GER, dietary protein intol-

Table 1. Differential Diagnosis of Vomiting by SystemsGastrointestinal Neurologic Endocrine

● Esophagus: Stricture, web, ring, ● Tumor ● Diabetic ketoacidosisatresia, tracheoesophageal ● Cyst ● Adrenal insufficiencyfistula, achalasia, foreign body ● Hematoma

Respiratory● Stomach: pyloric stenosis, web, ● Cerebral edemaduplication, peptic ulcer, ● Hydrocephalus ● Pneumoniagastroesophageal reflux ● Pseudotumor cerebri ● Sinusitis

● Intestine: duodenal atresia, ● Migraine headache ● Pharyngitismalrotation, duplication, ● Abdominal migraine

Miscellaneousintussusception, volvulus, ● Seizureforeign body, bezoar, pseudo-obstruction, ● Meningitis ● Sepsis syndromes

Renal ● Pregnancy● Colon: Hirschsprung disease,

● Obstructive uropathy: Ureteropelvic● Rumination

necrotizing enterocolitis

imperforate anus, foreign body, bezoarjunction obstruction,

● Bulimia

hydronephrosis, nephrolithiasis● Psychogenic● Acute gastroenteritis

● Renal insufficiency● Cyclic vomiting syndrome● Helicobacter pylori infection

● Glomerulonephritis ● Overfeeding● Parasitic infections: ascariasis, giardiasis

● Urinary tract infection ● Medications/vitamin/drug toxicity● Appendicitis

● Renal tubular acidosis ● Superior mesenteric artery● Celiac disease

Metabolicsyndrome● Milk/soy protein allergy

● Child abuse● Inflammatory bowel disease

● Galactosemia● Pancreatitis

● Hereditary fructosemia● Cholecystitis or cholelithiasis

● Amino acidopathy● Infectious and noninfectious hepatitis

● Organic acidopathy● Peritonitis● Trauma: Duodenal hematoma

● Urea cycle defects● Fatty acid oxidation disorders● Lactic adidosis● Lysosomal storage disorders● Peroxisomal disorders





Table 2. Age-related Differential Diagnosis of Vomiting in ChildrenYounger Than12 Months of Age

Age Common Causes Type of Vomiting Comment/Associated Features

Newborn Intestinal atresia/webs Bilious, depending on level oflesion

May occur at level of esophagus,duodenum, jejunum

Meconium ileus Bilious Strongly associated with cysticfibrosis; genetic testingsuggested

Hirschsprung disease Bilious or nonbilious History of non-passage of stoolsin nursery suggestive; suctionrectal biopsy may demonstratelack of intestinal ganglioncells

Necrotizingenterocolitis

Bilious or nonbilious Plain films of abdomen mayreveal intestinal pneumatoses

Inborn errors ofmetabolism

Bilious or nonbilious May have acidosis orhypoglycemia

0 to 3 months Pyloric stenosis Nonbilious Hypochloremic metabolicalkalosis

Malrotation withmidgut volvulus

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

Inborn errors ofmetabolism

Bilious or nonbilious Newborn metabolic screen maybe abnormal; acidosis orhypoglycemia may be present

Milk/soy protein allergy Bilious or nonbilious; mayhave gross or occult blood

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

Gastroesophagealreflux

Nonbilious; may have grossor occult blood

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

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

3 to 12months

Gastroenteritis Nonbilious initially; mayprogress to bilious

Stool studies may help establishoffending pathogen

Intussusception Bilious 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 bereduced by contrast enema

Child abuse Nonbilious Anterior fontanelle fullness maybe present; CNS imagingstudies may reveal acute orsubacute bleeding

Intracranial mass lesion Nonbilious Anterior fontanelle fullness maybe present; CNS imagingstudies diagnostic





erance, and IHPS are discussed in greater detail in thissection. Intussusception is another important cause ofvomiting in the young infant that is discussed in the nextsection because it also may present beyond infancy. Themanagement of acute gastroenteritis is discussed in thesection on management.

Gastroesophageal RefluxGER is the most common cause of recurrent nonbiliousemesis in infancy. It involves the retrograde movement ofgastric contents into the esophagus as a result of anabnormally functioning lower esophageal sphincter(LES). Under normal circumstances, the LES relaxesafter swallowing to allow passage of ingested food intothe stomach. Patients who have GER have transient

relaxations of the LES that are not precipitated by aswallow, allowing gastric contents to move freely backinto the esophagus from an area of higher to lowerpressure. In young infants, such relaxation often resultsfrom developmental immaturity of the LES, which mayimprove over time. Infants who have GER present withrecurrent postprandial regurgitation of ingested food ormilk, most often within 30 minutes of a feeding. Affectedchildren may appear irritable during or after feedings,and stereotypic opisthotonic movements with extensionand stiffening of arms and legs and extension of the head(Sandifer syndrome) occasionally may be observed. In-fants who have severe GER can have recurrent microaspi-ration into their lungs, resulting in chronic wheezing,respiratory symptoms, and even failure to thrive.

Infants who have the classic history of recurrent eme-sis but who are thriving and have normal physical exam-ination findings do not need specific treatment. Thick-ening the formula or human milk by adding cereal mayhelp reduce vomiting in such infants, but elevating thehead in the supine position has no proven beneficialeffect. (2) Infants who are irritable during feedings andthose who have respiratory or growth problems may

Figure 1. “Double bubble” sign on plain radiograph, whichrepresents air in the stomach and proximal duodenum andindicates duodenal atresia.

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

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





need pharmacologic intervention. Acid blockade withhistamine2 receptor antagonists or proton-pump inhibi-tors may help lessen the burning sensation caused by thegastric refluxant. Prokinetic agents such as metoclopra-mide and erythromycin may help decrease the physicalprocess of GER by targeting the LES.

A Cochrane meta-analysis reviewing seven random-ized control trials showed that metoclopramide was su-perior to placebo in reducing daily symptoms of GER.(2) However, its use must be weighed against the poten-tial adverse effects of extrapyramidal symptoms, head-ache, and drowsiness. Recent studies have suggested thatbaclofen, a GABA receptor agonist, may lessen the num-ber of transient LES relaxations via vagal-mediatedmechanisms and, thus, improve the pathophysiologicprocess associated with GER. (3) Additional investiga-tion into this agent’s overall efficacy for the treatment ofGER is necessary.

Dietary Protein IntoleranceDietary protein intolerance is a non-immunoglobulinE-mediated type of food hypersensitivity that typicallypresents in infants in the first postnatal year, shortly afterexposure to the offending allergen. Commonly impli-cated proteins include cow milk protein, soy protein, andegg protein. Among the clinical symptoms are irritability,feeding intolerance, recurrent vomiting and diarrhea,and in severe cases, failure to thrive. Occasionally, pa-tients may present with Heiner syndrome, manifesting aspulmonary hemosiderosis (due to recurrent microhem-orrhages into the lungs), iron deficiency anemia, andfailure to thrive. Examination of stools in patients whohave protein intolerance may reveal occult blood, withpolymorphonuclear cells, lymphocytes, and eosinophils.Stool-reducing substances may be positive due to carbo-hydrate malabsorption. Intestinal biopsies may revealflattened villi and colitis with infiltration of lymphocytes,eosinophils, and mast cells.

Treatment of dietary protein intolerance involves re-moval of the allergen from the diet. In the case of cowmilk protein allergy, 80% of patients respond to hydro-lyzed casein formula; the remaining 20% requireL-amino acid-based formulas or intravenous nutrition.(4) Once elimination has occurred, symptoms usuallyresolve in 3 to 10 days. The dietary protein intolerancetypically subsides by 18 to 24 months of age. (4)

Infantile Hypertrophic Pyloric StenosisInfants who have pyloric stenosis typically present tomedical attention with persistent projectile nonbiliousemesis between 2 and 6 weeks of age. Males, especially

those who are firstborn, are affected approximately fourtimes as often as females. The incidence is approximately3 per 1,000 live births. The exact cause of pyloric stenosisremains unclear. The relaxation mechanism of the pyloricsmooth muscle depends on nonadrenergic noncholin-ergic inhibitory innervation, mediated by vasoactive in-testinal peptide and nitric oxide (NO). Deficiencies inneuropeptidergic innervation and NO have been impli-cated in cases of pyloric stenosis, but neither has beensubstantiated as etiologic. Very early exposure to eryth-romycin (within the first 2 weeks after birth) also hasbeen associated with an eightfold increased risk of pyloricstenosis. (5) It is hypothesized that erythromycin inter-acts with intestinal motilin receptors, causing stronggastric and pyloric contractions and subsequent pyloricmuscle hypertrophy.

Pyloric stenosis usually is diagnosed by a typical his-tory and physical findings. Inspection of the abdomenshortly after an infant feeding may reveal a peristalticwave because the stomach muscles contract in an attemptto pass ingested milk past the pylorus. A palpable “olive”in the mid-epigastric region represents the hypertrophicpyloric muscle and strongly supports the diagnosis ofpyloric stenosis. Repeated episodes of vomiting of thegastric contents due to pyloric stenosis may result incharacteristic electrolyte abnormalities, although serumelectrolyte values may be normal if the patient is diag-nosed in the early stages.

The classic electrolyte abnormality is a hypochloremichypokalemic metabolic alkalosis. Normal acid produc-tion in the stomach is accompanied by the release ofbicarbonate ions into the blood as a result of the action ofcarbonic anhydrase. Because of the loss of the hydrogenions, this bicarbonate is unbuffered, resulting in an en-suing metabolic alkalosis. Under normal conditions, theexcess bicarbonate is excreted in the urine. However,affected infants also lose significant amounts of fluid inaddition to the electrolytes. The subsequent volumecontraction triggers a renal response of enhanced proxi-mal tubular reabsorption of bicarbonate and activation ofthe 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 tubule excretes large amounts ofpotassium and hydrogen ions in exchange of sodium.Lack of hydrogen ions results in enhanced excretion ofpotassium, leading to significant hypokalemia.

When the diagnosis of pyloric stenosis is being con-sidered, ultrasonography of the pyloric muscle can con-





firm the clinical suspicion, with sensitivity rates rangingfrom 85% to 100%. (6) Pyloric muscle thickness of 4 mmor more and muscle length of 14 mm or more arediagnostic of pyloric stenosis (Fig. 4). If ultrasono-graphic examination findings are normal, an upper GIradiographic series can be performed. The radiographicseries has a slightly higher sensitivity for pyloric stenosis(89% to 100%) and can aid in the diagnosis of othercauses of progressive emesis in this age group, such asantral web and other structural abnormalities. Surgicalpyloromyotomy is the definitive treatment of pyloricstenosis and is being performed laparoscopically at manycenters.

Vomiting in Older ChildrenVomiting occurs most commonly in older children in thesetting of an acute gastroenteritis accompanied by feverand 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 bacterialmeningitis can present with vomiting, usually accompa-nied by complaints of headache, fever, and neck stiffness.Elevation of intracranial pressure from entities such as abrain tumor or an intracranial hemorrhage also maypresent with a chief complaint of vomiting in associationwith a severe, progressive headache. Vomiting in suchpatients often occurs shortly after waking in the morningbecause of a gradual rise in intracranial pressure as thechild sleeps in the supine position. Inadvertent toxicingestions also should be considered, especially in tod-dlers.

IntussusceptionAcquired bowel obstructions such as intussusceptionmay present in the older infant and young child, with thepeak incidence occurring between 3 months and 3 years

of age. Intussusception is the telescoping of one portionof the bowel into its distal segment. Most commonly, theterminal ileum invaginates into the cecum, often as aresult of lymphatic hypertrophy in the Peyer patchesfrom a recent viral infection. A history of intermittentepisodes of severe and crampy abdominal pain with bil-ious emesis is classic. Parents often report that their childis lethargic in between episodes of pain and may describeblood-tinged, “currant jelly” stools. Physical examina-tion may reveal intestinal obstruction with a sausage-shape mass palpable in the right lower quadrant. Rapidconsultation with a pediatric surgeon is warranted. Con-trast or air enemas can be diagnostic, with the contrastoutlining the lead portion of the intussusception, givingthe typical “coiled spring” appearance (Fig. 5). In addi-tion, the hydrostatic pressure from the contrast enemamay reduce telescoping of the intestine. Surgical reduc-tion of the intussusception is indicated when the contrastenema is not successful.

Cyclic Vomiting SyndromeCyclic vomiting syndrome (CVS) is characterized bystereotypic recurrent episodes of nausea and vomitingwithout an identifiable organic cause. It is an idiopathicdisorder that usually begins in early childhood; relativelylittle is known about its pathogenesis or cause. Thediagnosis is based on several characteristic features:1) three or more episodes of recurrent vomiting, 2) in-tervals of normal health between episodes, 3) episodesthat are stereotypic with regard to symptom onset andduration, and 4) lack of laboratory or radiographic evi-dence to support an alternative diagnosis. Vomiting ep-isodes are of rapid onset and persist for hours to days,separated by symptom-free intervals that can range fromweeks to years. Treatment is supportive, focused on fluidmanagement in cases where dehydration and electrolyte

Figure 5. Contrast outlining the lead portion of the intussus-ception, giving the typical “coiled spring” appearance.

Figure 4. Thickened and lengthened pyloric muscle that ischaracteristic of pyloric stenosis.





imbalance occur. Amitriptyline and propranolol havebeen described as effective for prophylactic therapy (an-tiemetics may be of benefit during an acute episode).

Abdominal MigraineAbdominal migraines involve episodic attacks of epigas-tric or periumbilical abdominal pain and are believed toshare pathophysiologic mechanisms with CVS. Abdom-inal migraines are more common in females than inmales, with a ratio of 3:2, and the onset is primarilybetween 7 and 12 years. A family history of migraineheadaches may be present. Episodes of abdominal painare acute in onset and last for 1 hour or more. The pain isso intense that it interferes with the performance ofnormal activities and is associated with anorexia, nausea,vomiting, headache, photophobia, and pallor. Much likethose who have CVS, patients who have abdominalmigraines report intervals of completely normal healthbetween the episodes of pain. Diagnostic evaluationlooking for alternative organic conditions yields negativeresults. The diagnosis of abdominal migraine is sup-ported by a favorable response to medications used fortreatment of migraine headaches. Patients should beadvised about trigger avoidance, specifically caffeine-containing foods, altered sleep patterns, prolonged fast-ing, emotional stress, and exposure to flickering lights.

RuminationRumination is the repeated and painless regurgitation ofingested food into the mouth beginning soon after foodintake. The food is re-chewed and swallowed or spit out.Symptoms do not occur during sleep and do not respondto the standard treatment of GER. To qualify for thediagnosis, symptoms must be present for longer than8 weeks. Rumination is not associated with retching andoften is viewed as a behavioral entity, typically seen inmentally retarded children, neonates during prolongedhospitalization, and children and infants who have GER.Rumination also has been described in cases of childneglect and in older children and adolescents who havebulimia or are depressed. Most commonly, rumination isseen 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 benecessary.

Superior Mesenteric Artery SyndromeSuperior mesenteric artery (SMA) syndrome, otherwiseknown as Wilkie syndrome or cast syndrome, is a func-tional upper intestinal obstructive condition. Normally,the SMA forms a 45-degree angle, with the abdominalaorta at its origin and the third portion of the duodenumcrossing between the two structures. When the anglebetween the SMA and the aorta is narrowed to less than25 degrees, the duodenum may become entrapped andcompressed. This condition most commonly is describedin patients who have experienced rapid weight loss, im-mobilization in a body cast, or surgical correction ofspinal deformities.

SMA syndrome typically presents with epigastric ab-dominal pain, early satiety, nausea, and bilious vomiting.Patients experience worsening pain in the supine posi-tion, which may be relieved in the prone or knee-chestposition. Diagnosis usually is confirmed by upper GIradiographic series (Fig. 6) or computed tomographyscan (Fig. 7) with failure of contrast to pass beyond thethird portion of the duodenum. Conservative initialmanagement of SMA syndrome focuses on gastric de-compression, followed by the establishment of adequatenutrition and proper positioning after meals. Placementof an enteral feeding tube distal to the obstruction orparenteral nutrition may be needed in severe cases. Sur-gical correction with a duodenojejunostomy is a lastresort.

Figure 6. Severely dilated stomach and proximal duodenumindicative of high obstruction consistent with superior mes-enteric artery syndrome.





General Principles in the Management ofVomitingTherapy to alleviate vomiting should be directed at thespecific cause, when possible. Gastrointestinal obstruc-tions should be corrected, as deemed appropriate by thepediatric surgery team. Management of nonsurgicalcauses of vomiting include steps to correct fluid andelectrolyte imbalances that result from prolonged orexcessive vomiting and to identify and treat the underly-ing disorder causing the symptom. The 2003 Centers forDisease Control and Prevention practice guidelines forthe management of acute gastroenteritis in children,endorsed by the American Academy of Pediatrics, rec-ommend oral rehydration therapy (ORT) in cases ofmild-to-moderate dehydration from acute gastroenteri-tis. (7) Using an appropriate glucose-electrolyte solu-tion, 50 to 100 mL/kg of fluid should be administeredto the child over the course of 4 hours, along withreplacement of continuing losses from stool and emesis.This is most effective when the ORT is administered insmall, 5-mL increments every 1 to 2 minutes. In cases ofsevere dehydration, ileus, or persistent vomiting despiteadequate attempts at ORT, parenteral fluids must beadministered.

Although the previously cited guidelines do 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, promethazine,and chlorpromazine are antiemetics that act as D2-

receptor antagonists at the chemoreceptor trigger zone.Such drugs rarely are used in pediatric patients because oftheir extrapyramidal and sedative adverse effects. Antihis-tamines such as diphenhydramine, hydroxyzine, and di-menhydrinate also may help alleviate nausea and vomit-ing but have a sedative effect that makes clinical re-evaluation difficult. A newer class of antiemetics is the5HT3-receptor antagonists, ondansetron and granis-etron. The 5HT3 blockade occurs both at the entericlevel and at the chemoreceptor trigger zone. Thesedrugs, unlike the phenothiazines and antihistamines, donot have central nervous system adverse effects, makingthem more attractive options. The 5HT3-receptor an-tagonists have been approved for the management ofchemotherapy-induced nausea and vomiting and forpregnancy-associated and postoperative vomiting inadults. For children, however, there is no substantivescientific 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 wide variety of GI and extraintestinal disorders. Seriousextraintestinal causes of vomiting include brain tumorand meningitis; congenital or acquired intestinal ob-structive syndromes are the most serious intestinalcauses. Associated fluid and electrolyte imbalances alwaysmust be considered when assessing a child who has ahistory of vomiting. Conditions such as mild GER mayonly necessitate reassurance, but symptoms of biliousvomiting should prompt immediate referral to a pediatricsurgeon. Results of the history and physical examination,keeping in mind the nature of the vomiting and age ofthe child, may help the clinician determine the likelycause and the need for emergent treatment.

ACKNOWLEDGMENT. The authors would like to ex-press their gratitude to Dr Dvorah Balsam for the imagesand the descriptions of the findings.

References1. Godbole P, Stringer MD. Bilious vomiting in the newborn: howoften is it pathologic? J Ped Surg. 2002;37:909–9112. Craig WR, Hanlon-Dearman A, Sinclair C, Taback S, MoffattM. Metoclopramide, thickened feedings, and positioning forgastro-oesophageal reflux in children under two years. CochraneDatabase Syst Rev. 2004;4:CD0035023. Di Lorenzo C. Gastroesophageal reflux: not a time to “relax.”J Pediatr. 2006;149:436–438

Figure 7. Computed tomography scan of the abdomen revealsdilated stomach and duodenum with air-fluid levels. Theduodenum tapers abruptly (arrow) as it crosses the midlinebetween the aorta and the superior mesenteric artery.





4. Scurlock AM, Lee LA, Burks AW. Food allergy in children.Immunol Allergy Clin North Am. 2005;25:369–3885. Cooper WO, Griffin MR, Arbogast P, Hickson GB, Gautam S, RayWA. Very early exposure to erythromycin and infantile hypertrophicpyloric stenosis. Arch Pediatr Adolesc Med. 2002;156:647–6506. Mandell GA, Wolfson PJ, Adkins ES, et al. Cost-effective imagingapproach to the nonbilious vomiting infant. Pediatrics. 1999;103:1198–12027. King CK, Glass R, Bresee JS, Duggan C. Managing acute gastro-enteritis among children: oral hydration maintenance and nutritionaltherapy. MMWR Morbid Mortal Wkly Rep. 2003;52(RR16):1–16

Suggested ReadingBiank V, Werlin S. Superior mesenteric artery syndrome in children:

a 20 year experience. J Pediatr Gastroenterol Nutr. 2006;42:522–525

Haghighat M, Rafie SM, Dehghani SM, Fallahi GH, Nejabat M.Cyclic vomiting syndrome in children: experience with 181cases from southern Iran. World J Gastroenterol. 2007;13:1833–1836

Hulka F, Campbell TJ, Campbell JR, Harrison MW. Evolution inthe recognition of infantile hypertrophic pyloric stenosis. Pedi-atrics. 1997;100:e9

Kapfer SA, Rappold JF. Intestinal malrotation–not just thepediatric surgeon’s problem. J Am Coll Surg. 2004;199:628–635

Kimura K, Loaning-Baucke V. Bilious vomiting in the newborn:rapid diagnosis of intestinal obstruction. Am Fam Physician.2000;61:2791–2798

Rasquin A, DiLorenzo C, Forbes D, et al. Childhood functionalgastrointestinal disorders: child/adolescent. Gastroenterology.2006;130:1527–1537

PIR QuizQuiz also available online at www.pedsinreview.org.

Match the clinical finding with the most likely condition. Each answer may be used once, more than once, ornot 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. Intussusception.D. Protein intolerance.E. Pyloric stenosis.





DOI: 10.1542/pir.29-6-1832008;29;183Pediatrics in Review

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

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DOI: 10.1542/pir.29-6-1832008;29;183Pediatrics in Review

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

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