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DOI: 10.1542/pir.33-5-2072012;33;207Pediatrics in Review
Garrett C. Zella and Esther J. IsraelChronic Diarrhea in
Children
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Chronic Diarrhea in ChildrenGarrett C. Zella, MD,*
Esther J. Israel, MD*
Author Disclosure
Drs Zella and Israel
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.
Educational Gap
It is estimated that diarrheal illnesses are responsible for w2
to 4 million childhood
deaths worldwide each year, representing 13.2% of all childhood
deaths worldwide.
Objectives After completing this article, readers should be able
to:
1. Understand the pathophysiologic mechanisms involved in
chronic diarrhea.
2. Know how to evaluate a child who has chronic diarrhea,
including appropriate
elements of history, physical examination, stool analysis, and
blood testing.
3. Be familiar with the many disorders that cause chronic
diarrhea, both with and
without failure to thrive.
4. Know the therapies for the many causes of chronic
diarrhea.
DefinitionsChronic diarrhea is a common complaint in pediatric
medicine and can pose a complexsituation for practitioners and
families. This complaint is both a symptom and a sign.(1) Although
patients or their parents often assess the presence of diarrhea by
reportingstool consistency and frequency, one can more scientically
dene diarrhea as stool vol-ume >10 g/kg per day in infants and
toddlers, and >200 g/day in older children. (2)However, diarrhea
should not be dened solely by stool weight. Some adolescents
andadults may have up to 300 g of formed stool per day without any
complaints. (3) Theduration of symptoms necessary to dene diarrhea
as chronic also is not denitive.Most authors agree that 14 days of
symptoms meets criteria, although others use a cut-off of 4 weeks.
(4) An additional term, persistent diarrhea, acknowledges
diarrhealasting more than 14 days but implies a more abrupt onset
compared with chronic di-arrhea. Regardless of the specic term or
number of days of symptoms, it should beunderstood that this
denition should allow for the usual resolution of most causesof
acute diarrhea.
EpidemiologyIt is estimated that diarrheal illnesses are
responsible for w2 to 4 million childhooddeaths worldwide each
year. (5)(6) In 2002, the World Health Organization estimated
that 13.2% of all childhood deaths worldwide were causedby
diarrheal diseases, 50% of which were chronic diarrhealillnesses.
(7) Large-scale studies indicate that the preva-lence of chronic
diarrheal illnesses worldwide ranges from3% to 20%, and the
incidence is w3.2 episodes per child-year. (4)(8) Estimates in the
United States are substan-tially lower at 0.18 episodes per
child-year in children ages6 months to 3 years. (9) In the United
States, onlyw25%of cases present for medical care, and fewer than
1%of children are hospitalized for diarrheal diseases. (10)The
rotavirus vaccine may decrease hospitalizations byup to 66% in
developing countries, because a substantialnumber of these
hospitalizations are for rotavirus-associateddiarrhea. (11)
Abbreviations
CCD: congenital chloride diarrheaCF: cystic brosisCNSD: chronic
nonspecic diarrheaCSD: congenital sodium diarrheaIBD: inammatory
bowel diseaseIBS: irritable bowel syndromeIDI: intractable diarrhea
of infancyTTG IgA: tissue transglutaminase immune globulin AZES:
Zollinger-Ellison syndrome
*Pediatric Gastroenterology and Nutrition, Massachusetts General
Hospital, Boston, MA.
Article gastrointestinal disorders
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Pathophysiology
The many causes of chronic diarrhea can be divided intofour
principle pathophysiologic mechanisms: osmotic, se-cretory,
dysmotility associated, and inammatory. Often,a single disorder
will involve multiple overlapping mech-anisms. Regardless of the
cause, water in the intestinal lu-men is incompletely absorbed
either because net waterabsorption is decreased or because water is
being heldwithin the lumen by an osmotic gradient. Reduction innet
water absorption by as little as 1% may be sufcientto cause
diarrhea. (12)
Osmotic diarrhea is caused by a failure to absorb a lu-minal
solute, resulting in secretion of uids and net waterretention
across an osmotic gradient. This outcome canresult from either
congenital or acquired disease and isbest exemplied by the common
disorder of lactose mal-absorption. (13) Other carbohydrates may be
malab-sorbed, either because of dissacharidase deciencies orbecause
the absorptive capacity of the intestine for thatsugar may be
overwhelmed by excessive consumption,eg, fructose and sorbitol.
(14) Such excessive intakemay be seen in young children drinking
fruit juices. Dis-sacharidase deciencies, such as lactase deciency,
arerarely congenital but more often are a result of gutmucosal
injury secondary to some process later in in-fancy, such as an
enteritis. (2) Pure osmotic diarrheashould cease when the offending
dietary nutrients areremoved. (1)
Secretory diarrhea occurs when there is a net secretionof
electrolyte and uid from the intestine without com-pensatory
absorption. Endogenous substances, oftencalled secretagogues,
induce uid and electrolyte secre-tion into the lumen even in the
absence of an osmoticgradient. Children with a pure secretory
diarrhea willtherefore continue to experience diarrhea even
whilefasting. Typically, secretagogues affect ion transport inthe
large and small bowel both by inhibiting sodiumand chloride
absorption and by stimulating chloride se-cretion via cystic brosis
(CF) transmembrane regulatoractivation. Examples of secretory
diarrhea include multiplecongenital diarrheal disorders associated
with identiedgenetic mutations that affect gut epithelial ion
transport.(1) Congenital chloride diarrhea (CCD) is one
suchdisorder.
Chronic diarrhea associated with intestinal dysmotilitytypically
occurs in the setting of intact absorptive abilities.Intestinal
transit time is decreased, the time allowed forabsorption is
minimized, and uid is retained withinthe lumen. High-amplitude
propagated contractions playa key role in motility disorders of the
gut and have been
found to be more frequent in patients with diarrhea-predominant
irritable bowel syndrome (IBS). (15) Al-though diarrhea-predominant
IBS may be diagnosedin older adolescents, toddlers commonly present
withchronic nonspecic diarrhea (CNSD). Changes in smallintestinal
motility also have been implicated in causingCNSD. (16)
Inammatory diarrhea may encompass all of the path-ophysiologic
mechanisms. Inammation with resultantinjury to the intestine may
lead to malabsorption of die-tary macronutrients which, in turn,
creates a luminal os-motic gradient. Additionally, particular
infectious agentsmay induce secretion of uid into the lumen, and
bloodin the gut may alter intestinal motility. Diseases such
asinammatory bowel disease (IBD) and celiac disease ex-emplify this
inammatory mechanism. (13)
Evaluation of Chronic DiarrheaHistory and Physical
Examination
A careful history of the characteristics of the diarrhea
isimportant in assessing the severity of the illness and in
for-mulating a differential diagnosis. Stool frequency, vol-ume,
and appearance; the presence of blood or mucus;and the relationship
to feeding or dietary intake shouldbe documented. Also important is
the presence or absenceof abdominal pain, weight loss, rash,
fatigue, vomiting,joint aches, or oral ulcers, among other
extraintestinalsymptoms. A 3-day diary of stool pattern, dietary
in-take, and associated symptoms can be helpful. One shouldinquire
also about recent travel, exposure to new watersources, family
history, and sick contacts.
Physical examination should include plotting ofweight, height,
and head circumference on a standardizedgrowth chart. Signs of
nutrient deciencies should besought, such as perianal dermatitis in
zinc deciency andleg deformity in vitamin D deciency. The
abdomenmay reveal distension in malabsorption syndromes or
smallbowel bacterial overgrowth or may be exquisitely tender inan
inammatory state. Examination of the rectum is im-portant also and
may reveal perianal disease in IBD, guaiacpositive stool in many
disease states, or loss of surroundingsubcutaneous tissue in celiac
disease and other states ofmalnutrition.
Examination of Stool and BloodLaboratory examination should
begin with microbiologicstudies for bacteria and parasites in the
stool. Infectionwith bacteria such as Yersinia, Escherichia coli,
and Sal-monella may develop into chronic illness and can be
de-tected by routine stool culture. Additionally, some stool
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cultures may include testing for diarrhea-causingAeromonas and
Plesiomonas. Clostridium difcile toxinassay should be performed,
especially in the setting ofrecent antibiotic use. Antigen
detection for Giardia andCryptosporidium are more sensitive and
specic than rou-tine microscopy-based ova and parasite
examinationsand therefore may be helpful if these infections are
sus-pected. (17)
Analysis of the stool for electrolyte content and osmo-larity
may be helpful in distinguishing an osmotic froma secretory
diarrhea. If there is a difference betweenthe stool osmolarity and
twice the sum of the concen-trations of sodium and potassium in the
stool of>50mOsm, the diarrhea is osmotic in nature. If
thisosmotic gap is 30 g/day in infants and >50 g/day
inschool-age children) and a coefcient of fat malabsorp-tion of
>5% is considered abnormal past infancy. Thenormal percentage
can be up to 15% during infancy.
Blood tests should include routine complete bloodcell count to
evaluate for anemia and thrombocytosis,suggesting blood loss and
inammation, respectively.Evaluation of red blood cell
characteristics may suggestvitamin B12 or folate deciency in
malnutrition. Whiteblood cell count and differential and
immunoglobulinanalysis screen for immune disorders. Erythrocyte
sedi-mentation rate and C-reactive protein support inamma-tion but
are nonspecic. Elevated tissue transglutaminaseimmune globulin A
(TTG IgA) antibody is sensitive andspecic for celiac disease, but a
low total serum IgA levelmay result in a false-negative test.
Measurements of albu-min and prealbumin may be obtained to reect
low die-tary protein intake. (13) Levels of the fat soluble
vitaminsA, 25-OH vitamin D, vitamin E, and vitamin K (reectedby
prothrombin time) may be measured if fat malabsorp-tion is
suspected.
Additional TestingThe value of radiologic studies in the context
of chronicdiarrhea is limited. Abdominal radiographs may show
con-stipation or dilated small bowel loops. Computed tomog-raphy
and MRI may be useful in IBD to show bowel wallthickening
suggestive of mucosal inammation. Breath hy-drogen analysis, or
breath testing, can be used to ex-amine for carbohydrate
malabsorption. If not absorbed,lactose, sucrose, or lactulose given
at the onset of testingreaches colonic bacteria, producing hydrogen
that is mea-sured in the breath. Endoscopy may be useful to reveal
du-odenal villous blunting and intraepithelial lymphocytes inceliac
disease or evidence of ileal or colonic inammationin infectious
colitis or IBD. Small bowel biopsy during en-doscopy also may
reveal evidence of duodenitis in parasiticinfections. However,
stool testing for parasites is much lessinvasive and is more
sensitive and specic than endoscopy.
Differential DiagnosisIt may be helpful to separate the wide
differential diagno-sis of pediatric chronic diarrhea into those
illnesses thatresult in poor weight gain and those in which weight
typ-ically is maintained. The Table presents the features of
themain causes of chronic diarrhea.
Chronic Diarrhea Without Failure to ThriveChronic Nonspecific
Diarrhea of Childhood orInfancy
CNSD is the most common form of persistent diarrhea inthe rst 3
years after birth. (18) The typical time of onsetmay range from 1
to 3 years of age and can last from in-fancy until age 5 years.
Patients with CNSD usually passstool that is different in both
consistency and frequencyfrom that of other children. Affected
children may pass 4to 10 loose bowel movements per day without
blood ormucus. Specic to CNSD is the pattern that these pa-tients
pass stools only during waking hours, typically be-ginning with a
large formed or semiformed stool afterawakening. As the day
progresses, stools become morewatery and smaller in volume. Transit
time of enteral con-tents may be especially short, and parents
frequently describeundigested food remnants in the stool. By
denition, chil-dren with CNSD maintain their weights and heights.
Al-though some affected children describe mild abdominaldiscomfort,
most typically appear healthy and maintaina normal appetite and
activity level. (19)(20)
Potential pathophysiologic mechanisms for CNSD in-clude
increased intestinal motility and osmotic effects ofintraluminal
solutes (eg, carbohydrates). (16) The role ofingested carbohydrates
in CNSD has been emphasized in
gastrointestinal disorders chronic diarrhea
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Table. Causes of Chronic Diarrhea
Without Failure to Thrive Major Clinical Features Major
Laboratory and Imaging Findings
CNSD Daytime nonbloody, nonmucousy stools Normal laboratory and
imaging resultsNormal growthOccurs in the first few years after
birth
Infectious colitis Possible blood and/or mucus in stoolPossible
fever and/or abdominal painExposure to undercooked meatContaminated
waterOccurs at any age
Positive stool culture, ova and parasiteexamination, or stool
antigen test
Lactose malabsorption Abdominal discomfort,
bloating,flatulence
Elevated breath hydrogen concentrationafter lactose
ingestion
Nonbloody stoolsOccurs beyond infancy
Small bowel bacterialovergrowth
Abdominal discomfortIncreased risk if ileocecal valve
removedOccurs at any age
Elevated fasting breath hydrogenconcentration (>20 ppm)
Elevated early and late breath hydrogenconcentration
After lactulose ingestionIBS Alternating constipation with
diarrhea Normal laboratory and imaging results
Abdominal pain relieved by defecationAbsence of weight loss,
bloody stool,
fever, or anemiaTypically diagnosed in adolescence
or later
With Failure to ThriveIDI Infectious colitis ruled out
Enteropathy by histology
Higher risk in malnourished orimmunodeficient patients
In need of prompt nutritional supportAllergic enteropathy Most
commonly in response to cow or
soy milkGrowth failure is in sharp contrast to
well infant with allergic colitisStool may be guaiac
positive
May have hypoalbuminemia and anemiaElectrolyte abnormalities
from diarrhea/
vomitingSerum IgE may be elevated
Celiac disease Up to 1/100 prevalenceSevere cases have abdominal
distensionMyriad of presenting features
Elevated TTG IgA, antiendomysial IgAantibodies
May be IgA deficient*Histologic villous blunting and
intraepithelialLymphocytes
IBD Bloody stool more common in colitisEnteritis may cause
nonbloody stoolStooling urgency, abdominal pain,
fatigue
Elevated erythrocyte sedimentation rate,thrombocytosis
Iron-deficiency anemiaHypoalbuminemia
Immunodeficiency state(various diseases)
Recurrent infectionsYoung age, typically in infancy
Abnormal immunoglobulins (eg, low IgG,low IgA, high IgM)
LymphopeniaLow antigen titers to previous
immunizationsCongenital secretory diarrhea(Chronic chloride and
chronicsodium diarrhea)
Maternal polyhydramniosSevere secretory diarrhea at birthSevere
dehydration
CCD: hypochloremia and metabolicalkalosis
CSD: hyponatremia and metabolicacidosis
Continued
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light of a typical toddlers affection for fruit juices.
Exces-sive intake of fruit juices, particularly those
containingsorbitol or fructose (eg, apple, pear, cherry, and
prunejuices), may contribute to the stool osmotic load, thuscausing
or worsening diarrhea. (21)(22)
Reassurance is the cornerstone of therapy for CNSD.Parents
should be reassured that their child is growing welland is healthy.
Although no precise treatment for CNSDhas been established, dietary
intervention may be prudent.Fruit juice intake should beminimized
or changed to typesof juice with low sucrose and fructose loads.
Beyond therestriction of fruit juice, possible helpful changes may
beto liberalize fat to encourage normal caloric intake and toslow
intestinal transit time, not to restrict ber, and to assureadequate
but not overhydration. (21)
Infectious ColitisAlthough many infectious causes of diarrhea
result in anacute presentation and short course, other
pathogenicbacteria and parasites may cause chronic diarrhea.
Virusesrarely cause diarrhea lasting more than 14 days and
moretypically range from 2 days (eg, Norwalk-like virus) to 11days
(enteric adenoviruses) in duration. (6) Rotavirusmay cause diarrhea
lasting up to 20 days. (11)
Salmonella is one of the most common causes oflaboratory-conrmed
cases of food-borne intestinal disease
reported to the Centers for Disease Control and Preven-tion each
year. (23) The infection usually is contractedfrom exposure to food
of animal origin related to poultry,eggs, beef, and dairy products.
Nontyphoidal Salmonellaorganisms typically cause gastroenteritis
with diarrhea,abdominal cramping, and fever. Salmonella organisms
typ-ically are detected in routine stool culture for up to 5
weeksbut may be excreted in stool for >1 year in 5% of
patients.(24) Antibiotic therapy for uncomplicated
nontyphoidalserotypes is not indicated because it does not
shortenthe disease duration and may prolong the duration of
ex-cretion of bacteria in the stool. (25) Antibiotics are
appro-priate, however, for treating children younger than 3months
of age or those with immunosuppressive diseases,given the increased
risk for invasive disease (bacteremia, os-teomyelitis, abscess,
meningitis) in these populations. (23)
Yersinia enterocolitica and Y pseudotuberculosis causechronic
diarrhea less commonly than Salmonella in childrenin the United
States. Infection typically occurs via expo-sure to food products,
specically pork (a major Yersiniareservoir) and dairy products but
may occur with inges-tion of other foods contaminated by these
products. Di-arrheal stool may contain blood, mucus, and
leukocytes,reecting mucosal inammation. Symptoms may
mirrorappendicitis or ileal Crohn disease because Yersinia
mayaffect the terminal ileum. Often the organism needs to
Table. (Continued)
With Failure to ThriveTufting enteropathy Intractable watery
diarrhea Electrolyte abnormalities
Severe growth failure Small bowel villous atrophy and
crypthyperplasia without inflammation
Microvillous inclusiondisease
Diarrhea within first week afterbirth
Small bowel villous atrophy but no crypthyperplasia or
inflammation
No history of polyhydramniosAutoimmune enteropathy Secretory
diarrhea
May coexist with otherendocrinopathies
May have positive antienterocyte,antigoblet cell, or
anticolonocyteserum antibodies
Neuroendocrine tumors Secretory diarrhea VIPoma: elevated serum
VIPZES: elevated fasting serum gastrinCarcinoid: elevated urine
5-
hydroxyindoleacetic acidElevated prostaglandin E2
Hirschsprung disease Delayed passage of meconium Abnormal barium
enemaDistended abdomen Absent ganglion cells on rectal
biopsyExplosive stool with rectal
examinationCF Malabsorption of carbohydrate/
fat/proteinDecreased fecal elastaseElevated fasting breath
hydrogen if
small bowel bacterial overgrowth present
IgEimmune globulin E; VIPvasoactive intestinal
polypeptide-secreting tumor.* Leads to false-negative IgA-based
antibody tests: TTG IgG may be useful in this setting.
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be sought specically by laboratory personnel because itmay not
be part of each institutions routine stool culture.The efcacy of
antibiotics in treating uncomplicatedYersinia infection has not
been established. (26)
Other bacterial causes of chronic diarrhea includeEscherichia
coli, Campylobacter, Aeromonas, and Ple-siomonas. Enteropathogenic
E coli is a leading causeof chronic diarrhea in developing
countries, sometimes as-sociated with fever, abdominal pain, and
vomiting. (27)Enteropathogenic E coli is one type of E coli disease
inwhich antibiotic therapy has been shown to reduce mor-bidity and
mortality in uncomplicated diarrheal disease.(28) Persistent bloody
diarrhea with abdominal painshould raise suspicion for
enterohemorrhagic E coli, par-ticularly because enterohemorrhagic E
coli may result inhemolytic-uremic syndrome, a potentially
dangerouscomplication.Campylobacter often originates from
poultryand may cause diarrhea for only 4 to 5 days, but relapsesare
common. Both E coli and Campylobacter can be iso-lated by routine
stool culture.
Aeromonas, long considered a normal commensal or-ganism, has
been shown recently to cause secretory diar-rhea with up to 20
watery stools per day. Symptoms arepersistent in approximately
one-third of patients. Antibi-otics do not seem to be helpful in
uncomplicated Cam-pylobacter and Aeromonas illnesses. Pleisomonas
can befound in sh, shellsh, cats, and dogs; also causes secre-tory
diarrhea; and has a course that may be shortened byantibiotic
therapy. (29)
The protozoa Giardia intestinalis and Cryptosporid-ium may
affect immunocompetent as well as immunode-cient children and
adolescents. Both infections mayaffect the duodenum and upper small
bowel, leading tomild villous blunting, dissacharidase deciency,
and resul-tant osmotic and secretory diarrhea. Malabsorption of
fat,protein, and carbohydrates may occur, worsening diar-rhea. Both
infections are linked to contaminated waterand may be associated
with childcare centers, exposureto wild animals, swimming in water
parks or pools,or recent travel to developing countries.
Symptomaticgiardiasis should be treated, even in
immunocompetentchildren, with tinidazole, metronidazole, or
nitazoxanideas possible agents. Cryptosporidium infection
generallydoes not need to be treated unless the patient is
immu-nocompromised. However, nitazoxanide has been ap-proved for
treating immunocompetent children withdiarrhea associated with
Cryptosporidium. (30)
Disaccharide IntoleranceLactose malabsorption is, by far, the
most common typeof disaccharide intolerance. Approximately 70% of
the
worlds adult population has primary acquired lactase de-ciency,
resulting in lactose intolerance. Age of onsetvaries among
populations, with one-fth of Hispanic,Asian, and African American
children becoming lactoseintolerant before age 5 years. White
children typicallydo not lose lactase function until after age 5
years, andoften much later, during later teenage years or
beyond.(31) Molecular studies have elucidated differences
inmessenger RNA expression among races that mightexplain
population-based variations in lactase activity.(32) Congenital
lactase deciency is exceedingly rareand only a handful of cases
have been published inthe literature.
Secondary lactase deciency results from small intesti-nal
mucosal injury when lactase enzyme is lost from thetips of the
villi. Causes include rotaviral infection, para-sitic infection,
celiac disease, Crohn disease, and otherenteropathies. Many studies
question the clinical signif-icance of secondary lactase deciency
in diarrheal illnessesexcept in children who are
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during adolescence. Without any one specic pathophys-iologic
cause identied, IBS is considered a functionaldisorder dened by
symptom criteria. (35)(36) TheRome III criteria dene IBS as
abdominal pain or dis-comfort at least 3 days per month in the last
3 monthsassociated with two or more of the following
features:improvement with defecation, onset associated witha change
in frequency of stooling, and onset associatedwith change in the
form of the stool. This strict denitionmay be used to dene the
syndrome precisely but typi-cally is more useful in research rather
than in everydayclinical medicine. The history often suggests the
diag-nosis, with abdominal pain often relieved with defeca-tion.
These patients do not have rectal bleeding,anemia, weight loss, or
fever. It should be determinedthat celiac disease is not present.
Treatment is oftenchallenging. Antispasmodic agents, tricyclic
antide-pressants, and selective serotonin-reuptake inhibitorsmay
improve symptoms. Some probiotics have beenuseful in adult and
pediatric IBS, but results are notconsistent. (37)
Chronic Diarrhea With Failure to ThriveIntractable Diarrhea of
Infancy
Persistent diarrhea after an acute episode of presumedinfectious
diarrhea is known as intractable diarrhea of in-fancy (IDI),
postenteritis or postgastroenteritis diarrhea,postenteritis
enteropathy, or slick gut. This disorder isunique compared with
CNSD because in IDI there isweight loss associated with
malabsorption and histologicevidence of enteropathy. (38) IDI
remains an importantcause of morbidity and mortality in developing
countrieswhere children may be at nutritional risk. Children at
par-ticular risk include those who are young, who suffer
mal-nutrition, or who have an altered immune state. (39)Osmotic
diarrhea with increased uid requirements sec-ondary to carbohydrate
malabsorption is common. With-out nutritional support, patients may
become severely ill.
IDI should be suspected in any infant with persistentdiarrhea
after an acute gastroenteritis. Other causes ofchronic diarrhea
should be sought but not at the expenseof promptly supporting
caloric needs. (6) Small bowel bi-opsy may reveal patchy villous
atrophy and inammatoryinltrates in epithelial and lamina propria
layers. Cautionshould be exercised in obtaining biopsies because
malnu-trition increases the risks associated with
endoscopy.Breastfeeding should continue unless lactose
malabsorp-tion is strongly suspected.
To prevent IDI, guidelines for managing acute gastro-enteritis
should be followed, which recommend avoiding
formula dilution and promoting early feeding that re-duces
intestinal permeability and illness duration and im-proves
nutritional outcomes. (40) Dietary protein andfat are important in
recovery, but simple carbohydratesshould be minimized. The BRAT
diet (bananas, rice, ap-plesauce, toast) in the management of
diarrhea is unnec-essary and nutritionally suboptimal. Refeeding
syndromeis a risk for severely malnourished patients.
Intravenoushydration may be necessary in treating IDI. Toleranceof
enteral feeds and resolution of diarrhea typically occurwithin 2 to
3 weeks.
Allergic EnteropathyAllergic enteropathy, or eosinophilic
enteropathy, associ-ated with failure to thrive, vomiting, and
diarrhea, shouldbe distinguished from allergic colitis occurring in
other-wise healthy and thriving infants. As in allergic colitis,
al-lergic enteropathy is induced by food proteins withthe most
common being cow milk and soy proteins.In allergic enteropathy,
however, there is small intestinalmucosal damage resulting in
malabsorption of protein,carbohydrate, and fat. Protein
malabsorption may leadto hypoalbuminemia and diffuse swelling.
Profuse vom-iting and diarrhea may lead to severe dehydration,
leth-argy, and hypotension, mimicking sepsis in a younginfant.
Serum IgE levels may or may not be elevated.Protein hydrolysate or
amino acid-based elemental for-mulas are necessary if breastfeeding
on a restricted diet isnot possible. Once the inciting dietary
protein is re-moved, the enteropathy will resolve.
Celiac DiseaseCeliac disease is an immune-mediated enteropathy
thatoccurs in the setting of gluten ingestion in a
geneticallysusceptible individual. With its prevalence in adultsand
children approaching 1% worldwide, celiac diseasehas become a more
commonly diagnosed disorder. (41)However, the classic presentation
of celiac disease inchildren with the triad of failure to thrive,
diarrhea,and abdominal distension is being seen less
frequently.(42) Because of family screening, more sensitive
andeasily accessible testing, and the recognition of thewide
variety of presenting symptoms, identication ofpatients presenting
with atypical symptoms is on therise. (43)
Diagnosis should begin with establishing the presenceof
antiendomysial IgA antibodies, which have near 100%specicity, or
employing newer and less expensive tech-niques for measuring
enzyme-linked immunosorbentassay-based anti-TTG IgA antibodies.
Diagnosis is con-rmed by particular histologic ndings in the
duodenum,
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including villous blunting and prominent
intraepitheliallymphocytosis. Current treatment is with a diet free
ofwheat, rye, and barley. New potential therapies are beingsought,
including the use of gliadin-digesting recombi-nant enzymes.
Inflammatory Bowel DiseaseChildren and adolescents suffering
from diarrhea, with orwithout weight loss, must be evaluated for
IBD. Approx-imately 50% to 80% of children with Crohn disease
willpresent with diarrhea, among other symptoms. In Crohndisease,
stool may contain microscopic blood but maynot be grossly bloody,
especially in the absence of signif-icant left-sided colonic
disease. Diarrhea is more commonin colonic disease and may be
absent altogether in cases ofisolated small bowel inammation. In
ulcerative colitis,diarrhea is a more consistent presenting
feature, often in-sidious in its development but eventually
developinghematochezia. Nocturnal diarrhea with urgency may bea
sign of left-sided colonic inammation in either Crohndisease or
ulcerative colitis. Diarrhea associated with IBDtypically improves
with therapy as mucosal inammationresolves.
Immunodeficiency StatesChildren with primary immunodeciency
states oftenpresent with chronic diarrhea. (44) X-linked
agamma-globulinemia may result in diarrhea secondary to
chronicrotaviral infections or recurrent giardiasis. IgA
deciencymay lead to recurrent giardiasis and bacterial
overgrowth,and is associated with a 10- to 20-fold increased
incidenceof celiac disease. (45) Chronic diarrhea is common alsoin
hyper-IgM and human immunodeciency virus syn-dromes and may be
caused by infection withCryptosporid-ium parvum in these diseases.
Children with commonvariable immunodeency often present with
diarrheaand signicant malabsorption along with severe recur-rent
life-threatening infections during the rst monthsafter birth.
Intractable diarrhea with neonatal insulin-dependent diabetes
should raise suspicion for the syn-drome of immune dysregulation,
polyendocrinopathy,and enteropathy (autoimmune), X-linked (IPEX
syn-drome). Glycogen storage disease type 1B and
chronicgranulomatous disease may present very similarly toCrohn
disease, likely related to defective intestinal mu-cosal immunity.
(46)
Congenital Secretory DiarrheaTwo very rare causes of secretory
diarrhea in early infancyare CCD and congenital sodium diarrhea
(CSD). Fewerthan 15 patients with CSD and w250 with CCD have
been reported in the literature. (47) Both diseases
presentbefore birth with polyhydramnios resulting from in
uterodiarrhea. At birth, high-volume secretory diarrhea con-tinues
despite bowel rest and may cause life-threateningdehydration and
electrolyte disturbances. CCD causes se-vere hypochloremia and a
unique metabolic alkalosis,whereas CSD causes hyponatremia with
alkaline stoolsresulting in metabolic acidosis. Stool electrolytes
oftenaid in the diagnosis, and genetic testing can identify
defec-tive chloride transport genes in some patients with
CCD.Aggressive uid and electrolyte replacement is the main-stay of
therapy for both diseases.
Tufting EnteropathyTufting enteropathy, also known as intestinal
epithelialdysplasia, presents in the rst few months after birth
withgrowth failure and intractable watery diarrhea. (48) Sig-nicant
electrolyte abnormalities may occur even beforethe severity of
illness is recognized by caretakers. His-tology of the small bowel
reveals a unique picture ofvillous atrophy and crypt hyperplasia
without signi-cant inammation. Closely packed enterocytes appearto
create focal epithelial tufts. A recent genomicstudy of children
born with tufting enteropathy re-vealed mutations in the epithelial
cell adhesion mole-cule EpCAM. (49) Affected infants typically
becomedependent on parenteral nutrition to allow normalgrowth and
development. Small bowel transplant is po-tentially curative, but
the associated morbidity and mor-tality are high.
Microvillous Inclusion DiseaseAnother rare cause of chronic
secretory diarrhea in theneonatal period is microvillous inclusion
disease, present-ing with diarrhea so watery that it may be
mistaken forurine. (48) Microvillous inclusion disease is the
secondmost common cause of severe, protracted diarrhea inthe rst
week after birth, after infectious causes are ex-cluded. Contrary
to what occurs in CCD and CSD, poly-hydramnios typically is not
seen. Histology reveals smallbowel villous atrophy but without
inammation or ex-pected crypt hyperplasia. Villin substance can be
seenby immunostaining in affected cell cytoplasm, creatingthe
microvillous inclusions. Aggressive intravenous re-hydration and
electrolyte replacement are necessary tomaintain life during
infancy, followed by lifelong paren-teral nutrition in most
cases.
Autoimmune EnteropathyChildren with autoimmune enteropathy
usually developsecretory diarrhea after the rst 8 weeks after
birth.
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Another autoimmune disease, such as insulin-dependentdiabetes,
may be present in the setting of chronic diar-rhea and poor growth,
which should raise suspicion forIPEX syndrome. (48) However,
autoimmune enterop-athy may exist without extraintestinal
manifestations.Diagnosis is made by documenting
antienterocyte,anticolonocyte, or antigoblet cell antibodies in
theblood, although the number of centers that performthis test is
limited and the specicity of the test is un-clear. Treatment is
difcult but may be accomplishedwith immunosuppressive agents such
as corticoste-roids, 6-mercaptopurine, tacrolimus, and
iniximab.(50)
Neuroendocrine TumorsNeuroendocrine tumors affecting the
gastrointestinaltract in children are rare. These tumors produce
symp-toms by the systemic effect of their secretory products.The
neuroendocrine tumors produce secretory diarrheaand include
vasoactive intestinal polypeptide-secretingtumor, or VIPoma;
Zollinger-Ellison syndrome (ZES);tumors secreting prostaglandin E2;
and carcinoid syn-drome. VIP stimulates cyclic adenosine
monophosphateactivity, eventually resulting in intestinal
secretion, similarto the effects of the cholera toxin. Therefore,
the classicpresentation of VIPoma is with profuse watery
diarrhea(usually >20 cc/kg per day), hypokalemia, and
achlor-hydria (WDHA syndrome). ZES causes diarrhea becauseof high
intestinal gastrin levels. Carcinoid tumorsmay secrete serotonin,
bradykinin, and histamine, alsoleading to gastric acid
hypersecretion and diarrhea.Once secretory diarrhea is established,
the evaluationmay include measuring the concentrations of serumVIP,
fasting gastrin, and prostaglandin E2 levels,along with 24-hour
urine 5-hydroxyindoleacetic acidfor carcinoid tumor. Most VIPomas
in children areganglioneuromas or ganglioneuroblastomas, whichcan
be identied radiographically. Operative resectionis imperative but
not always curative if the tumor hasmetastasized. (51)
Hirschsprung DiseaseDiarrhea is present in approximately
one-third of neo-nates born with Hirschsprung disease. (52) The
diarrheausually is a consequence of enterocolitis that occurs in
thesetting of bacterial stasis in the lumen. (53) Children
maypresent with fever, diarrhea, and abdominal distension.Some
children may appear acutely ill with explosive diar-rhea, vomiting,
rectal bleeding, and lethargy, whereasothers may present with only
loose stools and perianal
excoriation. Hirschsprung disease should be suspectedin any
infant who does not pass meconium within the rst24 hours, which is
the case in 94% of affected infants butin only 10% of healthy
infants. Older infants may havepoor growth, a distended abdomen,
and explosive pas-sage of stool with rectal examination. Older
childrenwith Hirschsprung disease usually do not have the fe-cal
soiling and stool withholding behaviors that arecommon in
functional constipation. Enterocolitis rep-resents the most
signicant source of morbidity andmortality in Hirschsprung disease
and deserves im-mediate treatment with intravenous antibiotics
andsupportive care.
Cystic FibrosisDiarrhea occurs in CF most commonly as a result
of pan-creatic insufciency. Approximately 90% of patients withCF
have pancreatic insufciency. (54) Loss of exocrinepancreatic
function leads to malabsorption of carbohy-drates, fat, and protein
because of dysfunctional amylases,lipases, and proteases,
respectively. Such malabsorptionleads to poor growth in addition to
chronic diarrhea andpossible steatorrhea. Patients with CF also
have an in-creased incidence of small bowel bacterial
overgrowth,possibly secondary to altered motility and thickened
se-cretions, among other complex factors. (55) Fecal elas-tase can
be used as a predictor of pancreatic exocrinefunction, with low
levels indicating possible pancreaticinsufciency. Pancreatic enzyme
replacement therapymay improve malabsorptive diarrhea in patients
withCF.
Factitious DiarrheaWhen inconsistencies arise among a patients
history,physical signs, and laboratory ndings, the
practitionershould consider the possibility of a factitious
disorder.Many cases of factitious diarrhea induced by either
thepatient or patients parents have been reported in the
lit-erature. (56)(57) Although laxative ingestion is the mostcommon
cause of factitious diarrhea, the ingestion of os-motic agents or
even feces may induce diarrhea. Patientsalso may dilute stool to
create the appearance of diarrhea.Munchausen by proxy syndrome
(factitious disorder byproxy per Diagnostic and Statistical Manual
criteria), inwhich the caregiver creates the childs illness, often
in-cludes factitious diarrhea induced with stimulant laxativesor
even by syrup of ipecac poisoning. Such cases usuallyrequire
hospital admission with careful observation aftera full evaluation
for organic causes of chronic diarrhea hasbeen completed.
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Summary
The differential diagnosis for chronic diarrhea inchildren is
broad. Pediatric clinicians can narrow thesepossible diagnoses
beginning with a detailed historyand physical examination.
Particular attention should be paid to growthmeasurements to
distinguish between chronicdiarrhea with and without associated
growth failure.
Understanding the four basic pathophysiologicmechanisms of
diarrhea also may aid in makinga diagnosis. The four categories are
osmotic, secretory,dysmotility associated, and inflammatory.
Although specific therapies vary for each disease, theimportance
of maintaining nutrition demandsparticular emphasis. Whatever the
cause of thediarrhea, each patient requires adequate caloric
intaketo allow healing of the initial insult, or at least tosupport
the child while pursuing diagnostic andtherapeutic
interventions.
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2001;33(5):607609
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1. A 2-year-old girl has had daily diarrhea for the past 3
months. She has a soft but formed stool in the morningand then has
seven to eight episodes of increasingly soft-to-watery stools. Her
parents at times see undigestedfood in her stools. She does not
have loose stools at night. She eats a regular diet, drinks milk,
water, and juice.She is growing well. She has not had blood or
mucus in her stools and does not complain of abdominal pain.
Herparents ask what is the next step in the evaluation and
management of her diarrhea. Your best response is torecommend which
of the following?
A. Bowel rest with restricted caloric intake for 2 weeks.B.
Eliminating juice intake.C. Hydrogen breath testing.D. Initiating
treatment with artificial lactase enzymes.E. Obtaining stool
cultures.
2. A 14-year-old girl has abdominal pain approximately weekly.
During these episodes, she has multiple bowelmovements that are
looser than her usual stools. She relates that she feels better
after she has a bowelmovement. She has had no fever, rectal
bleeding, or mucus in her stool. She has not lost weight. Her
physicalexamination is normal. The best next step in the evaluation
of her abdominal pain is
A. Endoscopy.B. Upper gastrointestinal series with small bowel
follow-through.C. Stool electrolyte content and osmolarity.D.
Tissue transglutaminase immune globulin A test.E. 72-hour stool
collection for measurement of fecal fat.
3. An 8-month-old girl is seen for daily loose stools for 4
weeks. Her older siblings also had diarrhea butrecuperated after 10
days of illness. The infant has lost weight and is hospitalized for
further evaluation.The diet you are most likely to recommend for
this infant is
A. Bowel rest with parenteral nutrition.B. BRAT diet (bananas,
rice, applesauce, toast).C. Breastfeeding or regular formula.D.
Oral rehydration fluids only.E. Restricted protein and fat
intake.
4. A 5-month-old boy has been hospitalized for pneumonia. He has
had diarrhea for 3 months, with frequentwatery stools daily. He is
losing weight. On physical examination, he is afebrile, thin, and
listless. Theevaluation you are most likely to initiate
includes
A. Enteral transit time study.B. Hydrogen breath testing.C.
Immunoglobulin levels.D. Lactulose testing.E. 3-day dietary
history.
5. A 3-month-old infant boy has emesis and diarrhea and is
losing weight. His formula was changed to a soy-based product and
after rehydration he is admitted to the hospital for further
evaluation. The diet you are mostlikely to request for this infant
is
A. Bowel rest with parenteral nutrition.B. Cows milk-based
formula with artificial lactase enzyme.C. Diluted soy formula.D.
Oral rehydration solution.E. Protein hydrolysate or amino
acid-based elemental formula.
gastrointestinal disorders chronic diarrhea
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DOI: 10.1542/pir.33-5-2072012;33;207Pediatrics in Review
Garrett C. Zella and Esther J. IsraelChronic Diarrhea in
Children
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