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Enfoque diagnóstico de la diarrea en niños de entornos ricos en


recursos
AUTOR: Jason Levy, MD, RDMS
EDITORES DE SECCIÓN: Stephen J. Teach, MD, MPH, Teresa K Duryea, MD
EDITOR ADJUNTO: James F. Wiley, II, MD, MPH

Todos los temas se actualizan a medida que hay nueva evidencia disponible y nuestro proceso de revisión por pares se completa.

Revisión de la literatura vigente hasta: agosto de 2023.


Este tema se actualizó por última vez: 27 de julio de 2022.

INTRODUCCIÓN

Este tema discutirá el enfoque de la diarrea en niños que viven en entornos ricos en recursos. El abordaje de la
diarrea en niños que viven en entornos con recursos limitados se analiza por separado. (Ver "Abordaje del niño
con diarrea aguda en entornos de recursos limitados" y "Diarrea persistente en niños en entornos de recursos
limitados" .)

DEFINICIÓN

La diarrea se refiere al paso de heces blandas o acuosas. La Organización Mundial de la Salud (OMS) define un
caso como la evacuación de tres o más deposiciones blandas o acuosas por día [ 1 ]. Sin embargo, los límites
absolutos de la normalidad son difíciles de definir; cualquier desviación del patrón habitual del niño debe
generar preocupación (particularmente por la mala apariencia, el paso de sangre o moco, o la deshidratación),
independientemente del número real de deposiciones o su contenido de agua.

CAUSAS

La gastroenteritis infecciosa aguda debida a virus representa la mayoría de los episodios de diarrea en
entornos ricos en recursos, lo que genera más de 1,5 millones de visitas ambulatorias y 200.000
hospitalizaciones anualmente en los Estados Unidos [1 ] . Sin embargo, las deposiciones acuosas y/o
frecuentes pueden ser la manifestación inicial de un amplio espectro de otros trastornos agudos y crónicos (
tabla 1 ) [ 2 ]. El norovirus ha superado al rotavirus como el patógeno más común en regiones donde la
vacunación contra el rotavirus se ha convertido en una rutina [ 3 ].

Condiciones potencialmente mortales : varios trastornos que causan diarrea pueden poner en peligro la
vida de los niños y, ocasionalmente, los pacientes con diarrea por cualquier causa pueden desarrollar
deshidratación grave ( tabla 1 y algoritmo 1A ) [ 4 ].

Sepsis : la diarrea se asocia comúnmente con la sepsis causada por Salmonella spp y cepas toxigénicas de
Staphylococcus aureus (síndrome de shock tóxico estafilocócico [SST]):

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● Salmonella bacteremia and sepsis occurs in 1 percent of all patients with nontyphoidal Salmonella
gastroenteritis, respectively. Infants younger than one year of age and immunocompromised children
(eg, patients with primary immunodeficiency, human immunodeficiency virus [HIV] infection,
transplantation, or receiving tumor necrosis factor blocking agents such as etanercept or infliximab) are
at higher risk. Affected patients typically have fever, diarrhea, and ill appearance. Septic shock may be
present. Blood cultures provide the diagnosis and should be obtained in all children with fever and bloody
diarrhea who are ill enough to require hospitalization. (See "Nontyphoidal Salmonella bacteremia".)

● Profuse non-bloody and watery diarrhea frequently occurs as part of the initial presentation in patients
with staphylococcal TSS. Hypotension is often severe and unresponsive to aggressive fluid resuscitation.
The diagnosis of TSS is based upon clinical presentation ( table 2). The isolation of S. aureus is not
required for the diagnosis of staphylococcal TSS. S. aureus is recovered from wound or mucosal sites in 80
to 90 percent of patients with TSS and recovered from blood cultures in approximately 5 percent of cases.
(See "Staphylococcal toxic shock syndrome", section on 'Clinical manifestations' and "Staphylococcal toxic
shock syndrome", section on 'Diagnosis'.)

Intussusception — Intussusception is most common from 6 to 12 months of age, and the vast majority of
cases occur in the first two years of life. Most children with intussusception develop sudden onset of
intermittent, severe, crampy abdominal pain, accompanied by inconsolable crying and drawing up of the legs
toward the abdomen. Bloody diarrhea is often a late finding, although rarely may be the sole presenting
feature. The episodes of pain usually occur at 15- to 20-minute intervals. They become more frequent and may
be followed initially by emesis of gastric contents. Bilious emesis may develop as the obstruction progresses.
Between the painful episodes, the child may behave normally. As a result, initial symptoms can be confused
with gastroenteritis. As symptoms progress, there may be intermittent episodes of lethargy that worsen over
time, which can be mistaken for meningitis. A sausage-shaped abdominal mass may be felt, on occasion, in the
right side of the abdomen. Abdominal radiographs may reveal a paucity of gas on the right, which may be
better visualized with left lateral decubitus imaging. The diagnosis is established by abdominal ultrasound or
air contrast enema. (See "Intussusception in children", section on 'Evaluation' and "Intussusception in children",
section on 'Ultrasonography'.)

Hemolytic uremic syndrome — Healthy cattle are the main vectors of Shiga toxin-producing
enterohemorrhagic Escherichia coli (STEC), with the bacteria being present in the cattle intestine and feces.
Infection in humans occurs following ingestion of contaminated undercooked meat, unpasteurized milk or milk
products, water, fruits or vegetables, or coming into contact with animals in petting zoos. (See "Shiga toxin-
producing Escherichia coli: Microbiology, pathogenesis, epidemiology, and prevention", section on
'Transmission'.)

Hemolytic uremic syndrome (HUS), although uncommon, merits consideration in any child with bloody
diarrhea, particularly in the first five years of life, because it is a potentially fatal illness. It complicates 6 to 9
percent of enterohemorrhagic E. coli infections with the 0157:H7 strain and usually begins 5 to 10 days after
the onset of diarrhea. HUS, which has a sudden onset, is characterized by the triad of (see "Clinical
manifestations and diagnosis of Shiga toxin-producing Escherichia coli (STEC) hemolytic uremic syndrome
(HUS) in children", section on 'Typical course'):

● Microangiopathic hemolytic anemia


● Thrombocytopenia
● Acute renal failure

Children typically have a prodromal illness with abdominal pain, vomiting, and bloody diarrhea that precedes
the development of HUS by several days to weeks, as a result of which a patient may have no signs of

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hemolysis or renal failure when seen earlier in the course. The diarrhea and associated gastrointestinal
complaints may mimic those of ulcerative colitis, other enteric infections, and appendicitis. The diagnosis of
HUS in children is generally made on clinical grounds based on the characteristic clinical and laboratory
findings previously described: a prodrome of diarrhea due to a Shiga toxin-producing E. coli, followed by abrupt
onset of the characteristic triad of microangiopathic hemolytic anemia, thrombocytopenia, and acute kidney
injury. (See "Clinical manifestations and diagnosis of Shiga toxin-producing Escherichia coli (STEC) hemolytic
uremic syndrome (HUS) in children", section on 'Diagnosis'.)

Antibiotic treatment should be avoided in patients with HUS because it may cause relatively rapid worsening of
clinical status or prolong the course of disease. (See 'Therapeutic interventions' below.)

The treatment of HUS is discussed separately. (See "Treatment and prognosis of Shiga toxin-producing
Escherichia coli (STEC) hemolytic uremic syndrome (HUS) in children".)

Fulminant C. difficile colitis (pseudomembranous colitis) — This disorder results from an overgrowth of
toxin-producing clostridial organisms in the bowel. The typical presentation is acute watery diarrhea with lower
abdominal pain, low-grade fever, and leukocytosis, starting during or shortly after antibiotic administration.
Occasionally the course can be fulminant, progressing from diarrhea to toxic megacolon and shock.
Community-associated infection with a highly toxigenic strain of Clostridioides difficile has been reported in
otherwise healthy children who had minimal or no exposure to antibiotics. (See "Clostridioides difficile infection
in children: Clinical features and diagnosis" and "Clostridioides difficile infection in children: Microbiology,
pathogenesis, and epidemiology", section on 'Toxins'.)

The approach to diagnosis for C. difficile in children depends upon the age of the patient and clinical findings
and is discussed separately. (See "Clostridioides difficile infection in children: Clinical features and diagnosis",
section on 'Approach to diagnosis'.)

Appendicitis — Appendicitis typically begins with diffuse abdominal pain followed by vomiting, often in
association with constipation. The three classic clinical features are (see "Acute appendicitis in children: Clinical
manifestations and diagnosis", section on 'Clinical manifestations'):

● Periumbilical pain that subsequently migrates to the right lower quadrant


● Tenderness in the right lower quadrant
● Abdominal guarding and rebound

Observational studies suggest that children younger than five years of age are more likely to have diarrhea at
presentation than school-aged children. The presumed mechanism for the diarrhea is irritation of the colon by
the inflamed appendix. The stools are usually of low volume and with mucus. (See "Acute appendicitis in
children: Clinical manifestations and diagnosis", section on 'Clinical features by age'.)

The diagnosis of appendicitis as the cause of diarrhea may be delayed because the classic constellation of
findings is absent. This is particularly true in very young children or among patients of any age who have both
a perforated appendix and a long duration of illness. However, abdominal tenderness may be greater than
would be expected with gastroenteritis. An approach to the diagnosis of appendicitis is provided in the
algorithm ( algorithm 2). (See "Acute appendicitis in children: Clinical manifestations and diagnosis", section
on 'Clinical features by age'.)

Toxic megacolon — Toxic megacolon is a potentially lethal complication of preexisting bowel disease or
infectious colitis that is characterized by total or segmental nonobstructive colonic dilatation plus systemic
toxicity. Signs and symptoms of acute colitis that are frequently resistant to therapy are often present for at
least one week prior to the onset of acute dilatation. Severe bloody diarrhea is the most common presenting

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symptom, while improvement of diarrhea may herald the onset of megacolon. Physical examination invariably
reveals a toxic appearing patient with altered sensorium, tachycardia, fever, postural hypotension, lower
abdominal distension and tenderness, with or without signs of localized or generalized peritonitis. However,
large doses of steroids, analgesics, or a clouded sensorium may mask the signs or symptoms of toxic
megacolon. (See "Toxic megacolon", section on 'Clinical manifestations'.)

The diagnosis of toxic megacolon should be considered in all patients presenting with abdominal distension
and acute or chronic diarrhea. The diagnosis is clinical, based upon the finding of an enlarged dilated colon on
abdominal imaging accompanied by severe systemic toxicity. (See "Toxic megacolon", section on 'Diagnosis'.)

Toxic megacolon can occur as a complication of Shigella infection, pseudomembranous colitis, Hirschsprung
disease, or inflammatory bowel disease. These conditions are reviewed separately. (See "Congenital
aganglionic megacolon (Hirschsprung disease)" and "Management of the hospitalized child or adolescent with
acute severe ulcerative colitis" and "Shigella infection: Epidemiology, clinical manifestations, and diagnosis",
section on 'Intestinal complications'.)

Congenital secretory diarrheas — Congenital secretory diarrheas are characterized by profuse watery
diarrhea beginning at or shortly after birth and are rare. They are caused by a variety of inherited disorders
that disrupt nutrient digestion, absorption, or transport, enterocyte development and function, or
enteroendocrine function. Although they are not usually life-threatening, congenital secretory diarrheas may
lead to profound dehydration in the young infant over a short course of time. (See "Approach to chronic
diarrhea in neonates and young infants (<6 months)", section on 'Congenital diarrheas and enteropathies'.)

Common conditions — The most common causes of diarrhea are infections with viruses and bacteria,
diarrhea due to a systemic infection other than gastrointestinal, diarrhea associated with antibiotic
administration, and feeding-related diarrhea [4].

Viral gastroenteritis — Viral gastroenteritis is, by far, the single most common diarrheal disorder seen in the
emergency department and in general practice. Based upon prospective series of infants and children using
various highly accurate methods for identification of viral infection, a viral pathogen is identified in up to 60
percent of all children with isolated diarrhea and over 75 percent of children with vomiting and diarrhea [5-7].
Since 2020, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has emerged as an important viral
etiology of diarrhea in children. The incubation time from exposure, predominant season, severity and
duration of illness depends upon the specific virus ( table 3). Stool testing for specific viruses is typically not
necessary but may be employed during outbreaks to determine the etiology. (See "Acute viral gastroenteritis in
children in resource-rich countries: Clinical features and diagnosis", section on 'Etiology' and "COVID-19:
Clinical manifestations and diagnosis in children".)

Non-bloody diarrhea, vomiting, and fever are the most common findings in children with viral gastroenteritis.
Gross blood or mucus in the stool are uncommon in viral gastroenteritis and should prompt consideration of
bacterial enteritis or other etiology. (See "Acute viral gastroenteritis in children in resource-rich countries:
Clinical features and diagnosis", section on 'Clinical presentation'.)

Bacterial enteritis — Bacterial enteritis typically affects children older than two years of age and occurs
through oral-fecal contamination and after exposure to poultry, other farm animals, or contaminated meat or
produce. Bacterial enteritis is a less frequent cause of diarrhea in children in resource-rich regions than viral
infection but has been identified in 17 percent of children with isolated diarrhea and 8 percent of those with
vomiting and diarrhea; Salmonella spp and Campylobacter spp were most frequently recovered with isolated
diarrhea [7].

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Clinical features can include high fever, tenesmus, severe abdominal pain, and gross blood or mucus in the
stool. Seizures may be associated with Shigella gastroenteritis. However, bacterial enteritis can be
indistinguishable from viral gastroenteritis. Diagnosis is made by stool culture. (See "Acute viral gastroenteritis
in children in resource-rich countries: Clinical features and diagnosis", section on 'Bacterial or parasitic
gastroenteritis'.)

Common bacterial causes of acute gastroenteritis in children include:

● Some E. coli spp (see "Shiga toxin-producing Escherichia coli: Microbiology, pathogenesis, epidemiology,
and prevention" and "Shiga toxin-producing Escherichia coli: Clinical manifestations, diagnosis, and
treatment" and "Clinical manifestations and diagnosis of Shiga toxin-producing Escherichia coli (STEC)
hemolytic uremic syndrome (HUS) in children")

● Salmonella strains (see "Nontyphoidal Salmonella: Microbiology and epidemiology" and "Enteric (typhoid
and paratyphoid) fever: Epidemiology, clinical manifestations, and diagnosis" and "Nontyphoidal
Salmonella: Gastrointestinal infection and asymptomatic carriage")

● Shigella spp (see "Shigella infection: Epidemiology, clinical manifestations, and diagnosis")

● C. difficile (see "Clostridioides difficile infection in children: Microbiology, pathogenesis, and epidemiology"
and "Clostridioides difficile infection in children: Clinical features and diagnosis")

● Campylobacter jejuni (see "Campylobacter infection: Microbiology, pathogenesis, and epidemiology" and
"Campylobacter infection: Clinical manifestations, diagnosis, and treatment")

● Yersinia enterocolitica

Less common causes include Aeromonas hydrophila and Campylobacter upsaliensis. (See "Campylobacter:
Infection with less common species and related bacteria", section on 'Campylobacter upsaliensis'.)

Extraintestinal infections — Extraintestinal infections (such as otitis media, urinary tract infections [UTIs],
and pneumonia) can cause acute diarrhea without blood that is usually mild and self-limited and accompanied
by fever or vomiting. (See "Acute otitis media in children: Clinical manifestations and diagnosis", section on
'Clinical presentation'.)

Diagnosis of these infections can usually be made by their extraintestinal manifestations and/or specific
ancillary studies (eg, urinalysis, urine or blood culture, or chest radiograph):

● Bacterial sepsis – Patients with sepsis may have accompanying diarrhea but, with the exception of
Salmonella sepsis and staphylococcal TSS, they do not present with diarrhea as a chief complaint or
predominant symptom. (See "Systemic inflammatory response syndrome (SIRS) and sepsis in children:
Definitions, epidemiology, clinical manifestations, and diagnosis".)

● UTI – Clinical features of UTI include suprapubic and/or flank tenderness, dysuria, urgency, and
frequency; however, diarrhea, with or without fever, may be the only symptom of an otherwise
asymptomatic UTI in infants and young children. (See "Urinary tract infections in infants and children
older than one month: Clinical features and diagnosis", section on 'Clinical presentation'.)

● Otitis media – Symptoms and signs of otitis media include ear pain, fussiness, bulging of the tympanic
membrane, and hearing loss. Young children, usually under one to two years of age, with otitis media
may present with diarrhea rather than ear pain. (See "Acute otitis media in children: Clinical

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manifestations and diagnosis", section on 'Clinical diagnosis' and "Acute otitis media in children: Clinical
manifestations and diagnosis", section on 'Clinical presentation'.)

● Pneumonia – Clinical features of pneumonia include fever and symptoms or signs of respiratory distress
(eg, tachypnea, nasal flaring, grunting, retractions, crackles, decreased breath sounds). (See "Community-
acquired pneumonia in children: Clinical features and diagnosis", section on 'Clinical presentation'.)

Antibiotic-associated diarrhea — Antibiotic-associated diarrhea (AAD) occurs commonly with many


antibiotics prescribed for children, including amoxicillin, amoxicillin with clavulanic acid, cephalosporins, and
clindamycin. In one prospective series, 18 percent of children less than two years of age developed diarrhea
associated with antibiotic use [8]. The pathophysiology of AAD is poorly understood but is likely related to
disruption in fecal flora with overgrowth of enteropathogens [9]. C. difficile is the specific pathogen that is most
associated with AAD and has the greatest potential for severe outcomes. (See 'Fulminant C. difficile colitis
(pseudomembranous colitis)' above.)

The diagnosis of AAD should be suspected in any child who develops diarrhea while on antibiotics. The
approach to diagnosis for C. difficile in children depends upon the age of the patient and clinical findings and is
discussed separately. (See "Clostridioides difficile infection in children: Clinical features and diagnosis", section
on 'Approach to diagnosis'.)

Functional diarrhea — Increased intake of hyperosmolar fluids such as fruit juices in toddlers and young
school children may cause diarrhea as the result of an increased osmotic load. When associated with excess
carbohydrate intake, functional diarrhea also been called toddler's diarrhea or nonspecific diarrhea of
childhood. Patients have painless passage of four or more large, unformed stools per day. Early morning stools
are typically more formed than stools passed later in the day. Diarrhea typically improves when the volume of
formula volume or intake of osmotically active carbohydrates (eg, fruit juice, sorbitol, or fructose) is reduced.
(See "Overview of the causes of chronic diarrhea in children in resource-abundant settings", section on
'Functional diarrhea in young children'.)

Starvation stools — Diarrhea may also occur when intake of solid foods is limited (sometimes referred to as
"starvation stools"). Although typically referring to a type of chronic diarrhea in malnourished children,
diarrhea can also persist in well-nourished children with acute viral gastroenteritis who are only given clear
liquids during the course of their illness. After fluid repletion is complete, resumption of a normal diet in
patients with viral gastroenteritis helps to avoid this condition. (See "Acute viral gastroenteritis in children in
resource-rich countries: Management and prevention", section on 'Diet'.)

Treatment of children with severe malnutrition and starvation stools is discussed separately. (See
"Management of complicated severe acute malnutrition in children in resource-limited settings", section on
'Overview of inpatient management'.)

Lactase deficiency — Lactase deficiency, when it occurs in younger children, is usually a transient problem
caused by mucosal injury from an enteric infection. The lactose intolerance associated with acute viral
gastroenteritis usually is mild and self-limiting, lasting several days to one to two weeks. Breastfeeding and
infant formula can be resumed when severe dehydration is corrected and can continue without change for the
child with mild dehydration. (See "Acute viral gastroenteritis in children in resource-rich countries:
Management and prevention", section on 'Diet'.)

In older children and adolescents, a primary lactase deficiency can causes chronic lactose intolerance.
Ingestion of lactose may result in symptoms of abdominal pain, bloating, flatulence, and diarrhea. In addition,
adolescents may have symptoms of vomiting. The abdominal pain may be cramping in nature and is often
localized to the periumbilical area or lower quadrants. In children, the stools may be bulky, frothy, and watery.
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A presumptive diagnosis of lactose intolerance can be made in patients with mild symptoms that occur within a
few hours after significant lactose ingestion (eg, >2 servings of dairy/day or >1 serving in a single dose that is
not associated with a meal) and resolve after five to seven days of avoidance of lactose-containing foods. The
diagnostic approach to lactose intolerance is discussed in greater detail separately. (See "Lactose intolerance
and malabsorption: Clinical manifestations, diagnosis, and management", section on 'Diagnostic evaluation'.)

Other conditions

● Parasitic infections – Parasitic infections are uncommon among immunocompetent children in resource-
rich settings but may occur in those patients with recent immigration, travel to an underdeveloped
country, backcountry camping, exposure to poultry or other farm animals, or consumption of processed
meat. Parasitic infections are also more frequently seen in immunocompromised patients and can cause
severe illness. In immunocompetent hosts, parasitic infections typically cause watery diarrhea, abdominal
cramping, vomiting, and low-grade fever.

Typical parasitic causes of acute gastroenteritis in immunocompetent children include:

• Giardia (see "Giardiasis: Epidemiology, clinical manifestations, and diagnosis")

• Cryptosporidium (see "Cryptosporidiosis: Epidemiology, clinical manifestations, and diagnosis")

• Cystoisospora belli (formerly known as Isospora belli) (see "Epidemiology, clinical manifestations, and
diagnosis of Cystoisospora (Isospora) infections")

• Microsporidia and Cyclospora (see "Microsporidiosis" and "Cyclospora infection")

• Amebiasis (children or immigrants from endemic areas such as India, Africa, Mexico, Central and
South America and, less commonly, among travelers to these regions; diarrhea may contain blood or
mucus) (see "Intestinal Entamoeba histolytica amebiasis", section on 'Clinical manifestations')

• Intestinal tapeworms (see "Tapeworm infections")

In immunocompetent patients, the diagnosis of parasitic infection should be pursued when history
uncovers risk factors for exposure and when diarrhea is persistent without an etiology. The evaluation
typically begins with stool microscopy for ova and parasites. However, more sensitive and specific testing
is also available for giardia and cryptosporidium. Such testing is indicated when stool microscopy is
negative and an alternative diagnosis is not found as discussed separately.(See "Giardiasis: Epidemiology,
clinical manifestations, and diagnosis", section on 'Diagnosis' and "Cryptosporidiosis: Epidemiology,
clinical manifestations, and diagnosis", section on 'Diagnosis'.)

● Toxic exposures – Toxic exposures to contaminated food, toxic plants, toxic mushrooms,
organophosphates, and carbamates can also cause diarrhea. History of exposure is key to making the
diagnosis:

• Foodborne disease – Foodborne disease that presents with profuse watery diarrhea is characteristic of
Clostridium perfringens (meat, poultry, and gravy) or enterotoxigenic E. coli (ETEC; potato salad and
cruise ship diarrhea). (See "Causes of acute infectious diarrhea and other foodborne illnesses in
resource-rich settings", section on 'Watery diarrhea'.)

• Plant poisoning – Self-limited vomiting and diarrhea can be expected after ingestions of flower bulbs
of the Amaryllidaceae family (narcissus, daffodil, and amaryllis), plant berries (eg, Ilex spp [holly],
Phoradendron spp [mistletoe], Pyracantha spp, and poinsettia plants). More severe gastrointestinal

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toxicity can occur after ingestion of pokeweed (Phytolacca americana), castor bean (Ricinus communis),
jequirity bean (Abrus precatorius), solanaceous plants ("nightshades"; eg, Solanum dulcamara or S.
niger), and autumn crocus (Colchicum autumnale). (See "Potentially toxic plant ingestions in children:
Clinical manifestations and evaluation", section on 'Gastrointestinal toxicity'.)

• Mushroom poisoning – A variety of mushroom species cause acute gastroenteritis soon after
ingestion without any further toxicity. Often these exposures occur when children take a bite of a "little
brown mushroom" while playing outside in the backyard. With ingestion of these mushrooms,
symptoms occur within one to three hours and include nausea, vomiting, and abdominal cramping as
well as diarrhea. Close attention to the history of ingestion and the timing associated with the onset of
symptoms is important to differentiate acute gastroenteritis from the more concerning delayed
gastroenteritis that may indicate consumption of a more lethal variety of mushroom toxins (eg,
amatoxins, gyromitrin, orellanine). (See "Clinical manifestations and evaluation of mushroom
poisoning", section on 'Acute gastroenteritis' and "Clinical manifestations and evaluation of mushroom
poisoning", section on 'Delayed symptom onset (>6 hours after ingestion)'.)

• Organophosphate or carbamate compound poisoning – Diarrhea is a component of the cholinergic


excess seen after ingestion, inhalation, or skin contamination of organophosphates and carbamates.
Toxicity typically occurs within minutes to hours of exposure. Other findings include salivation, tearing,
vomiting, bronchorrhea, bronchospasm, and bradycardia. Weakness, fasciculations, and paralysis may
also develop. In addition, the patient may have a petroleum distillate or garlic odor. Diagnosis is made
on clinical grounds. Direct measurement of red blood cell acetylcholinesterase activity provides a
measure of the degree of toxicity. (See "Organophosphate and carbamate poisoning", section on
'Clinical features' and "Organophosphate and carbamate poisoning", section on 'Diagnosis'.)

● Laxative-induced diarrhea – Caregivers may give children laxatives in an attempt to treat constipation
or, rarely, as a form of medical child abuse. Adolescents with eating disorders may misuse laxatives in an
attempt to lose weight. The physician should inquire about laxative use when diarrhea is persistent or
when other signs of an eating disorder are present. When intentional laxative use is suspected but is not
disclosed on history, suggestive laboratory findings include hypokalemia, metabolic alkalosis, a positive
laxative screen for diphenolic laxatives (eg, bisacodyl) and polyethylene glycol-containing laxatives,
elevated stool magnesium or phosphate, or an elevated stool osmotic gap. (See "Eating disorders:
Overview of epidemiology, clinical features, and diagnosis" and "Factitious diarrhea: Clinical
manifestations, diagnosis, and management", section on 'Diagnosis'.)

A number of conditions in resource-rich settings can present with diarrhea that is usually chronic ( table 1).
They include (see "Overview of the causes of chronic diarrhea in children in resource-abundant settings"):

● Primary immunodeficiencies (see "Approach to the child with recurrent infections", section on 'The child
with an immunodeficiency')

● Diarrhea related to HIV infection (see "Evaluation of the patient with HIV and diarrhea")

● Food allergies including milk protein allergy (see "Clinical manifestations of food allergy: An overview",
section on 'Gastrointestinal symptoms' and "Milk allergy: Clinical features and diagnosis", section on
'Clinical features')

● Celiac disease (see "Diagnosis of celiac disease in children", section on 'Patients with symptoms
suggesting celiac disease')

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● Inflammatory bowel disease (see "Clinical presentation and diagnosis of inflammatory bowel disease in
children", section on 'Clinical manifestations')

● Cystic fibrosis (see "Cystic fibrosis: Clinical manifestations and diagnosis", section on 'Pancreatic disease')

● Acrodermatitis enteropathica (see "Zinc deficiency and supplementation in children", section on


'Acrodermatitis enteropathica')

● Neuroendocrine secretory tumors (eg, gastrinoma, VIPoma, and mastocytosis) (see "Zollinger-Ellison
syndrome (gastrinoma): Clinical manifestations and diagnosis", section on 'Clinical manifestations' and
"VIPoma: Clinical manifestations, diagnosis, and management", section on 'Clinical features' and
"Mastocytosis (cutaneous and systemic) in children: Epidemiology, clinical manifestations, evaluation, and
diagnosis", section on 'Gastrointestinal complaints' and "Mastocytosis (cutaneous and systemic) in
children: Epidemiology, clinical manifestations, evaluation, and diagnosis", section on 'Signs and
symptoms')

● Endocrine disorders (particularly hyperthyroidism but also hypoparathyroidism and congenital adrenal
hyperplasia) (see "Clinical manifestations of hypocalcemia", section on 'Hypoparathyroidism')

● Neonatal drug withdrawal (see "Prenatal substance exposure and neonatal abstinence syndrome (NAS):
Management and outcomes" and "Prenatal substance exposure and neonatal abstinence syndrome
(NAS): Clinical features and diagnosis", section on 'Clinical manifestations of NAS')

● Short gut syndrome (see "Chronic complications of short bowel syndrome in children", section on 'Chronic
diarrhea')

● Small intestinal bacterial overgrowth (see "Small intestinal bacterial overgrowth: Clinical manifestations
and diagnosis", section on 'Clinical features')

● Factitious diarrhea (in adolescents engaging in laxative abuse) (see "Factitious diarrhea: Clinical
manifestations, diagnosis, and management", section on 'Clinical manifestations')

● Irritable bowel syndrome (see "Chronic abdominal pain in children and adolescents: Approach to the
evaluation", section on 'Diagnosis of functional abdominal pain')

ACUTE DIARRHEA (TYPICAL DURATION <5 DAYS)

History — There are a number of historical factors to identify:

● Immune status of the child – Immunocompromise increases the risk of infection by unusual organisms,
the prevalence of which varies with the degree of immunosuppression and the nature of the underlying
condition.

● Fever and bloody or mucousy diarrhea – These two features of the diarrheal illness, either alone or in
combination, are particularly helpful in sorting through the differential diagnosis in otherwise healthy
children. (See 'Algorithmic approach to the patient' below.)

● Potential for dehydration – The number of episodes of diarrhea per day, the amount of oral fluid intake,
and urine output (eg, number of wet diapers or frequency of urination in the past 24 hours) and a recent
weight (if available) help identify patients who are likely to be dehydrated.

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● Duration of diarrhea – An acute diarrheal illness is typically defined as a duration of five days or less but
return to normal stool consistency after viral gastroenteritis, the most common etiology in resource-rich
regions may take longer. Diarrhea that has persisted beyond five days may warrant consideration of
other diagnoses, especially in children who are ill-appearing, have bloody diarrhea in association with
weight loss, or other findings suggesting a more serious underlying condition such as those discussed
below. (See 'Chronic diarrhea (duration >1 month)' below.)

● Institutionalized children and those recently returning from resource-limited settings are more likely to
have bacterial or parasitic pathogens. (See "Travelers' diarrhea: Epidemiology, microbiology, clinical
manifestations, and diagnosis".)

● Recent antibiotic use – Recent exposure to antibiotics suggests the possibility of antibiotic-associated
diarrhea and, in patients with a fulminant course, pseudomembranous colitis. (See "Clostridioides difficile
infection in children: Clinical features and diagnosis", section on 'Symptomatic disease'.)

● Dietary history – Diarrhea in patients taking large amounts of formula, fruit juices, or sorbitol suggests
overfeeding or functional diarrhea. Pain, bloating, flatulence, and diarrhea after eating lactose-containing
food supports the diagnosis of primary lactase deficiency in older children and adolescents.

Physical examination — The patient who requires volume resuscitation must be quickly identified.

Mild dehydration (less than 5 percent body weight) is often not discernable by physical examination but may be
suggested by a history of decreased oral intake, increased losses (eg, vomiting or diarrhea), and decreased
urine output. Clinical evidence of moderate (5 to 10 percent) or severe (>10 percent) dehydration membranes is
usually apparent ( table 4). The most useful signs for predicting a volume deficit of 5 percent or more include
a tired or fatigued general appearance, delayed capillary refill time greater than two seconds, dry mucous
membranes, and decreased tears. However, no single physical examination finding is particularly predictive,
and a combination of findings should be present for children with moderate to severe dehydration. When
available, comparison of current weight with a recently obtained prior weight can also help define the percent
of dehydration. (See "Clinical assessment of hypovolemia (dehydration) in children", section on 'Estimating
degree of hypovolemia'.)

In addition to identifying volume depletion, a thorough examination must be performed:

● Systemic, non-enteric infections, particularly otitis media, may cause diarrhea.

● A palpable mass or peritonitis suggests appendicitis, intussusception or, less commonly, toxic megacolon.

● Generalized toxicity and/or shock may occur with hemolytic uremic syndrome (HUS) or with sepsis, such
as from Salmonella or staphylococcal toxic shock syndrome (TSS) [10]. (See "Clinical manifestations and
diagnosis of Shiga toxin-producing Escherichia coli (STEC) hemolytic uremic syndrome (HUS) in children",
section on 'Typical course'.)

Laboratory testing and imaging — Otherwise well children with acute, non-bloody diarrhea and no exposure
to increase the risk of bacterial enteritis are usually managed without any ancillary studies. (See 'Common
conditions' above.)

The laboratory evaluation of children with chronic diarrhea in resource-rich settings is discussed separately.
(See "Approach to chronic diarrhea in children >6 months in resource-abundant settings".)

Additional studies are warranted for the following children:

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● Ill-appearing – Ancillary studies that help distinguish among life-threatening conditions in ill-appearing
patients with diarrhea include (see 'Life-threatening conditions' above):

• Complete blood count with differential


• Peripheral blood smear
• Reticulocyte count
• Rapid blood glucose
• Serum electrolytes, blood urea nitrogen (BUN), and creatinine
• Blood culture
• Stool culture
• Stool for C. difficile toxin
• Plain abdominal radiographs (upright or left lateral decubitus and AP views) in patients with signs of
toxic megacolon, peritonitis, or perforation
• Abdominal ultrasound in patients with findings suggesting intussusception or appendicitis

● Significant dehydration – Children with significant dehydration requiring intravenous rehydration


should have serum electrolytes, including a rapid blood glucose, since hypoglycemia occurs not
infrequently in this setting, BUN, and creatinine measured. (See "Clinical assessment of hypovolemia
(dehydration) in children".)

● Fever and blood or mucus in the stool but without toxic appearance:

• Stool culture for Salmonella, Shigella, Campylobacter spp, Yersinia, and Shiga toxin-producing Escherichia
coli (STEC); if a stool specimen is not immediately available, a rectal swab coated with stool may be
sent. In settings where multiplex stool tests are used, a high degree of clinical correlation and a
confirmatory stool culture are required before any treatment is provided. (See "Approach to the adult
with acute diarrhea in resource-rich settings", section on 'Multipathogen molecular panels'.)

• C. difficile toxin (only for patients older than one year of age with compatible clinical features antibiotic
exposure or other risk factors or predisposing conditions). (See "Clostridioides difficile infection in
children: Clinical features and diagnosis", section on 'Indications for testing'.)

A bacterial pathogen will be identified in 15 to 20 percent of cases [11-13]. Stool for ova and parasites is
indicated for children who have traveled to or reside in an endemic area.

● Recent immigration, travel to an underdeveloped country, backcountry camping, exposure to


poultry or other farm animals, or consumption of processed meat – Stool for ova and parasites

● Fever and no source (children younger than two years of age) – Urine dipstick or urinalysis and urine
culture. (See "Urinary tract infections in infants and children older than one month: Clinical features and
diagnosis", section on 'Decision to obtain urine sample'.)

Algorithmic approach to the patient — An algorithmic approach provides clinical guidance to the diagnostic
approach of diarrhea in children ( algorithm 1A and algorithm 1B and algorithm 3) [4].

First, the physician should determine whether the child appears seriously ill ( algorithm 1A) or has signs of a
surgical abdominal process.

● A palpable mass or peritonitis suggests appendicitis, intussusception, or, less commonly, toxic
megacolon. (See 'Intussusception' above and 'Appendicitis' above and 'Toxic megacolon' above.)

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● Generalized toxicity and/or shock may occur with HUS and with sepsis, such as from Salmonella or
staphylococcal TSS. (See 'Sepsis' above and 'Hemolytic uremic syndrome' above.)

● Seizures may be seen with shigellosis, occasionally before the onset of diarrhea. (See "Shigella infection:
Epidemiology, clinical manifestations, and diagnosis", section on 'Neurologic disease'.)

● Altered mental status with tenting of the skin and parched mucous membranes suggest severe
dehydration.

● Immunocompromised patients ( algorithm 1B) are at risk for unusual infections and require a rigorous
approach in accordance with protocols specific to the underlying disorder. (See "Evaluation of the patient
with HIV and diarrhea".)

● Profuse diarrhea in association with excessive salivation, lacrimation, and urination suggests
organophosphate ingestion. (See 'Other conditions' above.)

Next, the physician focuses on those with acute diarrhea ( algorithm 1B), as these patients are more likely to
require a diagnostic or therapeutic intervention. Immunocompromised patients are at risk for unusual
infections and require a rigorous approach in accordance with protocols specific to the underlying disorder.
(See "Evaluation of the patient with HIV and diarrhea".)

Fever and bloody or mucousy diarrhea, either alone or in combination, are particularly helpful in sorting
through the differential diagnosis ( algorithm 1B):

● Blood is seen in the stool of up to 10 percent of children with diarrhea. In most cases, the blood appears
in small quantities as drops on the surface of the stool and should not be construed as ominous.

● A small percentage of children with diarrhea, however, have more profuse rectal bleeding. Particularly in
these patients, one must exclude life-threatening disorders such as intussusception, HUS, and
pseudomembranous colitis. (See 'Intussusception' above and 'Hemolytic uremic syndrome' above and
'Fulminant C. difficile colitis (pseudomembranous colitis)' above.)

● Mucousy diarrhea, with or without blood, suggests bacterial enteritis [12,13].

Febrile with non-bloody diarrhea — The presence of fever in an immunocompetent child with diarrhea is
the hallmark of infection. Most febrile children with non-bloody diarrhea have viral enteritis. Although children
with SARS-CoV-2 most often present with respiratory complaints, fever and diarrhea can be the sole presenting
symptoms in infants and young children. (See "Acute viral gastroenteritis in children in resource-rich countries:
Clinical features and diagnosis".)

Afebrile with non-bloody diarrhea — Many afebrile children with non-bloody diarrhea will also have viral
enteritis. For those taking antibiotics, such as amoxicillin, the diarrhea may be related to the medication [8,9].

Overfeeding may cause diarrhea during the first 6 to 12 months of life. The history of excessive formula intake
in an overweight child indicates this diagnosis [14]. Excessive intake of fruit juices or sorbitol may cause
functional diarrhea in older children.

Febrile with bloody diarrhea — Febrile children with bloody and/or mucousy diarrhea typically have
infectious bacterial enteritis, although some may have viral infections. (See 'Bacterial enteritis' above and
"Causes of acute infectious diarrhea and other foodborne illnesses in resource-rich settings", section on
'Severe or bloody diarrhea'.)

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Pseudomembranous colitis is an important consideration in febrile children with bloody diarrhea who have
also received antibiotic therapy, especially if systemic toxicity, abdominal distension, and gross blood in the
stools are present. (See "Clostridioides difficile infection in children: Clinical features and diagnosis", section on
'Symptomatic disease'.)

Possible exceptions include the following:

● Amebiasis merits consideration in children or immigrants from endemic areas (eg, India, Africa, Mexico,
Central and South America) and, less commonly, among travelers to these regions. (See "Intestinal
Entamoeba histolytica amebiasis", section on 'Epidemiology'.)

● Children with inflammatory bowel disease may present with an initial episode of acute, bloody diarrhea.
In most of these cases, the physician can elicit a preceding history of weight loss and/or recurrent
abdominal pain. (See "Clinical presentation and diagnosis of inflammatory bowel disease in children",
section on 'Findings suggesting colitis'.)

Afebrile with bloody diarrhea — Afebrile children with bloody diarrhea represent the most worrisome
category because most patients with intussusception or HUS have this symptom constellation:

● Intussusception is a major concern in any child less than two years of age with grossly bloody diarrhea
that does not appear to have an infectious cause. A history of severe, colicky abdominal pain in a lethargic
child warrants an abdominal ultrasound or contrast enema. (See "Intussusception in children", section on
'Clinical manifestations'.)

● Bloody diarrhea with pallor, purpura, and hematuria with elevated serum BUN or creatinine and
thrombocytopenia point to HUS. (See "Clinical manifestations and diagnosis of Shiga toxin-producing
Escherichia coli (STEC) hemolytic uremic syndrome (HUS) in children", section on 'Typical course'.)

The most common diagnosis, infectious bacterial enteritis, should be made only after exclusion of the more
serious disorders by history, physical examination, and occasionally, laboratory or imaging studies.

Therapeutic interventions — Children with life-threatening causes for diarrhea warrant specific therapy
dictated by the underlying condition. (See 'Life-threatening conditions' above.)

● Fluid resuscitation – Parenteral fluid resuscitation with an isotonic solution (eg, normal saline) should be
initiated promptly in children with severe dehydration or circulatory compromise and may be particularly
important in preventing oliguric renal failure in those patients with HUS. Patients with toxic megacolon
and intussusception may also have significant ongoing third space losses that must be replaced. (See
"Treatment and prognosis of Shiga toxin-producing Escherichia coli (STEC) hemolytic uremic syndrome
(HUS) in children", section on 'Fluid management' and "Hypovolemic shock in children: Initial evaluation
and management", section on 'Management'.)

Most children with diarrhea will not require intravenous fluid repletion. Treatment with oral rehydration
solutions should be encouraged as the first line therapy for both rehydration and maintenance therapy in
patients who have mild to moderate dehydration and can drink. (See "Oral rehydration therapy".)

● Antibiotics – Antibiotics should not be used routinely for well-appearing children with acute bloody
diarrhea unless a specific pathogen has been isolated. Antibiotic therapy may be a risk factor for the
development of HUS in patients with bloody diarrhea due to E. coli O157:H7, which may be
indistinguishable from bloody diarrhea seen with other non-E. coli bacterial etiologies [15]. (See "Shiga
toxin-producing Escherichia coli: Clinical manifestations, diagnosis, and treatment", section on
'Antibiotics'.)
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However, antibiotics are essential to the proper treatment of sepsis, peritonitis, and staphylococcal TSS.
(See "Septic shock in children: Rapid recognition and initial resuscitation (first hour)", section on 'Empiric
antibiotic therapy'.)

Indications for antibiotic therapy in patients with specific gastrointestinal pathogens are discussed
separately:

• (See "Shigella infection: Treatment and prevention in children", section on 'Antibiotic therapy'.)
• (See "Nontyphoidal Salmonella: Gastrointestinal infection and asymptomatic carriage", section on
'Clinical approach'.)
• (See "Campylobacter infection: Clinical manifestations, diagnosis, and treatment", section on
'Indications'.)
• (See "Treatment and prevention of Yersinia enterocolitica and Yersinia pseudotuberculosis infection",
section on 'Treatment'.)

● Probiotics – Probiotics refer to products derived from food sources, especially cultured milk products. The
list of such microorganisms continues to grow and includes a variety of different strains of bacteria.
Probiotics appear to have only a modest effect on recovery from infectious diarrhea. Systematic reviews
also suggest that probiotics (including various bacterial species and the yeast S. boulardii) are effective in
reducing the incidence of diarrhea in patients who are taking antibiotics. However, discordant data have
been published and there is little detailed information regarding the optimal dose or timing of
supplementation or the effects on subgroups of patients. The use of probiotics for these indications is
discussed in more detail separately. (See "Probiotics for gastrointestinal diseases", section on 'Infectious
diarrhea'.)

Disposition — The majority of children with infectious diarrhea have mild to moderate dehydration and can be
managed as outpatients after receiving appropriate assessment and have proven oral rehydration therapy will
be successful. (See "Treatment of hypovolemia (dehydration) in children in resource-abundant settings".)

Hospital admission is warranted in children with any one of the following findings:

● Diagnosis of or strong clinical suspicion for a life-threatening cause of diarrhea, such as HUS or other
systemic illnesses (see 'Life-threatening conditions' above)

● Severe dehydration or significant electrolyte abnormalities upon presentation (see "Clinical assessment of
hypovolemia (dehydration) in children", section on 'Estimating degree of hypovolemia')

● Lack of improvement with rehydration

● Continued copious diarrhea that is likely to lead to recurrent dehydration if intravenous replacement of
ongoing losses does not occur

● Inability to drink

● Caregiver inability to manage the child’s condition or recognize deterioration

Persistent diarrhea — The child who returns with the persistence of an acute diarrheal illness, initially
presumed to be viral in origin and with no evidence of malnutrition or dehydration, often can be managed
without an extensive evaluation.

Common causes, in addition to persistent viral infection, are:

● Starvation stools due to excessive use of a clear liquid diet for several days

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● Secondary lactase deficiency following viral enteritis


● Bacterial infections

A stool culture should be obtained and testing for C. difficile toxin is indicated in children older than one year of
age who have had recent antibiotic therapy or bloody diarrhea.

Gradual refeeding is recommended if starvation stools are suspected (ie, the child has remained on a clear
liquid diet).

In those children with diarrhea of intermediate duration (one to four weeks), the potential etiologies include:

● Appendiceal abscess (particularly in patients with fever associated with abdominal tenderness or a history
of abdominal pain) (see "Acute appendicitis in children: Clinical manifestations and diagnosis")

● Bacterial enteritis or parasitic infestations (see "Acute viral gastroenteritis in children in resource-rich
countries: Clinical features and diagnosis", section on 'Bacterial or parasitic gastroenteritis')

CHRONIC DIARRHEA (DURATION >1 MONTH)

A brief initial evaluation of the child with chronic diarrhea in the acute setting (eg, emergency department) is
described below. An expanded differential diagnosis and more comprehensive diagnostic approach to chronic
diarrheal diseases in resource-rich settings is discussed in detail separately. (See "Overview of the causes of
chronic diarrhea in children in resource-abundant settings" and "Approach to chronic diarrhea in children >6
months in resource-abundant settings" and "Approach to chronic diarrhea in neonates and young infants (<6
months)".)

A child with chronic diarrhea who presents in an acute care setting is often not seriously ill. The evaluation
usually requires a period of observation and ancillary studies based upon the most likely underlying etiology
rather than urgent diagnostic and therapeutic intervention. Urgent conditions are suggested by a history of
bloody diarrhea or the physical finding of abdominal tenderness ( algorithm 3).

In resource-limited settings, chronic diarrhea typically is associated with serial enteric infections and
malnutrition. This common pathophysiology calls for a distinct approach to diagnosis and treatment, which is
discussed separately. (See "Persistent diarrhea in children in resource-limited settings".)

The following findings may indicate serious underlying disease in the child with chronic diarrhea:

● A history of delayed passage of meconium, constipation since birth, and abdominal distension are
compatible with Hirschsprung disease. (See "Congenital aganglionic megacolon (Hirschsprung disease)",
section on 'Clinical features'.)

● Malabsorptive stools (steatorrhea) and respiratory infections suggest cystic fibrosis. (See "Cystic fibrosis:
Clinical manifestations and diagnosis", section on 'Pancreatic disease'.)

● Failure to thrive, thrush, and pneumonia occur in association with human immunodeficiency virus (HIV)
infection or primary immunodeficiency. (See "Pediatric HIV infection: Classification, clinical
manifestations, and outcome", section on 'Clinical manifestations' and "Severe combined
immunodeficiency (SCID): An overview", section on 'Clinical manifestations'.)

● Bloody diarrhea with weight loss points to inflammatory bowel disease, particularly if the diarrhea is
bloody, or to irritable bowel syndrome. (See "Clinical presentation and diagnosis of inflammatory bowel
disease in children", section on 'Clinical manifestations'.)
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● Congenital secretory diarrheas begin at or shortly after birth with profuse, watery diarrhea.

The extent of ancillary testing depends upon the degree of illness and the suspected underlying
diagnosis. (See "Approach to chronic diarrhea in children >6 months in resource-abundant settings".)

At minimum, a stool culture and a stool for ova and parasites would aid in the diagnosis of infections of the
gastrointestinal tract and provide a head start on the evaluation for the physician who subsequently sees the
child.

The child with chronic diarrhea who is well-appearing and tolerates oral fluids can be managed as an
outpatient. The key factor in successfully diagnosing the etiology of the diarrhea is reliable follow-up with a
primary care provider or, when serious underlying disease is suspected, referral to a pediatric specialist.

SOCIETY GUIDELINE LINKS

Links to society and government-sponsored guidelines from selected countries and regions around the world
are provided separately. (See "Society guideline links: Acute diarrhea in children".)

INFORMATION FOR PATIENTS

UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics
patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer
the four or five key questions a patient might have about a given condition. These articles are best for patients
who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient
education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to
12th grade reading level and are best for patients who want in-depth information and are comfortable with
some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these
topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on
"patient info" and the keyword(s) of interest.)

● Basics topic (see "Patient education: Diarrhea in children (The Basics)")

● Beyond the Basics topic (see "Patient education: Acute diarrhea in children (Beyond the Basics)")

SUMMARY AND RECOMMENDATIONS

● Diagnostic approach – The approach to the evaluation of acute diarrhea in resource-rich settings is
summarized in the algorithms ( algorithm 1A-B). The table summarizes the causes of diarrhea,
highlighting the most common and the most life-threatening pediatric conditions ( table 1). (See 'Acute
diarrhea (typical duration <5 days)' above and 'Causes' above.)

The presence of fever and diarrhea with blood or mucus are two features of acute diarrheal illness, either
alone or in combination, that are particularly helpful in sorting through the differential diagnosis,
particularly in otherwise healthy, well-appearing children. (See 'History' above and 'Algorithmic approach
to the patient' above.)

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● Acute diarrhea – The patient with acute diarrhea who requires volume resuscitation must be quickly
identified. Clinical evidence of dehydration is already apparent at a deficit of 5 percent of body weight,
except in rare cases of hypernatremia ( table 4). A combination of historical and physical examination
findings rather than one single feature provides the most useful model for predicting a volume deficit of 5
percent or more. (See 'Physical examination' above.)

A palpable mass or peritonitis suggests appendicitis, intussusception or, less commonly, toxic megacolon.
Generalized toxicity and/or shock may occur with hemolytic uremic syndrome (HUS), severe dehydration,
or with sepsis, such as from Salmonella or staphylococcal toxic shock syndrome (TSS). (See 'Physical
examination' above and 'Life-threatening conditions' above.)

In addition to identifying volume depletion and life-threatening conditions, a thorough examination must
be performed because systemic, non-enteric infections, particularly otitis media, may cause acute
diarrhea. (See 'Extraintestinal infections' above.)

Ancillary studies in children with acute diarrhea are based upon a careful history and physical
examination. Most previously healthy children with self-limited diarrhea (eg, viral gastroenteritis,
extraintestinal infections, functional diarrhea, starvation stools, or transient lactase deficiency) and no
exposures to bacterial pathogens require no specific testing. (See 'Laboratory testing and imaging'
above.)

An acute diarrheal illness is typically defined as a duration of five days or less but return to normal stool
consistency after viral gastroenteritis, the most common etiology in resource-rich regions may take
longer. Diarrhea that has persisted beyond five days may warrant consideration of and evaluation for
other diagnoses, especially in children who are ill-appearing, have bloody diarrhea in association with
weight loss, or other findings suggesting a more serious underlying condition.

● Chronic diarrhea – A brief initial evaluation of the child with chronic diarrhea in the acute setting (eg,
emergency department) is described above ( algorithm 3). (See 'Chronic diarrhea (duration >1 month)'
above.)

A more comprehensive diagnostic approach to chronic diarrheal diseases in resource-rich and resource-
limited settings is discussed in greater detail separately. (See "Overview of the causes of chronic diarrhea
in children in resource-abundant settings" and "Approach to chronic diarrhea in children >6 months in
resource-abundant settings" and "Approach to chronic diarrhea in neonates and young infants (<6
months)" and "Persistent diarrhea in children in resource-limited settings".)

Use of UpToDate is subject to the Terms of Use.

REFERENCES

1. King CK, Glass R, Bresee JS, et al. Managing acute gastroenteritis among children: oral rehydration,
maintenance, and nutritional therapy. MMWR Recomm Rep 2003; 52:1.

2. Cohen MB. Etiology and mechanisms of acute infectious diarrhea in infants in the United States. J Pediatr
1991; 118:S34.

3. Becker-Dreps S, Bucardo F, Vilchez S, et al. Etiology of childhood diarrhea after rotavirus vaccine
introduction: a prospective, population-based study in Nicaragua. Pediatr Infect Dis J 2014; 33:1156.

4. Pereira F, Hsu D. Diarrhea. In: Textbook of Pediatric Emergency Medicine, 7th ed, Shaw KN, Bachur RG (Ed
s), Wolters Kluwer, Philadelphia, PA 2016. p.135.

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5. Pang XL, Honma S, Nakata S, Vesikari T. Human caliciviruses in acute gastroenteritis of young children in
the community. J Infect Dis 2000; 181 Suppl 2:S288.

6. Denno DM, Shaikh N, Stapp JR, et al. Diarrhea etiology in a pediatric emergency department: a case
control study. Clin Infect Dis 2012; 55:897.

7. Freedman SB, Xie J, Lee BE, et al. Microbial Etiologies and Clinical Characteristics of Children Seeking
Emergency Department Care Due to Vomiting in the Absence of Diarrhea. Clin Infect Dis 2021; 73:1414.

8. Turck D, Bernet JP, Marx J, et al. Incidence and risk factors of oral antibiotic-associated diarrhea in an
outpatient pediatric population. J Pediatr Gastroenterol Nutr 2003; 37:22.

9. Surawicz CM. Antibiotic-associated diarrhea in children: how many dirty diapers? J Pediatr Gastroenterol
Nutr 2003; 37:2.

10. Torrey S, Fleisher G, Jaffe D. Incidence of Salmonella bacteremia in infants with Salmonella gastroenteritis.
J Pediatr 1986; 108:718.

11. Finkelstein JA, Schwartz JS, Torrey S, Fleisher GR. Common clinical features as predictors of bacterial
diarrhea in infants. Am J Emerg Med 1989; 7:469.

12. Gupta DN, Sircar BK, Sengupta PG, et al. Epidemiological and clinical profiles of acute invasive diarrhoea
with special reference to mucoid episodes: a rural community-based longitudinal study. Trans R Soc Trop
Med Hyg 1996; 90:544.

13. Dutta P, Mitra U, Saha DR, et al. Mucoid presentation of acute enterocolitis in children: a hospital-based
case-control study. Acta Paediatr 1999; 88:822.

14. Issenman RM, Hewson S, Pirhonen D, et al. Are chronic digestive complaints the result of abnormal dietary
patterns? Diet and digestive complaints in children at 22 and 40 months of age. Am J Dis Child 1987;
141:679.

15. Wong CS, Jelacic S, Habeeb RL, et al. The risk of the hemolytic-uremic syndrome after antibiotic treatment
of Escherichia coli O157:H7 infections. N Engl J Med 2000; 342:1930.
Topic 6456 Version 32.0

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GRAPHICS

Etiología de la diarrea en niños por edad.

Causa Bebés y niños pequeños Niños mayores y adolescentes

Infecciones gastrointestinales Virus* Virus*

Bacterias* Bacterias*

parásitos parásitos

Infecciones no gastrointestinales Otitis media* Systemic infections


(diarrea parenteral) Urinary tract infections* Staphylococcal toxic shock
syndrome ¶
Other systemic infections

Dietary disturbances Functional diarrhea (eg, excess Starvation stools*


fructose and/or sorbitol intake [fruit
juices])/overfeeding*

Food allergy*

Starvation stools*

Anatomic abnormalities Intussusception ¶ Appendicitis ¶

Hirschsprung-associated enterocolitis Partial obstruction ¶


(±toxic megacolon ¶ )
Blind loop syndrome
Partial bowel obstruction ¶

Blind loop syndrome (also in patients


with dysmotility)

Intestinal lymphangiectasis

Short gut syndrome

Inflammatory bowel disease Early onset inflammatory bowel Ulcerative colitis (±toxic megacolon ¶ )
disease (rare, monogenic)
Crohn disease (±toxic megacolon ¶ )

Malabsorption or increased secretion Cystic fibrosis Celiac disease

Celiac disease Disaccharidase deficiency (primary or


secondary)*
Disaccharidase deficiency (eg, lactase
deficiency due to infectious Acrodermatitis enteropathica
diarrhea)*
Neuroendocrine secretory tumors
Acrodermatitis enteropathica

Congenital secretory diarrhea

Immunodeficiency Severe combined immunodeficiencies HIV infection


and other genetic disorders

HIV infection

Endocrinopathy Congenital adrenal hyperplasia Hyperthyroidism

Hypoparathyroidism

Miscellaneous Antibiotic-associated diarrhea* Antibiotic-associated diarrhea*

Clostridioides difficile C. difficile colitis


colitis (±pseudomembranous colitis ¶ ) (±pseudomembranous colitis ¶ )

Toxins Δ Toxins Δ

Hemolytic uremic syndrome ¶ Irritable bowel syndrome*

Neonatal drug withdrawal Psychogenic disturbances*

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HIV: human immunodeficiency virus.

* Common cause.

¶ Life-threatening cause.

Δ Potential toxins include foodborne toxin disease, poisonous plants or mushrooms, and organophosphates or
carbamates.

Courtesy of Gary R Fleisher, MD.

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Diarrhea in the seriously ill child

* More likely in older children and adolescents.

¶ More likely in infants and young children.

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Clinical criteria for staphylococcal toxic shock syndrome (issued by the United States
Centers for Disease Control and Prevention)

Clinical criteria

Fever – Temperature ≥38.9°C (102.0°F)

Rash – Diffuse macular erythroderma

Desquamation – 1 to 2 weeks after onset of rash

Hypotension:
For adults – Systolic blood pressure ≤90 mmHg
For children <16 years of age – Systolic blood pressure less than 5 th percentile by age

Multisystem involvement (3 or more of the following organ systems):


Gastrointestinal – Vomiting or diarrhea at onset of illness
Muscular – Severe myalgia or creatine phosphokinase elevation >2 times the upper limit of normal
Mucous membranes – Vaginal, oropharyngeal, or conjunctival hyperemia
Renal – Blood urea nitrogen or serum creatinine >2 times the upper limit of normal or pyuria (>5
leukocytes/high-power field) in the absence of urinary tract infection
Hepatic – Bilirubin or transaminases >2 times the upper limit of normal
Hematologic – Platelets <100,000/microL
Central nervous system – Disorientation or alterations in consciousness without focal neurologic signs when
fever and hypotension are absent

Laboratory criteria
Cultures (blood or cerebrospinal fluid) negative for alternative pathogens (blood cultures may be positive for
Staphylococcus aureus)

Serologic tests negative (if obtained) for Rocky Mountain spotted fever, leptospirosis, or measles

Case classification
Probable case – A case which meets the laboratory criteria and 4 of the 5 clinical criteria

Confirmed case – A case which meets the laboratory criteria and all 5 of the clinical criteria, including desquamation
(unless the patient dies before desquamation occurs)

The above criteria were established for epidemiologic surveillance; they should be not be used to exclude a case that
is highly suspicious for toxic shock syndrome, even if all criteria are not met.

Adapted from: Centers for Disease Control and Prevention. Toxic shock syndrome (other than streptococcal) (TSS): 2011 case definition. Available
at: https://ndc.services.cdc.gov/case-definitions/toxic-shock-syndrome-2011/ (Accessed on February 11, 2022).

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Diagnostic approach to pediatric appendicitis

PAS: Pediatric Appendicitis Score; WBC: white blood cell count; ANC: absolute neutrophil count;
CRP: C-reative protein; RLQ: right lower quadrant.

* Classic signs of early appendicitis consist of abdominal pain for less than two days that begins
periumbilically and then begins to radiate and localize to the right lower quadrant. The pain is
associated with anorexia, vomiting, and low grade fever. RLQ tenderness is present on physical
examination and the white blood cell count, absolute neutrophil count, and/or c-reactive protein
are elevated.

¶ For components of the pediatric appendicitis score refer to UpToDate graphics on pediatric
appendicitis score and to the UpToDate topic on clinical manifestations and diagnosis of
appendicitis in children.

Δ Diagnostic imaging prior to surgical consultation is typically performed for these patients. For
specific discussion of which imaging tests to order, refer to UpToDate topics on diagnostic imaging
in pediatric appendicitis. If local resources are insufficient to adequately perform or interpret
pediatric diagnostic imaging or if surgeons with pediatric expertise are not available, the patient
should be transferred to a facility with pediatric radiologic and surgical capability and no imaging
should be performed at the local institution.

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Epidemiologic and clinical features of common causes of acute viral gastroenteritis in


children*

Common
Possibility
modes of
Predominant Incubation of transient Othe
Virus transmission Age Duration
season period lactose feature
in order of
intolerance ¶
frequency

Rotavirus Fall/winter in 1 to 3 days Fecal-oral 6 to 24 5 to 7 days Yes Causes s


middle- to Respiratory? months childhoo
high-income diarrhea
countries Endemic
with season
temperate broaden
climates mass
Throughout immuniz
the year in
low- and
middle-low-
income
countries
with tropical
climates

Norovirus All year 12 to 48 Fecal-oral All ages 1 to 4 days No Vomiting


(winter) hours Water be the
Shellfish promine
symptom
Other foods
Causes m
Respiratory?
outbreak
nonbacte
gastroen
Endemic
epidemic

Sapovirus All year 1 to 2 days Fecal-oral Infants 3 to 4 days Endemic


and epidemic
toddlers

Astrovirus Winter 4 to 5 days Fecal-oral All ages 5 to 6 days Yes Endemic


Water epidemic

Enteric Summer 3 to 10 days Fecal-oral Children 6 to 9 days Yes Endemic


adenovirus
(types 40
and 41)

SARS-CoV-1: severe acute respiratory syndrome coronavirus 1; SARS-CoV-2: severe acute respiratory syndrome virus
2.

* Viruses that typically have extraintestinal manifestations (eg, coxsackievirus, echovirus, poliovirus, SARS-CoV-1,
SARS-CoV-2, influenza virus type B) also may cause gastroenteritis.

¶ It is not necessary to switch to lactose-free formula.

Data from:
1. Dennehy PH. Viral gastroenteritis in children. Pediatr Infect Dis J 2011; 30:63.
2. Lee RM, Lessler J, Lee RA, et al. Incubation periods of viral gastroenteritis: A systematic review. BMC Infect Dis 2013; 13:446.

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3. Public Health Agency of Canada. Adenovirus (serotypes 40 & 41). Available at: www.phac-aspc.gc.ca/lab-bio/res/psds-ftss/adenovirus-
eng.php (Accessed on August 5, 2015).

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Physical findings of volume depletion in infants and children

Mild Moderate Severe


Finding
(3 to 5%) (6 to 9%) (≥10%)

Pulse Full, normal rate Rapid* Rapid* and weak or absent

Systolic pressure Normal Normal to low Low

Respirations Normal Deep, rate may be Deep, tachypnea or


increased decreased to absent

Buccal mucosa Tacky or slightly dry Dry Parched

Anterior fontanelle Normal Sunken Markedly sunken

Eyes Normal Sunken Markedly sunken

Tears (in infants) Present Decreased Absent

Skin turgor Normal Reduced Tenting

Skin temperature and Normal Cool Cool, mottled, acrocyanosis


appearance

Urine output Normal or mildly reduced Markedly reduced Anuria

Systemic signs Increased thirst Listlessness, irritability Grunting, lethargy, coma

* Tachycardia may be the first sign of hypovolemic shock in infants.

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Acute diarrhea in children

* An acute diarrheal illness is typically defined as a duration of five days or less, but return to normal stool consistency after v
gastroenteritis, the most common etiology in resource-rich regions, may take longer. Diarrhea that has persisted beyond five
may warrant consideration of other diagnoses, especially in children who are ill-appearing, have bloody diarrhea in associatio
weight loss, or other findings suggesting a more serious underlying condition.

¶ More likely in older children and adolescents.

Δ More likely in infants and young children.

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Chronic diarrhea in children

* Symptoms typically >1 month in duration.

¶ More likely in older children and adolescents.

Δ Only in infants.

◊ More likely in infants and young children.

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Contributor Disclosures
Jason Levy, MD, RDMS No relevant financial relationship(s) with ineligible companies to disclose. Stephen J Teach, MD,
MPH Grant/Research/Clinical Trial Support: Novartis [Pediatric asthma]. All of the relevant financial relationships listed have
been mitigated. Teresa K Duryea, MD No relevant financial relationship(s) with ineligible companies to disclose. James F
Wiley, II, MD, MPH No relevant financial relationship(s) with ineligible companies to disclose.

El grupo editorial revisa las divulgaciones de los contribuyentes para detectar conflictos de intereses. Cuando se
encuentran, estos se abordan mediante un proceso de revisión de varios niveles y mediante requisitos de referencias que
se deben proporcionar para respaldar el contenido. Se requiere que todos los autores tengan contenido con las referencias
adecuadas y deben cumplir con los estándares de evidencia de UpToDate.

Política de conflicto de intereses

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