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Pediatric Gastroenteritis
Gilberto Rivera-Dominguez; Gabriel Castano; Lakmal S. Ekanayake; Amandeep Goyal.
Author Information
Last Update: July 22, 2019.

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Introduction
Gastroenteritis in the pediatric population is a very common disease that could be lethal. It
accounts for around 10% of pediatric deaths, estimating 70 million deaths per year around
the globe making it the second cause of death worldwide. The most common cause in infants
younger than 24 months old is rotavirus, after 24 months of age, Shigella displaces it to
second most common.[1][2][3]
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Etiology
Gastroenteritis occurs when there is a fecal-oral contact, ingestion of contaminated water or
food and person to person, been this the most common way of acquiring this infection and
making it the main cause for norovirus and shigella outbreaks. This disease is associated with
bad hygiene and poverty.[4][5]
In the United States, rotavirus and noroviruses (accountable for almost 58% of all cases) are
the most common viral agent that causes diarrhea, followed by enteric
adenoviruses, Sapovirus, and astroviruses.
The main risk factors for gastroenteritis are environmental, seasonal, and demographics,
being you children more susceptible. Other diseases like measles and immunodeficiencies
put the patient at a higher risk for a gastrointestinal (GI) infection. Malnutrition is another
significant risk factor, like vitamin-A deficiency or zinc deficiency.
Most of the episodes are acute diarrheas, lasting less than one week. When diarrhea lasts
more than 14 days, it is considered persistent diarrhea and accounts for 3% to 19% of
episodes. Around 50% of death cases due to diarrhea.
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Epidemiology
Children under 5 years of age are the most affected population, and the diarrheal episodes
happen more frequently in Asia and Africa, accounting for 80% of annual incidence.[6]
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Pathophysiology
The pathophysiology depends on the organism causing the disease. It can caused by toxins
like Staphylococcus aureus, while others increase secretion leading to dehydration, for
example, Salmonella. Cytotoxins like Shigella and Clostridium difficile can invade the more
susceptible tissue and cause inflammatory diarrhea. Enterotoxin production agents cause
noninflammatory diarrhea; the virus frequently destroys the villus surface, and parasites
adhere to the mucosa.
In the case of inflammatory diarrhea, there are fluid, proteins, and leukocytes entering the
interstitial lumen. Viruses like adenovirus can directly invade the microvillus or through
calcium-dependent endocytosis, causing the loss in the ability to absorb.
On a molecular level, agents affect the interstitial lumen by activating enterocyte intracellular
signal transduction, affecting the cytoskeleton of the host cells. This will alter the water and
electrolyte fluxes across the enterocytes. For toxic diarrhea, there is an increase of cAMP and
inhibition of NaCl abortion. When infiltration occurs, there is histologic damage that will
reduce glucose, stimulated Na, and electroneutral NaCl absorption.
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History and Physical

The clinical manifestations will be related to the pathogen. Ingestion of toxins (S. aureus)
can lead to rapid onset of nausea and vomiting within 6 hours of digestion. Patients may have
fever, cramps, and diarrhea within 8 to 72 hours.
Enterotoxins like Clostridium perfringens and Bacillus cereus cause watery diarrhea within 8
to 16 hours of ingestion. Viral infections are associated with cramps and watery diarrhea
after 16 to 48 hours. There are some pathogens that are related to bloody diarrhea. These
agents can cause symptoms up to 120 hours after ingestion. Some agents can cause
manifestations within minutes, for example, copper, shellfish toxins, tin, and other seafood
(puffer fish) through tetrodotoxin or scombroid with histamine release.
Overall symptomatology is not the best way to narrow a possible etiology. Fever is not
always present; although, this does not mean that there is no infection. The positive
predictive value of dysentery is reduced as well. In the suspicion of acute gastroenteritis,
appropriate laboratory testing is needed if the healthcare professional needs to verify the
causative agent.
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Evaluation
An evaluation with a proper clinical history is essential for every disease. Specific to a
gastroenteritis episode is a history of contact, child-care attendance, travel, and exposure.
Despite non-specific symptomatology, healthcare professionals can still narrow their options
by correctly analyzing the symptoms. For example, nausea and vomiting indicate upper
intestine; fever suggests inflammation (tissue invasion, dehydration or coinfection). Severe
abdominal pain and tenesmus indicate large intestine involvement. The presence of nausea,
vomiting with absent fever, periumbilical pain, and watery diarrhea suggest a non-serious
small intestine infection.[7][8][9][10]
Patients with diarrhea have the risk of dehydration; initial evaluation is to identify the
presence and severity. Addressing the level of acidosis can provide valuable information to
determine if fluid resuscitation is needed and if it should be oral or intravenous.
Microscopic stool examination and culture can narrow the causative agent. Mucus, blood or
leukocytes may indicate the agent. The problem with this technique is that there can be false
negatives at the early stage of the disease. Therefore, an XTAG GPP panel that is FDA
approved uses multiplex nucleic acid technology that can detect C. difficile, toxin
A/B, Campylobacter, Escherichia coli, Shigella and Shiga-like
toxins, Salmonella, Rotavirus, Norovirus, Giardia, and Cryptosporidium.
Cultures should be done as promptly as possible in children that present leukocytes in the
microscopic evaluation and have bloody diarrhea. Also, patients that are immunosuppressed
should get a culture. This now is done with (PCR).
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Treatment / Management
Overall, treatment and management of children with acute gastroenteritis involve rehydration
(oral or IV), diet selection, zinc supplementation, and additional therapies like probiotics.
IV rehydration is needed in babies under 6 months, patients with chronic illness, prematurity,
fever above 38 C (100.4 F) if younger than 3 months, or between 3 months and 36 months if
the patient has more than 39 C (102.2 F). Persistent emesis, bloody diarrhea, altered mental
status (consciousness) sunken eyes, and decrease urine output are also red flags that may lead
the clinician to consider giving the patient IV fluids.[11][12][13]
The treatment of choice is a low-osmolarity fluid, with 75 mEq of Na, 64 mEq of Cl, 20 mEq
of K and 75 mmol of glucose per liter, the total osmolarity should be 245 mOsm/L. In mild
to moderate emesis, give ondansetron (4 mg for children 4 to 11 years, and double the doses
for older children) is often considered for better oral rehydration. IV rehydration is done with
a lactated ringer or normal saline in 20 mL/Kg body weight.
Antibiotics are considered in certain situations. They may result in the reduction of severity
and duration, even the prevention of some complications like the spread infection. Among
the most used antibiotics are ciprofloxacin, TMP-SMX, erythromycin, and metronidazole.
However, antibiotics should be avoided when the following causative agents are
known: Bacillus cereus, Clostridium, and some Salmonella species.
The use of probiotics has not yet been scientifically proven to assist in the recovery or the
symptomatology; studies have been inconclusive. It is believed that when the illness is
caused by C. difficile, antibiotics might prevent diarrhea, and in the case of rotavirus,
antibiotics could cause a reduction in the diarrheal duration. Antispasmodic agents like
loperamide are contraindicated in children presenting dysentery.
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Differential Diagnosis
When diagnosing acute gastroenteritis there are several differential etiological agents to
consider:
 Norovirus, Rotavirus
 Shigella
 Hepatitis A
 Listeria
 Clostridium
 S. Aureus
 V. Cholerae
 Giardia
 E. Coli
 Campylobacter
 Ciliary dysentery
 Typhoid fever
 Vibriosis
 Yersiniosis
 C. Difficile
Proctitis can also be another differential diagnosis that can be caused by Gonococcus, herpes
simplex, Chlamydia, and Syphilis for example.
Other syndromes to consider are necrotizing enterocolitis, chronic inflammatory processes
like parasites, Crohn's, ischemic colitis, and allergic enteritis.
There are also noninfectious illnesses that can lead to GI infection: arsenic, cadmium,
copper, mercury, pesticides, and zinc.
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Prognosis
Prognosis and complications are directly related to access to care and treatment.
Go to:
Enhancing Healthcare Team Outcomes
The diagnosis and management of pediatric gastroenteritis requires an interprofessional team
that includes an emergency department physician, pediatrician, infectious disease nurse, and
an internist. Unlike adults, children are frail and do not tolerate dehydration well. The key,
therefore, is hydration. Children with severe dehydration and are febrile need to be admitted.
Depending on the cause, the child may require an antibiotic.
The outcomes of pediatric gastroenteritis depend on the severity of the diarrhea and time to
treat. Children who have delayed treatment can develop multiorgan failure, leading to death.
There are not many options when it comes to treatment in the active set of gastroenteritis, but
there are some measurements that can help prevent this disease. In newborns, exclusive
breastfeeding for the first 6 months prevents diarrheal episodes. There are also studies that
show vitamin-A supplementation reduces mortality in a diarrheal episode up to 30%. Other
more well-known measurements are the rotavirus vaccine and the ingestion of clean water
and food.[14][2]
Go to:

Questions
To access free multiple choice questions on this topic, click here.
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References
1.

Yang WC, Chang YJ, Lin YC, Chen CY, Peng YC, Wu HP. Survey of nil per os duration of
patients admitted to the emergency department due to vomiting. Medicine
(Baltimore). 2019 Apr;98(14):e15087. [PMC free article] [PubMed]

2.

Muhsen K, Kassem E, Rubenstein U, Goren S, Ephros M, Shulman LM, Cohen D. No

evidence of an increase in the incidence of norovirus gastroenteritis hospitalizations
in young children after the introduction of universal rotavirus immunization in
Israel. Hum Vaccin Immunother. 2019;15(6):1284-1293. [PMC free article] [PubMed]

3.

Koutri E, Papadopoulou A. Eosinophilic Gastrointestinal Diseases in Childhood. Ann.

Nutr. Metab. 2018;73 Suppl 4:18-28. [PubMed]
4.

Jeffs E, Williman J, Martin N, Brunton C, Walls T. The epidemiology of non-viral

gastroenteritis in New Zealand children from 1997 to 2015: an observational
study. BMC Public Health. 2019 Jan 05;19(1):18. [PMC free article] [PubMed]

5.

Neu J, Pammi M. Necrotizing enterocolitis: The intestinal microbiome, metabolome

and inflammatory mediators. Semin Fetal Neonatal Med. 2018 Dec;23(6):400-
405. [PubMed]

6.

Simwaka JC, Mpabalwani EM, Seheri M, Peenze I, Monze M, Matapo B, Parashar UD,
Mufunda J, Mphahlele JM, Tate JE, Mwenda JM. Diversity of rotavirus strains
circulating in children under five years of age who presented with acute
gastroenteritis before and after rotavirus vaccine introduction, University Teaching
Hospital, Lusaka, Zambia, 2008-2015. Vaccine. 2018 Nov 12;36(47):7243-
7247. [PubMed]

7.

Lo Vecchio A, Buccigrossi V, Fedele MC, Guarino A. Acute Infectious Diarrhea. Adv.

Exp. Med. Biol. 2019;1125:109-120. [PubMed]

8.

Raval MV, Kwan AB, Travers CD, Heiss KF. Importance of Compliance Audits for a
Pediatric Complicated Appendicitis Clinical Practice Guideline. J Med Syst. 2018 Nov
07;42(12):257. [PubMed]

9.

Guarino A, Lo Vecchio A, Dias JA, Berkley JA, Boey C, Bruzzese D, Cohen MB, Cruchet
S, Liguoro I, Salazar-Lindo E, Sandhu B, Sherman PM, Shimizu T. Universal
Recommendations for the Management of Acute Diarrhea in Nonmalnourished
Children. J. Pediatr. Gastroenterol. Nutr. 2018 Nov;67(5):586-593. [PubMed]

10.
 Cohen R, Raymond J, Gendrel D. Antimicrobial treatment of diarrhea/acute
gastroenteritis in children. Arch Pediatr. 2017 Dec;24(12S):S26-S29. [PubMed]

11.

Grigsby A, Herron J, Hunter BR. Does the addition of dextrose to IV crystalloid

therapy provide clinical benefit in acute dehydration? A systematic review and meta-
analysis. CJEM. 2019 Sep;21(5):638-645. [PubMed]

12.

Romano C, Dipasquale V, Scarpignato C. Antiemetic Drug Use in Children: What the

Clinician Needs to Know. J. Pediatr. Gastroenterol. Nutr. 2019 Apr;68(4):466-
471. [PubMed]

13.

Freedman SB, Williamson-Urquhart S, Farion KJ, Gouin S, Willan AR, Poonai N, Hurley
K, Sherman PM, Finkelstein Y, Lee BE, Pang XL, Chui L, Schnadower D, Xie J, Gorelick
M, Schuh S., PERC PROGUT Trial Group. Multicenter Trial of a Combination Probiotic
for Children with Gastroenteritis. N. Engl. J. Med. 2018 Nov 22;379(21):2015-
2026. [PubMed]

Copyright © 2020, StatPearls Publishing LLC.

This book is distributed under the terms of the Creative Commons Attribution 4.0 International License

(http://creativecommons.org/licenses/by/4.0/), which permits use, duplication, adaptation, distribution, and reproduction in

any medium or format, as long as you give appropriate credit to the original author(s) and the source, a link is provided to

the Creative Commons license, and any changes made are indicated.

Bookshelf ID: NBK499939PMID: 29763114

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 In this Page
 Introduction
 Etiology
 Epidemiology
 Pathophysiology
 History and Physical
 Evaluation
 Treatment / Management
 Differential Diagnosis
 Prognosis
 Enhancing Healthcare Team Outcomes
 Questions
 References

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