Diarrhea

Back

Practice Essentials

Diarrhea is the reversal of the normal net absorptive status of water and electrolyte absorption to secretion. The augmented water content in the stools (above the normal value of approximately 10 mL/kg/d in the infant and young child, or 200 g/d in the teenager and adult) is due to an imbalance in the physiology of the small and large intestinal processes involved in the absorption of ions, organic substrates, and thus water.

Essential update: Children with diarrhea may benefit from green tea and pomegranate extract

Research conducted in a community clinic in Nicaragua demonstrates that green tea and pomegranate extract combined with a standard oral rehydration solution help children with diarrhea improve faster.[1]

The study involved 61 children, 2 to 17 years of age, who had uncontrolled diarrhea in the previous 48 hours. All patients received an oral rehydration solution for 2 days. In addition, 30 patients received the extract on day 1. The remaining 31 children, serving as the control group, received the extract on day 2. Researchers observed patients in the first 24 hours and rated their bowel movements on the Bristol Stool Scale (BSS).

Results showed the average time to achieve a BSS score of 4 or less was significantly shorter in the extract group than in the control group (3.1 vs 9.2 hours; P = .002).

In addition, a BSS score of 4 or less in the first bowel movement after treatment was achieved by more patients in the extract group than the control group (60% vs 29%). BSS scores in the extract group were maintained on day 2.[1]

Signs and symptoms

Acute diarrhea is defined as the abrupt onset of 3 or more loose stools per day and lasts no longer than 14 days; chronic or persistent diarrhea is defined as an episode that lasts longer than 14 days. The distinction has implications not only for classification and epidemiologic studies but also from a practical standpoint, because protracted diarrhea often has different etiologies, poses different management problems, and has a different prognosis.

The clinical presentation and course of diarrhea therefore depend on its cause and on the host. Consider the following to determine the source/cause of the patient’s diarrhea:

Signs and symptoms of diarrhea may include the following:

See Clinical Presentation for more detail.

Diagnosis

Fecal laboratory studies include the following:

Other laboratory studies may include the following:

See Workup for more detail.

Management

Acute-onset diarrhea is usually self-limited; however, an acute infection can have a protracted course. Management is generally supportive: In most cases, the best option for treatment of acute-onset diarrhea is the early use of oral rehydration therapy (ORT).[2]

Pharmacotherapy

Vaccines (eg, rotavirus) can help increase resistance to infection. Antimicrobial and antiparasitic agents may be used to treat diarrhea caused by specific organisms and/or clinical circumstances. Such medications include the following:

See Treatment and Medication for more detail.

Background

Acute diarrhea is defined as the abrupt onset of 3 or more loose stools per day. The augmented water content in the stools (above the normal value of approximately 10 mL/kg/d in the infant and young child, or 200 g/d in the teenager and adult) is due to an imbalance in the physiology of the small and large intestinal processes involved in the absorption of ions, organic substrates, and thus water. A common disorder in its acute form, diarrhea has many causes and may be mild to severe.

Childhood acute diarrhea is usually caused by infection of the small and/or large intestine; however, numerous disorders may result in diarrhea, including a malabsorption syndrome and various enteropathies. Acute-onset diarrhea is usually self-limited; however, an acute infection can have a protracted course. By far, the most common complication of acute diarrhea is dehydration.

Although the term "acute gastroenteritis" is commonly used synonymously with "acute diarrhea," the former term is a misnomer. The term gastroenteritis implies inflammation of both the stomach and the small intestine, whereas, in reality, gastric involvement is rarely if ever seen in acute diarrhea (including diarrhea with an infectious origin); in addition, enteritis is also not consistently present. Examples of infectious acute diarrhea syndromes that do not cause enteritis include Vibrio cholerae– induced diarrhea and Shigella -induced diarrhea. Thus, the term acute diarrhea is preferable to acute gastroenteritis.

Diarrheal episodes are classically distinguished into acute and chronic (or persistent) based on their duration. Acute diarrhea is thus defined as an episode that has an acute onset and lasts no longer than 14 days; chronic or persistent diarrhea is defined as an episode that lasts longer than 14 days. The distinction, supported by the World Health Organization (WHO), has implications not only for classification and epidemiological studies but also from a practical standpoint because protracted diarrhea often has a different set of causes, poses different problems of management, and has a different prognosis.

Pathophysiology

Diarrhea is the reversal of the normal net absorptive status of water and electrolyte absorption to secretion. Such a derangement can be the result of either an osmotic force that acts in the lumen to drive water into the gut or the result of an active secre­tory state induced in the enterocytes. In the former case, diarrhea is osmolar in nature, as is observed after the ingestion of nonabsorbable sugars such as lactulose or lactose in lactose malabsorbers. Instead, in the typical active secretory state, enhanced anion secretion (mostly by the crypt cell compartment) is best exemplified by enterotoxin-­induced diarrhea.

In osmotic diarrhea, stool output is proportional to the intake of the unabsorbable substrate and is usually not massive; diarrheal stools promptly regress with discontinuation of the offending nutrient, and the stool ion gap is high, exceeding 100 mOsm/kg. In fact, the fecal osmolality in this circumstance is accounted for not only by the electrolytes but also by the unabsorbed nutrient(s) and their degradation products. The ion gap is obtained by subtracting the concentration of the elec­trolytes from total osmolality (assumed to be 290 mOsm/kg), according to the formula: ion gap = 290 – [(Na + K) × 2].

In secretory diarrhea, the epithelial cells’ ion transport processes are turned into a state of active secretion. The most common cause of acute-onset secretory diarrhea is a bacterial infection of the gut. Several mechanisms may be at work. After colonization, enteric pathogens may adhere to or invade the epithelium; they may produce enterotoxins (exotoxins that elicit secretion by increasing an intracellular second messenger) or cytotoxins. They may also trigger release of cytokines attracting inflammatory cells, which, in turn, contribute to the acti­vated secretion by inducing the release of agents such as prostaglandins or platelet-activating factor. Features of secretory diarrhea include a high purg­ing rate, a lack of response to fasting, and a normal stool ion gap (ie, 100 mOsm/kg or less), indicating that nutrient absorption is intact.

Frequency

United States

In the United States, one estimate before the introduction of specific antirotavirus immunization in 2006 assumed a cumulative incidence of 1 hospitalization for diarrhea per 23-27 children by age 5 years, with more than 50,000 hospitalizations. By these estimates, rotavirus was associated with 4-5% of all childhood hospitalizations and a cost of nearly $ 1 billion.[3] Furthermore, acute diarrhea is responsible for 20% of physician referrals in children younger than 2 years and for 10% in children younger than 3 years.

The impact of vaccination on rotavirus morbidity has been remarkable, with significant reduction of diarrhea-associated hospitalizations and visits to emergency departments in children in the years 2007-2008 compared with the prevaccine period.[4]

International

In developing countries, an average of 3 episodes per child per year in children younger than 5 years is reported; however, some areas report 6-8 episodes per year per child. In these settings, malnutrition is an important additional risk factor for diarrhea, and recurrent episodes of diarrhea lead to growth faltering and substantially increased mortality.[5] Childhood mortality associated with diarrhea has constantly but slowly declined during the past 2 decades, mostly because of the widespread use of oral rehydration solutions; however, it appears to have plateaued over the past several years.

Because the single most common cause of infectious diarrhea worldwide is rotavirus, and because a vaccine has been in use for over 3 years now, a reduction in the overall frequency of diarrheal episodes is hoped for in the near future.

Mortality/Morbidity

Mortality from acute diarrhea is overall globally declining but remains high. Most estimates have diarrhea as the second cause of childhood mortality, with 18% of the 10.6 million yearly deaths in children younger than age 5 years.

Despite a progressive reduction in global diarrheal disease mortality over the past 2 decades, diarrhea morbidity in published reports from 1990-2000 slightly increased worldwide compared with previous reports. In the United States, an average of 369 diarrhea-associated deaths/year occurred among children aged 1-59 months during 1992-1998 and 2005-2006.[6] The vast majority of diarrhea-associated infant deaths were reported in 2005-2007, with 86% of deaths occurring among low-birthweight (< 2500 g) infants.[7]

Furthermore, in countries in which the toll of diarrhea is highest, poverty also adds an enormous additional burden, and long-term consequences of the vicious cycle of enteric infections, diarrhea, and malnutrition are devastating.[5]

Sex

Most cases of infectious diarrhea are not sex specific. Females have a higher incidence of Campylobacter species infections and hemolytic uremic syndrome (HUS).

Age

Viral diarrhea is most common in young children. Rotavirus and adenovirus are particularly prevalent in children younger than 2 years. Astrovirus and norovirus usually infect children younger than 5 years. Yersinia enterocolitis typically infects children younger than 1 year, and the Aeromonas organism is a significant cause of diarrhea in young children.

Very young children are particularly susceptible to secondary dehydration and secondary nutrient malabsorption. Age and nutritional status appear to be the most important host factors in determining the severity and the duration of diarrhea. In fact, the younger the child, the higher is the risk for severe, life-threatening dehydration as a result of the high body-water turnover and limited renal compensatory capacity of very young children. Whether younger age also means a risk of run­ning a prolonged course is an unsettled issue. In developing countries, persis­tent postenteritis diarrhea has a strong inverse correlation with age.

History

Acute diarrhea in developed countries is almost invariably a benign, self-limited condition, subsiding within a few days. The clinical presentation and course of illness depend on the etiology of the diarrhea and on the host. For example, rotavirus is more commonly associated with vomiting, dehydration, and a greater number of work days lost than nonrotavirus gastroenteritis.

Table 1. Stool Characteristics and Determining Their Source


View Table

See Table

Table 2. Organisms and Frequency of Symptoms


View Table

See Table

Physical

The following may be observed:

Table 3. Dehydration Severity, Signs, and Symptoms


View Table

See Table

Causes

Although infectious agents are by far the most common cause for sporadic or endemic episodes of acute diarrhea, one should not dismiss other causes that can lead to the same presentation.

Laboratory Studies

The following may be noted in patients with diarrhea:

Table 4. Common Bacteria and Optimum Culture Mediums


View Table

See Table

Other Tests

Because the pathogenesis of diarrhea can be either osmolar (due to the presence of an excess of unabsorbed substrates in the gut lumen) or secretory (due to active anion secretion from the enterocytes), the anion gap in the stools is occasionally used to ascertain the nature of the diarrhea. The stool anion gap is calculated according to the formula: 290 - [(Na+K) X 2]. If the value is more than 100, osmolar diarrhea can be assumed to be present. If the value is less than 100, the diarrhea has a secretory origin.

Procedures

Intestinal biopsy is not required in evaluating an otherwise healthy child with acute-onset diarrhea, but it may be indicated in the presence of chronic or protracted diarrhea, as well as in cases in which a search for a cause is believed to be mandatory (eg, in patients with acquired immunodeficiency syndrome [AIDS] or patients who are otherwise severely immunocompromised).

Medical Care

In 2003 the Center for Disease Control (CDC) put forth recommendations for the management of acute pediatric diarrhea in both the outpatient and inpatient settings including indication for referral.[2]

Indications for medical evaluation of children with acute diarrhea include the following:

The report also includes information on assessment of dehydration and what steps should be taken to adequately treat acute diarrhea.

Treatment of dehydration due to diarrhea includes the following:

ORT is the cornerstone of treatment, especially for small-bowel infections that produce a large volume of watery stool output. ORT with a glucose-based oral rehydration syndrome must be viewed as by far the safest, most physiologic, and most effec­tive way to provide rehydration and maintain hydration in children with acute diarrhea worldwide, as recommended by the WHO; by the ad hoc committee of European Society for Pediatric Gastroenterology, Hepatology and Nutrition (ESPGHAN); and by the American Academy of Pediatrics.[9] However, the global use of ORT is still insufficient. Developed countries, in particular the United States, seem to be lagging behind despite studies that demonstrate beyond doubt the efficacy of ORT in emergency care settings, in which intravenous rehydration unduly continues to be widely privileged.

Not all commercial ORT formulas promote optimal absorption of electrolytes, water, and nutrients. The ideal solution has a low osmolarity (210-250) and a sodium content of 50-60 mmol/L. Administer maintenance fluids plus replacement of losses. Educate caregivers in methods necessary to replace this amount of fluid. Administer small amounts of fluid at frequent intervals to minimize discomfort and vomiting. A 5-mL or 10-mL syringe without a needle is a very useful tool. The syringe can be quickly used to place small amounts of fluid in the mouth of a child who is uncooperative. Once the child becomes better hydrated, cooperation improves enough to take small sips from a cup. This method is time intensive and requires a dedicated caregiver. Encouragement from the physician is necessary to promote compliance. Oral rehydration is now universally recommended to be completed within 4 hours.

The addition of zinc to oral rehydration solution has been proven effective in children with acute diarrhea in developing countries and is recommended by the WHO.[10] However, no evidence suggests efficacy in children living in developed countries, in which the prevalence of zinc deficiency is assumed to be extremely low.

The composition of almost all other beverages (carbonated or not) that are commercially available and frequently used in children with diarrhea is completely inadequate for rehydration or for maintaining hydration, considering the sodium content, which is invariably extremely low, and osmolarity that is often dangerously elevated. For instance, Coca-Cola, Pepsi-Cola, and apple juice have an osmolarity of 493, 576, and 694-773, respectively.

At completion of hydration, resumption of feeding is strongly recommended. In fact, many studies convincingly demonstrate that early refeeding hastens recovery. Also, robust evidence suggests that, in the vast majority of episodes of acute diarrhea, refeeding can be accomplished without the use of any special (eg, lactose-free or soy-based) formulas.

Antimotility agents are not indicated for infectious diarrhea, except for refractory cases of Cryptosporidium infection. Antimicrobial therapy is indicated for some nonviral diarrhea because most is self-limiting and does not require therapy.

Therapies recommended for some nonviral diarrheas include the following:

Consultations

Diet

Breastfed infants with acute diarrhea should be continued on breast milk without any need for interruption. In fact, breastfeeding not only has a well-known protective effect against the development of enteritis, it also promotes faster recovery and provides improved nutrition. This is even more important in developing countries, where with­drawal of breastfeeding during diarrhea has been shown to have a deleterious effect on the development of dehydra­tion in infants with acute watery diarrhea.

Medication Summary

Diarrheal diseases have been the object of numerous forms of treatment, both dietetic and pharmacologic, for centuries. However, the evidence is now clear that, in most cases, the best option for treatment of acute-onset diarrhea is the early use of oral rehydration therapy (ORT).[2] Pharmacological treatment is rarely of any use, and antidiarrheal drugs are often harmful.

In terms of recommended antimicrobial treatment in the immunocompetent host, enteric bacterial and protozoan pathogens can be grouped as follows:

Agents for whom antimicrobial therapy is always indicated: The consensus includes only V cholerae, Shigella species, and G lamblia.

Agents for whom antimi­crobial therapy is indicated only in selected circumstances, include the following:

Probiotics

Recently, some strains of probiotics (defined as live microorganisms that when ingested in adequate doses, provide a benefit to the host) have been found to be effective as an adjunct when treating children with acute diarrhea. Data from well-conducted randomized controlled trials on efficacy of probiotics in children with diarrhea are definitely positive. They consistently show a statistically significant benefit and moderate clinical benefit of a few, now well-identified probiotic strains (mostly Lactobacillus GG and Saccharomyces boulardii but also Lactobacillus reuteri) in the treatment of acute watery diarrhea (primarily rotaviral) in infants and young children in developed countries.

Such a beneficial effect seems to result in a reduction of the duration of diarrhea of about one day and seems to be exerted mostly on rotaviral diarrhea, with much less evidence of efficacy in invasive bacterial diarrhea. The effect is not only strain-dependent but also dose-dependent, with doses of at least 5 billion/d being required for effect.[11] Shortening the duration of diarrhea by one day may not appear to be hugely beneficial. However, in consideration of the high morbidity of the infection, even a reduction of this order is indeed desirable because it affords considerable savings in terms of loss of working days and direct health costs.

Furthermore, probiotics may reduce the risk of spreading rotavirus infection by shortening diarrhea duration and volume of watery stool output and by reducing the fecal shedding of rotavirus, and they have been found useful in preventing the dissemination of hospital-acquired diarrheas.

A recent position paper jointly published by the ESPGHAN and the European Society for Pediatric Infectious Disease (ESPID) stated, ‘‘Probiotics may be an effective adjunct to the management of diarrhea. However, because there is no evidence of efficacy for many preparations, we suggest the use of probiotic strains with proven efficacy and in appropriate doses for the management of children with acute gastroenteritis as an adjunct to rehydration therapy (II, B). The following probiotics showed benefit in meta-analyses of randomized controlled trials: Lactobacillus GG (I, A) and S boulardii (II, B).’’

Table 5 illustrates current assessment of the efficacy of probiotics in conditions characterized by diarrhea.

Table 5. Probiotic Efficacy in Diarrhea


View Table

See Table

Cefixime (Suprax)

Clinical Context:  Potent long-acting oral cephalosporin with increased gram-negative coverage. Inhibits bacterial cell wall synthesis by binding to 1 or more PBPs. Bacteria eventually lyse because of ongoing activity of cell wall autolytic enzymes while cell wall assembly is arrested.

Ceftriaxone (Rocephin)

Clinical Context:  A third-generation cephalosporin antibiotic with activity against gram-positive and some gram-negative bacteria. Binds to PBPs, inhibiting bacterial cell wall growth.

Cefotaxime (Claforan)

Clinical Context:  Third-generation cephalosporin antibiotic with activity against gram-positive and some gram-negative bacteria. Binds to PBPs, inhibiting bacterial cell wall growth.

Erythromycin (E.E.S., E-Mycin, Eryc, Ery-Tab, Erythrocin)

Clinical Context:  Bacteriostatic macrolide with activity against most gram-positive organisms and atypical respiratory organisms. Useful for Campylobacter species and vibrio enteritis.

Furazolidone (Furoxone)

Clinical Context:  Antiparasitic agent with wide coverage. Nitrofuran with antiprotozoal activity. Alternative drug for children because availability in liquid suspension. Most common adverse effects are GI upset and brown discoloration of urine.

Iodoquinol (Vytone, Yodoxin)

Clinical Context:  Antiparasitic agents with wide coverage.

Metronidazole (Flagyl)

Clinical Context:  Very active against Giardia species, gram-negative anaerobes, and Entamoeba species. Imidazole ring-based antibiotic active against various anaerobic bacteria and protozoa. Often used in combination with other antimicrobial agents except for C difficile enterocolitis).

Paromomycin (Humatin)

Clinical Context:  Amebicidal and antibacterial aminoglycoside obtained from a strain of Streptomyces rimosus, active in intestinal amebiasis. Recommended for treatment of Diphyllobothrium latum, Taenia saginata, T solium, Dipylidium caninum, and Hymenolepis nana.

Quinacrine (Atabrine)

Clinical Context:  Very effective antiparasitic against Giardia species.

Sulfamethoxazole and trimethoprim (Bactrim, Septra, Cotrim)

Clinical Context:  Folate-synthesis blocker with wide antibiotic coverage. Inhibits bacterial growth by inhibiting synthesis of dihydrofolic acid. Effective in E coli infections. Dosage form contains 5:1 ratio of sulfamethoxazole to trimethoprim.

Vancomycin (Vancocin)

Clinical Context:  Effective treatment (when PO) for antibiotic-associated colitis due to C difficile. However, reserve for individuals whose symptoms are not responding to less expensive and almost equally effective metronidazole.

Tetracycline (Sumycin)

Clinical Context:  Treats gram-positive and gram-negative organisms as well as mycoplasmal, chlamydial, and rickettsial infections. Good agent in older children who present with severe Yersinia species infection.

Nitazoxanide (Alinia)

Clinical Context:  Inhibits growth of C parvum sporozoites and oocysts and G lamblia trophozoites. Elicits antiprotozoal activity by interfering with pyruvate-ferredoxin oxidoreductase (PFOR) enzyme-dependent electron transfer reaction, which is essential to anaerobic energy metabolism. Available as a 20-mg/mL oral susp.

Rifaximin (Xifaxan, RedActiv, Flonorm)

Clinical Context:  Nonabsorbed (< 0.4%), broad-spectrum antibiotic specific for enteric pathogens of the gastrointestinal tract (ie, Gram-positive, Gram-negative, aerobic and anaerobic). Rifampin structural analog. Binds to beta-subunit of bacterial DNA-dependent RNA polymerase, thereby inhibiting RNA synthesis. Indicated for E coli (enterotoxigenic and enteroaggregative strains) associated with travelers' diarrhea.

Class Summary

Antimicrobial agents, in addition to the immune system, help destroy offending organisms. Their use is confined to specific etiologies and/or clinical circumstances.

Rotavirus vaccine (RotaTeq, Rotarix)

Clinical Context:  Currently, 2 PO administered live-virus vaccines are marketed in the United States. Both are indicated to prevent rotavirus gastroenteritis, a major cause of severe diarrhea in infants.

RotaTeq is a pentavalent vaccine that contains 5 live reassortant rotaviruses and is administered as a 3-dose regimen against G1, G2, G3, and G4 serotypes, the 4 most common rotavirus group A serotypes. It also contains attachment protein P1A (genotype P[8]).

Rotarix protects against rotavirus gastroenteritis caused by G1, G3, G4, and G9 strains and is administered as a 2-dose series in infants aged 6-24 wk.

Clinical trials found that the vaccines prevented 74-78% of all rotavirus gastroenteritis cases, nearly all severe rotavirus gastroenteritis cases, and nearly all hospitalizations.

Class Summary

These agents elicit active immunization to increase resistance to infection. Vaccines consist of microorganisms or cellular components, which act as antigens. Administration of the vaccine stimulates the production of antibodies with specific protective properties.

Further Inpatient Care

Admit neonates or young infants with moderate dehydration, suspected infection with enterohemorrhagic E coli, or bloody diarrhea.

Oral rehydration therapy (ORT) is the universally recommended form of treatment, proven to be successful even in children who vomit or have mild-to-moderate dehydration. Admit a child with severe dehydration. Also, ORT requires vigilance. If the caregiver cannot comply with protocol, consider admission.

Further Outpatient Care

Follow-up care depends on the severity of diarrhea and the child's age. Uncomplicated diarrhea in a school-aged child may not require follow-up care if the caregiver is reliable and has quick access to a physician. Closely monitor young children to ensure that complications do not occur. Closely monitor children who require labor-intensive ORT. Neonates require strict follow-up care within a few days of illness to ensure that malabsorption and dehydration do not occur.

Deterrence/Prevention

Vaccines are indicated for persons with high risk of exposure to some pathogens.

Complications

Common complications include the following:

Enteric fever is caused by S typhi. This syndrome has an insidious onset of malaise, fever, abdominal pain, and bradycardia. Diarrhea and rash (rose spots) appear after 1 week of symptoms. Bacteria may have disseminated at that time, and treatment is required to prevent systemic complications such as hepatitis, myocarditis, cholecystitis, or GI bleeding.

HUS is caused by damage to vascular endothelial cells by verotoxin (released by enterohemorrhagic E coli and by Shigella organisms). Thrombocytopenia, microangiopathic hemolytic anemia, and acute renal failure characterize HUS. Symptoms usually develop one week after onset of diarrhea, when the organism may be absent.

RS can complicate acute infections and is characterized by arthritis, urethritis, conjunctivitis, and mucocutaneous lesions. Individuals with RS usually do not demonstrate all features.

Carrier states are observed after some bacterial infections.

Prognosis

In developed countries, with proper management, prognosis is very good. However, data show an increase in diarrhea-associated deaths among US children from the mid-1980s through 2006. During 2005-2007, 1087 diarrhea-associated infant deaths were reported with 86% of deaths occurring among low birthweight (< 2500g) infants. Risk factors for these infants included male sex, black race, and low 5-minute Apgar score (< 7).[7]

Death is caused predominantly by dehydration and secondary malnutrition from a protracted course. Severe dehydration must be managed with parenteral fluids. Once malnutrition from secondary malabsorption begins, prognosis turns grim unless the patient is hospitalized and supplemental parenteral nutrition is started. Neonates and young infants are at particular risk of dehydration, malnutrition, and malabsorption syndromes.

Even though the mortality rate is low in developed countries, children can die from complications; however, prognosis for children in countries without modern medical care and children with comorbid conditions is more guarded.

Author

Stefano Guandalini, MD, Founder and Medical Director, Celiac Disease Center, Chief, Section of Pediatric Gastroenterology, Hepatology and Nutrition, Department of Pediatrics, University of Chicago Medical Center; Professor, Department of Pediatrics, Section of Gastroenterology, Hepatology and Nutrition, University of Chicago Division of the Biological Sciences, The Pritzker School of Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

M Akram Tamer, MD, Professor, Program Director, Department of Pediatrics, University of Miami, Leonard M Miller School of Medicine

Disclosure: Nothing to disclose.

Richard E Frye, MD, PhD, Associate Professor, Department of Pediatrics, University of Arkansas for Medical Sciences

Disclosure: Nothing to disclose.

Specialty Editors

Chris A Liacouras, MD, Director of Pediatric Endoscopy, Division of Gastroenterology and Nutrition, Children's Hospital of Philadelphia; Associate Professor of Pediatrics, University of Pennsylvania School of Medicine

Disclosure: Nothing to disclose.

Mary L Windle, PharmD, Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Steven M Schwarz, MD, FAAP, FACN, AGAF, Professor of Pediatrics, Children's Hospital at Downstate, State University of New York Downstate Medical Center

Disclosure: Curemark, LLC Consulting fee Board membership; Centocor, Inc. Grant/research funds Independent contractor

Chief Editor

Carmen Cuffari, MD, Associate Professor, Department of Pediatrics, Division of Gastroenterology/Nutrition, Johns Hopkins University School of Medicine

Disclosure: Prometheus Laboratories Honoraria Speaking and teaching; Abbott Nutritionals Honoraria Speaking and teaching

References

  1. Kling J. Green Tea and Pomegranate Extract Help Fight Diarrhea in Children. Medscape Medical News. Available at http://www.medscape.com/viewarticle/833747. Accessed October 24, 2014.
  2. King CK, Glass R, Bresee JS, Duggan C. Managing acute gastroenteritis among children: oral rehydration, maintenance, and nutritional therapy. MMWR Recomm Rep. Nov 21 2003;52:1-16. [View Abstract]
  3. Fischer TK, Viboud C, Parashar U, Malek M, Steiner C, Glass R, et al. Hospitalizations and deaths from diarrhea and rotavirus among children < 5 years of age in the United States, 1993-2003. J Infect Dis. Apr 15 2007;195(8):1117-25. [View Abstract]
  4. Cortese MM, Tate JE, Simonsen L, Edelman L, Parashar UD. Reduction in gastroenteritis in United States children and correlation with early rotavirus vaccine uptake from national medical claims databases. Pediatr Infect Dis J. Jun 2010;29(6):489-94. [View Abstract]
  5. Talbert A, Thuo N, Karisa J, Chesaro C, Ohuma E, Ignas J, et al. Diarrhoea complicating severe acute malnutrition in kenyan children: a prospective descriptive study of risk factors and outcome. PLoS One. 2012;7(6):e38321. [View Abstract]
  6. Esposito DH, Holman RC, Haberling DL, Tate JE, Podewils LJ, Glass RI, et al. Baseline estimates of diarrhea-associated mortality among United States children before rotavirus vaccine introduction. Pediatr Infect Dis J. Nov 2011;30(11):942-7. [View Abstract]
  7. Mehal JM, Esposito DH, Holman RC, Tate JE, Sinden LL, Parashar UD. Risk Factors for Diarrhea-Associated Infant Mortality in the United States, 2005-2007. Pediatr Infect Dis J. Mar 9 2012;[View Abstract]
  8. Vernacchio L, Vezina RM, Mitchell AA, Lesko SM, Plaut AG, Acheson DW. Diarrhea in American infants and young children in the community setting: incidence, clinical presentation and microbiology. Pediatr Infect Dis J. Jan 2006;25(1):2-7. [View Abstract]
  9. Guarino A, Albano F, Ashkenazi S, et al. European Society for Paediatric Gastroenterology, Hepatology, and Nutrition/European Society for Paediatric Infectious Diseases evidence-based guidelines for the management of acute gastroenteritis in children in Europe: executive summary. J Pediatr Gastroenterol Nutr. May 2008;46(5):619-21. [View Abstract]
  10. [Guideline] Atia AN, Buchman AL. Oral rehydration solutions in non-cholera diarrhea: a review. Am J Gastroenterol. Oct 2009;104(10):2596-604; quiz 2605. [View Abstract]
  11. Guandalini S. Probiotics for prevention and treatment of diarrhea. J Clin Gastroenterol. Nov 2011;45 Suppl:S149-53. [View Abstract]
  12. [Best Evidence] Ruiz-Palacios GM, Perez-Schael I, Velazquez FR, et al. Safety and efficacy of an attenuated vaccine against severe rotavirus gastroenteritis. N Engl J Med. Jan 5 2006;354(1):11-22. [View Abstract]
  13. Soares-Weiser K, MacLehose H, Bergman H, Ben-Aharon I, Nagpal S, Goldberg E, et al. Vaccines for preventing rotavirus diarrhoea: vaccines in use. Cochrane Database of Systematic Reviews. 2012.
  14. Abubakar I, Aliyu SH, Arumugam C, Usman NK, Hunter PR. Treatment of cryptosporidiosis in immunocompromised individuals: systematic review and meta-analysis. Br J Clin Pharmacol. Apr 2007;63(4):387-93. [View Abstract]
  15. Barclay L. Zinc supplements reduce diarrhea in children. Medscape Medical News [serial online]. May 15, 2014;Accessed May 28, 2014. Available at http://www.medscape.com/viewarticle/825203
  16. Bellemare S, Hartling L, Wiebe N, et al. Oral rehydration versus intravenous therapy for treating dehydration due to gastroenteritis in children: a meta-analysis of randomised controlled trials. BMC Med. Apr 15 2004;2:11. [View Abstract]
  17. Bryce J, Boschi-Pinto C, Shibuya K, Black RE,. WHO estimates of the causes of death in children. Lancet. Mar 26-Apr 1 2005;365(9465):1147-52. [View Abstract]
  18. Charles MD, Holman RC, Curns AT, et al. Hospitalizations associated with rotavirus gastroenteritis in the United States, 1993-2002. Pediatr Infect Dis J. Jun 2006;25(6):489-93. [View Abstract]
  19. Coffin SE, Elser J, Marchant C, et al. Impact of acute rotavirus gastroenteritis on pediatric outpatient practices in the United States. Pediatr Infect Dis J. Jul 2006;25(7):584-9. [View Abstract]
  20. Girard MP, Steele D, Chaignat CL, Kieny MP. A review of vaccine research and development: human enteric infections. Vaccine. Apr 5 2006;24(15):2732-50. [View Abstract]
  21. Guandalini S. Treatment of acute diarrhea in the new millennium. J Pediatr Gastroenterol Nutr. May 2000;30(5):486-9. [View Abstract]
  22. Guandalini S, Dincer AP. Nutritional management in diarrhoeal disease. Baillieres Clin Gastroenterol. Dec 1998;12(4):697-717. [View Abstract]
  23. Guandalini S, Kahn S. Acute diarrhea. In: Walker A, Goulet O, Kleinman J, et al eds. Pediatric Gastrointestinal Disease. Vol 1. Ontario, Canada: Brian C. Decker; 2008:252-64/Chapter 15.
  24. Matson DO, Staat MA, Azimi P, Itzler R, Bernstein DI, Ward RL, et al. Burden of rotavirus hospitalisations in young children in three paediatric hospitals in the United States determined by active surveillance compared to standard indirect methods. J Paediatr Child Health. Apr 25 2012;[View Abstract]
  25. Mayo-Wilson E, Junior JA, Imdad A, Dean S, Chan XH, Chan ES, et al. Zinc supplementation for preventing mortality, morbidity, and growth failure in children aged 6 months to 12 years of age. Cochrane Database Syst Rev. May 15 2014;5:CD009384. [View Abstract]
  26. Miller RC, Petereit DG, Sloan JA, et al. A phase III randomized study of sulfasalazine versus placebo in the prevention of acute diarrhea in patients receiving pelvic radiation therapy [abstract LBA2]. Presented at American Society for Radiation Oncology (ASTRO) 55th Annual Meeting; September 22, 2013; Atlanta, Georgia.
  27. Mulcahy N. Recommended drug may cause diarrhea with radiation. October 3, 2013. Medscape Medical News. Available at http://www.medscape.com/viewarticle/812057. Accessed October 7, 2013.
  28. Sandhu BK, Isolauri E, Walker-Smith JA, et al. A multicentre study on behalf of the European Society of Paediatric Gastroenterology and Nutrition Working Group on Acute Diarrhoea. Early feeding in childhood gastroenteritis. J Pediatr Gastroenterol Nutr. May 1997;24(5):522-7. [View Abstract]
  29. Sullivan PB. Nutritional management of acute diarrhea. Nutrition. Oct 1998;14(10):758-62. [View Abstract]
  30. [Guideline] Walker-Smith JA, Sandhu BK, Isolauri E, et al. Guidelines prepared by the ESPGAN Working Group on Acute Diarrhoea. Recommendations for feeding in childhood gastroenteritis. European Society of Pediatric Gastroenterology and Nutrition. J Pediatr Gastroenterol Nutr. May 1997;24(5):619-20. [View Abstract]
Stool CharacteristicsSmall BowelLarge Bowel
AppearanceWateryMucoid and/or bloody
VolumeLargeSmall
FrequencyIncreasedHighly increased
BloodPossibly positive but never gross bloodCommonly grossly bloody
pHPossibly < 5.5>5.5
Reducing substancesPossibly positiveNegative
WBCs< 5/high power fieldCommonly >10/high power field
Serum WBCsNormalPossible leukocytosis, bandemia
OrganismsViral
  • Rotavirus
  • Adenovirus
  • Calicivirus
  • Astrovirus
  • Norovirus
Invasive bacteria
  • Escherichia Coli (enteroinvasive, enterohemorrhagic)
  • Shigella species
  • Salmonella species
  • Campylobacter species
  • Yersinia species
  • Aeromonas species
  • Plesiomonas species
Enterotoxigenic bacteria
  • E coli
  • Klebsiella
  • Clostridium perfringens
  • Cholera species
  • Vibrio species
Toxic bacteria
  • Clostridium difficile
Parasites
  • Giardia species
  • Cryptosporidium species
Parasites
  • Entamoeba organisms
OrganismIncubationDurationVomitingFeverAbdominal Pain
Rotavirus1-7 d4-8 dYesLowNo
Adenovirus8-10 d5-12 dDelayedLowNo
Norovirus1-2 d2 dYesNoNo
Astrovirus1-2 d4-8 d+/-+/-No
Calicivirus1-4 d4-8 dYes+/-No
Aeromonas speciesNone0-2 wk+/-+/-No
Campylobacter species2-4 d5-7 dNoYesYes
C difficileVariableVariableNoFewFew
C perfringensMinimal1 dMildNoYes
Enterohemorrhagic E coli1-8 d3-6 dNo+/-Yes
Enterotoxigenic E coli1-3 d3-5 dYesLowYes
Plesiomonas speciesNone0-2 wk+/-+/-+/-
Salmonella species0-3 d2-7 dYesYesYes
Shigella species0-2 d2-5 dNoHighYes
Vibrio species0-1 d5-7 dYesNoYes
Y enterocoliticaNone1-46 dYesYesYes
Giardia species2 wk1+ wkNoNoYes
Cryptosporidium species5-21 dMonthsNoLowYes
Entamoeba species5-7 d1-2+ wkNoYesNo
Hydration0-5% Dehydration

(Mild)

5-10% Dehydration

(Moderate)

10% or More

(Severe)

GeneralWellRestlessLethargic
EyesNormalSunkenVery sunken
TearsPresentAbsentAbsent
MouthMoistDryVery dry
ThirstDrinks normallyThirstyDrinks poorly
SkinPinch retracts immediatelyPinch retracts slowlyPinch stays folded
OrganismDetection MethodMicrobiologic Characteristics
Aeromonas speciesBlood agarOxidase-positive flagellated gram-negative bacillus (GNB)
Campylobacter speciesSkirrow agarRapidly motile curved gram-negative rod (GNR); Campylobacter jejuni 90% and Campylobacter coli 5% of infections
C difficileCycloserine-cefoxitin-fructose-egg (CCFE) agar; enzyme immunoassay (EIA) for toxin; latex agglutination (LA) for proteinAnaerobic spore-forming gram-positive rod (GPR); toxin-mediated diarrhea; produces pseudomembranous colitis
C perfringensNone availableAnaerobic spore-forming GPR; toxin-mediated diarrhea
E coliMacConkey eosin-methylene blue (EMB) or Sorbitol-MacConkey (SM) agarLactose-producing GNR
Plesiomonas speciesBlood agarOxidase-positive GNR
Salmonella speciesBlood, MacConkey EMB, xylose-lysine-deoxycholate (XLD), or Hektoen enteric (HE) agarNonlactose non–H2S-producing GNR
ConditionPatients and ControlsMost-Studied ProbioticsEvidence of Efficacy

(- to +++)

Prevention of Daycare Diarrhea2000Lactobacillus GG

Bifidobacterium lactis

Lactobacillus reuteri

Lactobacillus casei

Bifidobacterium bifidum + Streptococcus thermophilus

+
Prevention of Nosocomial Diarrhea1000Lactobacillus GG++
Prevention of Antibiotic-Associated Diarrhea2000Lactobacillus GG

Saccharomyces boulardii

+++
Infectious Diarrhea3500Lactobacillus GG

Saccharomyces boulardii

+++
Persistent Diarrhea460Lactobacillus GG+