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Diarrhea

  • Author: Stefano Guandalini, MD; Chief Editor: Carmen Cuffari, MD  more...
 
Updated: Aug 19, 2015
 

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:

  • Stool characteristics (eg, consistency, color, volume, frequency)
  • Presence of associated enteric symptoms (eg, nausea/vomiting, fever, abdominal pain)
  • Use of child daycare (common pathogens: rotavirus, astrovirus, calicivirus; Campylobacter, Shigella, Giardia, and Cryptosporidium species [spp])
  • Food ingestion history (eg, raw/contaminated foods, food poisoning)
  • Water exposure (eg, swimming pools, marine environment)
  • Camping history (possible exposure to contaminated water sources)
  • Travel history (common pathogens affect specific regions; also consider rotavirus and Shigella, Salmonella, and Campylobacter spp regardless of specific travel history, as these organisms are prevalent worldwide)
  • Animal exposure (eg, young dogs/cats: Campylobacter spp; turtles: Salmonella spp)
  • Predisposing conditions (eg, hospitalization, antibiotic use, immunocompromised state)

Signs and symptoms of diarrhea may include the following:

  • Dehydration: Lethargy, depressed consciousness, sunken anterior fontanel, dry mucous membranes, sunken eyes, lack of tears, poor skin turgor, delayed capillary refill
  • Failure to thrive and malnutrition: Reduced muscle/fat mass or peripheral edema
  • Abdominal pain/cramping
  • Borborygmi
  • Perianal erythema

See Clinical Presentation for more detail.

Diagnosis

Fecal laboratory studies include the following:

  • Examination for ova and parasites
  • Leukocyte count
  • pH level: A pH level of 5.5 or less or the presence of reducing substances indicates carbohydrate intolerance, which is usually secondary to viral illness
  • Examination of exudates for presence/absence of leukocytes
  • Cultures: Always culture for Salmonella, Shigella, and Campylobacter spp and Y enterocolitica in the presence of clinical signs of colitis or if fecal leukocytes are present; look for Clostridium difficile in those with diarrhea characterized by colitis and/or bloody stools; assess for Escherichia coli, particularly O157:H7, with bloody diarrhea and a history of eating ground beef; screen for Vibrio and Plesiomonas spp with a history of eating raw seafood or foreign travel
  • Enzyme immunoassay for rotavirus or adenovirus antigens
  • Latex agglutination assay for rotavirus

Other laboratory studies may include the following:

  • Serum albumin levels: Low in protein-losing enteropathies from enteroinvasive intestinal infections (eg, Salmonella spp, enteroinvasive E coli)
  • Fecal alpha1-antitrypsin levels: High in enteroinvasive intestinal infections
  • Anion gap to determine nature of the diarrhea (ie, osmolar vs secretory)
  • Intestinal biopsy: 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)

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:

  • Cefixime
  • Ceftriaxone
  • Cefotaxime
  • Erythromycin
  • Furazolidone
  • Iodoquinol
  • Metronidazole
  • Paromomycin
  • Quinacrine
  • Sulfamethoxazole and trimethoprim
  • Vancomycin
  • Tetracycline
  • Nitazoxanide
  • Rifaximin

See Treatment and Medication for more detail.

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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.

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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.

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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.

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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.

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Contributor Information and Disclosures
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

Stefano Guandalini, MD is a member of the following medical societies: American Gastroenterological Association, North American Society for Pediatric Gastroenterology, Hepatology and Nutrition, European Society for Paediatric Gastroenterology, Hepatology & Nutrition, North American Society for the Study of Celiac Disease

Disclosure: Received consulting fee from AbbVie for consulting.

Coauthor(s)

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

Richard E Frye, MD, PhD is a member of the following medical societies: American Academy of Neurology, Child Neurology Society, International Neuropsychological Society, American Academy of Pediatrics

Disclosure: Nothing to disclose.

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

M Akram Tamer, MD is a member of the following medical societies: American Medical Association, Florida Medical Association

Disclosure: Nothing to disclose.

Specialty Editor Board

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.

Chief Editor

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

Carmen Cuffari, MD is a member of the following medical societies: American College of Gastroenterology, American Gastroenterological Association, North American Society for Pediatric Gastroenterology, Hepatology and Nutrition, Royal College of Physicians and Surgeons of Canada

Disclosure: Received honoraria from Prometheus Laboratories for speaking and teaching; Received honoraria from Abbott Nutritionals for speaking and teaching.

Additional Contributors

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

Chris A Liacouras, MD is a member of the following medical societies: American Gastroenterological Association

Disclosure: Nothing to disclose.

References
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Table 1. Stool Characteristics and Determining Their Source
Stool Characteristics Small Bowel Large Bowel
Appearance Watery Mucoid and/or bloody
Volume Large Small
Frequency Increased Highly increased
Blood Possibly positive but never gross blood Commonly grossly bloody
pH Possibly < 5.5 >5.5
Reducing substances Possibly positive Negative
WBCs < 5/high power field Commonly >10/high power field
Serum WBCs Normal Possible leukocytosis, bandemia
Organisms Viral
  • 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
Table 2. Organisms and Frequency of Symptoms
Organism Incubation Duration Vomiting Fever Abdominal Pain
Rotavirus 1-7 d 4-8 d Yes Low No
Adenovirus 8-10 d 5-12 d Delayed Low No
Norovirus 1-2 d 2 d Yes No No
Astrovirus 1-2 d 4-8 d +/- +/- No
Calicivirus 1-4 d 4-8 d Yes +/- No
Aeromonas species None 0-2 wk +/- +/- No
Campylobacter species 2-4 d 5-7 d No Yes Yes
C difficile Variable Variable No Few Few
C perfringens Minimal 1 d Mild No Yes
Enterohemorrhagic E coli 1-8 d 3-6 d No +/- Yes
Enterotoxigenic E coli 1-3 d 3-5 d Yes Low Yes
Plesiomonas species None 0-2 wk +/- +/- +/-
Salmonella species 0-3 d 2-7 d Yes Yes Yes
Shigella species 0-2 d 2-5 d No High Yes
Vibrio species 0-1 d 5-7 d Yes No Yes
Y enterocolitica None 1-46 d Yes Yes Yes
Giardia species 2 wk 1+ wk No No Yes
Cryptosporidium species 5-21 d Months No Low Yes
Entamoeba species 5-7 d 1-2+ wk No Yes No
Table 3. Dehydration Severity, Signs, and Symptoms
Hydration 0-5% Dehydration



(Mild)



5-10% Dehydration



(Moderate)



10% or More



(Severe)



General Well Restless Lethargic
Eyes Normal Sunken Very sunken
Tears Present Absent Absent
Mouth Moist Dry Very dry
Thirst Drinks normally Thirsty Drinks poorly
Skin Pinch retracts immediately Pinch retracts slowly Pinch stays folded
Table 4. Common Bacteria and Optimum Culture Mediums
Organism Detection Method Microbiologic Characteristics
Aeromonas species Blood agar Oxidase-positive flagellated gram-negative bacillus (GNB)
Campylobacter species Skirrow agar Rapidly motile curved gram-negative rod (GNR); Campylobacter jejuni 90% and Campylobacter coli 5% of infections
C difficile Cycloserine-cefoxitin-fructose-egg (CCFE) agar; enzyme immunoassay (EIA) for toxin; latex agglutination (LA) for protein Anaerobic spore-forming gram-positive rod (GPR); toxin-mediated diarrhea; produces pseudomembranous colitis
C perfringens None available Anaerobic spore-forming GPR; toxin-mediated diarrhea
E coli MacConkey eosin-methylene blue (EMB) or Sorbitol-MacConkey (SM) agar Lactose-producing GNR
Plesiomonas species Blood agar Oxidase-positive GNR
Salmonella species Blood, MacConkey EMB, xylose-lysine-deoxycholate (XLD), or Hektoen enteric (HE) agar Nonlactose non–H2S-producing GNR
Table 5. Probiotic Efficacy in Diarrhea
Condition Patients and Controls Most-Studied Probiotics Evidence of Efficacy



(- to +++)



Prevention of Daycare Diarrhea 2000 Lactobacillus GG



Bifidobacterium lactis



Lactobacillus reuteri



Lactobacillus casei



Bifidobacterium bifidum + Streptococcus thermophilus



+
Prevention of Nosocomial Diarrhea 1000 Lactobacillus GG ++
Prevention of Antibiotic-Associated Diarrhea 2000 Lactobacillus GG



Saccharomyces boulardii



+++
Infectious Diarrhea 3500 Lactobacillus GG



Saccharomyces boulardii



+++
Persistent Diarrhea 460 Lactobacillus GG +
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