Background
Acute diarrhea is defined as the abrupt onset of abnormally high fluid content in the stool: more than the normal value of approximately 10 mL/kg/d in the infant and young child, and more than 200 g/d in the teenager and adult. This situation typically implies an increased frequency of bowel movements, which can range from 4-5 to more than 20 times per day. The augmented water content in the stools 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; however, numerous disorders may cause this condition, 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); 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.
Epidemiology
Frequency
United States
In the United States, one estimate assumes a cumulative incidence of 1 hospitalization for diarrhea per 23-27 children by age 5 years, with more than 50,000 hospitalizations in 2000. By these estimates, rotavirus is associated with 4-5% of all childhood hospitalizations, and 1 in 67 to 1 in 85 children are hospitalized due to rotavirus by age 5 years. 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.
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. 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 few 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.
Furthermore, in countries where 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.
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.
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. [Medline].
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. [Medline].
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. [Medline].
[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. [Medline].
Guandalini S. Probiotics for children with diarrhea: an update. J Clin Gastroenterol. Jul 2008;42 Suppl 2:S53-7. [Medline].
Guandalini S. Probiotics for children with diarrhea: an update. J Clin Gastroenterol. Jul 2008;42 Suppl 2:S53-7. [Medline].
[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. [Medline]. [Full Text].
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. [Medline].
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. [Medline]. [Full Text].
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. [Medline].
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. [Medline].
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. [Medline].
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. [Medline].
Guandalini S. Treatment of acute diarrhea in the new millennium. J Pediatr Gastroenterol Nutr. May 2000;30(5):486-9. [Medline].
Guandalini S, Dincer AP. Nutritional management in diarrhoeal disease. Baillieres Clin Gastroenterol. Dec 1998;12(4):697-717. [Medline].
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.
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. [Medline].
Sullivan PB. Nutritional management of acute diarrhea. Nutrition. Oct 1998;14(10):758-62. [Medline].
[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. [Medline].
| 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
| Invasive bacteria
|
Enterotoxigenic bacteria
| Toxic bacteria
| |
Parasites
| Parasites
|
| 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 |
| 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 |

