Diarrhea Follow-up

  • Author: Stefano Guandalini, MD; Chief Editor: Carmen Cuffari, MD   more...
 
Updated: Apr 8, 2010
 

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.

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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.

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Deterrence/Prevention

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

  • In February 2006, the United States Food and Drug Administration (FDA) approved an oral vaccine for rotavirus (RotaTeq). Soon thereafter, the AAP and the Advisory Committee on Immunization Practices (ACIP) recommended RotaTeq to be part of regularly scheduled childhood immunizations. RotaTeq is administered in a 3-dose series starting between age 6-12 weeks and completing before 32 weeks. An older rotavirus vaccine (RotaShield) was associated with an increased incidence of intussusception and is no longer on the market, but RotaTeq did not show an increased risk compared with placebo in clinical trials.
  • In April 2008, the FDA approved Rotarix, another oral vaccine, for prevention of rotavirus gastroenteritis. The current recommendation is to administer 2 separate doses of Rotarix to patients aged 6-24 weeks. Rotarix was efficacious in a large study, which reported that Rotarix protected patients with severe rotavirus gastroenteritis and decreased the rate of severe diarrhea or gastroenteritis of any cause.[7]
  • A study that involved over 63,000 patients who received Rotarix or placebo at age 2 months and at age 4 months reported a decreased risk of intussusception in patients who received Rotarix.[7] The intussusception data was determined over a 31-day observation period (inpatient or outpatient) after each dose of the Rotarix vaccine; this also included a 100-day surveillance period for all serious adverse events. Although more patients who received Rotarix were observed to have seizures or pneumonia-related deaths, this link has not been directly established to Rotarix. However, on March 22, 2010, the FDA recommended the temporary discontinuation of its use, pending further studies on the reported presence of an apparently benign pig virus in the Rotarix vaccine.
  • The Salmonella typhi vaccine is recommended for travelers to countries with a high risk of this infection, persons with intimate exposure to a documented typhoid fever carrier, and workers with frequent exposure to this bacteria. Live-attenuated, killed whole-cell, and capsular polysaccharide vaccines are available.
  • The Vibrio species vaccine is available but only protects 50% of immunized persons for 3-6 months. It is not indicated for use.
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Complications

Common complications include the following:

  • Aeromonas caviae - Intussusception, gram-negative sepsis, hemolytic-uremic syndrome (HUS)
  • Campylobacter species -Bacteremia, meningitis, cholecystitis, urinary tract infection, pancreatitis, Reiter syndrome (RS)
  • C difficile - Chronic diarrhea
  • C perfringens serotype C - Enteritis necroticans
  • Enterohemorrhagic E coli - Hemorrhagic colitis
  • Enterohemorrhagic E coli O157:H7 - HUS
  • Plesiomonas species - Septicemia
  • Salmonella species - Seizures, HUS, perforation, RS
  • Vibrio species - Rapid dehydration
  • Y enterocolitica - Appendicitis, perforation, intussusception, peritonitis, toxic megacolon, cholangitis, bacteremia, RS
  • Rotavirus - Isotonic dehydration, carbohydrate intolerance
  • Giardia species - Chronic fat malabsorption
  • Cryptosporidium species - Chronic diarrhea
  • Entamoeba species - Colonic perforation, liver abscess

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.

  • After diarrhea caused by Salmonella organisms, 1-4% of individuals with nontyphoid and enteric fever infections become carriers. The carrier stage for Salmonella organisms is more likely for females, infants, and individuals with biliary tract disease.
  • Asymptomatic C difficile carriage may be observed in as many as 20% of hospitalized patients receiving antibiotics and in 50% of infants.
  • Rotavirus is excreted asymptomatically in feces of children who were previously infected, typically for as long as 1-2 weeks.
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Prognosis

In developed countries, with proper management, prognosis is very good.

  • 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.
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Patient Education

Education is most important for prevention and treatment. Proper ORT prevents dehydration, and early refeeding speeds recovery of intestinal mucosa. With caregiver, emphasize proper hygiene and food preparation practices to prevent future infections and spread.

For excellent patient education resources, visit eMedicine's Esophagus, Stomach, and Intestine Center. Also, see eMedicine's patient education articles Irritable Bowel Syndrome, Inflammatory Bowel Disease, and Diarrhea.

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Contributor Information and Disclosures
Author

Stefano Guandalini, MD  Director, University of Chicago Celiac Disease Program, Section Chief of Gastroenterology, Hepatology and Nutrition; Professor, Department of Pediatrics, University of Chicago Comer Children's Hospital

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

Disclosure: Nothing to disclose.

Coauthor(s)

Richard E Frye, MD, PhD  Assistant Professor, Departments of Pediatrics and Neurology, University of Texas Health Science Center at Houston

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

Disclosure: Nothing to disclose.

M Akram Tamer, MD  Program Director, Professor, Department of Pediatrics, University of Miami

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

Disclosure: Nothing to disclose.

Specialty Editor Board

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

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

Disclosure: Nothing to disclose.

Mary L Windle, PharmD  Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Pharmacy Editor, eMedicine

Disclosure: Nothing to disclose.

Steven M Schwarz, MD, FAAP, FACN, AGAF  Professor of Pediatrics, Children's Hospital at Downstate, SUNY-Downstate Medical Center

Steven M Schwarz, MD, FAAP, FACN, AGAF is a member of the following medical societies: American Academy of Pediatrics, American College of Nutrition, American College of Physician Executives, American Gastroenterological Association, American Pediatric Society, Gastroenterology Research Group, New York Academy of Medicine, North American Society for Pediatric Gastroenterology and Nutrition, and Society for Pediatric Research

Disclosure: TAP Pharmaceuticals Honoraria Speaking and teaching; Curemark, LLC Consulting fee Board membership; Centocor, Inc. Grant/research funds Independent contractor; Johnson & Johnson, 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

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, and Royal College of Physicians and Surgeons of Canada

Disclosure: Nothing to disclose.

References
  1. 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].

  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. [Medline].

  3. 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].

  4. [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].

  5. Guandalini S. Probiotics for children with diarrhea: an update. J Clin Gastroenterol. Jul 2008;42 Suppl 2:S53-7. [Medline].

  6. Guandalini S. Probiotics for children with diarrhea: an update. J Clin Gastroenterol. Jul 2008;42 Suppl 2:S53-7. [Medline].

  7. [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].

  8. 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].

  9. 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].

  10. 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].

  11. 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].

  12. 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].

  13. 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].

  14. Guandalini S. Treatment of acute diarrhea in the new millennium. J Pediatr Gastroenterol Nutr. May 2000;30(5):486-9. [Medline].

  15. Guandalini S, Dincer AP. Nutritional management in diarrhoeal disease. Baillieres Clin Gastroenterol. Dec 1998;12(4):697-717. [Medline].

  16. 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.

  17. 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].

  18. Sullivan PB. Nutritional management of acute diarrhea. Nutrition. Oct 1998;14(10):758-62. [Medline].

  19. [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].

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Table 1. Stool Characteristics and Determining Their Source
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
Table 2. Organisms and Frequency of Symptoms
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
Table 3. Common Bacteria and Optimum Culture Mediums
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
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