Gastroenteritis in Emergency Medicine 

  • Author: Arthur Diskin, MD; Chief Editor: Steven C Dronen, MD, FAAEM   more...
 
Updated: Mar 19, 2012
 

Background

Gastroenteritis is a nonspecific term for various pathologic states of the gastrointestinal tract. The primary manifestation is diarrhea, but it may be accompanied by nausea, vomiting, and abdominal pain. A universal definition of diarrhea does not exist, although patients seem to have no difficulty defining their own situation. Although most definitions center on the frequency, consistency, and water content of stools, the author prefers defining diarrhea as stools that take the shape of their container.

The severity of illness may vary from mild and inconvenient to severe and life threatening. Appropriate management requires extensive history and assessment and appropriate, general supportive treatment that is often etiology specific. Diarrhea associated with nausea and vomiting is referred to as gastroenteritis.

Diarrhea is one of the most common reasons patients seek medical care. In the developed world, it is one of the most common reasons for missing work, while in the developing world, it is a leading cause of death. In developing countries, diarrhea is a seasonal scourge usually worsened by natural phenomena, as evidenced by monsoon floods in Bangladesh in 1998 or the recent earthquake in Haiti. An estimated 100 million cases of acute diarrhea occur every year in the United States. Of these patients, 90% do not seek medical attention, and only 1-2% require hospital admission. Diarrheal diseases can quickly reach epidemic proportions, rapidly overwhelming public health systems in even the most advanced societies.

Next

Pathophysiology

Infectious agents usually cause acute gastroenteritis. These agents cause diarrhea by adherence, mucosal invasion, enterotoxin production, and/or cytotoxin production.

These mechanisms result in increased fluid secretion and/or decreased absorption. This produces an increased luminal fluid content that cannot be adequately reabsorbed, leading to dehydration and the loss of electrolytes and nutrients.

Diarrheal illnesses may be classified as follows:

  • Osmotic, due to an increase in the osmotic load presented to the intestinal lumen, either through excessive intake or diminished absorption
  • Inflammatory (or mucosal), when the mucosal lining of the intestine is inflamed
  • Secretory, when increased secretory activity occurs
  • Motile, caused by intestinal motility disorders

The small intestine is the prime absorptive surface. The colon then absorbs additional fluid, transforming a relatively liquid fecal stream in the cecum to well-formed solid stool in the rectosigmoid.

Disorders of the small intestine result in increased amounts of diarrheal fluid with a concomitantly greater loss of electrolytes and nutrients.

Microorganisms may produce toxins that facilitate infection. Enterotoxins, generated by some bacteria (ie, enterotoxigenic Escherichia coli, Vibrio cholera) act directly on secretory mechanisms and produce typical, copious watery (rice water) diarrhea. No mucosal invasion occurs. The small intestines are primarily affected, and elevation of the adenosine monophosphate (AMP) levels is the common mechanism.

Cytotoxin production by other bacteria (ie, Shigella dysenteriae, Vibrio parahaemolyticus, Clostridium difficile, enterohemorrhagic E coli) results in mucosal cell destruction that leads to bloody stools with inflammatory cells. A resulting decreased absorptive ability occurs.

Enterocyte invasion is the preferred method by which microbes such as Shigella and Campylobacter organisms and enteroinvasive E coli cause destruction and inflammatory diarrhea. Similarly, Salmonella and Yersinia species also invade cells but do not cause cell death. Hence, dysentery does not usually occur. However, these bacteria invade the bloodstream across the lamina propria and can cause enteric fevers such as typhoid.

Diarrheal illness occurs when microbial virulence overwhelms normal host defenses. A large inoculum may overwhelm the host capacity to mount an effective defense. Normally, more than 100,000 E coli are required to cause disease, while only 10 Entamoeba or Giardia cysts may suffice to do the same. Some organisms (eg, V cholera, enterotoxigenic E coli) produce proteins that aid their adherence to the intestinal wall, thereby displacing the normal flora and colonizing the intestinal lumen. As few as 10 norovirus viral particles may cause disease.

In addition to the ingestion of pathogenic organisms or toxins, other intrinsic factors can lead to infection. An alteration of normal bowel flora can create a biologic void that is filled by pathogens. This occurs most commonly after antibiotic administration, but infants are also at risk prior to colonization with normal bowel flora.

The normally acidic pH of the stomach and colon is an effective antimicrobial defense. In achlorhydric states (ie, caused by antacids, histamine-2 [H2] blockers, gastric surgery, decreased colonic anaerobic flora), this defense is weakened.

Hypomotility states may result in colonization by pathogens, especially in the proximal small bowel, where motility is the major mechanism in the removal of organisms. Hypomotility may be induced by antiperistaltic agents (eg, opiates, diphenoxylate and atropine [Lomotil], loperamide) or anomalous anatomy (eg, fistulae, diverticula, antiperistaltic afferent loops) and is inherent in disorders such as diabetes mellitus or scleroderma.

The immunocompromised host is more susceptible to infection, as evidenced by the wide spectrum of diarrheal pathogens in patients with AIDS.

The exact mechanism of vomiting in acute diarrheal illness is not known, although serotonin release has been postulated as a cause, stimulating visceral afferent input to the chemoreceptor trigger zone in the lower brainstem. Preformed neurotoxins produced by Staphylococcus aureus and Bacillus cereus, when ingested, can cause severe vomiting.

Previous
Next

Epidemiology

Frequency

United States

Frequency is difficult to determine because of underreporting, especially of mild illness, resulting in wide variations of estimated numbers of cases, hospitalizations, and deaths. As many as 100 million cases occur per year with several million healthcare visits and thousands of hospitalizations; children account for more than 1.5 million outpatient visits. It is estimated that the norovirus is responsible for a large percent of GI illnesses in the United States. According to the Centers for Disease Control and Prevention (CDC), probably more than 21 million cases a year and nearly 50% of foodborne outbreaks are caused by norovirus. In Great Britain, it has been known as "winter vomiting disease." Whether the increased incidence of norovirus is real or simply a result of increased awareness, surveillance, and reporting is unclear.

Food and water represent important vehicles for pathogens and are linked to several illnesses that cause gastroenteritis. In 2008, foodborne agents were responsible for 48 million illnesses and 1,034 reported outbreaks in the United States. The following are examples of sporadic common source outbreaks:

  • Gastroenteritis associated with V parahaemolyticus infection from Gulf Coast oysters has been reported.
  • Salmonella gastroenteritis from reptilian pets has been reported.
  • A religious cult in Oregon intentionally contaminated salad with Salmonella typhimurium, which resulted in 751 victims who developed acute gastroenteritis.
  • In July 1998, more than 60 persons in Wyoming were infected with E coli O157:H7 from a contaminated water supply.
  • In 1993, E coli O157:H7–contaminated fast-food hamburger meat in the Pacific Northwest infected 500 persons, 4 of whom died.
  • From 1981-1994, 333 cases of Vibrio vulnificus infection associated with raw oyster consumption were reported in Florida. Two persons died from gastroenteritis, and 50 persons died from septicemia.
  • In January 1995, 322 cases of norovirus, formerly known as Norwalk virus (calicivirus), infection–associated acute gastroenteritis resulted from the consumption of raw oysters in Florida.
  • In October 1996, 629 children and staff members at one elementary school in Florida were infected in a point-source outbreak of norovirus.
  • In July 1995, 77 cases of cryptosporidiosis at a day camp in Florida were reported, most likely secondary to contamination involving a water hose.
  • In April 1994, 96 cases of Campylobacter infection were reported in Florida. The common source was ingested, contaminated commercial ice cubes.
  • In 1996, norovirus–associated gastroenteritis resulted from the ingestion of raw oysters in Louisiana.
  • From May 1996 to June 1996, E coli O157:H7 infections secondary to consumption of mesclun lettuce from a single producer were reported in multiple states (first identified in Connecticut and Illinois).
  • In August and September of 1999, E coli O157:H7 infections secondary to contaminated well water at the Washington County Fair (New York) were reported.
  • In 2002, norovirus was attributed to 9 of the 21 outbreaks of acute gastroenteritis on cruise ships reported to the CDC's Vessel Sanitation Program in this period.
  • While cruise ship outbreaks get the most publicity, norovirus outbreaks have also been reported in various locations including casinos, airplanes, nursing homes, hospitals, amusement parks, camps, military facilities, and schools.
  • In 2005, E coli O157:H7 infections secondary to contaminated animals were reported at Florida fairs.
  • Between January 1996 and November 2000, 348 outbreaks of norovirus were reported to the CDC.
  • Amongst all cruise ship voyages under the auspices of the CDC's Vessel Sanitation Program (VSP), 14 reported outbreaks occurred in 2010 (and an additional 9 have been reported through June 2011).[1] The CDC posts outbreaks as occurring on voyages from 3-21 days, on ships carrying 100 or more passengers in which 3% or more of passengers or crew reported symptoms of diarrheal disease to the ships medical staff during the voyage, and are gastrointestinal illness outbreaks of public health significance.
  • The CDC has a very active Vessel Sanitation Program, which inspects cruise ships and issues scores, with a score of 85 or less being unsatisfactory.[2] These inspections cover issues of food safety, potable and recreational water treatment, outbreak prevention and reporting policies, and pest management programs, amongst other issues.
  • In September 2006, there were 4 cases of botulism associated with commercial carrot juice; all 4 patients were hospitalized. Three individuals were in Georgia and 1 in Florida.
  • In 2008, there were 1,442 infections, 286 hospitalizations, and 2 possible deaths distributed among 43 states and Canada, caused by the uncommonly detected serotype Salmonellasaintpaul. The outbreak was associated with multiple raw produce items, including jalapeño pepper, Serrano pepper, and possibly tomatoes.
  • Between April and August of 2008, an E coli (O157:H7) multistate outbreak associated with contaminated bagged spinach resulted in 205 confirmed illnesses and 3 deaths.
  • Between November 2008 and April 2009, there were 714 cases (9 deaths) of Salmonellatyphimurium reported in 46 states due to contaminated peanut products, such as peanut butter and peanut-containing products, precipitating a major recall of affected products.[3]
  • From May to November 2010, there were approximately 1,939 infections of Salmonellaenteritidis associated with shell eggs among 11 states.
  • In 2010, there were 9 individuals infected with Salmonella t yphi as a result of consuming contaminated frozen mamey fruit pulp in California and Nevada. The product was voluntarily recalled by 2 companies.
  • From November 2010 to February 2011, 140 individuals from 26 states became infected with Salmonella serotype I 4,[5],12:I, linked to the consumption of tiny green alfalfa sprouts or spicy sprouts from a chain restaurant.
  • As of October 2011, 133 people have become ill (including 28 deaths) in multiple states as a result of becoming infected with 4 strains of Listeria monocytogenes from contaminated cantaloupes.

International

There are an estimated 1.5 billion cases of diarrhea that occur yearly, and it is the leading cause of death in many underdeveloped countries. It is the second leading cause of death in children younger than 5 years, taking the lives of approximately 1.5-2 million children each year. Approximately 30-50% of visitors to developing countries develop, and perhaps return with, diarrhea.

In 2001 and 2002, outbreaks of gastroenteritis caused by norovirus were reported in diverse locations such as the American Midwest; Boston; Northern Europe; St. Petersburg, Russia; Canada; and Alaska.

In May 2011, an outbreak originating in Germany and spreading throughout 15 other countries was caused by the unusual shiga-toxin–producing E coli O104:H4, eventually classified as enteroaggregative pathotype. It resulted in over 3,000 cases without the hemolytic-uremic syndrome and more than 900 cases developed hemolytic-uremic syndrome (a very high percentage), with an unusual number of adults affected and a high mortality rate compared with prior shiga-producing E coli strains. In the German outbreak, horizontal genetic exchange appears to have resulted in this unique O104:H4 strain, which has a prophage encoding shiga toxin 2 virulence and antibiotic resistance factors.[4]

Mortality/Morbidity

Estimates for mortality and morbidity widely vary. In the United States, approximately 900,000, including 200,000 pediatric, hospitalizations occur yearly, with as many as 6,000 deaths.[5] Internationally, the mortality rate is 1.4-2.5 million deaths each year.

The CDC reported enteritis deaths more than doubled in the United States, an increase to 17,000 in 2007 from about 7,000 in 1999. Adults over 65 years of age accounted for 83% of deaths. Clostridium difficile (C difficile) and norovirus were the most common infectious causes of gastroenteritis-associated deaths. C difficile was tied to 14,500 of these deaths, up from 2,700 in 1999. Norovirus was associated with about 800 deaths annually, though there were 50% more deaths in years when epidemics were caused by new strains of the virus.[6]

Age

  • Pediatric gastroenteritis is discussed in Pediatrics, Gastroenteritis.
  • Gastroenteritis may occur at any age. Morbidity and mortality are much higher in the very young and the very old.
Previous
 
 
Contributor Information and Disclosures
Author

Arthur Diskin, MD  Vice-President, Global Chief Medical Officer, Royal Caribbean Cruise Lines; Voluntary Associate Professor, University of Miami, Leonard M Miller School of Medicine

Arthur Diskin, MD is a member of the following medical societies: American College of Emergency Physicians

Disclosure: Royal Caribbean Cruise Lines Salary Employment

Specialty Editor Board

Michelle Ervin, MD  Chair, Department of Emergency Medicine, Howard University Hospital

Michelle Ervin, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, National Medical Association, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Eugene Hardin, MD, FAAEM, FACEP  Former Chair and Associate Professor, Department of Emergency Medicine, Charles Drew University of Medicine and Science; Former Chair, Department of Emergency Medicine, Martin Luther King Jr/Drew Medical Center

Disclosure: Nothing to disclose.

John D Halamka, MD, MS  Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center

John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Chief Editor

Steven C Dronen, MD, FAAEM  Chair, Department of Emergency Medicine, LeConte Medical Center

Steven C Dronen, MD, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

References
  1. Centers for Disease Control and Prevention. Vessel Sanitation Program: Cruise Ship Outbreak Updates. Available at http://www.cdc.gov/nceh/vsp/surv/GIlist.htm.

  2. Centers for Disease Control and Prevention. Vessel Sanitation Program: Cruise Ship Inspection. Available at http://wwwn.cdc.gov/InspectionQueryTool/Forms/InspectionSearch.aspx.

  3. Centers for Disease Control and Prevention. Investigation Update: Outbreak of Salmonella Typhimurium Infections, 2008-2009. Available at http://www.cdc.gov/salmonella/typhimurium/update.html.

  4. Rasko DA, Webster DR, Sahl JW, et al. Origins of the E. coli strain causing an outbreak of hemolytic-uremic syndrome in Germany. N Engl J Med. Aug 25 2011;365(8):709-17. [Medline]. [Full Text].

  5. Farthing M, Lindberg G, Dite P, et al. World Gastroenterology Organisation practice guideline: Acute diarrhea. World Gastroenterology Organisation. Available at http://www.worldgastroenterology.org/acute-diarrhea-in-adults.html. Accessed September 2011.

  6. CDC research shows outbreaks linked to imported foods increasing. Available at http://www.cdc.gov/media/releases/2012/p0314_foodborne.html. Accessed March 14, 2012.

  7. Belliot G, Lavaux A, Souihel D, Agnello D, Pothier P. Use of murine norovirus as a surrogate to evaluate resistance of human norovirus to disinfectants. Appl Environ Microbiol. May 2008;74(10):3315-8. [Medline]. [Full Text].

  8. [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].

  9. DuPont HL, Jiang ZD, Okhuysen PC, Ericsson CD, de la Cabada FJ, Ke S, et al. A randomized, double-blind, placebo-controlled trial of rifaximin to prevent travelers' diarrhea. Ann Intern Med. May 17 2005;142(10):805-12. [Medline].

  10. Caeiro JP, DuPont HL. Management of travellers' diarrhoea. Drugs. Jul 1998;56(1):73-81. [Medline].

  11. Centers for Disease Control and Prevention. Outbreaks of gastroenteritis associated with noroviruses on cruise ships--United States, 2002. MMWR Morb Mortal Wkly Rep. Dec 13 2002;51(49):1112-5. [Medline]. [Full Text].

  12. Heymann DL. Control of communicable diseases manual. 19th ed. Washington, DC: American Public Health Association; 2008:258-260, 534-539.

  13. Dolin R. Noroviruses--challenges to control. N Engl J Med. Sep 13 2007;357(11):1072-3. [Medline].

  14. DuPont HL. Clinical practice. Bacterial diarrhea. N Engl J Med. Oct 15 2009;361(16):1560-9. [Medline].

  15. [Guideline] DuPont HL. Guidelines on acute infectious diarrhea in adults. The Practice Parameters Committee of the American College of Gastroenterology. Am J Gastroenterol. Nov 1997;92(11):1962-75. [Medline].

  16. Glass RI, Parashar UD, Estes MK. Norovirus gastroenteritis. N Engl J Med. Oct 29 2009;361(18):1776-85. [Medline].

  17. Gonenne J, Pardi DS. Clostridium difficile: an update. Compr Ther. Fall-Winter 2004;30(3):134-40. [Medline].

  18. [Guideline] Guerrant RL, Van Gilder T, Steiner TS, Thielman NM, Slutsker L, Tauxe RV, et al. Practice guidelines for the management of infectious diarrhea. Clin Infect Dis. Feb 1 2001;32(3):331-51. [Medline].

  19. Health Protection Agency Centre for Infections. Guidance for the Management of Norovirus Infection in Cruise Ships - Norovirus Working Group. Available at http://www.hpa.org.uk/publications/2007/cruiseliners/cruiseliners.pdf.

  20. Hom J. Do probiotics reduce the duration and symptoms of acute infectious diarrhea?. Ann Emerg Med. November 2011;58:445-446.

  21. Musher DM, Musher BL. Contagious acute gastrointestinal infections. N Engl J Med. Dec 2 2004;351(23):2417-27. [Medline].

  22. Seamens CM, Schwartz G. Food-borne illness: differential diagnosis and targeted management. Emerg Med Rep. 1998;19:120-131.

  23. Teitelbaum JE. Probiotics and the treatment of infectious diarrhea. Pediatr Infect Dis J. Mar 2005;24(3):267-8. [Medline].

  24. Thielman NM, Guerrant RL. Clinical practice. Acute infectious diarrhea. N Engl J Med. Jan 1 2004;350(1):38-47. [Medline].

  25. Widdowson MA, Glass R, Monroe S, Beard RS, Bateman JW, Lurie P, et al. Probable transmission of norovirus on an airplane. JAMA. Apr 20 2005;293(15):1859-60. [Medline].

Previous
Next
 
Hektoen enteric agar with Escherichia coli colonies. Different growth media are necessary for identifying different enteric pathogens, suppressing the growth of nonpathogens, and allowing for chemical reactions to assist in identification. The appearance results from the organism's ability to ferment lactose placed in the medium. This results in the production of acid, which lowers the pH and causes a change in the pH indicator placed in the medium. Salmonella and Shigella organisms do not ferment lactose.
Example of Salmonella on Hektoen enteric agar. The medium also contains ferric ammonium citrate, which indicates the production of hydrogen sulfide by the appearance of a black precipitate.
The MacConkey medium is commonly used and differentiates lactose fermenters, which produce acid, decrease the pH, and cause the neutral red indicator to give the colonies a pink-to-red color.
The Christensen method is used to determine if an organism produces the enzyme urease (Yersinia) or not (Salmonella, Shigella, Vibrio). Hydrolysis of urea produces ammonia and carbon dioxide, alkalinizing the medium and turning the phenol red from light orange to magenta (pink).
Often, a combination of methods may be used for identification. The tube on the left is triple sugar iron (TSI) agar. The alkaline slant and acid butt (K/A) indicates an organism that ferments glucose only (not lactose or sucrose). The middle tube is indole positive, as indicated by the pink ring, and indicates the organism's ability to split tryptophan to form indole. The tube on the right is urease negative. Taken together, these tests indicate the organism is likely Shigella.
Gram stain may be helpful in identifying an etiologic agent. This stain shows gram-negative bacilli, which could be Salmonella or Shigella with 2 polymorphonucleocyte cells (PMNs).
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2012 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.

DISCLAIMER: The content of this Website is not influenced by sponsors. The site is designed primarily for use by qualified physicians and other medical professionals. The information contained herein should NOT be used as a substitute for the advice of an appropriately qualified and licensed physician or other health care provider. The information provided here is for educational and informational purposes only. In no way should it be considered as offering medical advice. Please check with a physician if you suspect you are ill.