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Emergent Treatment of Gastroenteritis

  • Author: Arthur Diskin, MD; Chief Editor: Steven C Dronen, MD, FAAEM  more...
Updated: Jan 02, 2015


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 earthquake in Haiti in 2010. An estimated 179 million cases of acute gastroenteritis occur every year in the United States.[1] Of these patients, 80-85% 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.



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,Giardia cysts, or norovirus particles 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.

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.




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 179 million cases occur per year with several million healthcare visits and thousands of hospitalizations; children account for more than 1.5 million outpatient visits of which nearly 1 million are associated with norovirus.[2]

It is estimated that the norovirus is responsible for a large percent of GI illnesses in the United States and possibly worldwide. One contributing factor to its frequency is the mutability of its genome[3] and another is the low minimal infective dose. 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 confirmed to be caused by norovirus or norovirus was the only suspected etiology. 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.

Acute gastroenteritis outbreaks have been associated with many modes of transmission, including foodborne, waterborne, person-to-person, animal contact, and environmental. Food and water represent important vehicles for pathogens and are linked to several illnesses that cause gastroenteritis. In 2009 alone, foodborne agents were responsible for 13,497 illnesses from 668 reported outbreaks in the United States. There were 2,259 reported acute gastroenteritis outbreaks attributed to person-to-person transmission in the United States between 2009 and 2010. Among the reported settings, nursing homes and other long-term care facilities ranked most common, followed by childcare settings, hospitals, and schools.[1]

Public vomit incidents have also been known to be a source of transmission of acute gastroenteritis in outbreaks, in particular those caused by norovirus. In fact, studies demonstrate that norovirus particles can travel up to 3 meters during such incidents.

The following are examples of outbreaks that have occurred over the years:

  • Gastroenteritis associated with V parahaemolyticus infection from Gulf Coast oysters has been reported.
  • A religious cult in Oregon intentionally contaminated salad with Salmonella typhimurium, which resulted in 751 victims who developed acute gastroenteritis.
  • 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 1993, E coli O157:H7–contaminated fast-food hamburger meat in the Pacific Northwest infected 500 persons, 4 of whom died.
  • In April 1994, 96 cases of Campylobacter infection were reported in Florida. The common source was contaminated commercial ice cubes.
  • 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 July 1995, 77 cases of cryptosporidiosis at a day camp in Florida were reported, most likely secondary to contamination involving a water hose.
  • 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 October 1996, 629 children and staff members at one elementary school in Florida were infected in a point-source outbreak of norovirus.
  • In July 1998, more than 60 persons in Wyoming were infected with E coli O157:H7 from a contaminated water supply.
  • 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 2005, E coli O157:H7 infections secondary to contaminated animals were reported at Florida fairs.
  • After Hurricane Katrina struck the Gulf Coast in September 2005, an evacuation site in Houston, Texas reported 1,169 cases of acute gastroenteritis; of 44 stool samples tested by reverse transcription-polymerase chain reaction, norovirus was confirmed in 22.
  • 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 Salmonella saintpaul. 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 Salmonella typhimurium reported in 46 states due to contaminated peanut products, such as peanut butter and peanut-containing products, precipitating a major recall of affected products.
  • From May to November 2010, there were approximately 1,939 infections of Salmonella enteritidis 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, 147 people had become ill (including 28 deaths) in multiple states as a result of becoming infected with 4 strains of Listeria monocytogenes from contaminated cantaloupes.
  • In April 2012, 14 individuals became ill with norovirus after consuming contaminated oysters in a restaurant in New Orleans. Oysters were harvested off the Louisiana coast; the shellfish harvesting zone was closed for 3 weeks.
  • One individual spread norovirus to 7 others through contamination of a reusable grocery bag in Washington state.
  • In January 2012, 90 individuals in Indiana became ill with norovirus after eating at a chain restaurant where an infected food handler reported to work. All 6 stool samples collected from employees resulted positive for norovirus. Of the 90 ill, 3 were hospitalized and 2 were treated in an emergency department.
  • In February 2012, 242 persons attending a boy's basketball tournament became ill with acute gastroenteritis; tests confirmed the cause was norovirus GII.7, which is a rare strain. No common source was determined, but there was a public vomit incident where many individuals were exposed.
  • In July 2012, over 200 became ill after eating salad or salsa in a Mexican self-service restaurant.
  • A chain restaurant in Indiana was reported to be the source of norovirus illness for 20 individuals who attended a Red Cross event for rescue workers; an additional 40 close contacts were infected via person-to-person transmission.

While norovirus-associated outbreaks of acute gastroenteritis gain the most publicity when they occur on board cruise ships, these actually occur most commonly in long-term care facilities such as nursing homes, schools, and daycare centers. The CDC has established the Vessel Sanitation Program, which monitors gastrointestinal illness on board cruise ships that carry more than 13 passengers and have a foreign itinerary and US port.[4] The Health Protection Agency, which is a division of Public Health England, has published evidence-based practice parameters for health professionals and ship crew members on the identification and management of norovirus outbreaks aboard cruise ships at sea and on sanitation procedures after ships return to port.[5]

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.

Amongst all cruise ship voyages under the auspices of the CDC's Vessel Sanitation Program, the number of reported outbreaks occurred as follows: 14 in 2010, 14 in 2011, 16 in 2012 and 9 in 2013.[6]


There are an estimated 2 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 1.9 million children each year.[7, 8] Approximately 30-50% of visitors to developing countries develop return with diarrhea.

In May 2011, a shiga-toxin–producing E coli (O104:H4), eventually classified as enteroaggregative pathotype, started in Germany and affected 3000 or more individuals, with 900 or more developing hemolytic–uremic syndrome (a very high percentage) and with an unusual number of adults affected and a high mortality rate compared with prior shiga-producing E coli strains. The German outbreak is unique as horizontal genetic exchange appears to have resulted in this unique O104:H4 strain, which has a prophage encoding shiga toxin 2 and additional virulence and antibiotic-resistance factors. Fieldwork suggested the source was fresh vegetables.[9]


Most cases of gastroenteritis are self-limited with an excellent prognosis.

Estimates for mortality and morbidity widely vary. In the United States, approximately 900,000, including 200,000 pediatric, hospitalizations occur yearly, with an average of 11,255 deaths.[10] 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 older than 65 years accounted for 83% of deaths and the majority of hospitalizations. Clostridium difficile and norovirus were the most common infectious causes of gastroenteritis-associated deaths. C difficile was associated with 14,500 of these deaths, up from 2,700 in 1999. Norovirus was associated with an estimated 797 deaths annually, causing the majority of gastroenteritis outbreaks,[10] although 50% more deaths occurred in years when epidemics were caused by new strains of the virus.[11]


Complications of gastroenteritis include the following:

  • Dehydration
  • Malabsorption
  • Transient lactose intolerance
  • Chronic diarrhea
  • Systemic infection (meningitis, arthritis, pneumonia) especially with Salmonella infections
  • Sepsis ( Salmonella, Yersinia, Campylobacter organisms)
  • Hemolytic-uremic syndrome (much more common in children, especially with E coli O157:H7)
  • Reactive arthritides ( Salmonella, Shigella, Yersinia, Campylobacter, Giardia organisms)
  • Persistent diarrhea
  • Thrombotic thrombocytopenic purpura or TTP ( E coli O157:H7)
  • Guillain-Barré syndrome ( Campylobacter organisms)


Significantly higher mortality is observed among non-Hispanic whites.[10]


Significantly higher mortality is observed among women.[10]


Pediatric gastroenteritis is discussed in Pediatric Gastroenteritis.

Gastroenteritis may occur at any age. Morbidity and mortality are much higher in the very young and the very old. It is a major cause of mortality among children younger than 5 years in developing countries, and persons aged 65 years or older account for the majority of hospitalizations and deaths in the United States.[10]

Norovirus has become the leading cause of acute gastroenteritis in children younger than 5 years seeking medical attention in the United States since the introduction of the rotavirus vaccine.[2]

Contributor Information and Disclosures

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: Nothing to disclose.


Lillian Gutierrez-Alvarez, MPH Public Health Analyst, Medical and Public Health Department, Royal Caribbean Cruises, Ltd

Lillian Gutierrez-Alvarez, MPH is a member of the following medical societies: American Public Health Association, Golden Key International Honour Society

Disclosure: Nothing to disclose.

Specialty Editor Board

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

Disclosure: Received salary from Medscape for employment. for: Medscape.

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, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.


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.

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.

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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).
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