Emergent Treatment of Gastroenteritis

Updated: Oct 27, 2023
Author: Arthur Diskin, MD; Chief Editor: Steven C Dronen, MD, FAAEM 



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; appropriate, general supportive treatment 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,  Hurricane Katrina in 2005, or the earthquake in Haiti in 2010.[1] Prior to the coronavirus disease 2019 (COVID-19) pandemic, an estimated 179 million cases of acute gastroenteritis occurred every year in the United States.[2] Of these patients, 80-85% did not seek medical attention, and only 1-2% require hospital admission.[3] Diarrheal diseases can quickly reach epidemic proportions, rapidly overwhelming public health systems in even the most advanced societies.

A sharp decline in the incidence of norovirus outbreaks was observed in early 2020 owing to COVID-19–related measures, including limiting travel, physical distancing, mask-wearing, handwashing, and surface disinfection.[4, 5] As such measures are increasingly relaxed, an uptick in cases has occurred, and it is projected that norovirus cases will return to pre-pandemic levels by 2026.[6]


Infectious agents are the usual cause of acute gastroenteritis. These agents cause diarrhea by several mechanisms, including 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 of the gastrointestinal tract. 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 a typical, copious watery (rice water) diarrhea. No mucosal invasion occurs. The small intestines are primarily affected, and an elevation of the adenosine monophosphate (AMP) levels is the common pathogenic 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 the 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 the 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 the 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, proton pump inhibitors [PPIs], 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 for 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 acquired immunodeficiency syndrome (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.


Viral (50-70%) causes of gastroenteritis


Norovirus is the leading cause of viral gastroenteritis in the United States. Noroviruses (formerly known as Norwalk virus in the United States and as small, round structured virus [SRSV] in the United Kingdom), along with the sapoviruses (formerly known as Sapporo-like viruses), are members of the Caliciviridae family of viruses. The norovirus is a small, 26-40 nm, nonenveloped, single-stranded RNA virus classified as a Calicivirus. Sapoviruses, a cause of gastroenteritis, predominantly in children, are also in the Caliciviridae family. Five norovirus genogroups have been identified: GI, GII, GIII, GIV, and GV; many clusters (genotypes) have also been identified. In 2010, the land-based experience was far busier than usual. The dominating strain was GII-4 (New Orleans). Norovirus is often called the "winter vomiting disease" in Britain and the incidence seems to be higher in colder weather.

It is a highly infectious virus—with as few as 10-100 particles necessary for transmission—and is quite resistant to quaternary ammonia compounds, alcohol, detergent-based compounds, freezing, and heat (to 60o C). It is a very difficult virus to culture and measure; thus, studies on norovirus are limited, with researchers using a "surrogate," nonenveloped virus, Feline calicivirus (FCV), to assess the efficacy of disinfectants and other mitigation strategies. Some researchers have questioned the use of FCV as a surrogate since FCV is a respiratory virus and norovirus is a gastrointestinal (GI) virus and likely is more resilient than FCV due to the need for norovirus to survive in the hostile environment of the gut. Therefore, the results of testing performed to validate the efficacy of disinfectants and hand sanitizers possibly overestimate the actual effectiveness of these products on human norovirus.

It has been suggested that murine norovirus (MNV) can serve as a useful tool in assessing the risk of infection with human norovirus. It has been used as a surrogate to evaluate the resistance of human norovirus to disinfectants due to its similar characteristics (ie, resistance to basic and acidic pHs, capsid structure, genomic organization, and replication cycle) to human norovirus.[7]

Various modes of transmission exist including fecal-oral transmission (predominant), person to person, fecal contamination of food and/or water, fomite transmission, and airborne spread when in close proximity to someone vomiting, as the virus is easily aerosolized.

Between January 1996 and November 2000, 348 outbreaks of norovirus were reported to the Centers for Disease Control and Prevention (CDC). Of these, 39% of patients were contaminated by food, 12% by person to person, 3% by water, and 18% by unidentified sources.[8] Most of the food sources responsible were identified as oysters, salads, salad dressing, sandwiches, deli meats, cake and frosting, raspberries, drinking water, and ice. Shellfish have been implicated in some outbreaks, but it is not a frequent source on cruise ships, where the predominant mode of infection is believed to be fecal-oral and person-to-person from individuals who come onto the ships ill and do not report the illness or quarantine themselves in their cabins.[9]

Public vomiting episodes with aerosolization of the virus is likely a major source of spread in congested public locations such as cruise ships, schools, and casinos. The same study reveals that 39% contracted the disease in restaurants, 30% in nursing homes, 12% at school, 10% on vacation, and 9% remain unidentified.[9]

The CDC launched the National Outbreak Reporting System (NORS), a web-based platform for reporting waterborne, foodborne, and enteric disease outbreaks in 2009. Between 2009 and 2013, 10,756 acute gastroenteritis outbreaks were reported, with primary transmission modes of person-to-person contact, environmental contamination, and unknown. Norovirus accounted for largest percentage of cases (84$).[2]

The incubation period for the norovirus is between 12 and 48 hours. Some of the early symptoms include nausea, a sudden onset of vomiting, moderate diarrhea, headache, fever (~50%), chills, and myalgia and will last 12-60 hours. The clinical features suggestive of norovirus include the patient's presentation and the sudden onset of symptoms, with uncontrolled vomiting being a classic sign. Usually, more vomiting than diarrhea occurs. The virus is noninvasive of the colon; therefore, white blood cells (WBCs) are not seen in the stool, and hematochezia is rare. The severity and length of illness seen is often related to the then current predominant strain.

The natural course of this illness usually provides resolution within 36 hours. Unless the patient is very young, very old, debilitated with severe underlying disease, or immunocompromised, they usually do very well with this self-limited illness responding to oral rehydration and a rapid return to a normal diet once the vomiting has ceased. The only therapy is oral and/or intravenous hydration with occasional need for antiemetics. The usual cautions concerning the use of antiemetics in very young patients apply. Although viral shedding has been reported for up to 2 weeks or more, the polymerase chain reaction (PCR) testing used to determine this may just be detecting inactivated RNA. The length of viral shedding, the large number of viruses shed in stool (millions) relative to the number required for infection (10-100) explains the communicability and the need for education as to meticulous hand hygiene.

There are many norovirus strains with no cross-immunity, so repeat infections are possible throughout one's lifetime.


Various caliciviruses, other than norovirus, are likely responsible for many outbreaks of previously unidentified viral gastroenteritis.


Rotavirus may cause severe dehydration. (See Pediatric Gastroenteritis.)

Rotavirus is a nonenveloped, double-stranded RNA virus of the Reoviridae family with a wheel-like appearance under electron microscopy—hence the name. The virus is extremely contagious. Nearly all children are infected with rotavirus at some point before age 5 years, unless immunized. There are two commercially available vaccines in the United States, each with antibodies to multiple strains. Prior to this, there were 55,000–70,000 hospitalizations per year in United States.[10] The illness lasts 3-8 days and usually starts with some vomiting, followed by severe foul-smelling (distinctive) diarrhea, potentially leading to severe dehydration.

Adults can be infected with rotavirus, although symptoms are usually not as severe. Those adults most likely to be infected include people with children affected by the virus, elderly persons, and the immunocompromised. There are multiple strains (4 are common in the United States), so people can be infected with rotavirus multiple times. Usually, the first infection is the most severe. Most initial infections occur by age 2 years. Rotavirus is considered the most significant etiological agent for acute GI illness in children worldwide, with up to 500,000 deaths annually worldwide.[10] The peak rotavirus season is November to April (cooler weather) in temperate weather and year-round in tropical climates.

Other viruses that can also cause gastroenteritis include the following:

  • Adenovirus

  • Parvovirus

  • Astrovirus

  • Coronavirus

  • Pestivirus

  • Torovirus

Bacterial (15-20%) causes of gastroenteritis


Salmonella appears as the second most common agent among outbreaks with known pathogens. It is manifested by acute enterocolitis, with abdominal pain, diarrhea, nausea, headache, sometimes vomiting, and almost always fever. Infected persons may develop a localized infection or septicemia. Salmonellosis is predominantly foodborne, and, on average, the onset of symptoms occurs 12-36 hours after ingestion of the contaminated source. It is estimated that Salmonella is responsible for approximately 1.35 million infections in the United States each year, with 26,500 hospitalizations and 420 deaths.[11] Over 2,500 serotypes of Salmonella have been described, but S typhimurium and S enteritidis are the most commonly detected in infected persons.

The incidence of S typhimurium has increased since 1997, and it was the cause of a multistate outbreak associated with peanut butter and other peanut-containing products that resulted in 714 cases across 46 states. The outbreak began in the summer of 2008; however, the epidemiologic investigation was initiated in November due to the inherent time lag in reporting (stool sample results may take 2 wk). The problem became evident when there was a growing cluster of Salmonella serotype typhimurium isolates with the same pulsed-field gel electrophoresis (PFGE) pattern in several states.

Review of detailed epidemiologic questionnaires, assessment of foods, and results of case-control studies in industrialized settings where clusters appeared led to the assumption of peanut butter being the common source of the outbreak. The FDA inspected the facility where the peanut butter was produced and positive test results from finished peanut butter obtained on site confirmed the presence of the outbreak strain. Being an ingredient-driven outbreak, many products distributed through various channels had the potential of being contaminated. As a result of the findings, recalls of peanut butter and peanut-containing foods were issued for products dated as far back as January 2007. In addition, the producing facility was directed to stop production and distribution of all products.[12]

C difficile

Clostridium difficile, often referred to as “C diff,” is a gram-positive, spore-forming, toxin-producing bacillus that typically affects patients receiving antibiotic treatment, especially with broad-spectrum drugs (eg, cephalosporins, clindamycin, fluoroquinolones). Clinical symptoms of C difficile infection include watery diarrhea, fever, nausea, loss of appetite, and abdominal pain or tenderness. Complications that may result from infection include pseudomembranous colitis, toxic megacolon, perforations of the colon, sepsis, and even death, although it is rare. In some cases, infection resolves within 2-3 days of discontinuing the offending antibiotic. However, there are cases that require a full course of an appropriate antibiotic; several antibiotics are effective against C difficile. Severe cases may require surgery to remove the infected portion of the intestine.

Incidence and severity have increased during recent years due to the emergence of a more virulent epidemic strain. It is the leading cause of hospital-acquired gastrointestinal illness in the United States, with costs of 3.2 billion dollars annually.[13] A recent study reported that of 320 patients admitted to a tertiary care center, 31 (9.7%) tested positive for C difficile but had no symptoms of infection.[14] Host susceptibility is greater in hospitalized persons and those with underlying medical conditions. The bacterium is shed in feces and can be acquired from contact with contaminated surfaces, devices, or hands; it is considered to be a healthcare-associated infection.

Elderly individuals are more commonly affected; however, infection may occur at any age and over the last few years its appearance in populations considered low risk has increased (ie, healthy outpatients, children, and people with no recent history of taking antibiotics). In cases of community-acquired infection, obesity has been reported to be a possible risk factor.[15] The use and application of evidence-based management and prevention strategies are important factors in the collaboration to reduce incidence of C difficile. New treatment strategies are currently under study.

Other bacterial causes include the following:

  • Shigella

  • C jejuni

  • Yersinia enterocolitica

  • E coli: Enterohemorrhagic O157:H7, enterotoxigenic, enteroadherent, enteroinvasive

  • V cholera

  • Aeromonas

  • B cereus

  • Clostridium perfringens

  • Listeria

  • M avium-intracellulare (MAI), immunocompromised

  • Providencia

  • V parahaemolyticus

  • V vulnificus

Parasitic (10-15%) causes of gastroenteritis


Giardia lamblia (also called Giardia intestinalis), a flagellate protozoan parasite, lives primarily in the upper part of the small intestine of an organism. Some infected individuals present with symptoms including diarrhea, bloating, greasy stools that tend to float, abdominal cramps, nausea/vomiting, and dehydration, while others may be asymptomatic. The average incubation period is 7-10 days, and symptoms may persist for 1-2 weeks. Most infections occur in children aged 1-9 years, but predominantly in those younger than 5 years. It is also seen in adults aged 25-44 years.

Infected persons may excrete cysts intermittently, making it difficult to diagnose. Several stool samples should be collected on various days and enzyme-linked immunosorbent assay (ELISA) or direct fluorescent antibody methods are usually performed to identify the parasite.

Transmission occurs from person to person or even from animals to humans via the fecal-oral route, through the ingestion of contaminated water. For example, it can be acquired from drinking downstream where a cow or other animal(s) may have contaminated the water. The risk of becoming infected is higher for travelers around the world, persons participating in outdoor activities/recreational water facilities, and those who consume unfiltered/untreated water (ie, hikers, campers).

The majority of cases are observed during the months of June to October, coinciding with the months of increased travel and outdoor/recreational water activities. There is increased risk in daycare centers and for close contacts of infected persons as well. Giardiasis occurs worldwide, with higher prevalence in areas where there is poor hygiene and sanitation. However, it is the most common intestinal parasitic disease in the United States, with an excess of 19,000 infections reported each year.

It has two stages, cyst and trophozoite. Both forms are passed in feces; however, the cyst is the infective stage and the one that can survive outside of a host and in the environment for weeks or months. It has moderate tolerance to chlorine and is capable of living in cold water for significant periods. Individuals infected with Giardia may shed 1 to 10 billion cysts daily, while the infectious dose is approximately 10 cysts, sometimes even as few as 1 or 2.

Other parasitic causes include the following:

  • Amebiasis

  • Cryptosporidium

  • Cyclospora

Food-borne toxigenic diarrhea

Preformed toxins include S aureus and B cereus

Postcolonization toxins include V cholera, C perfringens, enterotoxigenic E coli, and Aeromonas.

Shellfish poisoningand poisoning from other marine animals

Shellfish and marine animal poisoning include the following:

  • Paralytic shellfish poisoning (PSP) - Saxitoxin

  • Neurologic shellfish poisoning (NSP) - Brevetoxin

  • Diarrheal shellfish poisoning (DSP) - Okadaic acid

  • Amnesic shellfish poisoning - Domoic acid

  • Ciguatera (ciguatoxins)

  • Scombroid (conversion of histidine to histamine)

Drug-associated diarrhea

Medications associated with diarrhea include the following:

  • Antibiotics, due to alteration of normal flora

  • Laxatives, including magnesium-containing antacids

  • Colchicine

  • Quinidine

  • Cholinergics

  • Sorbitol

  • Proton pump inhibitors (PPIs): In a prospective population-based study of 38,109 middle-aged and older Australian adults, there was an association between use of PPIs and a significantly higher risk of hospitalization for infectious gastroenteritis, regardless of the PPI used.[16] There was a dose-response relationship noted.

Pseudomembranous colitis

Pseudomembranous colitis occurs as an overgrowth of C difficile.C difficile assay findings are positive.

Other causes

Other causes of diarrhea include the following:

  • Unknown agents, especially in developing countries

  • Ischemic colitis

  • Ulcerative colitis

  • Crohn disease

  • Carcinoid tumor or vasoactive intestinal peptide tumor (VIPoma)

  • Acquired immunodeficiency syndrome (AIDS)

  • Dumping or short bowel syndrome

  • Radiation or chemotherapy


United States data

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.[17]

It is estimated that the norovirus is responsible for a large percentage of gastrointestinal (GI) illnesses in the United States and possibly worldwide. One contributing factor to its frequency is the mutability of its genome[18] and another is the low minimal infective dose. According to the Centers for Disease Control and Prevention (CDC), 19 to 21 million cases a year and more than 50% of foodborne outbreaks are confirmed to be caused by norovirus or norovirus was the only suspected etiology.[19] 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.[3]

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 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.

  • 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 typhi 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.

  • Data for selected foodborne disease outbreaks by year (from 2006 forward) and by pathogen are available at the CDC site for foodborne outbreaks.

Although 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 GI illness on board cruise ships that carry more than 13 passengers and have a foreign itinerary and US port.[20] 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.[21]

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 GI 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 each in 2010 and 2011, 16 in 2012, 9 each in 2013 and 2014, 12 in 2015, 13 in 2016, 11 each in 2017 and 2018, 10 in 2019, 4 in 2020, 1 in 2021, 4 in 2022, and 13 in the first three quarters of 2023.[22]

International data

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.[23, 24] Approximately 30-50% of visitors to developing countries 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 (30%) 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.[25]

In a systematic review and meta-analysis of data on the prevalence or incidence of norovirus and acute gastroenteritis in Latin America, the overall prevalence of norovirus in acute gastroenteritis cases was 15%, and 37%-100% of cases were associated with GII.4 strains (but only 7% of asymptomatic norovirus patients were affected with this strain).[26]

In a 2017 report that estimated the healthcare costs of acute gastroenteritis and human Campylobacter infection in Switzerland, investigators reported an annual cost of approximately 29-45 million euros, of which about 9 to 24.2 million euros related to physician visits without a stool diagnostic test being obtained; about 12.3 million euros for patients with negative Campylobacter species stool tests and 1.8 million euros for those with positive Campylobacter species stool tests; and 6.5 million euros for inpatients with Campylobacter infection.[27]

Race-, sex-, and age-related demographics

Significantly higher mortality is observed among women and non-Hispanic white individuals.[28]

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.[28]

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.[17]

Pediatric gastroenteritis is discussed in the Medscape Drugs & Diseases article Pediatric Gastroenteritis.



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.[28] Internationally, the mortality rate is 1.4-2.5 million deaths each year.

The Centers for Disease Control and Prevention (CDC) reported that 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. C 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,[28] although 50% more deaths occurred in years when epidemics were caused by new strains of the virus.[29]


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)

  • Toxic megacolon

  • Reactive arthritides (Salmonella, Shigella, Yersinia, Campylobacter, Giardia organisms)

  • Persistent diarrhea

  • Thrombotic thrombocytopenic purpura or TTP (E coli O157:H7)

  • Guillain-Barré syndrome (Campylobacter organisms)

Patient Education

Patients should be educated on the importance and proper methods of oral rehydration and early appropriate feeding.

All patients, especially the parents of infants and young children, must be extensively educated about the signs and symptoms of dehydration.

Patients with food-borne exposures should be educated on deterrence.

Immunocompromised patients and individuals with liver disease should be educated not to consume raw shellfish, especially oysters.

Travelers to underdeveloped areas should be made aware of proper avoidance measures, appropriate treatment, and current endemic illnesses.




A well-taken history, considering important epidemiologic factors, can help to identify not only the cause of diarrhea but also if the patient is at risk for complications. History in infectious and food poisoning cases varies depending on the agent, with variation in the onset; the frequency and consistency of the stools; the presence or absence of blood and mucus, and associated vomiting, cramps, or fever. The history should also identify risk factors for unusual causes of acute gastroenteritis and possible reasons to suspect noninfectious etiologies. Indications of dehydration or sepsis should also be sought.

As an example, norovirus is usually diagnosed by history. The incubation period for the norovirus is between 12 and 48 hours. Some of the early symptoms include nausea, a sudden onset of vomiting, moderate diarrhea, headache, fever (~50%), chills, and myalgia and will last 12-60 hours. The clinical factors suggestive of norovirus include the patient's presentation and the sudden onset of symptoms, with uncontrolled vomiting being a classic sign. Usually, more vomiting than diarrhea occurs. The natural course of this illness usually provides resolution within 36 hours.

The following discussion involves elements of the history to obtain.

Duration of illness

Duration and rapidity of symptom onset are important in determining the incubation period and possible infecting organism and in directing further care.

Diarrhea that lasts longer than a month requires consideration of a different spectrum of etiologic factors than diarrhea that lasts less than 1-2 weeks.


The presence of high fever (with or without chills) generally suggests that an invasive organism is the cause of diarrhea, although many extraintestinal illnesses can present with both fever and diarrhea, especially in children.


Vomiting, a symptom common to a host of illnesses, implies proximal bowel involvement, especially with preformed neurotoxin, as elaborated by S aureus and B cereus.

Vomiting is a leading symptom of intestinal obstruction, usually coupled with distention or if the patient has had gastric bypass surgery; however, distention may not be significant if the obstructing lesion is very proximal. Vomiting without diarrhea must always prompt a search for noninfectious causes and cannot be referred to as gastroenteritis.


The location and character of pain may be indicative of the area of infection because colonic involvement is usually associated with tenesmus and pain in either of the lower quadrants or the lower back, whereas jejunoileal infection may result in periumbilical pain.

Cramps may be caused by an electrolyte imbalance.

Pain, especially in patients older than 50 years, should raise the suspicion of an ischemic process.


Note the following:

  • Frequency, amount, color, consistency (ie, watery, semisolid, odor), and presence of blood and/or mucus are factors that can help to determine the causative agent.

  • Large volumes of stool are usually associated with enteric infection, whereas colonic infection results in several small stools.

  • The presence of blood may indicate colonic ulceration (bacterial infection, inflammatory disease, ischemia).

  • White bulky feces that float (high fat content) are due to a small bowel pathology that leads to malabsorption.

  • Copious (rice water) diarrhea is a hallmark of cholera.

Extraintestinal causes

Obtain a history of any nonintestinal illnesses that can lead to diarrhea. Vomiting and/or diarrhea may be a manifestation of that illness or a result of its treatment. Obtaining a history of recent surgery or radiation, food or drug allergies, and endocrine or gastrointestinal disorders is extremely important. The patient should always be questioned regarding prior episodes.

Malaria, Whipple disease, irritable bowel, incomplete bowel obstruction, inflammatory bowel disease, nutritional disease, carcinoid and malabsorption syndromes can all result in diarrhea and are examples of the numerous possible noninfectious causes.

Drugs such as colchicine, quinidine, antimicrobials, cancer chemotherapeutic agents, and magnesium-containing antacids frequently cause diarrhea.


Orthostasis, lightheadedness, diminished urine formation, and a change in mentation are symptoms of marked dehydration, requiring aggressive treatment. These symptoms are particularly important in elderly patients, a group that is most at risk from diarrhea.

Severe dehydration may also be associated with significant electrolyte imbalances.

Epidemiologic factors

Note the following:

  • A number of historical questions may provide clues to the etiology of the illness, including foreign travel, recent camping, recent antibiotic use, daycare attendance, and/or ingestion of raw, possibly spoiled, or new marine products, as well as similar illnesses in family, friends, or close contacts.

  • An epidemiologic factor may be travel to developing countries where bacterial or parasitic agents are endemic and can cause infection or to campgrounds in developed regions, where agents such as Giardia lamblia, Aeromonas, and Cryptosporidium can contaminate untreated water.

  • Enterotoxigenic E coli is the most frequent cause of traveler's diarrhea. Symptoms usually begin within days of arrival in the region and can last from 5 days to 2 weeks.

  • Vibrio species are more common in Asia, although epidemics have occurred in Central America within the last 10 years.

  • As many as 12% of diarrheal illness cases may be caused by rotavirus in travelers to Asia, Africa, and South America.

  • Men who are homosexual are more prone to infection by the usual pathogens (ie, Shigella, Campylobacter jejuni, Salmonella, protozoalike Entamoeba) via the fecal-oral route. Anal receptive intercourse may result in the direct inoculation of Neisseria gonorrhoeae, Chlamydia trachomatis, Treponema pallidum, and herpes simplex virus. Severely immunocompromised states (CD4 cell count < 200) increase the risk of infection by agents such as Mycobacterium avium complex, microsporidia, cytomegalovirus (CMV), and Isospora belli.

  • Recent use of antimicrobial drugs increases the risk of C difficile infection.

  • A common source outbreak from contaminated water and food may cause gastroenteritis either by infection (eg, C jejuni, G lamblia) or by ingestion of a preformed toxin (eg, E coli O157:H7, scombroid, ciguatera).

  • Infections via the fecal-oral route are prevalent in children who attend daycare centers. Rotavirus has an infection rate of nearly 100% in exposed children younger than 2 years. Other family members are also at risk for infection.

  • Exposure to a public vomiting episode in a public location such as cruise ship or casino can lead to exposure to aerosolized norovirus infection.

Physical Examination

A thorough physical examination is essential to assess the general state of hydration and nutrition and to exclude extraintestinal causes of diarrhea. Usually, the cause of diarrhea cannot be determined based on the physical findings present, which may be few.

The most important element of the physical examination is the assessment of the patient's hydration status. (Dehydration in children, for example, is classified according to the degree of hydration/percentage deficit as < 3%, none; 3-6%, mild; 6-9%, moderate; and >10%, severe.)[30] Additionally, signs of bacteremia or sepsis should be sought. Patients with chronic diarrhea may need an evaluation of their nutritional status.

A rectal examination should be performed, involving checking for blood and mucus. Rectal examination may reveal abscesses, fistulae, and fissures, which may indicate inflammatory bowel disease. A partially obstructing tumor or a fecal impaction may be discovered as a cause of diarrhea. Finally, the stool can be examined for the presence of blood and pus.

Hydration and nutritional status

Diminished skin turgor, weight loss, resting hypotension and tachycardia, dry mucus membranes, decreased frequency of urination, changes in mental status, and orthostasis can be used to gauge dehydration.

In children, the absence of tears, poor capillary refill, sunken eyes, depressed fontanelles, increased axillary skin folds, and dry diapers all may reflect a dehydrated state. Capillary refill time is a simple and effective assessment to identify children in need of prompt rehydration.[31]

Muscle wasting and signs of neural dysfunction due to nutritional depletion may be observed in patients with chronic diarrhea.

Abdominal examination

A careful abdominal examination is necessary to exclude causes of diarrhea that may require surgical intervention.

The examiner should look for signs of an acute abdomen, listening for bowel sounds, determining the location of any tenderness, and palpating for masses or organomegaly, rebound, guarding, distension, or rigidity.

Appendicitis in children may manifest as diarrhea.

Extreme caution should be exercised in post gastric bypass bariatric surgery patients, as they may not manifest typical signs/symptoms such as vomiting or distension with obstruction or ischemia.



Diagnostic Considerations

Other conditions to consider in the differential diagnosis of gastroenteritis include the following:

  • Various infectious etiologies

  • Pseudomembranous colitis

  • Food-borne toxigenic diarrhea

  • Toxins

  • Hormonal (vasoactive intestinal peptides)

  • Drugs (ie, sorbitol, cholinergics, caffeine)

  • Postsurgical complications

  • Radiation colitis

  • Carcinoid

  • Pediatrics: adrenogenital/cystic fibrosis

Important considerations

It is important to recognize/diagnose the following conditions in patients:

  • Dehydration or sepsis

  • Immunocompromised patients and their potential, unusual etiologies or propensity to develop complications

  • Hemolytic-uremic syndrome in patients with E coli infection

  • Pseudomembranous colitis (C difficile)

  • Toxic megacolon

  • Appendicitis in patients who present with vomiting and diarrhea

  • Noninfectious etiology, such as ischemic bowel, bowel obstruction, or other etiologies for abdominal symptomatology

Note the following:

  • Avoid diagnosing gastroenteritis in a patient who is only vomiting when the vomiting is due to a nongastrointestinal and possibly life-threatening etiology

  • Complications may result from the inappropriate use of antimotility and antiemetic medications.

Special concerns

Pseudomembranous colitis (C difficile)

Note the following:

  • This condition occurs mostly in patients who are hospitalized or live in a nursing home and who have recently been on antibiotics and is due to infection with toxin-producing strains of C difficile. Toxins A and B damage the mucosa of the colon.

  • Symptoms may range from mild to severe bloody diarrhea and colitis, with pseudomembranous colitis being the most severe form.

  • Complications include dehydration, toxic megacolon, and perforation.

  • Stop any antibiotics.

  • Treat with intravenous fluids and vancomycin or metronidazole.

  • Condition is suspect with prior or current antibiotic therapy.

  • Diagnosis via assay or sigmoidoscopy.

Gastroenteritis in the elderly patient

Diagnosing complications, such as dehydration (may have chronic poor skin turgor and dry mucus membranes) is more difficult. Elderly patients may be unable to take needed medications. Electrolyte disorders and hypovolemia may have much more serious implications, and life-threatening abdominal emergencies, such as appendicitis, are easier to overlook. Fever may not be manifested, and pain sensation may be blunted.

Travelers' diarrhea

Note the following:

  • The condition is usually self-limited (3-5 d).

  • Onset is within 1 week of arrival.

  • Fever, vomiting, and bloody stools are uncommon.

  • Early treatment may decrease duration.

  • Loperamide is often useful.

  • If a lack of response to antibiotics is present, check for parasites.

  • Consider C difficile in patients taking antibiotics.

  • The use of probiotics, such as Lactobacillus GG, has had mixed results in treatment and prevention.

  • Rifaximin at 200 mg PO tid may be used for the treatment or prevention of travelers' diarrhea.[32]

Food-borne toxigenic diarrhea

Note the following:

  • The condition is usually self-limited and of short duration.

  • Stool analysis and culture are not helpful.

  • Perform supportive treatment only.

  • Antibiotics rarely are useful or indicated.

Diarrhea in patients with acquired immunodeficiency syndrome (AIDS)

Note the following:

  • The condition usually becomes more severe as the immune system deteriorates.

  • Patient may require antimotility agents only.

  • Consider drug-related and herb-related causes.

  • Start with empiric treatment with a quinolone and culture the stool.

  • Pursue diagnostic testing more aggressively because patients with AIDS are more likely to have an identifiable etiology.

  • Consider nonopportunistic bacterial and protozoal infections first, followed by etiologies such as Cytomegalovirus (CMV) and Mycobacterium infections.

  • Treatment must include nutritional and psychosocial support.

Differential Diagnoses



Laboratory Studies

Determination of laboratory tests

The patient's evaluation should be based on the clinical assessment and the need to do the following:

  • Further evaluate the seriousness of the condition (degree of dehydration and electrolyte derangement).

  • Determine a specific etiologic agent.

  • Evaluate the patient for noninfectious etiologies.

  • Patients who require further workup include those who appear seriously ill or dehydrated; those who have high fevers, bloody stools, severe abdominal pain, or persistent diarrhea; and those who are immunocompromised or whose condition is suspected of having an epidemic diarrheal etiology.

  • History, epidemiologic considerations, and the physical examination should be the primary guides in determining whether any further diagnostic evaluation is necessary, followed by microscopic examination of the stool.

Stool studies and culture

Note the following:

  • The presence of blood or leukocytes in stool is a strong indicator of inflammatory diarrhea.

  • Stool studies can be performed efficiently and inexpensively by using a Wright stain or methylene blue and directly observing for leukocytes and performing an occult blood test.

  • Fecal leukocytes are present in 80-90% of all patients with Salmonella or Shigella infections but are less common with other infecting organisms such as Campylobacter and Yersinia. They may also be present in ulcerative colitis and Crohn disease but are usually absent in viral infections, Giardia infection, enterogenic E coli infection, and toxigenic bacterial food poisoning.

  • A stool culture is not necessary or cost-effective in most cases of diarrhea unless an unusual bacterial cause is suspected and it may be needed for epidemiological purposes.

  • A lower threshold for performing stool cultures and examination for ova and parasites is indicated in immunocompromised, immunosuppressed patients and those who have recently traveled to remote locations or developing nations.

  • Fever, bloody stools, leukocytes in stool, pain resembling that associated with appendicitis (Yersinia), and diarrheal illness associated with partially cooked hamburger (cytotoxigenic E coli O157:H7) are all indications for culture. If possible, the laboratory should be informed of suspected organisms.

  • Frequently, stool cultures are obtained inappropriately in the United States. Consider whether obtaining a culture would change the therapy.

  • Specific indications for stool cultures include bloody stools, stools that test positive for occult blood or leukocytes, prolonged course of diarrhea that has not been treated with antibiotics, immunocompromised host, or for epidemiologic purposes, such as cases involving food handlers.

  • Routine stool cultures identify only Campylobacter, Shigella, Salmonella, Aeromonas, and Yersinia species.

  • Testing for other pathogens, such as Vibrio species, enterohemorrhagic E coli O157:H7, and other Shigatoxin-producing bacteria require special media. The laboratory should be informed regarding the need for appropriate media for suspected organisms (eg, MacConkey sorbitol agar for E coli O157:H7). Additionally, the laboratory may need to perform specialized testing to specifically identify the organism.

    Emergent Treatment of Gastroenteritis. The MacConk Emergent Treatment of Gastroenteritis. 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.
    Emergent Treatment of Gastroenteritis. Hektoen ent Emergent Treatment of Gastroenteritis. 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.
    Emergent Treatment of Gastroenteritis. Example of Emergent Treatment of Gastroenteritis. 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.
  • Studies of selected centers have shown that only 2% of stool culture results are positive as routinely obtained. The cost per positive stool culture result has been estimated to be at least $900-1200.

  • Similarly, if parasitic illness is in the differential or if the patient has recently traveled to an endemic region or has chronic diarrhea, the stool should be examined for parasites or their ova with the caveat that several samples may be required to make the diagnosis. Ova and parasite studies are indicated for patients who are immunocompromised, who have a persistent or prolonged course, or whose conditions are unresponsive to antibiotics.

  • Travel to endemic regions followed by chronic diarrhea without signs of acute bacterial diarrhea should prompt a search for a parasitic etiology.

  • Entamoeba histolytica can result in bloody stools, but a smear reveals a lack of leukocytes due to exotoxin produced by the parasite that lyses the cells.

  • Stool can be sent to reference labs for examination for norovirus by polymerase chain reaction (PCR). This is usually reserved for epidemiological purposes. Rapid assays are becoming available with varying sensitivities/specificities and questionable clinical applicability.

Routine laboratory tests

Routine laboratory tests (complete blood cell [CBC] count, levels of electrolytes, renal function studies) may not be helpful or indicated in making a diagnosis. These tests may be useful as indicators of severity of disease, especially in elderly or very young patients, although that determination is best made clinically.

Electrolytes and blood urea nitrogen (BUN) measurements are indicated in patients with severe diarrhea or dehydration to assess the state of hydration and to specifically rule out hyponatremia or hypernatremia. Decreased serum bicarbonate suggests severe dehydration, especially in children. Acidosis secondary to bicarbonate loss in the stools and/or from hypovolemia-induced lactic acidosis may be present. Hypokalemia may also occur.

A CBC count may be indicated with a prolonged course, severe diarrhea, or toxicity. The white blood cell (WBC) count is usually increased in Salmonella infections but normal or low with significant left shift in Shigella infections. The WBC count is otherwise variable. Eosinophilia may be present in parasitic infections.

Enzyme-linked immunosorbent assay (ELISA)

Commercially available immunofluorescent antibody and enzyme immunoassays are also available for Giardia and Cryptosporidium organisms. C difficile toxin assays can be performed when antibiotic-associated diarrhea is suspected.


Enzyme-linked immunosorbent assay (ELISA) is available in less than 2 hours but is not sensitive enough in adults.


ELISA is more than 90% sensitive in susceptible populations (eg, people who camp or travel to endemic areas). Consider ELISA prior to ova and parasite examination or string test.

Imaging Studies

An acute abdominal series is indicated only when bowel obstruction, toxic megacolon, or perforation is suspected.

A low threshold for CT scanning should be maintained in post gastric bypass patients and older patients with significant abdominal pain.


Sigmoidoscopy may be indicated if pseudomembranous colitis or inflammatory bowel disease is suspected. Sigmoidoscopy is useful in obtaining tissue for culture in patients with acquired immunodeficiency syndrome (AIDS) who have undiagnosed diarrhea or wasting syndrome.



Emergency Department Care

Prehospital care is directed toward early and aggressive fluid therapy in patients who are unstable.

The following discussion involves management in the emergency department (ED).

Goals of therapy

Goals of ED therapy include the following:

  • Rehydrate orally (PO) or intravenously (IV) as needed.

  • Treat symptoms (eg, fever, pain) as indicated.

  • Identify complications.

  • Prevent the spread of infections.

  • Identify public health concerns and treat certain cases with specific or empiric antibiotic therapy.


Note the following:

  • Administration of 1-2 L dextrose 5% in 0.5 isotonic sodium chloride solution with 50 mEq NaHCO3 and 10-20 mEq KCl over 30-45 minutes may be necessary in patients who are severely dehydrated.

  • Clinical assessment and serum electrolyte concentrations should guide therapy.

  • To give fluids more rapidly, KCl may be given orally or in the second or third liter bag or as a supplemental IV of 20 mEq KCl in 100 mL of isotonic sodium chloride solution over 1 hour. Ensure normal renal function prior to KCl administration.

  • Rehydrate patients until mental status and signs of perfusion and pulse are normal (caution in elderly patients with congestive heart failure [CHF]), such as a urine output of 1-2 mL/kg/h.

  • For pediatric patients, administer 20 mL/kg of isotonic sodium chloride solution initially for resuscitation. Repeat as necessary and add KCl as indicated.

  • Indications for IV rehydration include severe intractable vomiting, altered consciousness, severe dehydration, ileus, excessive choleralike stools, and time or environment not conducive to oral rehydration therapy (ORT).

Solutions for oral rehydration

Consider the following:

  • The World Health Organization solution is 90 mEq/L Na+, 20 mEq/L K+, 80 mEq/L Cl-, 20 g/L glucose; osmolarity is 310; CHO:Na = 1.2:1; administer 250 mL (approximately 8 oz) every 15 minutes until fluid balance is clinically restored, then 1.5 L of oral fluid per liter of stool.

  • Other oral rehydration products include Naturalyte, Cera Lyte, Rehydralyte, and Pedialyte.

  • Oral rehydration may not decrease the duration or volume of diarrhea.

  • Small amounts of oral fluids may be given repeatedly while the patient is still vomiting.

  • Oral rehydration has been largely responsible for the tremendous decrease in the death rate in underdeveloped countries from infectious diarrhea, including cholera.

  • The glucose/sodium transport mechanism remains intact despite enterotoxigenic illness. Coupled transport is one of several mechanisms of sodium and water absorption in the bowel. It is the direct entry of sodium and water across the cell at the intestinal brush border membrane via the linking (coupling) of 1 organic molecule, such as glucose, to 1 sodium molecule. This is the principle upon which ORT is based. Optimally, therefore, the ratio of carbohydrate to sodium should approach 1:1. Glucose is necessary to stimulate the absorption of water and electrolytes by the small intestines.

  • The solution must be iso-osmolar or hypo-osmolar to avoid an increased osmotic load in the small intestines contributing to an osmotic diarrheal effect, pulling fluid into the lumen.

  • Studies have shown oral and IV rehydration to be equivalent therapies in patients who can tolerate the oral fluid.

  • Although standard glucose-electrolyte solutions achieve and maintain rehydration, they may not reduce stool volume or duration of diarrheal illness, affecting compliance.

  • Newer solutions with complex carbohydrates and short chain polypeptides of cereals and legumes are now available to provide additional organic cotransport molecules with no increase in osmolarity. These appear to offer the advantage of decreased stool volumes and shortened duration of illness.


Early age-appropriate refeeding in children (and adults) is important to initiate as soon as rehydration is complete. Note the following:

  • Early refeeding with complex carbohydrates provides additional cotransport molecules without osmotic penalty and stimulates mucosal repair.

  • Consider rice, wheat, bread, potatoes, and lean meats, especially chicken.

  • Milk can be safely given early. Despite the potential for lactose intolerance, clinical evidence of acute lactase deficiency is uncommon, and most children can tolerate nonhuman milk without difficulty during acute diarrheal illnesses.

  • What has been learned from studies of early pediatric refeeding probably can be generalized to the adult population. Initiate early feeding with the above dietary recommendations once rehydration has been accomplished and vomiting is controlled.

Empiric therapy

Empiric therapy for infectious diarrhea is sometimes indicated. Food-borne toxigenic diarrhea usually requires only supportive treatment, not antibiotics. Note the following:

  • The duration of traveler's diarrhea (E coli, Shigella) can be shortened by half or more with trimethoprim-sulfamethoxazole (TMP/SMZ) or ciprofloxacin administered for 3 days. Single doses have also been used effectively. The duration of treatment may be extended by 2-3 days for moderate-to-severe cases.

  • Generally, fluoroquinolones are the drugs of choice for acute infectious gastroenteritis when used empirically. They do not appear to increase carrier states; however, they are contraindicated in pregnant women and in children.

  • Erythromycin or azithromycin is effective in Campylobacter infections, although erythromycin is not well tolerated in the patient who is vomiting.

  • Metronidazole (oral or parenteral) is effective in mild-to-moderate cases of C difficile diarrhea (in addition to discontinuance of the causative agent). Patients who are severely ill may require orally administered vancomycin, which may require delivery via nasogastric tube or colonoscope.

  • Mild cases of suspected Yersinia infection should be treated with TMP/SMZ or a fluoroquinolone, while patients who are more ill and require admission benefit from IV ceftriaxone.

  • Intestinal salmonellosis in an immunocompetent host does not require antimicrobials because they may prolong fecal shedding of organisms.

  • Metronidazole is effective against parasitic infestations with Giardia or Entamoeba.


Antiemetics may be useful in the treatment of nausea and vomiting in adults. They are usually not recommended in children.

In a multicenter Italian pediatric ED study that evaluated antiemesis in 832 children (aged 1-6 years) with acute gastroenteritis who underwent successful first attempt with oral rehydration solution, of which 356 were randomized to either placebo (n = 118) or domperidone (1 dose, 0.5 mg/kg) or ondansetron (1 dose, 0.15 mg/kg) (n = 119, each), ondansetron administration reduced the risk of IV hydration by half compared to placebo and domperidone.[33] The investigators suggested that in the emergency care setting, 60% of children in this age group with gastroenteritis-associated emesis without severe dehydration can be effectively managed with oral rehydration alone.[33]

Antidiarrheals (antimotility agents)

These agents have traditionally been discouraged because of concerns with causing bacteremia; however, they appear to have a role in the symptomatic treatment of mild-to-moderate diarrhea, especially with nonbloody and traveler's diarrhea.

The most common agents include bismuth subsalicylate (Pepto-Bismol). For patients older than 14 years, give 2 tablets or 20 mL PO q30min as needed to a maximum of 8 doses. Loperamide (Imodium) is useful as an adjunct to rehydration for symptomatic relief. The American Academy of Pediatrics (AAP) does not recommend this for children.

Octreotide (Sandostatin), an analog of somatostatin, may be used subcutaneously and intravenously to control severe secretory diarrhea. It has been approved for this purpose in the treatment of carcinoid tumors and VIPomas. Octreotide is under investigation for other uses, including secretory diarrhea associated with acquired immunodeficiency syndrome (AIDS), short bowel syndrome, dumping syndrome, radiation, and chemotherapy.

Inpatient care

If the patient is hospitalized, the following are treatment strategies in addition to those discussed above:

  • Continue rehydration and management of electrolytes if ED response is inadequate.

  • Manage sepsis in the toxic-appearing patient.

  • Evaluate for underlying etiology if the diagnosis is uncertain.

  • Manage complications.


Transfer of the unstable patient is inappropriate under Emergency Medical Treatment and Active Labor Act (EMTALA) regulations unless benefits clearly outweigh risks.

Unless the patient requires admission and has a complicated medical condition that would be better managed in another facility, transfer is neither necessary nor recommended.


A consultation with an infectious diseases specialist may be necessary for patients with chronic diarrhea, those who may have a parasitic infection, individuals infected with C difficile when vancomycin use is contemplated, patients who relapse, and those with acquired immunodeficiency syndrome (AIDS) who have diarrhea.

A consultation with a gastroenterologist may also be indicated in the above circumstances and when pseudomembranous colitis, ulcerative colitis, or Crohn disease are in the differential diagnosis.

If a surgical abdomen is suspected or if the patient is status post gastric bypass bariatric surgery, a consultation with a surgeon may be appropriate.

Outpatient Care

Outpatient care includes the following:

  • Rehydrate orally with balanced sodium and glucose solutions.

  • Ensure appropriate early oral refeeding.

  • Ensure appropriate deterrence and infection control procedures and activities, including notification of common source or close contact exposures, as appropriate.

  • Administer antibiotic, antimotility, and antiemetic treatment only as indicated and directed.

  • Wash buttocks after each diarrheal stool to avoid effects of stool enzyme on the skin.

  • Instruct the patient to return upon experiencing bloody stools, worsening abdominal pain, severe vomiting, and/or concerns regarding dehydration.

  • Instruct the patient to seek follow-up care if diarrhea persists longer than 10 days.

Outpatient medications may include antibiotics, antiemetics, and/or antimotility agents.



The following are factors to consider with breastfeeding:

  • Decreased incidence of rotavirus but does not eliminate this diagnosis

  • Formula supplementation with nonpathogenic bacteria such as Bifidobacterium bifidum


General precautions

Note the following:

  • Take enteric precautions to avoid spread to family members, especially by washing hands before eating and after each stool or diaper change.

  • Avoid shellfish served in unregulated environments, in areas with known red tides, or areas of recently reported outbreaks, including Vibrio species and Norwalk virus. Individuals with a history of any liver disease should avoid raw shellfish.

  • Wash all produce prior to consumption, especially if imported.

  • Avoid cross-contamination of foods during preparation (eg, cutting boards).

  • Avoid raw or undercooked eggs or poultry.


As many as 40% of travelers to high-risk areas (South and Southeast Asia, Africa, and Latin America) contract diarrhea. Dietary precautions, in addition to the above, which will reduce this risk are as follows:

  • Eat steaming hot foods (cooked foods) and drink steaming hot beverages (eg, coffee, tea).

  • Consume acidic foods, such as citrus.

  • Consume dry foods, such as bread and nuts.

  • Drink carbonated beverages.

  • Avoid water, ice, raw fruits without a skin or peel, raw vegetables, unpasteurized milk and dairy products, and foods sold in the streets.

  • Avoid moist foods served at room temperature, leafy green vegetables, and ripened fruit with broken skin.

  • Take the above precautions when aboard an aircraft leaving the high-risk area.

  • Travelers who request prophylaxis can take 2 tablets of Pepto-Bismol with each meal and at bedtime, not exceeding a daily dose of 8 tablets.

  • Although prophylactic antimicrobial therapy generally should be discouraged in the young and healthy traveler, if chemoprophylaxis is requested, a daily single dose of TMP/SMZ or a fluoroquinolone can be provided.

  • Travelers with certain underlying conditions should be encouraged to use prophylactic antibiotics. These include patients with AIDS, inflammatory bowel disease, systemic malignancy, insulin dependency, or achlorhydria and patients taking omeprazole or chronically using H2 antagonists. Sporadic or intermittent H2 antagonist use is not an indication for prophylaxis.

  • Avoid drinking from unfamiliar fresh water sources, such as lakes and rivers.


There are very few ways to entirely eliminate norovirus. Alcohol-based hand sanitizers, used by a number of cruise lines and recommended by hospital-based practices, need a minimum of 15-30 seconds of contact time to be effective and should not be considered a substitute for aggressive handwashing and mechanical drying. In addition, sanitizing the fingertips and under the finger nails with alcohol hand gels is difficult, and this may be another factor in their relative ineffectiveness in comparison to handwashing with soap and water. Because norovirus is an unencapsulated virus, alcohol-containing products are less effective and require higher concentrations of alcohol. Several popular commercially available products containing 62-70% alcohol demonstrate varying results, on average a log reduction between 2 and 4. Testing methodology and surrogates vary among the studies.

Alcohol-based hand gels are relatively ineffective in the disinfection and/or removal of norovirus from the hands. The recent increase in norovirus infection in acute care hospitals may be the result of the increased availability of alcohol-based hand gels, and the possible resultant reduction in the frequency of staff handwashing with soap and water and drying with a paper towel.

During an outbreak on board a cruise ship, most surfaces that can be safely disinfected are treated with sodium hypochlorite (bleach), with a concentration of 1000 ppm, freshly constituted (higher concentrations quoted are not freshly constituted and may have varying efficacy). A 1-minute contact time is required, and a >4.0 log reduction is anticipated. However, this concentration is not approved for food handling surfaces and cannot be used on fabrics and many other surfaces.

Steam cleaning to >70o C is recommended for carpets and certain furnishings.

Benzethonium chloride is a synthetic quaternary ammonium, surfactant, antiseptic, and anti-infective compound used as a topical antimicrobial agent and in antibacterial moist towelettes and wipes. While many of these compounds have limited efficacy for unencapsulated viruses, newer products seem more effective. However, studies show a contact time of >10 minutes may be required.

Accelerated and stabilized hydrogen peroxide is another product used for virucidal disinfecting. It requires a 5-minute contact time. It can be expensive, and, currently, no hand wipes are available.

Phenolic-based products have been used with some success in the past, but concerns about toxicity and their mucosal irritation when "fogged" have meant most cruise lines have moved away from their primary use in mitigating norovirus.

Oil of thyme, which has bactericidal and virucidal properties, is another hand wipe alternative.

Numerous new products are always becoming available, and objective third-party evaluations are critical in the decision-making processes.



Medication Summary

The goals of pharmacotherapy are to reduce morbidity, to prevent complications, and to possibly decrease the duration of illness.

In February 2006, the United States Food and Drug Administration (FDA) approved an oral vaccine for rotavirus (RotaTeq). RotaTeq is administered in a 3-dose series starting between age 6-12 weeks and completed before age 32 weeks. It protects against types G1, G2, G3 and G4.

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.[34] In March 2010, Rotarix was temporarily taken off the market due to concerns with contamination with porcine circovirus type 1 (PCV1), but in May 2010 the FDA cleared use of the product again. Rotarix should not be given to children with latex allergy. It protects against type G1, G3, G4, and G9. Rotashield, an earlier vaccine, was withdrawn from the market due to concerns with intussusception.


Class Summary

Therapy must cover all likely pathogens in the context of the clinical setting.

Ciprofloxacin (Cipro)

Fluoroquinolones are the agents of choice for the empiric treatment of invasive and traveler's diarrhea syndromes in adult patients. They are also the agents of choice when treatment is indicated and the organism involved is known to be Campylobacter, E coli (non-O157:H7), nontyphoid Salmonella (although antibiotic treatment may prolong bacterial shedding), Shigella, or Yersinia.

Trimethoprim-sulfamethoxazole (Bactrim)

Excellent second choice for empiric therapy, although it is not effective against Campylobacter organisms. Increasing resistance. First drug of choice for patients younger than 18 years. Specifically recommended for 5 d for shigellosis.

Rifaximin (Xifaxan, RedActiv, Flonorm)

Nonabsorbed (< 0.4%), broad-spectrum antibiotic specific for enteric pathogens of the gastrointestinal tract (ie, gram-positive, gram-negative, aerobic, and anaerobic). Rifampin structural analog. Binds to beta-subunit of bacterial DNA-dependent RNA polymerase, thereby inhibiting RNA synthesis. Indicated for E coli (enterotoxigenic and enteroaggregative strains) associated with travelers' diarrhea.


Class Summary

All these drugs are indicated in the control of nausea and vomiting. All have been associated with extrapyramidal adverse effects, especially in patients who are acutely ill, dehydrated, or children. They should be used with caution and only in the lowest effective dose. A weak association with Reye syndrome exists, and all may mask the vomiting associated with underlying CNS lesions.

Prochlorperazine (Compazine)

Antidopaminergic drug that blocks the postsynaptic mesolimbic dopamine receptors. Has an anticholinergic effect and can depress the reticular activating system, possibly responsible for relieving nausea and vomiting.

Promethazine (Phenergan)

Antidopaminergic agent effective in the treatment of emesis. Blocks postsynaptic mesolimbic dopaminergic receptors in the brain and reduces stimuli to the brainstem reticular system.

Trimethobenzamide (Tigan)

Has central effects in which it inhibits the medullary receptor trigger zone.

Ondansetron (Zofran)

Selective 5-HT3 receptor antagonist that blocks serotonin both peripherally and centrally. Indicated for nausea and vomiting due to radiation and/or chemotherapy and for postoperative nausea and vomiting. Cost considerations.

Antidiarrheal agents

Class Summary

These agents are used to decrease the frequency of diarrheal stools and possibly the duration. They should be used with caution in children and in patients with dysentery, as some reports of prolonged illness and development of toxic megacolon exist.

Loperamide (Imodium)

Antimotility DOC. Generally safe and indicated in the early treatment of travelers' diarrhea.

Diphenoxylate HCl 2.5 mg/atropine sulfate 0.025 mg (Lomotil)

Antidiarrheal agent chemically related to narcotic analgesic meperidine. A subtherapeutic dose of anticholinergic atropine sulfate is added to discourage overdosage, in which case diphenoxylate may clinically mimic the effects of codeine.

Each tab of Lomotil or 5 cc of elixir contains 2.5 mg diphenoxylate hydrochloride and 0.025 mg atropine sulfate.

Almost always the preferred antimotility agent.


Class Summary

Elicit active immunization to increase resistance to infection. Vaccines consist of microorganisms or cellular components, which act as antigens. Administration of the vaccine stimulates the production of antibodies with specific protective properties.

Rotavirus vaccine (RotaTeq, Rotarix)

Currently, 2 orally administered live-virus vaccines are marketed in the United States. Each is indicated to prevent rotavirus gastroenteritis, a major cause of severe diarrhea in infants.

RotaTeq is a pentavalent vaccine that contains 5 live reassortant rotaviruses and is administered as a 3-dose regimen against G1, G2, G3, and G4 serotypes, the 4 most common rotavirus group A serotypes. It also contains attachment protein P1A (genotype P[8]).

Rotarix protects against rotavirus gastroenteritis caused by G1, G3, G4, and G9 strains and is administered as a 2-dose series in infants aged 6-24 wk.

Clinical trials found that the vaccines prevented 74-78% of all rotavirus gastroenteritis cases, nearly all severe rotavirus gastroenteritis cases, and nearly all hospitalizations due to rotavirus.


Questions & Answers


What is gastroenteritis?

What is the pathophysiology of diarrhea in gastroenteritis?

Other than ingestion, which factors may lead to infections causing diarrhea in gastroenteritis?

What is the pathophysiology of vomiting in gastroenteritis?

What is the role of salmonella in the etiology of gastroenteritis?

What is the role of giardia lamblia in the etiology of gastroenteritis?

What is the role of norovirus in the etiology of gastroenteritis?

What is the role of non-norovirus caliciviruses in the etiology of gastroenteritis?

What is the role of rotavirus in the etiology of gastroenteritis?

Which viruses are less common causes of gastroenteritis?

What is the role of clostridium difficile (C diff) in the etiology of gastroenteritis?

What are less common bacterial causes of gastroenteritis?

What are the less common parasitic causes of gastroenteritis?

Which food-borne toxins cause gastroenteritis?

Which medications cause gastroenteritis?

What is the role of pseudomembranous colitis in the etiology of gastroenteritis?

What are the noninfectious causes of gastroenteritis?

What is the prevalence of gastroenteritis in the US?

What are documents outbreaks of gastroenteritis that have occurred in the US?

What is the prevalence of gastroenteritis outbreaks aboard cruise ships and how are they monitored?

What is the global prevalence of gastroenteritis?

Which patient groups have the highest prevalence of gastroenteritis?

What are the possible complications of gastroenteritis?

What is the prognosis of gastroenteritis?

What is included in patient education about gastroenteritis?


What is the focus of clinical history in the evaluation of gastroenteritis?

What is the importance of the duration of illness in the history of gastroenteritis?

What does the presence of high fever suggest in the evaluation of gastroenteritis?

What does a history of vomiting suggest in the evaluation of gastroenteritis?

How is pain characterized in gastroenteritis?

How is stool characterized in gastroenteritis?

How are possible extraintestinal causes of gastroenteritis evaluated?

What are the signs and symptoms of dehydration in gastroenteritis?

Which epidemiologic factors should be assessed in the evaluation of gastroenteritis?

What is included in the physical exam to evaluate gastroenteritis?

Which physical findings are characteristic of dehydration in gastroenteritis?

Which physical findings are characteristic of nutritional depletion in gastroenteritis?

What is included in the abdominal exam to evaluate gastroenteritis?


Which conditions are included in the differential diagnoses of gastroenteritis?

What are considerations in the diagnosis of gastroenteritis in patients with vomiting only?

How is pseudomembranous colitis diagnosed and treated?

How does the presentation of gastroenteritis differ between elderly patients and younger adults?

How is travelers&#39; diarrhea diagnosed and treated?

How is food-borne gastroenteritis diagnosed and treated?

How is gastroenteritis diagnosed and treated in patients with AIDS?

What are the differential diagnoses for Emergent Treatment of Gastroenteritis?


How are the lab tests for the workup of gastroenteritis determined?

What is the role of stool studies and culture in the workup of gastroenteritis?

What is the role of routine lab tests in the workup of gastroenteritis?

What is the role of enzyme-linked immunosorbent assay (ELISA) in the workup of gastroenteritis?

What is the role of imaging studies in the workup of gastroenteritis?

What is the role of sigmoidoscopy in the workup of gastroenteritis?


What is the role of empiric therapy in gastroenteritis treatment?

What is the role of antiemetics in gastroenteritis treatment?

What is included in prehospital care of gastroenteritis?

What is the goal of emergency department (ED) treatment for gastroenteritis?

How are patients with gastroenteritis rehydrated?

What are the solutions for oral rehydration used in gastroenteritis treatment?

What are the steps in refeeding patients with gastroenteritis following rehydration?

What is the role of antidiarrheals in gastroenteritis treatment?

What is included in inpatient care for gastroenteritis?

When is patient transfer indicated for the treatment of gastroenteritis?

Which specialist consultations are beneficial to patients with gastroenteritis?

What is included in outpatient care of gastroenteritis?

How is gastroenteritis prevented?

How is gastroenteritis prevented when traveling?

How is norovirus gastroenteritis prevented?


What is the role of medications in the treatment of gastroenteritis?

Which medications in the drug class Vaccines are used in the treatment of Emergent Treatment of Gastroenteritis?

Which medications in the drug class Antidiarrheal agents are used in the treatment of Emergent Treatment of Gastroenteritis?

Which medications in the drug class Antiemetics are used in the treatment of Emergent Treatment of Gastroenteritis?

Which medications in the drug class Antibiotics are used in the treatment of Emergent Treatment of Gastroenteritis?