Emergent Treatment of Gastroenteritis

2/25/2019 https://emedicine.medscape.
com/article/775277-print
emedicine.medscape.com
Emergent Treatment of
Gastroenteritis
Updated: Feb 10, 2017
Author: Arthur Diskin, MD; Chief Editor: Steven C Dronen, MD, FAAEM
Overview
Background
Gastroenteritis is a nonspecific term for various pathologic states of the gastrointestinal tract. The primary manifestation is
diarrhea, but it may be accompanied by nausea, vomiting, and abdominal pain. A universal definition of diarrhea does not exist,
although patients seem to have no difficulty defining their own situation. Although most definitions center on the frequency,
consistency, and water content of stools, the author prefers defining diarrhea as stools that take the shape of their container.
The severity of illness may vary from mild and inconvenient to severe and life threatening. Appropriate management requires
extensive history and assessment and appropriate, general supportive treatment that is often etiology specific. Diarrhea
associated with nausea and vomiting is referred to as gastroenteritis.
Diarrhea is one of the most common reasons patients seek medical care. In the developed world, it is one of the most common
reasons for missing work, while in the developing world, it is a leading cause of death. In developing countries, diarrhea is a
seasonal scourge usually worsened by natural phenomena, as evidenced by monsoon floods in Bangladesh in 1998 or the
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.
Pathophysiology
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.
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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.
Etiology
Viral (50-70%) causes of gastroenteritis
Norovirus
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.[2]
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, 54% of patients were contaminated by food, 17% by person to person, 4% by water, and 25% by
unidentified sources. 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.[3]
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.
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.
Caliciviruses
Various caliciviruses, other than norovirus, are likely responsible for many outbreaks of previously unidentified viral
gastroenteritis.
Rotavirus
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 now 2 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 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 800,000 annually. 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 include the following:
Salmonella
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 1.4 million infections in the United States each year, of which only about 40,000 are reported. 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.[4]
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.[5] 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.[6] 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.[7] 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
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 2 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 little 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.[8] 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 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
Epidemiology
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.[9]
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[10] 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 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 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.
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.[11] 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.[12]
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 in 2010, 14 in 2011, 16 in 2012 and 9 in 2013.[13]
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.[14, 15] 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.[16]
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).[17]
In a 2017 report that estimated the healthcare costs of acute gastroenteritis and human Campylobacter infection in Switzerland,
investigators reported an annual cost of approximatedly 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 positive Campylobacter species stool tests; and 6.5 million euros
for inpatients with Campylobacter infection.[18]
Race-, sex-, and age-related demographics
Significantly higher mortality is observed among women and non-Hispanic white individuals.[19]
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.[19]
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.[9]
Pediatric gastroenteritis is discussed in the Medscape Drugs & Diseases article Pediatric Gastroenteritis.
Prognosis
Morbidity/mortality
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.[19] 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,[19] although 50% more deaths occurred in
years when epidemics were caused by new strains of the virus.[20]
Complications
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.
For patient education resources, see the Digestive Disorders Center, as well as Gastroenteritis, Abdominal Pain in Adults,
Diarrhea, and Vomiting and Nausea.
Presentation
History
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.
Fever
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
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.
Pain
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.
Stools
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.
Dehydration
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.) 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.
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.
DDx
Diagnostic Considerations
Other conditions to consider in the differential diagnosis of gasteroenteritis include the following:
Various infectious etiologies
Pseudomembranous colitis
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.[21]
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
Appendicitis
CBRNE - Botulism
Giardiasis
Hemolytic Uremic Syndrome in Emergency Medicine
Hypovolemic Shock
Inflammatory Bowel Disease
Large-Bowel Obstruction
Pediatric Dehydration
Pediatric Gastroenteritis in Emergency Medicine
Salmonella Infection in Emergency Medicine
Small-Bowel Obstruction
Workup
Workup
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.
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.
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.
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.
Rotavirus
Enzyme-linked immunosorbent assay (ELISA) is available in less than 2 hours but is not sensitive enough in adults.
Giardia
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.
Procedures
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.
Treatment
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.
Rehydration
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.
Refeeding
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
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 gastrenteritis
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.[22] 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.[22]
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
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.
Consultations
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.
Prevention
Breastfeeding
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
Precautions
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.
Travelers
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.
Norovirus
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 finger tips 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
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.[23] 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 G 9. Rotashield, an earlier vaccine, was
withdrawn from the market due to concerns with intussusception.
Antibiotics
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.
Antiemetics
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.
Vaccines
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.
Contributor Information and Disclosures
Author
Arthur Diskin, MD Vice-President, Global Chief Medical Officer, Royal Caribbean Cruise Lines; Voluntary Associate Professor,
University of Miami, Leonard M Miller School of Medicine
Arthur Diskin, MD is a member of the following medical societies: American College of Emergency Physicians
Disclosure: Nothing to disclose.
Coauthor(s)
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
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.
BS Anand, MD Professor, Department of Internal Medicine, Division of Gastroenterology, Baylor College of Medicine
BS Anand, MD is a member of the following medical societies: American Association for the Study of Liver Diseases, American
College of Gastroenterology, American Gastroenterological Association, American Society for Gastrointestinal Endoscopy
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
Acknowledgements
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
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
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Emergent Treatment of Gastroenteritis

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2/25/2019 https://emedicine.medscape.

Diarrheal illnesses may be classified as follows:

Secretory, when increased secretory activity occurs

Motile, caused by intestinal motility disorders

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

Bacterial (15-20%) causes of gastroenteritis include the following:

Other bacterial causes include the following:

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

M avium-intracellulare (MAI), immunocompromised

Parasitic (10-15%) causes of gastroenteritis

Other parasitic causes include the following:

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:

Neurologic shellfish poisoning (NSP) - Brevetoxin

Diarrheal shellfish poisoning (DSP) - Okadaic acid

Amnesic shellfish poisoning - Domoic acid

Scombroid (conversion of histidine to histamine)

Medications associated with diarrhea include the following:

Antibiotics, due to alteration of normal flora

Laxatives, including magnesium-containing antacids

Other causes include the following:

Unknown agents, especially in developing countries

Carcinoid tumor or vasoactive intestinal peptide tumor (VIPoma)

Acquired immunodeficiency syndrome (AIDS)

Dumping or short bowel syndrome

Race-, sex-, and age-related demographics

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

Complications of gastroenteritis include the following:

Transient lactose intolerance

Systemic infection (meningitis, arthritis, pneumonia) especially with Salmonella infections

Sepsis (Salmonella, Yersinia, Campylobacter organisms)

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

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

Guillain-Barré syndrome (Campylobacter organisms)

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

The following discussion involves elements of the history to obtain.

Cramps may be caused by an electrolyte imbalance.

Note the following:

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

Severe dehydration may also be associated with significant electrolyte imbalances.

Note the following:

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

Hydration and nutritional status

Appendicitis in children may manifest as diarrhea.

Various infectious etiologies

Food-borne toxigenic diarrhea

Hormonal (vasoactive intestinal peptides)

Drugs (ie, sorbitol, cholinergics, caffeine)

Pediatrics - Adrenogenital/cystic fibrosis

Hemolytic-uremic syndrome in patients with E coli infection

Pseudomembranous colitis (C difficile)

Appendicitis in patients who present with vomiting and diarrhea

Note the following:

Note the following:

Complications include dehydration, toxic megacolon, and perforation.

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

Note the following:

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