Viral Gastroenteritis

Stuempfig ND, Seroy J.

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Introduction
Acute infectious gastroenteritis is a common illness seen around the world.
Viral pathogens cause most of these cases. The acute diarrheal disease is
generally self-limiting in industrialized nations but can have significant
morbidity for young and elderly patients. In underdeveloped countries, viral
diarrheal diseases are a significant cause of death, especially in infants [1][2].
According to the Centers for Disease Control, viral gastroenteritis infections can
account for over 200,000 deaths of children per year worldwide. Viral
gastroenteritis is a known cause of nausea, vomiting, diarrhea, anorexia, weight
loss, and dehydration. Isolated cases can occur, but viral gastroenteritis more
commonly occurs in outbreaks within close communities such as daycare
centers, nursing facilities, and cruise ships. Many different viruses can lead to
symptomatology, though in routine clinical practice the true causative virus is
generally not identified. Regardless of the viral cause, treatment is generally
uniform and directed toward symptomatic improvement with a focus on
hydration status [1][2]. In the United States and other industrialized countries,
the disease is most often self-limited and resolves in 1 to 3 days. However, in
susceptible patients including young children, elderly patients, and the
immunocompromised, hospitalization can occur without proper supportive care
leading to increased morbidity and mortality [3][4].

Etiology
Several different viruses including rotavirus, norovirus, adenovirus, and
astroviruses account for most cases of acute viral gastroenteritis. Most are
transmitted via the fecal-oral route, including contaminated food and water.
Transmission has also been shown to occur via fomites, vomitus, and possibly
airborne methods. Norovirus is more resistant to chlorine and ethanol
inactivation than other viruses.
Rotavirus
Rotavirus is a double-stranded RNA virus named for the wheel-like appearance
of its viral capsid on an electron micrograph. Rotavirus infection is universal
among humans, and almost all children acquire antibodies by age
3 [5]. Rotavirus infection usually presents with acute vomiting followed by
several days of diarrhea, crampy abdominal pain, anorexia, and low-grade
fevers. Infants and young children who develop severe dehydration are more
likely to have an infection from rotavirus than other viral gastroenteritis
pathogens. Viral shedding of infectious particles can occur in the stool for up to
10 days [6]. Adults are more likely to develop an asymptomatic infection with a
rise in antibody titer. Immunosuppressed individuals can experience more
prolonged and severe disease, with longer viral shedding [7]. Rotavirus
pathogenesis is complicated with several possible mechanisms including
malabsorption from mucosal damage, viral enterotoxin secretion, and enteric
secretions in response to the virus. Rotavirus increases electrolyte secretion
from the small intestine and decreases glucose cotransport of these
electrolytes [8].
Throughout recorded history, rotavirus has been the leading cause of episodic
infantile illness worldwide. However, in 2006 an oral vaccine was introduced.
Since the introduction and utilization of this vaccine, the United States and
many other industrialized countries have seen a sharp decline in the number and
severity of gastroenteritis cases caused by rotavirus. Before 2006, it was
estimated that over 3.5 million infants were affected annually in the United
States and that rotavirus led to 440,000 deaths annually worldwide in children
less than five years old [9]. Since the routine vaccination of children, each year
has seen a 58% to 90% reduction in cases [10]. Before vaccination, the United
States saw an estimated 55,000-70,000 hospitalizations of children under five
due to rotavirus. This number has decreased by 40,000-50,000 since the vaccine
became available, according to the Centers for Disease Control. Although the
incidence of rotavirus in the United States has been historically seasonal, with
peak seasonality being from December to April, this pattern has become very
inconsistent since vaccination became common [11]. Now, the virus tends to
infect sporadically throughout the year in the United States. Despite widespread
use of the vaccine in developed countries, rotavirus is still the leading cause of
infantile diarrheal illness worldwide. The Centers for Disease Control estimated
that there were still 215,000 rotavirus-related deaths in 2013. More than 40% of
World Health Organization member countries have initiated large-scale
vaccination of children. This number is anticipated to rise in the next few years.
In turn, infection and mortality caused by rotavirus are expected to continue
declining.
Norovirus
Norovirus is a single-stranded RNA member of the calicivirus family [12]. It is
the most common cause of epidemic diarrheal illness, accounting for over 90%
of viral gastroenteritis outbreaks and approximately 50% of
cases worldwide [13]. Norovirus can withstand freezing, heating, and common
disinfectant products containing alcohol or chlorine [14]. It is a frequent cause
of outbreaks within somewhat closed communities such as nursing homes,
schools, military populations, athletic teams, and cruise ships.
Norovirus presents most commonly with abdominal cramps and nausea
followed by vomiting and/or diarrhea. Onset can be abrupt. Symptoms also
include myalgias, malaise, and low-grade fevers up to 39 C. Diarrhea is non-
bloody and can consist of multiple bowel movements per day. The illness is
self-limiting, and most patients have recovered in 72 hours without sequelae [1].
Elderly individuals and immunocompromised patients may have more severe
and prolonged illness.
Norovirus infection causes histopathologic changes in the jejunum of blunted
villi with intact mucosa [15]. These changes occur quickly and usually resolve
by two weeks after the onset of illness. Fat and d-xylose absorption decrease as
does brush border enzyme activity leading to diarrhea [15]. Unlike rotavirus,
there does not seem to be enterotoxin production.
Since the advent of the rotavirus vaccine, norovirus has become the most
common cause of viral gastroenteritis in the United States, responsible for 19 to
21 million total illnesses per year. It is estimated to cause 56,000-71,000
hospitalizations and 570-800 deaths annually in the United States [13]. Because
of its relative stability in the environment, norovirus is implicated in nearly 50%
of all foodborne outbreaks [13]. Norovirus is present throughout the year,
despite initially being thought of as a disease that peaked in the winter months.
Other viral causes of acute viral gastroenteritis include adenovirus, sapovirus,
and astrovirus [16]. Each of these viruses can cause anywhere between 2% to
9% of viral gastroenteritis cases, with developing countries seeing a slightly
higher burden of disease from the astrovirus group. These viruses tend to affect
children more than adults.

Epidemiology
The most frequent cause of diarrheal disease worldwide is acute viral
gastroenteritis. Men and women are affected equally. Norovirus is the most
common viral cause. It is responsible for 90% of epidemic diarrheal cases
worldwide and approximately 50% of all viral gastroenteritis cases. It accounts
for 19 to 21 million cases of diarrheal illness annually in the United States
alone. Norovirus causes 50% of all foodborne diarrheal outbreaks [13]. Prior to
routine vaccination, rotavirus was the most common cause of diarrheal illness in
the pediatric population with roughly 3.5 million cases per year in the United
States. Nearly all children possessed rotavirus antibodies by age three.
Worldwide, rotavirus accounted for 440,000 deaths per year [9]. However, since
the implementation of vaccination in 2006, the number of cases seen annually in
the United States has declined 50% to 90% per year [11]. As more countries
adopt the standard practice of rotavirus vaccination, the overall number of cases
is expected to continue to decrease. Other viral causes such as adenovirus,
sapovirus, and astrovirus account for 2% to 9% of cases worldwide, with a
higher bias for children than adults [16].

Pathophysiology
The clinical manifestations for viral gastroenteritis are due to the effects that the
viruses, along with specific cytotoxins, have on the enterocytes of the intestine.
The virus uses the enterocyte to replicate, leading to interference with brush
border enzyme production, which in turn leads to malabsorption and osmotic
diarrhea [8]. Additionally, viral toxins lead to direct damage and cell lysis of
enterocytes and intestinal villa, causing a transudative loss of fluid into the
intestine [15]. The loss of cell function can lead to electrolyte abnormalities
which are caused by the loss of transporter functionality. That can lead to acid-
base disturbances as well. The virus is then shed through feces, and occasionally
in the vomitus. Peak viral load within the stool is anywhere between 24 to 48
hours after symptomatology. Some studies show viral shedding lasting for
several weeks past symptomatology [8][15].

History and Physical

Acute gastroenteritis is defined by loose or watery diarrhea that consists of 3 or
more bowel movements in a day. Other symptoms may include nausea,
vomiting, fever, or abdominal pain [3]. Symptoms usually last for less than a
week, most often improving after 1 to 3 days. Any signs of illness that persist
past two weeks are classified as chronic and therefore do not meet the
requirements for acute gastroenteritis. Patients often present with complaints of
a relatively sudden onset of symptoms, usually over the course of 1 to 2 hours.
Other people in the family or close contacts may have similar complaints. Mild
fever and mild abdominal pain are common. Vomiting is present in most but not
all cases. Concerning symptoms include high fever, bloody diarrhea, protracted
vomiting, or severe abdominal pain. These may indicate to the clinician that
another disease process may be the cause. It is important to elicit information
relevant to causes other than viral gastroenteritis, such as bacterial agents or
other acute abdominal pathology including acute appendicitis, bowel
obstruction, and diverticulitis. Travel history, recent antibiotic use, disease
exposure, occupational exposures, and immune status should all be
considered. Particular attention should be paid to infants, elderly patients, and
individuals who are immunosuppressed due to disease or medication usage.
Upon physical exam, it is important to address any abnormal vital signs. Mild
fever is common in viral gastroenteritis, but high fever (greater than 39 C)
should trigger concern for causes that are not viral in origin. Additionally,
tachycardia and tachypnea may be present due to fever and dehydration. An
assessment for dehydration is of the utmost importance, especially in patients
who demonstrate extremes of age, chronic illness, or immunosuppression.
These patient groups are at a much higher risk for severe complications due to
dehydration. Another physical exam finding may include mild, diffuse
abdominal tenderness. Significant tenderness to palpation, guarding, rebound, or
point-specific tenderness should lead the clinician to consider other causes of
symptomatology.

Evaluation
Due to the lack of readily available viral testing capabilities in most clinics and
emergency departments, acute viral gastroenteritis is a clinical diagnosis.
Therefore, patients who appear clinically well-hydrated and who lack risk
factors for severe disease do not necessarily warrant further testing. Diagnostics
are used to help rule out other causes of the patient’s symptoms. Complete
blood counts may reveal a mild leukocytosis in a patient with viral
gastroenteritis. Other serum inflammatory markers may also show mild
elevation. Patients who are suffering from significant dehydration may
demonstrate hemoconcentration on complete blood count testing as well as
electrolyte disturbances on chemistry panels. Dehydration may also present as
acute kidney injury, evidenced by changes in the BUN and creatinine on
chemistry panel.
Imaging studies of the abdomen most often appear normal. CT scans may reveal
mild, diffuse colonic wall thickening or other inflammatory changes of the
bowel. However, there are no specific findings, and CT scanning should be
performed to rule out other, more severe etiologies. Stool studies may be
obtained, but readily available laboratory testing assays assess only for bacterial
causes and do not diagnose specific viral causes. Patients with bloody stool,
high fever, severe abdominal pain, or severe dehydration warrant stool studies
as these symptoms are not consistent with simple viral gastroenteritis.

Treatment / Management
The treatment of viral gastroenteritis is based on symptomatic support [3][4].
The most important goal of treatment is to maintain hydration status and
effectively counter fluid and electrolyte losses. Fluid therapy is a fundamental
part of treatment. Intravenous fluids may be administered to those individuals
who appear dehydrated or to those unable to tolerate oral fluids. Antiemetic
medications such as ondansetron or metoclopramide may be used to assist with
controlling nausea and vomiting symptoms. Patients demonstrating severe
dehydration or intractable vomiting may require hospital admission for
continued intravenous fluids and careful monitoring of electrolyte status.
Electrolyte abnormalities may be addressed on an individual level, although
often these are caused by an overall fluid volume depletion which, when
corrected, will also cause electrolytes to normalize. Both saline and lactated
Ringer’s solutions appear to be effective for the treatment of dehydration due to
viral gastroenteritis.
Debate exists over antidiarrheal medication usage. Medications such
as diphenoxylate/atropine or loperamide are not recommended in patients who
are 65 or older. Younger patients may benefit from antimotility medications [4].
However, some feel that if a patient can maintain a well-hydrated status,
antidiarrheal treatment should not be initiated. For oral rehydration, some
studies have shown that commercially available oral rehydration solutions
containing electrolytes are superior to sports drinks and other forms of oral
rehydration [2]. However, a recent study using children with mild dehydration
demonstrated no differences between children receiving oral rehydration
solutions versus ad lib oral intake [17]. No specific nutritional recommendations
are universal for patients with viral gastroenteritis. A diet of banana, rice,
apples, tea, and toast is often advised, but several studies have failed to show
any significant outcome difference when compared to regular diets [18].
Most patients who present to outpatient clinics or the emergency department
with acute viral gastroenteritis can be discharged home safely. Adults often
benefit from antiemetic medications at home although home antiemetic
medication is not recommended in young children. Patients who may benefit
from hospital observation or admission are those that demonstrate signs or
symptoms of dehydration, intractable vomiting, severe electrolyte disturbances,
significant renal failure, severe abdominal pain, or pregnancy.

Differential Diagnosis
Although acute viral gastroenteritis is generally a self-limiting illness in the
industrialized world, it is essential for a clinician to be aware of and rule out
other, more severe causes of the patient’s symptoms. Food poisoning due to
bacterial toxins frequently causes symptoms very similar to viral gastroenteritis,
though the treatment for food poisoning often parallels that of viral
gastroenteritis. Bacterial and protozoal causes of gastroenteritis can potentially
mimic symptoms of viral gastroenteritis but often require a different treatment
approach and may carry higher morbidity potential. Pathogens such
as Salmonella, Escherichia coli, Shigella, Campylobacter, Giardia lamblia,
and Clostridium difficile may be potential causes in those patients who present
with atypical symptoms of viral gastroenteritis. Other acute abdominal
pathology including but not limited to acute appendicitis, diverticulitis,
inflammatory bowel disease, bowel obstruction, or cholecystitis needs to be
investigated if the patient’s history or physical exam warrants it. Many cases of
missed abdominal pathology are initially diagnosed as viral gastroenteritis.
Viral upper respiratory illnesses and certain types of bacterial pneumonia may
also present with symptoms similar to that of viral gastroenteritis.

Enhancing Healthcare Team Outcomes

The majority of patients with gastroenteritis present to the emergency room.
However, because there are so many causes of gastroenteritis, the emergency
department physician, nurse practitioner and internist need to rule out other
serious disorder first become making a diagnosis of viral gastroenteritis, which
is a clinical diagnosis aided with laboratory data.
Food poisoning due to bacterial toxins frequently causes symptoms very similar
to viral gastroenteritis, though the treatment for food poisoning often parallels
that of viral gastroenteritis. Bacterial and protozoal causes of gastroenteritis can
potentially mimic symptoms of viral gastroenteritis but often require a different
treatment approach and may carry higher morbidity potential.
If there is any doubt about the diagnosis, the infectious disease expert should be
consulted before discharging the patient. Most patients with viral gastroenteritis
improve with supportive measures including hydration and bowel rest.

Questions
To access free multiple choice questions on this topic, click here.

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Publication Details

Author Information

Authors
Nathan D. Stuempfig1; Justin Seroy2.

Affiliations
1 The Permanente Medical Group
2 Banner University Medical Center Phoenix

Publication History
Last Update: June 17, 2019.

Copyright
Copyright © 2019, StatPearls Publishing LLC.

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Publisher
StatPearls Publishing, Treasure Island (FL)

NLM Citation
Stuempfig ND, Seroy J. Viral Gastroenteritis. [Updated 2019 Jun 17]. In: StatPearls [Internet]. Treasure
Island (FL): StatPearls Publishing; 2019 Jan-.