Viral Gastroenteritis

Etiology

Several different viruses, including rotavirus, norovirus, adenovirus, and astrovirus, 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; 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 the 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, studies 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 younger than 5.[9] Since the routine vaccination of children, each year has seen a significant reduction in cases.[10][11][12] 

Before vaccination, the United States saw an estimated 55,000 to 70,000 hospitalizations of children younger than 5 due to rotavirus. According to the CDC, this number has decreased by 40,000 to 50,000 since the vaccine became available. 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.[13] Now, the virus tends to infect individuals in the United States sporadically throughout the year. Despite the widespread use of the vaccine in developed countries, rotavirus is still the leading cause of infantile diarrheal illness worldwide, with the CDC estimating that 215,000 rotavirus-related deaths occurred in 2013. Although there has been a continued decline in disease burden, some regions of the world are still disproportionately affected by this virus.[14] 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. Please see StatPearls' companion resource, "Rotavirus", for further information.

Norovirus

Norovirus is a single-stranded RNA member of the calicivirus family.[15] This viral pathogen is the most common cause of epidemic diarrheal illness, accounting for >90% of viral gastroenteritis outbreaks and approximately 50% of cases worldwide.[16][17] Norovirus can withstand freezing, heating, and common disinfectant products containing alcohol or chlorine.[18] Norovirus is a frequent cause of outbreaks within somewhat closed communities, eg, nursing homes, schools, military populations, athletic teams, and cruise ships.

Norovirus presents most commonly with abdominal cramps and nausea, followed by vomiting and diarrhea. Onset can be abrupt. Symptoms also include myalgias, malaise, and fevers up to 102.2 °F (39 °C). Diarrhea is non-bloody and can consist of multiple bowel movements per day. The illness is self-limiting, and most patients recover in 72 hours without sequelae.[1] Elderly individuals and immunocompromised patients may have a more severe and prolonged illness. 

Norovirus infection causes histopathologic changes in the jejunum of blunted villi with intact mucosa.[19] These changes occur quickly and usually resolve within 2 weeks after the onset of illness. Fat and d-xylose absorption decrease, as does brush border enzyme activity, leading to diarrhea.[19] Unlike rotavirus, enterotoxin production does not seem to occur.

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 annually. Norovirus is estimated to cause 103,000 hospitalizations and 900 deaths annually in the United States. A majority of these deaths occur in people older than 65.[17] Because of its relative environmental stability, norovirus is implicated in approximately 50% of all foodborne outbreaks.[17] Norovirus is present throughout the year, despite initially being thought of as a disease that peaks in the winter months. Please see StatPearls' companion resource, "Norovirus", for further information.

Other viral causes of acute viral gastroenteritis include adenovirus, sapovirus, and astrovirus.[20] 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. Norovirus accounts 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 58% of all foodborne diarrheal outbreaks.[17] 

Before routine vaccination, rotavirus was the most common cause of diarrheal illness in the pediatric population, with roughly 3.5 million cases yearly in the United States. Nearly all children possessed rotavirus antibodies by age 3. 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.[13] As more countries adopt the standard practice of rotavirus vaccination, the overall number of cases is expected to continue to decrease. Other viral causes, eg, adenovirus, sapovirus, and astrovirus, account for 2% to 9% of cases worldwide, with a higher bias for children than adults.[20]

Pathophysiology

The clinical manifestations of 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 leads to malabsorption and osmotic diarrhea.[8] Additionally, viral toxins lead to direct damage and cell lysis of enterocytes and intestinal villi, causing a transudative fluid loss into the intestine.[19] 

The loss of cell function can lead to electrolyte abnormalities 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][19]

History and Physical

Clinical History

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, often improving after 1 to 3 days. Any signs of illness that persist past 2 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 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.

Symptoms, eg, high fever, bloody diarrhea, protracted vomiting, or severe abdominal pain, are often indicative of an underlying etiology other than viral gastroenteritis. Therefore, clinicians should elicit information relevant to differential diagnoses of viral gastroenteritis, eg, 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, older patients, and immunosuppressed individuals secondary to disease or medication usage. 

Physical Examination

Addressing any abnormal vital signs noted on physical examination is also essential. Mild fever is common in viral gastroenteritis, but a high fever (>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 have a much higher risk of severe complications due to dehydration. Other physical exam findings associated with viral gastroenteritis include mild, diffuse abdominal tenderness. Significant tenderness to palpation, guarding, rebound, or point-specific tenderness should lead the clinician to consider other diagnoses that may cause these symptoms.

Evaluation

Laboratory Studies

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. Diagnostic laboratory studies may help exclude 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 suffering from significant dehydration may demonstrate hemoconcentration on complete blood count testing and electrolyte disturbances on chemistry panels. Dehydration may also present as acute kidney injury, evidenced by changes in the BUN and creatinine on a chemistry panel.

Diagnostic Imaging Studies

Imaging studies of the abdomen most often appear normal. Computed tomography (CT) scans may reveal mild, diffuse colonic wall thickening or other inflammatory changes of the bowel. However, no specific findings are diagnostic of viral gastroenteritis, 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

Viral gastroenteritis management primarily comprises supportive therapies.[3][4][21] The most important goal of treatment is to maintain hydration status and effectively counter fluid and electrolyte losses. Therefore, fluid management is a fundamental component of treatment. Intravenous fluids may be administered to those individuals who appear dehydrated or to those unable to tolerate oral fluids. Antiemetic medications (eg, ondansetron or metoclopramide) may be used to assist with controlling nausea and vomiting symptoms.(A1)

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 individually, although these are often 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, eg, diphenoxylate/atropine or loperamide, are not recommended for patients aged 65 or older. Younger patients may benefit from antimotility medications.[4] However, some feel that in patients who are able to 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.[22] 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 compared to regular diets.[23](A1)

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 antiemetic medication is often prescribed for home use in children, no clear evidence that it helps to prevent return visits to the emergency department has been established.[24][25] Patients who may benefit from hospital observation or admission are those who 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, a clinician must be aware of and rule out other, more severe causes of the patient’s symptoms. Food poisoning due to bacterial toxins frequently causes symptoms 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 frequently require a different treatment approach and may carry a higher morbidity potential.

Pathogens, eg, Salmonella, Escherichia coli, Shigella, Campylobacter, Giardia lamblia, and Clostridium difficile may be potential causes in patients 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 examination findings warrant 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 viral gastroenteritis.

Prognosis

The prognosis of viral gastroenteritis in most cases is excellent and self-limited. However, continued maintenance of oral hydration is essential, even if a patient does not seek medical care. Mortality does occur at extremes of age and in immunosuppressed individuals. Today, calciviruses are associated with more deaths than rotaviruses. Noroviruses have been involved in many nursing home outbreaks, and the diarrhea is often severe. Newer strains of norovirus have evolved and continue to be more virulent.