ﺑﺎﺯﮔﺸﺖ ﺑﻪ ﺻﻔﺤﻪ ﻗﺒﻠﯽ
خرید پکیج
تعداد آیتم قابل مشاهده باقیمانده : 3 مورد
نسخه الکترونیک
medimedia.ir

Acute viral gastroenteritis in children in resource-abundant countries: Clinical features and diagnosis

Acute viral gastroenteritis in children in resource-abundant countries: Clinical features and diagnosis
Literature review current through: Jan 2024.
This topic last updated: Sep 27, 2022.

INTRODUCTION — The epidemiology, clinical features, and diagnosis of acute viral gastroenteritis in children in resource-abundant countries will be discussed here. The prevention and treatment of acute viral gastroenteritis in children in resource-abundant countries, acute diarrhea in children in resource-limited countries, and chronic diarrhea in children are discussed separately.

(See "Acute viral gastroenteritis in children in resource-abundant countries: Management and prevention".)

(See "Approach to the child with acute diarrhea in resource-limited settings".)

(See "Overview of the causes of chronic diarrhea in children in resource-abundant settings" and "Approach to chronic diarrhea in children >6 months in resource-abundant settings" and "Persistent diarrhea in children in resource-limited settings".)

DEFINITIONS

Acute gastroenteritis – A clinical syndrome often defined by increased stool frequency with loose consistency with or without vomiting, fever, or abdominal pain [1-5]; examples of increased stool frequency include:

≥3 loose or watery stools in 24 hours

Number of loose/watery bowel movements that exceeds the child's usual number of daily bowel movements by two or more

Acute gastroenteritis usually lasts less than one week and not longer than two weeks. Most cases of acute gastroenteritis are caused by viruses, bacteria, and parasites, although noninfectious conditions can cause similar manifestations. (See 'Etiology' below.)

Acute viral gastroenteritis – Acute gastroenteritis caused by a viral pathogen

Persistent or chronic diarrhea – Diarrhea that lasts >14 days

Recurrent diarrhea – Diarrhea that recurs after seven days without diarrhea

PATHOGENESIS — The major clinical manifestations of viral gastroenteritis are caused by intestinal infection and destruction of enterocytes, which results in transudation of fluid into the intestinal lumen and net loss of fluid and salt in the stool [6-10]. Intestinal injury also decreases the ability to digest food, particularly complex carbohydrates, and to absorb digested food across the intestinal mucosa. The pathogenesis of acute diarrhea is discussed in detail separately. (See "Pathogenesis of acute diarrhea in children" and "Clinical manifestations and diagnosis of rotavirus infection", section on 'Pathogenesis and histopathology'.)

Factors associated with severe or prolonged clinical manifestations include [11-16]:

First infection with a particular pathogen

Malnutrition

Lack of maternally acquired immunity (eg, antibody acquired transplacentally or via human milk)

Immune compromise

Large inoculum of virus

EPIDEMIOLOGY — Acute viral gastroenteritis occurs throughout the year, with a fall and winter predominance in most temperate climates (table 1) [17-20]. During the first two years of the coronavirus disease 2019 (COVID-19) pandemic, there was a global decrease of acute childhood gastrointestinal infections, most likely related to the seclusion of children in households.

Acute viral gastroenteritis can be transmitted by asymptomatic carriers as well as by symptomatic patients before the onset of symptoms [4,21,22]. It is generally transmitted by the fecal-oral route. The possibility of airborne transmission of rotavirus and norovirus has been suggested in some outbreaks [23-25].

ETIOLOGY — The most common causes of acute viral gastroenteritis in children are described below (table 1).

In active surveillance in the United States during 2011 to 2016, a pathogen was detected in 51.2 percent of 660 children age 14 days to 11 years who were hospitalized with acute gastroenteritis and in 20.6 percent of 624 age-matched healthy controls [26]. The most commonly detected viruses were norovirus (18.5 percent of cases, 6.6 percent of controls), rotavirus (16.1 percent of cases, 9.8 percent of controls), and adenovirus (7.7 percent of cases, 1.4 percent of controls).

Rotavirus – Rotavirus gastroenteritis usually occurs in children between six months and two years of age [27,28]. It occurs in the fall and winter in middle- to high-income countries with temperate climates and throughout the year in low and middle-low income countries and countries with tropical climates (table 1). (See "Clinical manifestations and diagnosis of rotavirus infection".)

Rotavirus has historically been the most common cause of medically attended viral gastroenteritis in children. In countries that routinely immunize infants against rotavirus, rotavirus gastroenteritis has decreased substantially, although some older children and adults develop symptomatic rotavirus disease [29-31]. (See "Rotavirus vaccines for infants", section on 'Efficacy/effectiveness'.)

In the United States, laboratory surveillance during the prevaccine (2000 to 2006) and postvaccine (2007 to 2018) periods demonstrates decreases in rotavirus-positive laboratory tests (from 26 to 6 percent) and rotavirus-positive laboratory tests during the characteristic autumn-winter peak (from 43 to 14 percent) and in the duration of the "rotavirus season" (from 26 to 9 weeks), as well as the emergence of a biennial pattern with alternating years of low and high rotavirus activity (figure 1) [32]. In the United States, state-specific annual rotavirus season activity appears to be related to accumulation of susceptible children (ie, high birth rate and low rotavirus vaccination coverage) [33].

Norovirus – Norovirus gastroenteritis occurs in people of all ages. It occurs year-round [34]. Norovirus is highly contagious and the leading cause of outbreaks of gastroenteritis [22,35,36]. Older children and adolescents with severe acute gastroenteritis, especially as part of a common source outbreak (food, water source, or fomite), are more likely to have norovirus than other causes of acute gastroenteritis [22,37,38]. Norovirus also causes sporadic gastroenteritis, which occurs primarily in young children [39,40]. (See "Norovirus".)

Norovirus is, or is becoming, the leading cause of medically attended gastroenteritis in children in countries that immunize infants against rotavirus gastroenteritis [30,41-44]. In active surveillance in the United States during 2011 to 2016, norovirus was detected in 18.5 percent of children (age 14 days to 11 years) hospitalized with acute gastroenteritis compared with 6.6 percent of healthy controls [26].

Sapovirus – Sapovirus gastroenteritis mainly affects infants and toddlers [35,45,46]. It occurs year-round. The clinical illness is milder than that of rotavirus.

In laboratory surveillance from three counties in the United States during 2008 to 2009, sapovirus was isolated from 5.4 percent of 1281 children younger than five years with medically attended acute gastroenteritis [17]. It was detected throughout the year, with the highest proportion from March through July. In active surveillance in the United States during 2012, sapovirus was detected in 7 percent of children <2 years of age who were hospitalized or seen in the emergency department for acute diarrhea compared with 3 percent of healthy controls [47].

Astrovirus – Astrovirus occurs in people of all ages. It may cause outbreaks in closed populations [35]. Sporadic astrovirus gastroenteritis occurs primarily in children younger than four years. Astrovirus gastroenteritis usually occurs in the winter months.

Astrovirus is less frequently isolated from hospitalized children than rotavirus and norovirus. In laboratory surveillance from three counties in the United States during 2008 to 2009, astrovirus was isolated from 4.9 percent of 1281 children younger than five years with medically attended acute gastroenteritis [17]. Astrovirus was predominantly detected from November through May. In active surveillance in the United States during 2012, astrovirus was detected in 3 percent of children <2 years of age who were hospitalized or seen in the emergency department for acute diarrhea compared with 0.3 percent of healthy controls [47].

Enteric adenovirus – Adenovirus gastroenteritis predominantly affects children younger than four years [10,35]. It occurs throughout the year, with a peak in the summer [17,18,35]. (See "Pathogenesis, epidemiology, and clinical manifestations of adenovirus infection", section on 'Gastrointestinal system'.)

In laboratory surveillance from three counties in the United States during 2008-2009, enteric adenovirus was isolated from 11.8 percent of 1281 children younger than five years with medically attended acute gastroenteritis [17]. Enteric adenovirus was detected throughout the year, with the highest proportion in June. In active surveillance in the United States during 2012, adenovirus was detected in 23 percent of children <2 years of age who were hospitalized or seen in the emergency department for acute diarrhea compared with 16 percent of healthy controls [47].

Other viruses – Viruses that typically have extraintestinal manifestations (eg, coxsackievirus, echovirus, poliovirus, severe acute respiratory syndrome coronavirus 1 or 2, influenza virus type B) also may cause mild gastroenteritis.

Mixed viral infections – Mixed viral infections are common, but the clinical significance of coinfection with multiple viruses is unclear. In a 2014 literature review of studies using polymerase chain reaction to detect viral gastroenteritis pathogens, the prevalence of mixed infections in children with symptoms of gastroenteritis ranged from 5.7 to 17 percent [48]. Detection of more than one virus did not appear to influence clinical presentation or severity.

CLINICAL PRESENTATION — Although most viral enteric infections are asymptomatic, virtually every child has more than one symptomatic episode of acute gastroenteritis before two years of age [4,21].

Among symptomatic children, illness generally begins 12 hours to 10 days after exposure and lasts for 3 to 9 days (table 1) [6,8,9]. The typical presentation is diarrhea, vomiting, or both; additional manifestations may include fever, abdominal pain or cramps [49], anorexia, headache, and myalgia. The constellation of findings varies by age (young infants have less specific signs), from day to day, and from person to person. Children may have only diarrhea or vomiting at first but with progression can become sufficiently ill to require hospitalization. Other symptoms may develop as the disease evolves; approximately 10 percent of children hospitalized for rotavirus infection have only fever and/or vomiting at the time of admission [50]. In children, vomiting is a prominent feature in both rotavirus and norovirus gastroenteritis [51,52].

Vomiting usually lasts for one to two days and diarrhea for five to seven days [2,18,53]. Stools are typically loose or watery; however, they may be normal in color or relatively pale colored. They may be odorless or have a characteristic odor [54]. Visible blood or mucus in the stool are uncommon in viral gastroenteritis and should prompt consideration of a nonviral etiology. (See 'Bacterial or parasitic gastroenteritis' below.)

The clinical features of medically attended viral gastroenteritis in immune-competent children were described in a review of 135 cases of polymerase chain reaction-confirmed gastroenteritis from a tertiary care children's hospital between 2006 and 2009 (during which there was an outbreak of norovirus) [18]:

Diarrhea was present in 90 percent; the median duration of diarrhea was six days (interquartile range 3 to 14); the median maximum number of stools per day was six (interquartile range 4 to 10)

Vomiting was present in 56 percent; the median duration of vomiting was four days (interquartile range two to six); the median maximum number of episodes of emesis per day was three (interquartile range two to five)

Fever (>38.3°C [101°F]) was present in 42 percent

Abdominal cramping was reported in 12 percent; abdominal distension in 16 percent; and abdominal tenderness in 16 percent

COMPLICATIONS — Complications of acute viral gastroenteritis include [27]:

Hypovolemia/dehydration – Severe dehydration that is not promptly addressed with rehydration may lead to shock, multiorgan dysfunction, and death, particularly in immunocompromised patients. (See "Clinical assessment of hypovolemia (dehydration) in children" and "Hypovolemic shock in children in resource-abundant settings: Initial evaluation and management", section on 'Etiology'.)

Acute viral gastroenteritis that requires medical attention for dehydration occurs predominantly in young children, particularly those younger than two years. Young children are more susceptible to dehydration than older children because they have a higher body surface-to-volume ratio, a higher metabolic rate, lower fluid reserves, and depend upon others to provide fluids [3].

Electrolyte abnormalities – Acute viral gastroenteritis may be associated with electrolyte abnormalities and acid base disturbance (hypernatremia, hyponatremia, hypokalemia, metabolic acidosis). Hypokalemia may cause ileus, which can worsen emesis and impair fluid and electrolyte absorption. (See "Acid-base and electrolyte abnormalities with diarrhea" and "Hypokalemia in children", section on 'Muscular weakness'.)

Carbohydrate intolerance – Carbohydrate intolerance, particularly lactose intolerance (due to damage to and loss of mature enterocytes containing lactase) is uncommon. In one series of 107 children with acute gastroenteritis, lactose intolerance was demonstrated in 11 percent and lasted for ≤5 days [55]. The diagnosis of lactose intolerance is supported by reducing substances in the stool and/or stool pH <5.5. Lactose intolerance can be recognized at disease onset and when patients develop an exacerbation of diarrhea after introduction of lactose-containing foods and beverages (including infant formulas). (See "Lactose intolerance and malabsorption: Clinical manifestations, diagnosis, and management", section on 'Secondary lactose malabsorption'.)

Irritant diaper dermatitis – (See "Diaper dermatitis", section on 'Risk factors'.)

EVALUATION

Setting of evaluation — The evaluation of children with acute gastroenteritis may begin with a telephone call to assess whether the child needs to be seen in the office or the emergency department. The child's fluid status and the possibility of severe illness or condition other than acute gastroenteritis that requires specific therapy are the focus of this conversation. (See "Acute viral gastroenteritis in children in resource-abundant countries: Management and prevention", section on 'Severity assessment' and "Clinical assessment of hypovolemia (dehydration) in children" and "Hypovolemic shock in children in resource-abundant settings: Initial evaluation and management".)

Indications for a medical visit include [1-3,56]:

Age <6 months or weight <8 kg (17 pounds 10 ounces)

Temperature ≥38°C (100.4°F) for infants <3 months or ≥39°C (102.2°F) for children 3 to 36 months

Visible blood in stool or melena

Frequent vomiting over a period of several hours

Frequent and substantial volumes of diarrhea

Diarrhea for >7 days or persistent vomiting

Caregiver's report of symptoms of moderate to severe dehydration (table 2)

Multisystem compromise, cardiovascular instability (these children should be referred directly to the emergency department)

Inability of the caregiver to administer or failure of the child to tolerate or respond to oral rehydration therapy at home

Underlying immunodeficiency or condition complicating the treatment or course of illness (eg, malnutrition, diabetes mellitus or other metabolic disease)

Social circumstances that make telephone assessment unreliable

History and examination — The history (table 3) and examination (table 4) of children with symptoms and signs of gastroenteritis focus upon:

Determining the severity of illness; gastroenteritis severity is reflected by the degree of dehydration (table 2) [1,3,57]. The best individual signs of hypovolemia include (see "Clinical assessment of hypovolemia (dehydration) in children", section on 'Clinical assessment'):

Weight loss

Dry mucous membranes

Prolonged capillary refill time

Loss of skin turgor

Increased and deep respiratory pattern

Other important signs include elevated pulse, diminished systolic and/or diastolic blood pressure, and sunken fontanelle (in children whose fontanelle remains open) (table 2). Tachycardia may be the first sign of hypovolemic shock among infants.

Evaluating other causes of diarrhea and/or vomiting that require definitive therapy and can be confused with acute gastroenteritis in the first day or two of symptoms (eg, meningitis, acute abdominal processes, diabetic ketoacidosis, toxic ingestions, pneumonia, streptococcal pharyngitis) [2,3,27,57-59]. (See 'Differential diagnosis' below and "Diagnostic approach to diarrhea in children in resource-abundant settings" and "Approach to the infant or child with nausea and vomiting".)

Laboratory evaluation

Well-appearing immunocompetent children with typical presentation – Most immune-competent children older than one year of age with typical findings of acute gastroenteritis do not require laboratory evaluation. The results of laboratory tests are unlikely to change management, which focuses on fluid repletion and maintenance (even for bacterial and parasitic gastroenteritis).

Ill-appearing children and children with hypovolemia, atypical presentation, or uncertain diagnosis – For children who are ill appearing and/or who have hypovolemia, an atypical presentation (table 5), or uncertain diagnosis, laboratory evaluation may be helpful. The laboratory evaluation is guided by the clinical scenario and diagnostic considerations.

As examples:

During the COVID-19 pandemic, we suggest testing for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in children with diarrhea and exposure to a person with SARS-CoV-2 infection. (See "COVID-19: Clinical manifestations and diagnosis in children", section on 'Criteria for COVID-19 testing'.)

For children with moderate to severe volume depletion, who may require intravenous therapy (table 2), we suggest measurement of serum electrolytes. The serum sodium concentration guides fluid management. (See "Clinical assessment of hypovolemia (dehydration) in children", section on 'Laboratory testing' and "Treatment of hypovolemia (dehydration) in children in resource-abundant settings", section on 'Intravenous rehydration therapy'.)

Electrolyte abnormalities and acid-base disorders in patients with diarrhea are discussed separately. (See "Acid-base and electrolyte abnormalities with diarrhea".)

In children with volume depletion, a complete blood count (CBC) may show signs of hemoconcentration (eg, increased hemoglobin or hematocrit) but is not necessary for diagnosis or management.

For children with suspected bacterial gastroenteritis (eg, known outbreak; exposure to potentially contaminated food such as undercooked meats, eggs, or shellfish, unpasteurized milk (table 6); visible blood or mucus in stool; elevated band count [if CBC is obtained]), microscopic examination of a fecal smear stained with Wright stain or methylene blue for fecal leukocytes and/or stool cultures may be warranted. (See "Causes of acute infectious diarrhea and other foodborne illnesses in resource-abundant settings", section on 'Clinical clues to the microbial cause'.)

Fecal leukocytes indicate inflammation in the bowel wall, which is more characteristic of bacterial than viral gastroenteritis, but do not distinguish between infectious and noninfectious inflammatory processes. Most bacteria cause a polymorphonuclear inflammation, although Salmonella typhi may cause a mononuclear reaction.

For children with suspected bacterial gastroenteritis, we do not obtain markers of inflammation in the serum (C-reactive protein, procalcitonin) or stool (fecal lactoferrin, fecal calprotectin) because even if elevated they are unlikely to change the management of young children with acute gastroenteritis [1,57,60]. Stool lactoferrin may be falsely positive in breastfed infants.

For children with suspected parasitic gastroenteritis (eg, persistent diarrhea, immunocompromised host, travel to areas with inadequate handling of sewage, peripheral eosinophilia [if CBC is obtained], or eosinophils on Wright-stained fecal smear, uncertain diagnosis), we suggest obtaining stool studies for ova and parasites [61,62].

For children with suspected inflammatory bowel disease (eg, persistent or recurrent episodes of diarrhea, visible blood or mucus in the stool, poor growth, extraintestinal manifestations), microscopic examination of a fecal smear stained with Wright stain or methylene blue for fecal leukocytes may be warranted [63-65]. Fecal leukocytes indicate inflammation in the bowel wall but do not distinguish between infectious and noninfectious inflammatory processes. Eosinophils may suggest ulcerative colitis [66,67]. (See "Clinical presentation and diagnosis of inflammatory bowel disease in children", section on 'Clinical manifestations'.)

For children with suspected C. difficile (table 7), we obtain stool studies for C. difficile. (See "Clostridioides difficile infection in children: Clinical features and diagnosis", section on 'Testing for C. difficile'.)

Suspected urinary tract infection (eg, suprapubic or flank tenderness, dysuria, urgency, frequency or history of previous urinary tract infection) – Urinalysis and urine culture. (See "Urinary tract infections in infants and children older than one month: Clinical features and diagnosis", section on 'Clinical presentation'.)

DIAGNOSIS

Clinical diagnosis — The diagnosis of acute viral gastroenteritis is made clinically; laboratory studies are not routinely necessary. Clinical features suggestive of viral gastroenteritis include:

Diarrhea (eg, ≥3 loose or watery stools in 24 hours or a number of loose/watery bowel movements that exceeds the child's usual number of daily bowel movements by two or more), with or without vomiting, fever, or abdominal pain

Absence of visible blood and mucus in the stool

Absence of atypical features: findings more characteristic of bacterial or parasitic gastroenteritis, extraintestinal infections, or noninfectious conditions associated with diarrhea and vomiting (table 5) (see 'Differential diagnosis' below)

In children with atypical features, other causes of acute gastroenteritis, extraintestinal infections, and noninfectious causes of diarrhea and/or vomiting must be considered and may require exclusion (by history, examination, or targeted laboratory or imaging studies) before making the diagnosis of acute viral gastroenteritis. (See 'Differential diagnosis' below and "Diagnostic approach to diarrhea in children in resource-abundant settings" and "Approach to the infant or child with nausea and vomiting".)

Etiologic diagnosis — Microbiologic testing usually is not necessary in immunocompetent hosts with routine gastroenteritis; however, microbiologic testing, including virologic assays, bacterial stool cultures, testing for C. difficile toxins, and/or stool examination for ova and parasites, may be indicated in the following circumstances or patients [1,2,58]:

Children with a known in-person exposure to a laboratory-confirmed case of COVID-19 within the previous 14 days (see "COVID-19: Clinical manifestations and diagnosis in children", section on 'Criteria for COVID-19 testing')

During outbreaks of gastroenteritis, particularly in an institution with a closed population (hospital, childcare center, school)

For cohorting and isolation of hospitalized patients (see "Acute viral gastroenteritis in children in resource-abundant countries: Management and prevention", section on 'Prevention')

Patients with underlying conditions (eg, immune compromise, cancer, inflammatory bowel disease [IBD])

Patients with prolonged diarrhea (ie, >7 days)

Uncertain diagnosis (eg, acute viral gastroenteritis versus IBD)

Clinical features and the pattern of illness may suggest a particular virus (table 1), but confirmation requires microbiologic testing because no feature is pathognomonic [18]. Viral gastroenteritis pathogens are excreted in the stool. They can be detected one to two days before symptom onset through a week or two after symptom resolution. Diagnosis of most of the common causes of acute viral gastroenteritis in children is discussed separately:

Norovirus (see "Norovirus", section on 'Diagnosis')

Rotavirus (see "Clinical manifestations and diagnosis of rotavirus infection", section on 'Diagnosis')

Adenoviruses 40 and 41 (see "Diagnosis, treatment, and prevention of adenovirus infection", section on 'Diarrhea in young children')

Molecular methods such as multiplex real-time polymerase chain reaction (RT-PCR) are commercially available for the detection of fecal viral pathogens, including astrovirus, and are replacing traditional tests [48]. The major advantages of molecular diagnostic methods are increased sensitivity for common viruses, such as rotavirus and adenovirus, and the ability to detect uncultivable viruses such as norovirus, sapovirus, and astrovirus [68,69]. Interpretation of assay results may be complicated by the frequent detection of viruses in fecal samples from asymptomatic children and the detection of multiple viruses in a single sample [69-71]. When multiple pathogens are detected, the clinician should recognize that disease outbreaks in closed settings and individual cases in regions with poor water and sewage handling may be caused by multiple pathogens, with a clinical presentation of features of each pathogen, such as profuse and watery diarrhea, with blood apparent, in a patient simultaneously ill from rotavirus and hemorrhagic Escherichia coli infection.

DIFFERENTIAL DIAGNOSIS

Bacterial or parasitic gastroenteritis — Nonvirus enteritis pathogens (eg, bacteria and parasites) account for approximately 30 percent of cases of acute gastroenteritis in children; the proportion is lower in resource-abundant countries and higher in resource-limited countries [27]. Clinical features that favor bacterial or parasitic gastroenteritis over viral gastroenteritis include:

Age >2 years – Bacterial and parasitic agents generally cause gastroenteritis in children at an older age (eg, two to four years), whereas viral pathogens more frequently cause serious gastroenteritis in those younger than two years.

Visible blood or mucus in the stool – Visible blood or mucus in the stool is more suggestive of bacterial than viral gastroenteritis but may occasionally occur in viral gastroenteritis [18]; occult blood (detected only by stool guaiac test) does not help to distinguish viral from bacterial gastroenteritis.

High fever (ie, >40°C [104°F]), tenesmus, central nervous system symptoms (eg, seizures), severe abdominal pain, and smaller volume stools are more characteristic of bacterial pathogens [1,27,58,60], but high fever and seizures have been reported in rotavirus and norovirus gastroenteritis [72,73].

Exposures (eg, international travel, exposure to poultry or other farm animals, consumption of processed meat, consumption of unfiltered/untreated water, swimming in natural bodies of water).

An elevated band count (if complete blood count is performed) is suggestive of bacterial gastroenteritis.

Bacterial causes of acute gastroenteritis in children include:

Diarrheagenic E. coli (see "Shiga toxin-producing Escherichia coli: Microbiology, pathogenesis, epidemiology, and prevention" and "Shiga toxin-producing Escherichia coli: Clinical manifestations, diagnosis, and treatment" and "Clinical manifestations and diagnosis of Shiga toxin-producing Escherichia coli (STEC) hemolytic uremic syndrome in children")

Salmonella (see "Nontyphoidal Salmonella: Microbiology and epidemiology" and "Enteric (typhoid and paratyphoid) fever: Epidemiology, clinical manifestations, and diagnosis" and "Nontyphoidal Salmonella: Gastrointestinal infection and asymptomatic carriage")

Shigella (see "Shigella infection: Epidemiology, clinical manifestations, and diagnosis")

C. difficile (see "Clostridioides difficile infection in children: Microbiology, pathogenesis, and epidemiology" and "Clostridioides difficile infection in children: Clinical features and diagnosis")

Campylobacter jejuni (see "Campylobacter infection: Microbiology, pathogenesis, and epidemiology" and "Campylobacter infection: Clinical manifestations, diagnosis, and treatment")

Campylobacter upsaliensis (see "Campylobacter: Infection with less common species and related bacteria", section on 'Campylobacter upsaliensis')

Mycobacteria, such as Mycobacterium avium complex, particularly in immunocompromised patients (see "Disseminated nontuberculous mycobacterial (NTM) infections and NTM bacteremia in children", section on 'Clinical features')

Parasitic causes of acute gastroenteritis in children include:

Giardia (see "Giardiasis: Epidemiology, clinical manifestations, and diagnosis")

Cryptosporidium (see "Cryptosporidiosis: Epidemiology, clinical manifestations, and diagnosis")

C. belli (formerly known as I. belli) (see "Epidemiology, clinical manifestations, and diagnosis of Cystoisospora (Isospora) infections")

Microsporidia and Cyclospora (see "Microsporidiosis" and "Cyclospora infection")

Extraintestinal infections — Extraintestinal infections that may present with diarrhea and/or vomiting are listed below [27,59]. These infections can usually be differentiated from acute gastroenteritis by their extraintestinal manifestations and/or specific laboratory tests (eg, chemistry, cell count, and culture of cerebrospinal fluid; urinalysis and urine culture).

Meningitis – Characteristic features of meningitis include fever, altered level of consciousness, and meningeal signs. (See "Bacterial meningitis in children older than one month: Clinical features and diagnosis", section on 'Clinical features' and "Viral meningitis in children: Clinical features and diagnosis".)

Bacterial sepsis – Clinical features of sepsis include alterations in vital signs and white blood cell count indicating a systemic inflammatory response syndrome (SIRS) in the presence of clinical or laboratory findings of infection. (See "Sepsis in children: Definitions, epidemiology, clinical manifestations, and diagnosis".)

Pneumonia – Clinical features of pneumonia include fever and symptoms or signs of respiratory distress (eg, tachypnea, nasal flaring, grunting, retractions, crackles, decreased breath sounds). (See "Community-acquired pneumonia in children: Clinical features and diagnosis", section on 'Clinical presentation'.)

Urinary tract infection (UTI) – Clinical features of UTI include suprapubic or flank tenderness, dysuria, urgency, and frequency. (See "Urinary tract infections in infants and children older than one month: Clinical features and diagnosis", section on 'Clinical presentation'.)

Streptococcal tonsillopharyngitis – Clinical features of streptococcal tonsillopharyngitis include enlarged erythematous tonsils with exudate and palatal petechiae. (See "Group A streptococcal tonsillopharyngitis in children and adolescents: Clinical features and diagnosis", section on 'Clinical features'.)

Otitis media – Symptoms and signs of otitis media include ear pain, bulging of the tympanic membrane, and hearing loss. (See "Acute otitis media in children: Clinical manifestations and diagnosis", section on 'Clinical presentation' and "Acute otitis media in children: Clinical manifestations and diagnosis", section on 'Clinical diagnosis'.)

Noninfectious conditions — A number of noninfectious conditions can present with symptoms that mimic those of infectious gastroenteritis (table 8). The approach to distinguishing these conditions from acute viral gastroenteritis is discussed separately. (See "Diagnostic approach to diarrhea in children in resource-abundant settings" and "Approach to the infant or child with nausea and vomiting".)

INDICATIONS FOR REFERRAL — Urgent referral for diagnostic evaluation and therapy may be warranted in children with:

Severe dehydration (table 2) associated with cardiovascular instability and/or electrolyte/acid-basic imbalance (eg, hypernatremia, hypokalemia, metabolic acidosis) (see "Hypernatremia in children" and "Hypokalemia in children" and "Approach to the child with metabolic acidosis")

Clinical features suggesting extraintestinal involvement or another etiology (see 'Differential diagnosis' above)

Immune compromise

Diarrhea lasting more than seven days (see "Overview of the causes of chronic diarrhea in children in resource-abundant settings" and "Approach to chronic diarrhea in children >6 months in resource-abundant settings" and "Approach to chronic diarrhea in neonates and young infants (<6 months)")

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Acute diarrhea in children".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or email these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient education" and the keyword[s] of interest.)

Basics topics (see "Patient education: Viral gastroenteritis in adults (The Basics)" and "Patient education: Diarrhea in children (The Basics)" and "Patient education: Rotavirus infection (The Basics)")

Beyond the Basics topic (see "Patient education: Acute diarrhea in children (Beyond the Basics)")

SUMMARY AND RECOMMENDATIONS

Definitions – Acute gastroenteritis is a clinical syndrome often defined by increased stool frequency (eg, ≥3 loose or watery stools in 24 hours or a number of loose/watery bowel movements that exceeds the child's usual number of daily bowel movements by two or more), with or without vomiting, fever, or abdominal pain. Acute viral gastroenteritis is caused by a viral pathogen. (See 'Definitions' above.)

Epidemiology – Acute viral gastroenteritis occurs throughout the year with a fall and winter predominance in most temperate climates (table 1). It can be transmitted by asymptomatic carriers as well as by symptomatic patients before the onset of symptoms. It is generally transmitted by the fecal-oral route. (See 'Epidemiology' above.)

Etiology – The most common causes of acute viral gastroenteritis in children include rotavirus, norovirus, sapovirus, astrovirus, and enteric adenoviruses (table 1). Mixed viral infections are common, but the clinical significance of coinfection with multiple viruses is unclear. (See 'Etiology' above.)

Clinical presentation – Among symptomatic patients, the clinical manifestations include diarrhea, vomiting, fever, abdominal cramps, anorexia, headache, and myalgia. The constellation of symptoms varies from day to day and from person to person. (See 'Clinical presentation' above.)

Complications – Acute viral gastroenteritis may be complicated by dehydration, electrolyte and acid-base disturbances, and carbohydrate intolerance. Acute viral gastroenteritis that requires medical attention for dehydration occurs predominantly in young children, particularly those younger than two years. (See 'Complications' above.)

Evaluation

The history (table 3) and examination (table 4) of children with symptoms and signs of gastroenteritis focus upon determining the severity of illness, mainly dehydration (table 2) and evaluating other causes of diarrhea and/or vomiting that may be confused with viral gastroenteritis and require definitive therapy (eg, meningitis, acute abdominal processes, diabetic ketoacidosis, pneumonia, streptococcal pharyngitis, toxic ingestions,). (See 'History and examination' above.)

Most immune-competent children older than one year of age with typical findings of acute gastroenteritis do not require laboratory evaluation. For children who are ill appearing and/or who have hypovolemia, an atypical presentation (table 5), or uncertain diagnosis, laboratory evaluation may be helpful. The laboratory evaluation is guided by the clinical scenario and diagnostic considerations. (See 'Laboratory evaluation' above.)

Diagnosis – The diagnosis of acute viral gastroenteritis is made by the characteristic clinical features, including (see 'Diagnosis' above):

Diarrhea with or without vomiting, fever, or abdominal pain

Absence of visible blood or mucus

Absence of atypical findings (table 5)

Differential diagnosis – The differential diagnosis of acute viral gastroenteritis includes bacterial and parasitic gastroenteritis, extraintestinal infections, and noninfectious conditions. These conditions generally are associated with features that are atypical for acute viral gastroenteritis (table 5). (See 'Differential diagnosis' above.)

ACKNOWLEDGMENT — The editorial staff at UpToDate acknowledge David O Matson, MD, PhD, who contributed to an earlier version of this topic review.

  1. Guarino A, Ashkenazi S, Gendrel D, et al. European Society for Pediatric Gastroenterology, Hepatology, and Nutrition/European Society for Pediatric Infectious Diseases evidence-based guidelines for the management of acute gastroenteritis in children in Europe: update 2014. J Pediatr Gastroenterol Nutr 2014; 59:132.
  2. National Institute for Health and Care Excellence. Diarrhoea and vomiting in children: Diarrhoea and vomiting caused by gastroenteritis: diagnosis, assessment and management in children younger than 5 years. https://www.nice.org.uk/guidance/cg84 (Accessed on May 26, 2017).
  3. King CK, Glass R, Bresee JS, et al. Managing acute gastroenteritis among children: oral rehydration, maintenance, and nutritional therapy. MMWR Recomm Rep 2003; 52:1.
  4. Velázquez FR, Matson DO, Calva JJ, et al. Rotavirus infection in infants as protection against subsequent infections. N Engl J Med 1996; 335:1022.
  5. Bányai K, Estes MK, Martella V, Parashar UD. Viral gastroenteritis. Lancet 2018; 392:175.
  6. Schreiber DS, Blacklow NR, Trier JS. The mucosal lesion of the proximal small intestine in acute infectious nonbacterial gastroenteritis. N Engl J Med 1973; 288:1318.
  7. Agus SG, Dolin R, Wyatt RG, et al. Acute infectious nonbacterial gastroenteritis: intestinal histopathology. Histologic and enzymatic alterations during illness produced by the Norwalk agent in man. Ann Intern Med 1973; 79:18.
  8. Shepherd RW, Gall DG, Butler DG, Hamilton JR. Determinants of diarrhea in viral enteritis. The role of ion transport and epithelial changes in the ileum in transmissible gastroenteritis in piglets. Gastroenterology 1979; 76:20.
  9. Mebus CA, Wyatt RG, Kapikian AZ. Intestinal lesions induced in gnotobiotic calves by the virus of human infantile gastroenteritis. Vet Pathol 1977; 14:273.
  10. Wilhelmi I, Roman E, Sánchez-Fauquier A. Viruses causing gastroenteritis. Clin Microbiol Infect 2003; 9:247.
  11. Kaiser P, Borte M, Zimmer KP, Huppertz HI. Complications in hospitalized children with acute gastroenteritis caused by rotavirus: a retrospective analysis. Eur J Pediatr 2012; 171:337.
  12. Henke-Gendo C, Harste G, Juergens-Saathoff B, et al. New real-time PCR detects prolonged norovirus excretion in highly immunosuppressed patients and children. J Clin Microbiol 2009; 47:2855.
  13. Sugata K, Taniguchi K, Yui A, et al. Analysis of rotavirus antigenemia in hematopoietic stem cell transplant recipients. Transpl Infect Dis 2012; 14:49.
  14. Bok K, Green KY. Norovirus gastroenteritis in immunocompromised patients. N Engl J Med 2012; 367:2126.
  15. Morales E, García-Esteban R, Guxens M, et al. Effects of prolonged breastfeeding and colostrum fatty acids on allergic manifestations and infections in infancy. Clin Exp Allergy 2012; 42:918.
  16. Morrow AL, Ruiz-Palacios GM, Jiang X, Newburg DS. Human-milk glycans that inhibit pathogen binding protect breast-feeding infants against infectious diarrhea. J Nutr 2005; 135:1304.
  17. Chhabra P, Payne DC, Szilagyi PG, et al. Etiology of viral gastroenteritis in children <5 years of age in the United States, 2008-2009. J Infect Dis 2013; 208:790.
  18. Osborne CM, Montano AC, Robinson CC, et al. Viral gastroenteritis in children in Colorado 2006-2009. J Med Virol 2015; 87:931.
  19. Hall AJ, Rosenthal M, Gregoricus N, et al. Incidence of acute gastroenteritis and role of norovirus, Georgia, USA, 2004-2005. Emerg Infect Dis 2011; 17:1381.
  20. Zimmerman CM, Bresee JS, Parashar UD, et al. Cost of diarrhea-associated hospitalizations and outpatient visits in an insured population of young children in the United States. Pediatr Infect Dis J 2001; 20:14.
  21. Guerrero ML, Noel JS, Mitchell DK, et al. A prospective study of astrovirus diarrhea of infancy in Mexico City. Pediatr Infect Dis J 1998; 17:723.
  22. Barclay L, Park GW, Vega E, et al. Infection control for norovirus. Clin Microbiol Infect 2014; 20:731.
  23. Sawyer LA, Murphy JJ, Kaplan JE, et al. 25- to 30-nm virus particle associated with a hospital outbreak of acute gastroenteritis with evidence for airborne transmission. Am J Epidemiol 1988; 127:1261.
  24. Foster SO, Palmer EL, Gary GW Jr, et al. Gastroenteritis due to rotavirus in an isolated Pacific island group: an epidemic of 3,439 cases. J Infect Dis 1980; 141:32.
  25. Bonifait L, Charlebois R, Vimont A, et al. Detection and quantification of airborne norovirus during outbreaks in healthcare facilities. Clin Infect Dis 2015; 61:299.
  26. Harrison CJ, Hassan F, Lee B, et al. Multiplex PCR Pathogen Detection in Acute Gastroenteritis Among Hospitalized US Children Compared With Healthy Controls During 2011-2016 in the Post-Rotavirus Vaccine Era. Open Forum Infect Dis 2021; 8:ofab592.
  27. Elliott EJ. Acute gastroenteritis in children. BMJ 2007; 334:35.
  28. Parashar UD, Nelson EA, Kang G. Diagnosis, management, and prevention of rotavirus gastroenteritis in children. BMJ 2013; 347:f7204.
  29. Payne DC, Vinjé J, Szilagyi PG, et al. Norovirus and medically attended gastroenteritis in U.S. children. N Engl J Med 2013; 368:1121.
  30. Hemming M, Räsänen S, Huhti L, et al. Major reduction of rotavirus, but not norovirus, gastroenteritis in children seen in hospital after the introduction of RotaTeq vaccine into the National Immunization Programme in Finland. Eur J Pediatr 2013; 172:739.
  31. Gastañaduy PA, Curns AT, Parashar UD, Lopman BA. Gastroenteritis hospitalizations in older children and adults in the United States before and after implementation of infant rotavirus vaccination. JAMA 2013; 310:851.
  32. Hallowell BD, Parashar UD, Curns A, et al. Trends in the Laboratory Detection of Rotavirus Before and After Implementation of Routine Rotavirus Vaccination - United States, 2000-2018. MMWR Morb Mortal Wkly Rep 2019; 68:539.
  33. Burnett E, Parashar UD, Winn A, et al. Major Changes in Spatiotemporal Trends of US Rotavirus Laboratory Detections After Rotavirus Vaccine Introduction-2009-2021. Pediatr Infect Dis J 2022; 41:759.
  34. Chamberland RR, Burnham CA, Storch GA, et al. Prevalence and Seasonal Distribution of Norovirus Detection in Stools Submitted From Pediatric Patients for Enteric Pathogen Testing. J Pediatric Infect Dis Soc 2015; 4:264.
  35. Dennehy PH. Viral gastroenteritis in children. Pediatr Infect Dis J 2011; 30:63.
  36. Glass RI, Parashar UD, Estes MK. Norovirus gastroenteritis. N Engl J Med 2009; 361:1776.
  37. Green KY, Belliot G, Taylor JL, et al. A predominant role for Norwalk-like viruses as agents of epidemic gastroenteritis in Maryland nursing homes for the elderly. J Infect Dis 2002; 185:133.
  38. Vanden Esschert KL, Mattioli MC, Hilborn ED, et al. Outbreaks Associated with Untreated Recreational Water - California, Maine, and Minnesota, 2018-2019. MMWR Morb Mortal Wkly Rep 2020; 69:781.
  39. Shioda K, Kambhampati A, Hall AJ, Lopman BA. Global age distribution of pediatric norovirus cases. Vaccine 2015; 33:4065.
  40. Lucero Y, Lagomarcino AJ, Espinoza M, et al. Norovirus compared to other relevant etiologies of acute gastroenteritis among families from a semirural county in Chile. Int J Infect Dis 2020; 101:353.
  41. Doll MK, Gagneur A, Tapiéro B, et al. Temporal Changes in Pediatric Gastroenteritis after Rotavirus Vaccination in Quebec. Pediatr Infect Dis J 2016; 35:555.
  42. Operario DJ, Platts-Mills JA, Nadan S, et al. Etiology of Severe Acute Watery Diarrhea in Children in the Global Rotavirus Surveillance Network Using Quantitative Polymerase Chain Reaction. J Infect Dis 2017; 216:220.
  43. Halasa N, Piya B, Stewart LS, et al. The Changing Landscape of Pediatric Viral Enteropathogens in the Post-Rotavirus Vaccine Era. Clin Infect Dis 2021; 72:576.
  44. Burke RM, Mattison C, Marsh Z, et al. Norovirus and Other Viral Causes of Medically Attended Acute Gastroenteritis Across the Age Spectrum: Results from the MAAGE Study in the United States. Clin Infect Dis 2021.
  45. Rockx B, De Wit M, Vennema H, et al. Natural history of human calicivirus infection: a prospective cohort study. Clin Infect Dis 2002; 35:246.
  46. Pang XL, Joensuu J, Vesikari T. Human calicivirus-associated sporadic gastroenteritis in Finnish children less than two years of age followed prospectively during a rotavirus vaccine trial. Pediatr Infect Dis J 1999; 18:420.
  47. Hassan F, Kanwar N, Harrison CJ, et al. Viral Etiology of Acute Gastroenteritis in <2-Year-Old US Children in the Post-Rotavirus Vaccine Era. J Pediatric Infect Dis Soc 2019; 8:414.
  48. Corcoran MS, van Well GT, van Loo IH. Diagnosis of viral gastroenteritis in children: interpretation of real-time PCR results and relation to clinical symptoms. Eur J Clin Microbiol Infect Dis 2014; 33:1663.
  49. Ali S, Maki C, Xie J, et al. Characterizing Pain in Children with Acute Gastroenteritis Who Present for Emergency Care. J Pediatr 2021; 231:102.
  50. Staat MA, Azimi PH, Berke T, et al. Clinical presentations of rotavirus infection among hospitalized children. Pediatr Infect Dis J 2002; 21:221.
  51. Graham DY, Jiang X, Tanaka T, et al. Norwalk virus infection of volunteers: new insights based on improved assays. J Infect Dis 1994; 170:34.
  52. Robilotti E, Deresinski S, Pinsky BA. Norovirus. Clin Microbiol Rev 2015; 28:134.
  53. Colomba C, De Grazia S, Giammanco GM, et al. Viral gastroenteritis in children hospitalised in Sicily, Italy. Eur J Clin Microbiol Infect Dis 2006; 25:570.
  54. Poulton J, Tarlow MJ. Diagnosis of rotavirus gastroenteritis by smell. Arch Dis Child 1987; 62:851.
  55. Szajewska H, Kantecki M, Albrecht P, Antoniewicz J. Carbohydrate intolerance after acute gastroenteritis--a disappearing problem in Polish children. Acta Paediatr 1997; 86:347.
  56. Ho MS, Glass RI, Pinsky PF, et al. Diarrheal deaths in American children. Are they preventable? JAMA 1988; 260:3281.
  57. Shane AL, Mody RK, Crump JA, et al. 2017 Infectious Diseases Society of America Clinical Practice Guidelines for the Diagnosis and Management of Infectious Diarrhea. Clin Infect Dis 2017; 65:e45.
  58. Granado-Villar D, Cunill-De Sautu B, Granados A. Acute gastroenteritis. Pediatr Rev 2012; 33:487.
  59. World Gastroenterology Organisation Global Guidelines. Acute diarrhea in adults and children: A global perspective. February 2012. www.worldgastroenterology.org/acute-diarrhea-in-adults.html (Accessed on July 29, 2015).
  60. Wiegering V, Kaiser J, Tappe D, et al. Gastroenteritis in childhood: a retrospective study of 650 hospitalized pediatric patients. Int J Infect Dis 2011; 15:e401.
  61. Gill CJ, Lau J, Gorbach SL, Hamer DH. Diagnostic accuracy of stool assays for inflammatory bacterial gastroenteritis in developed and resource-poor countries. Clin Infect Dis 2003; 37:365.
  62. Kim MJ, Kim WH, Jung HC, et al. Isospora belli Infection with Chronic Diarrhea in an Alcoholic Patient. Korean J Parasitol 2013; 51:207.
  63. DeWitt TG, Humphrey KF, McCarthy P. Clinical predictors of acute bacterial diarrhea in young children. Pediatrics 1985; 76:551.
  64. Muñóz O, Coello-Ramírez P, Serafin F, et al. [Acute infectious gastroenteritis. Etiology and its correlation with clinical manifestations and fecal mucus]. Arch Invest Med (Mex) 1979; 10:135.
  65. Coello-Ramírez P, Movrín-Meleg JC, Díaz-Bensussen S. [Analysis of fecal mucus in children with prolonged and acute diarrhea]. Bol Med Hosp Infant Mex 1976; 33:61.
  66. Smyth CM, Akasheh N, Woods S, et al. Activated eosinophils in association with enteric nerves in inflammatory bowel disease. PLoS One 2013; 8:e64216.
  67. Sadi G, Yang Q, Dufault B, et al. Prevalence of Peripheral Eosinophilia at Diagnosis in Children With Inflammatory Bowel Disease. J Pediatr Gastroenterol Nutr 2016; 62:573.
  68. Cybulski RJ Jr, Bateman AC, Bourassa L, et al. Clinical Impact of a Multiplex Gastrointestinal Polymerase Chain Reaction Panel in Patients With Acute Gastroenteritis. Clin Infect Dis 2018; 67:1688.
  69. Mihala G, Ware RS, Lambert SB, et al. Potentially Pathogenic Organisms in Stools and Their Association With Acute Diarrheal Illness in Children Aged <2 Years. J Pediatric Infect Dis Soc 2022; 11:199.
  70. Nicholson MR, Van Horn GT, Tang YW, et al. Using Multiplex Molecular Testing to Determine the Etiology of Acute Gastroenteritis in Children. J Pediatr 2016; 176:50.
  71. Hanson KE, Couturier MR. Multiplexed Molecular Diagnostics for Respiratory, Gastrointestinal, and Central Nervous System Infections. Clin Infect Dis 2016; 63:1361.
  72. Johansen K, Hedlund KO, Zweygberg-Wirgart B, Bennet R. Complications attributable to rotavirus-induced diarrhoea in a Swedish paediatric population: report from an 11-year surveillance. Scand J Infect Dis 2008; 40:958.
  73. Ueda H, Tajiri H, Kimura S, et al. Clinical characteristics of seizures associated with viral gastroenteritis in children. Epilepsy Res 2015; 109:146.
Topic 5984 Version 43.0

References

آیا می خواهید مدیلیب را به صفحه اصلی خود اضافه کنید؟