Gastroenteritis: Overview

Gastroenteritis is a common clinical syndrome. It poses one of the world’s major clinical and public health problems, and in developing countries with poor-quality drinking water and low levels of sanitation it is a major cause of morbidity and mortality, especially among children and the elderly.

chiasmus diagram showing abba pattern
Figure X1 courtesy of Opens in new window

Gastroenteritis refers to inflammation and irritation of the gastrointestinal tract which includes the small intestine, large intestine, and the stomach. The condition disrupts the regular process of absorption of water in the intestines. As a result, water from the contents of the intestines does not get into the body; which is the primary function of the intestines. This condition is commonly known as stomach flu or gastric flu although it is not caused due to influenza virus at all. It is particularly common in children and extremely contagious as well (Medical News Today, 2009).

Gastroenteritis is caused by infection of the gastrointestinal tract by various viruses, bacteria and protozoa, which have most commonly been transmitted by the faecal-oral route. The syndrome consists of diarrhoea, abdominal cramping or pain, nausea and vomiting, lethargy, malaise and fever. Each of these features may be present to a varying degree, and may last from 1 day to more than 3 weeks.

In developed countries, even though serious morbidity and mortality are low, gastroenteritis may be an extremely painful and unpleasant event causing disruption to daily life and significant loss of working and school days. Patients often seek emergency medical care because of the acuteness of onset or the frequency of the diarrhoea, the severity of abdominal pain and cramps, and because of concerns regarding dehydration.

Gastroenteritis may occur in many settings. It may be a sporadic isolated event, a small outbreak either within a family or other close living group such as in a geriatric residential facility, or part of a larger community epidemic. The latter can place extreme strain upon emergency department (ED) resources. It may occur in a traveler, either while still overseas or on their return home. It is important to be aware of the circumstances and context in which the illness occurs, as these will often dictate the course of investigation or management.

Pathophysiology and Microbiology

Micro-organisms of all descriptions are constantly entering the gastrointestinal tract through the mouth. Extremely few of these progress to cause clinical illness. The natural defenses of the gastrointestinal tract against infection include gastric acid secretion, normal bowel flora, bile salt production, bowel motility, mucosal lymphoid tissue and secreted immunoglobulin A.

People with disturbances in any of these defenses are more prone to a clinical infection. For example, patients with achlorhydria, bowel stasis or blind loops, immunodeficiency states or recent antibiotic therapy that has disturbed bowel flora are prone to gastroenteritis. Some organisms such as rotavirus occur principally in children, as previous infection confers immunity.

A wide variety of viruses, bacteria and protozoa may cause gastroenteritis, and the list is continually growing. Viral agents include rotavirus, enteric adenovirus, astrovirus, calicivirus, Norwalk virus, coronavirus and cytomegalovirus. Bacteria include, Campylobacter jejuni, Staphylococcus aureus, Bacillus cereus, Escherichia coli, Vibrio cholera, Shigella dysenteriae, Salmonella enteriditis, Yersinia enterocolitica, Clostridium perfringens and C. difficile. Protozoa include Giardia lomblia, Cryptosporidium parvum and Entamoeba histolytica.

Micro-organisms cause gastroenteritis by a number of mechanisms. They may release preformed toxins prior to ingestion, multiply and produce toxins within the gastrointestinal lumen, directly invade the bowel wall, or use a combination of toxins and invasion. Staphylococcus aureus and Bacillus cereus produce a variety of toxins in stored food that are subsequently ingested. These toxins are absorbed and within hours act on the central nervous system to produce an illness characterized predominantly by vomiting and mild diarrhoea.

Invasive bacteria are characterized by Salmonella, which invades the mucosa, primarily of the distal ileum, producing cell damage and excessive secretion. Shigella likewise invades the mucosa but also produces toxins that have cytotoxic, neurotoxic and enterotoxic effects.

The many strains of E. coli have been divided into five groups, depending on the pathology of the diseases they cause. These are enteropathogenic, enterotoxigenic, enteroinvasive, enteroaggregative and enterohaemorrhagic. Enterohaemorrhagic E. coli is associated with haemorrhagic colitis and the haemolytic-uraemic syndrome, whereas enterotoxigenic E. coli is associated with traveler’s diarrhoea. The protozoan Giordia lambia adheres to the jejunum and upper ileum, causing mucosal inflammation, inhibition of disaccharidase activity and overgrowth of luminal bacteria.

Clinical Presentation

The clinical history and examination are directed at confirming the diagnosis of gastroenteritis, excluding other diagnoses, and determining the degree of dehydration.

The principal clinical manifestation of gastroenteritis is diarrhoea. The World Health Organization syndromic definition of gastroenteritis is ‘three or more abnormally loose or fluid stools over 24 hours’. The diarrhoea of gastroenteritis is often watery and profuse in the early stages of the illness, and may last for up to 3 weeks. It is important to determine as far as possible the frequency, volume and characteristics of the stool. Some organisms, such as enterohaemorrhagic E. Coli, Shigella, Salmonella, Campylobacter and Entamoeba histolytica, may cause acute and bloody diarrhoea, whereas others such as Giardia may cause loose, pale, greasy stools.

Adbdominal pain is common and is most often described as a diffuse intermittent colicky pain situated centrally in the abdomen. It may occur just prior to, and be partially relieved by, a bowel action. Severe pain is often caused by Campylobacter, Yersinia and E. coli. Abdominal pain is also the hallmark of many other forms of intra- and extra-abdominal pathology. Diagnoses other than gastroenteritis should be seriously considered if the pain is well localized, constant and severe, or radiates to the back or shoulder.

Vomiting may be present, particularly early in the illness, and can be variable in severity and persistence. The amount of vomiting and the ability to keep down clear fluids should be determined, as this will dictate the management of dehydration. Severe vomiting often occurs with organisms that produce preformed toxin, although it does not usually persist for longer than 24 hours.

Anorexia, nausea and lethargy are common. Fever and systemic symptoms such as headache are prominent with organisms that invade the bowel wall and enter the systemic circulation, such as Yersinia. Lethargy may be related to the dehydration or merely the strain of constant and persistent diarrhoea from any aetiology.

Specific inquiry regarding fluid status is essential. The aim should be to determine the amount of fluids that have been taken orally and kept down over the course of the illness, along with the estimated urine output. It is also important to ascertain pre-existing or intercurrent illness, such as diabetes or immunosuppression, which may alter management.

Clinical Examination

Suitable infection control procedures should be instituted prior to the examination to prevent spread to the examining doctor and hence to other patients. The patient should be in an isolated cubicle. Hand hygiene procedures before and after the consultation, the use of gloves and prompt disposal of soiled clothing and linen are important.

A careful clinical examination should be performed, concentrating on the abdomen and the circulatory state of the patient. The vital signs, temperature and urinalysis should be obtained.

In mild to moderate gastroenteritis the clinical examination is often unremarkable. There may be some general abdominal tenderness, active bowel sounds and facial pallor, but little else. In more severe disease the abdominal tenderness may be pronounced and signs of dehydration present. Of note, uncomplicated gastroenteritis is extremely unlikely if the abdominal examination reveals localized tenderness or signs of peritoneal irritation.

Fluid losses through diarrhoea, vomiting and fever, together with poor oral fluid intake, can lead to clinically apparent dehydration. This may be manifest as tachycardia, tachypnoea, reduced tissue turgor, delayed capillary return, reduced urine output and, in its more severe stages, hypotension, impaired conscious state and death.

Extra-abdominal signs of a primary gastroenteritis can occur. Campylobacter has been associated with reactive arthritis and Guillain-Barré syndrome. The clinical features, course and complications for various causative agents are summarized in Table X.

AdultsChildrenClinical FeaturesCausative Agents
1–10 days (usually 2–5 days)2–5 days occasionally >10 daysSudden onset of diarrhoea, abdominal pain, nausea, vomitingRaw or undercooked poultry, raw milk, raw or undercooked meat, untreated water
E. coli enterohaemorrhagic (STEC, VTEC)2–10 days5–10 daysSevere colic, mild to profuse bloody diarrhoea can lead to haemolytic uraemic syndromeMany raw foods (especially minced beef), unpasteurized milk, contaminated water
E. coli enteropathogenic, enterotoxigenic, enteroinvasive12–72 hrs (enterotoxigenic)3–14 daysSevere colic, watery to profuse diarrhoea, sometimes bloodyMany raw foods, food contaminated by faecal matter, contaminated water
Salmonella serovars (non-typhoid)6–72 hrs3–5 daysAbdominal pain, diarrhoea, chills, fever, malaiseRaw or undercooked meat & chicken, raw or undercooked eggs & eggs products
Shigella spp. 12–96 hrs4–7 daysMalaise, fever, vomiting, diarrhoea (blood & mucus)Foods contaminated by infected food handlers & untreated water contaminated by human faeces
Yersinia enterocolitica3–7 days1–21 daysAcute diarrhoea sometimes bloody, fever, vomitingRaw meat especially pork, raw or undercooked poultry, milk & milk products
Vibrio choleraA few hrs to 5 days3–4 daysAsymptomatic to profuse painless watery diarrhoea, dehydrationRaw seafood, contaminated water
Vibrio parahaemolyticus4–30 hrs (usually 12–24 hrs)1–7 daysAbdominal pain, diarrhoea, vomiting & sometimes fever, illness of moderate severityRaw & slightly cooked fish, shellfish, other seafoods
Norovirus (and other viral gastroenteritis)24–48 hrs12–60 hrsSevere vomiting, diarrhoeaOysters, clams, foods contaminated by infected food handlers and untreated water
Rotaviruses24–72 hrsUp to 7 daysMalaise, headache, fever, vomiting, diarrhoeaFoods contaminated by infected food handlers and untreated water contaminated by human faces
Cryptosporidium1–12 days4–21 daysProfuse watery diarrhoea, abdominal painFoods contaminated by infected food handlers & untreated water contaminated by human faeces
Giardia lambia1–3 weeks1–2 weeks to monthsLoose pale greasy stools, abdominal painFoods contaminated by infected food handlers and untreated water contaminated by human faeces
Entamoeba histolytica2&ndsh;4 weeksWeeks to monthsColic, mucous or bloody diarrhoeaFoods contaminated by infected food handlers and untreated water contaminated by human faeces
Toxin producing bacteria
B. cereus (toxin in food)1–6 hrs (vomiting) or 6–24 hrs (diarrhoea)<24 hrsTwo known toxins causing nausea and vomiting or diarrhoea & crampsCereals, rice, meat products, soups, vegetables
C. perfringes (toxin in gut)6–24 hrs24 hrsSudden onset colic, diarrhoeaMeals, poultry, stews, graves, (often inadequately reheated or held warm)
Staphylococcus aureus30 min-8 hrs24 hrsAcute vomiting, & cramps, may lead to collapseCold foods (much handled during preparation) milk products, salted meats
Table X1 | Adapted from Guidelines for the Control of Infectious Diseases — The Blue Book. Communicable Diseases Section, Public Health Group, Victorian Government Department of Human Services, 2005. (Reproduced with the kind of the Communicable Diseases Section, Public Health Group, Victorian Government Department of Human Services).


The principles of treatment for gastroenteritis are to replace fluid and electrolyte losses, minimize symptoms if possible, and in selected cases administer specific antimicrobial therapy. Clear fluids for 24 hours are often recommended, with the rationale that keeping the stomach empty will minimize vomiting. If the patient wishes to eat it is allowed. Strictly withholding feeding, especially from children, is not necessary.

Replacement of fluid losses may be achieved enterally, either by mouth or via a nasogastric tube, or intravenously. The method selected will depend on the cooperation of the patient, the degree of dehydration, the rate at which rehydration is desired, and the presence of other diseases such as diabetes.

Specific oral rehydration solutions are the most appropriate for oral or nasogastric use. There are a number of commercial preparations available through pharmacies without prescription. These consist of a balanced formula of glucose, sodium and potassium salts, and in worldwide trials have been shown to be extremely effective and safe, even when used in the most primitive of conditions.

Although many commonly available fluids may be used and will probably be effective in mild disease, fluids that contain large amounts of glucose, such as degassed lemonade or undiluted fruit juice, should not be encouraged in adults and are contraindicated in children. These fluids are hyperosmolar and deficient in electrolytes, thus prompting further fluid losses.

Glucose-containing electrolyte solutions use the gut’s co-transport system for glucose and sodium, thereby facilitating the absorption of water as well. Milk and other lactose containing products should be avoided during the acute phase of the illness, as viral or bacterial enteropathogens often result in transient lactose malabsorption. Caffeine-containing products should also be avoided. Caffeine increases cyclic AMP levels, thereby promoting the secretion of fluid and worsening diarrhoea.

Intravenous rehydration is necessary in patients who are shocked or who are becoming progressively more dehydrated despite oral or nasogastric fluids. Resuscitation should be commenced with normal saline at a rate which accounts for ongoing losses, as well as replacing the estimated fluid deficit. In severely dehydrated patients one or two 20 mL/kg boluses of normal saline may be necessary. Patients should also be encouraged to take oral fluids, unless vomiting is prohibitive. As soon as an adequate intake is achieved the intravenous fluids can be scaled back and ceased.

Close monitoring of the serum electrolytes is necessary during intravenous rehydration. In particular it is important to monitor serum sodium, as the exclusive use of normal saline for rehydration can lead to hypermatraemia. Potassium should be added to the fluid as determined by the serum potassium, remembering that a low serum potassium in this circumstance is indicative of a low total body potassium.

In adults, parenterally administered antiemetic drugs such as metoclopramide, prochlorperazine, or ondansetron may be useful in the management of severe vomiting. In children, an unacceptably high incidence of dystonic reactions precludes their use. Antimotility agents such as loperamide may be used, and have been shown to reduce the number of diarrhoeal stools and the duration of the illness. Antimotility agents have significant side effects and should only be used if it is essential.

Even though many bacteria that cause gastroenteritis respond to antibiotics they are rarely indicated. Recent antibiotic guidelines suggest that most infections with Campylobacter, Salmonella, Shigella, Yersinia and E. coli do not need antibiotics. In the majority of these cases the illness will be short-lived and mild. Because of the previous widespread use of antibiotics to treat gastroenteritis from any cause, and the current use of antibiotics in animals bred for food, many isolates of Campylobacter jejuni, Shigella and Salmonella are resistant to many antibiotics.

Choice of antibiotics should be based on antibiotic sensitivity patterns. Antibiotics may be indicated in Giardia infections, Shigella causing severe disease, Salmonella in infants, the immunosuppressed or the elderly, Campylobacter in food handlers, and in traveller’s diarrhoea. Antibiotics are contraindicated in uncomplicated Salmonella infections as they may prolong the carrier state. Recommended antibiotic regimens are summarized below.

Table X2 | Antibiotic treatment regimens
Giardia lamblia
Tinidazole 2 g (child: 50 mg/kg up to 2 g) orally, as a single dose. OR
Metronidazole 2 g (child: 30 mg/kg up to 2 g) orally, daily for 3 days.
Tinidazole 2 g (child: 50 mg/kg up to 2 g) orally, daily for 3 days. OR
Metronidazole 600 mg (child: 15 mg/kg up to 600 mg) orally, 8 hours for 7–10 days. PLUS
Paromycin 500 mg (child: 10 mg/kg up to 500 mg) orally 8 hourly for 7 days (to prevent relapse).
Norfloxacin 400 mg (child: 10 mg/kg up to 400 mg) orally, 12 hourly for 5 days. OR
Ampicillin 1 g (child: 25 mg/kg up to 1g) orally, 6 hourly for 5 days. OR
Co-trimoxacole 160/800 mg (child: 4/20 mg/kg up to 160/800 mg) orally, 12 hourly for 5 days.
Erythromycin 500 mg (child: 10 mg/kg up to 500 mg) orally, 6 hourly for 5–7 days.
Traveler’s diarrhoea
Norfloxacin 800 mg (child: 20 mg/kg up to 800 mg) orally, as a single dose. OR
Azithromycin 1 g (child: 20 mg/kg up to 1 g) orally, as a single dose.
Clostridium difficile
Metronidazole 400 mg (child: 10 mg/kg up to 400 mg) orally, 8 hourly for 7–10 days.
If unresponsive or severe disease: Vancomycin 125 mg (child: 3 mg/kg up to 125 mg) orally 6 hourly for 7–10 days.
Reference: Therapeutic Guidelines: Antibiotic. Version 13, 2006. Therapeutic Guidelines Limited. Antibiotic Expert Committee, Melbourne.
    Adapted from: Textbook of Adult Emergency Medicine E-Book. Authored By Peter Cameron, George Jelinek, Anne-Maree Kelly, Lindsay Murray, Anthony F. T. Brown. References as cited include:
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