Viral gastroenteritis

Rotavirus infection (Fig. 20.2.1) is the most common cause of acute gastroenteritis in children worldwide, with a peak incidence between 6 and 24  months of age. It is also a major cause of mortality in developing countries and is responsible for the majority of cases where hospital admission is required. In Australia, before routine infant rotavirus immunization was introduced in 2007, approximately 10 000 children aged under 5 years were hospitalized each year due to rotavirus infection, 115 000 visited a general practitioner, 22 000 required an emergency department visit and, on average, one Australian child died each year from the complications of dehydration and shock. Since 2007, these numbers have fallen dramatically.Infants in developing countries are more susceptible to severe infection causing life-threatening diarrhoea because of pre-existing malnutrition and poor access to primary care. Similarly, Indigenous Australian children require hospitalisation due to rotavirus gastroenteritis about three to five times more commonly than non-Indigenous children.

Fig. 20.2.1 The rotavirus (electron micrograph).

The mucosal damage caused by rotavirus (Fig. 20.2.2) occurs primarily in the small intestine. It results in villus destruction and loss of digestive enzymes found on the tips of villi. This causes impaired digestion of carbohydrates, impaired intestinal absorption of fluid and electrolytes, and fluid loss from the intestine. The need for structural repair places considerable nutritional demands on malnourished children. Repeated asymptomatic reinfection helps maintain immunity.

Fig. 20.2.2 Scanning electron microscope appearances of (A) normal and (B) rotavirus-infected calf jejunum. Villi are short, the epithelium is damaged, and crypts are deep.

(Courtesy of DGA Hall, Institute for Animal Health, Compton, UK. With permission from Walker et al 1991.)

The other major viral cause of hospital admissions is the enteric adeno family of viruses. Norovirus is also implicated in winter outbreaks of vomiting. Other less common viruses, such as calicivirus, astrovirus and other small viruses, have also been implicated in gastroenteritis requiring hospitalization. Cytomegalovirus (CMV) enteritis should be considered in immunocompromised patients.

Bacterial and parasitic gastroenteritis

Bacteria cause fewer episodes of acute gastroenteritis in developed countries than viruses. The main causes of bacterial infection are Campylobacter jejuni, Salmonella spp., Shigella spp. and various types of Escherichia coli, each accounting for a small percentage. Clostridium difficile, known to cause pseudomembranous colitis following systemic antibiotic therapy, is usually hospital-acquired and becoming increasingly resistant to first line treatment options.

In developing countries, E. coli (enterotoxigenic, enteropathogenic and enteroinvasive), Shigella spp. and Entamoeba histolytica are especially important: E. coli because of the large number of episodes it causes, Shigella because it causes prolonged, debilitating illness and antibiotic-resistant strains are emerging, and Entamoeba because it causes severe life- threatening dysentery. These organisms are rarely acquired in industrialized countries.

The parasite Giardia lamblia is a rare cause of acute dehydrating diarrhoea, but a common cause of persistent diarrhoea with flatulence and bloating. It is most common in toddlers and young children, and also in their parents and caregivers. It is also common in people who have travelled overseas especially to developing countries where drinking water supplies may be contaminated. Another parasite, Cryptosporidium, is another rare cause of acute diarrhoea in some infants admitted to hospital and should be considered in immunocompromised patients.

Clinical features

Acute gastroenteritis is a relatively common cause of presentation to medical attention, but it should remain a diagnosis of exclusion, because several systemic disorders and surgical emergencies can present with diarrhoea and/or vomiting (Box 20.2.1) and should be considered in the differential diagnosis.

Symptoms of acute gastroenteritis are watery diarrhoea (up to 10–20 stools daily) with or without vomiting and fever (to 39–40°C). Vomiting is often the predominant feature early in the illness, followed by diarrhoea. If both occur concurrently, there is an increased risk of dehydration. Maintaining hydration is easier after the cessation of vomiting. Blood, mucus and the passage of small frequent bowel actions accompanied by abdominal pain suggest a diagnosis of colitis due to bacterial gastroenteritis (‘bacterial dysentery’), amoebic dysentery or, potentially, inflammatory bowel disease.

Investigations

Stool samples should be sent for microscopy, bacterial culture and sensitivities (MC + S). Samples should also be sent for ova, cysts and parasites (OCP) and viral studies, which may include enzyme-linked immunosorbent assay (ELISA), polymerase chain reaction (PCR) and viral culture. Appropriate treatment should not be withheld pending results. Sending several stool samples from different bowel actions increases the positive yield of the test and is recommended.

Management

Once the diagnosis of acute gastroenteritis is made on thorough clinical history and physical examination, the next step is to assess the degree of dehydration and institute an appropriate plan for rehydration. This should be combined with nutritional support that aids the patient during the recovery phase.

Dehydration

The risk of dehydration is inversely related to age, with young infants being at greatest risk because they have a high surface area : body volume ratio, resulting in increased insensible fluid loss. They also tend to have more severe vomiting and diarrhoea than older children and adults.

Fluid loss is usually assessed on the basis of percentage body weight loss. Physical signs of dehydration are not usually apparent until 4% of body weight is lost.

The signs of dehydration traditionally described are outlined in Box 20.2.2. The three signs that discriminate best between dehydration and adequate hydration are deep breathing, decreased skin turgor and poor peripheral perfusion.

Electrolyte loss

Dehydration is usually isotonic (water and electrolytes being lost in equal amounts). Hypertonic hypernatraemic dehydration (fluid loss > electrolyte loss) occurs in 5–10% of children with acute gastroenteritis, and hypotonic hyponatraemic dehydration (electrolyte loss > fluid loss) can occur if the colon (a major site of sodium resorption) is out of circuit (e.g. in short gut syndrome).

If corrected too rapidly, hypernatraemic dehydration can cause convulsions due to rapid shifts of water into cells. Hyponatraemic dehydration can also cause significant neurological morbidity and mortality and, in contrast to the hypernatraemic state, requires vigorous replacement of sodium. Nasogastric rehydration has a much lower risk of these electrolyte complications than intravenous rehydration.

Rehydration guidelines

See also Chapter 6.1.

No dehydration

• Nutritional intake and fluids should not be modified and should be encouraged to keep up with ongoing losses, avoiding the need for rehydration via nasogastric or intravenous route.

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