Depending on the severity of diarrhea, treatment consists of oral rehydration, during which the child is given extra water to drink that contains small amounts of salt and sugar. Some infections are serious enough to warrant hospitalisation where fluids are given by intravenous drip or nasogastric tube, and the childs electrolytes and blood sugar are monitored. Antibiotics are not recommended. Prognosis
Rotavirus infections rarely cause other complications and for a well managed child the prognosis is excellent. Epidemiology
Rotavirus A, which accounts for more than 90% of rotavirus gastroenteritis in humans, is endemic worldwide. Each year rotavirus causes millions of cases of diarrhoea in developing countries, almost 2 million resulting in hospitalisation and an estimated 453,000 resulting in the death of a child younger than five. This is about 40 per cent of all hospital admissions related to diarrhea in children under five worldwide.In the United States alone—before initiation of the rotavirus vaccination programme—over 2.7 million cases of rotavirus gastroenteritis occurred annually, 60,000 children were hospitalised and around 37 died from the results of the infection. The major role of rotavirus in causing diarrhoea is not widely recognised within the public health community, particularly in developing countries. Almost every child has been infected with rotavirus by age five. It is the leading single cause of severe diarrhoea among infants and children, being responsible for about 20% of cases, and accounts for 50% of the cases requiring hospitalisation. Rotavirus causes 37% of deaths attributable to diarrhoea and 5% of all deaths in children younger than five.
An international panel of experts have developed recommendations for the management of IgG4-RD. They concluded that in all cases of symptomatic, active IgG4-RD that treatment is required. Some cases with asymptomatic IgG4-RD also require treatment, as some organs tend to not cause symptoms until the late stages of disease. Urgent treatment is advised with certain organ manifestations, such as aortitis, retroperitoneal fibrosis, proximal biliary strictures, tubulointerstitial nephritis, pachymeningitis, pancreatic enlargement and pericarditis. Induction of remission
In untreated patients with active disease, the recommended first-line agent for induction of remission is glucocorticoids unless contraindications exist. Glucocorticoids characteristically result in a rapid and often dramatic improvement in clinical features and often a resolution of radiographic features. However, where advanced fibrotic lesions have resulted in irreversible damage, the response to glucocorticoids and other current treatment options may be poor or even absent. Although not validated yet in clinical trials, the common induction regime is prednisolone 30–40 mg per day for 2–4 weeks, then gradually tapered over 3 to 6 months. Recurrences during or after tapering of glucocorticoids are frequent, however. Steroid-sparing immunosuppressive agents might be considered, depending on local availability of these drugs, for use in combination with glucocorticoids from the start of treatment in order to reduce the side-effects of prolonged glucocorticoid usage. Steroid-sparing agents that have been used include rituximab, azathioprine, methotrexate, and cyclophosphamide, although trials are needed to ascertain the effectiveness of each drug in IgG4-RD.