Hepatitis A in children Frequent asked Questions скачать в хорошем качестве

Hepatitis A in children Frequent asked Questions

The hepatitis A virus (HAV) is a positive-sense, single-stranded RNA virus that belongs to the family Picornaviridae. It replicates primarily within hepatocytes and is a common infectious etiology of acute hepatitis worldwide. Symptoms of acute infection include nausea, vomiting, fatigue, malaise, abdominal pain, poor appetite, and fever. This activity reviews the evaluation and management of hepatitis A and highlights the role of the interprofessional team in improving care for patients with this condition. Epidemiology Improved sanitation has resulted in a shift in the age group that acquires hepatitis A. In recent years there has been a decline in the incidence of a new infections. The United States has a low endemicity. Mexico has a high prevalence of individuals with the anti-HAV antibody indicating previous infection. The frequency of acute hepatitis is higher in those U.S. states that are adjacent to Mexico. The reported hepatitis A incidence has declined by 90% to as low as 1.2 cases per 100,000 population. The greatest reductions are seen in children and in those states where routine vaccination was started in 1999. Over the last 4 decades, the average age of hepatitis A infected individuals has increased. Individuals in high-risk populations account for most cases of HAV infection. These groups include foreign travelers to developing nations, gays, childcare workers, institutionalized individuals, and those living in poverty. Food handlers are an infrequent source of outbreaks in the United States. Virtually any food may be contaminated with HAV. International HAV is highest in resource-poor regions such as Africa, Asia, and South America, where evidence of past infection is nearly universal. Acquisition often occurs in childhood, and it is usually asymptomatic. Sex There is no sexual predilection. It is most common in aid workers, gays, and around sewage. Age With increasing age symptomatic disease and adverse sequelae increases. Mortality from fulminant hepatic failure increases with increasing age. History and Physical Acute HAV infection is typically a self-limited illness characterized by nausea, vomiting, right upper quadrant abdominal discomfort, malaise, anorexia, myalgia, fatigue, and fever. Patients may develop dark urine and pale stools within a week, followed by jaundice, icteric (yellow-tinted) sclera, and pruritus. Patients usually have elevated levels of serum alanine aminotransferase, aspartate aminotransferase, bilirubin, alkaline phosphatase, and lambda-glutamyl transpeptidase. These lab abnormalities typically resolve within 1 to 6 weeks following the onset of symptoms. The incubation period usually ranges from 14 to 28 days but can last up to 50 days. The severity of symptoms varies with age and comorbidities, particularly underlying chronic liver disease. Most children with acute HAV infection are asymptomatic. Extra-hepatic manifestations rarely occur but may include pancreatitis, rash, acute kidney injury with interstitial nephritis or glomerular nephritis, pneumonitis, pericarditis, hemolysis, and acute cholecystitis. Neurologic complications have also been reported such as mononeuritis, Guillan-Barre, encephalitis and central myelitis. There were two reported cases in 1991 of autoimmune hepatitis triggered by acute HAV infection. Lemon et al. describe five clinical patterns: Asymptomatic infection Symptomatic infection with jaundice, dark urine, and clay-colored stool Cholestatic hepatitis with prolonged alkaline phosphatase and bilirubin elevation and pruritus Relapsing infection Fulminant hepatitis. Evaluation Acute hepatitis A is diagnosed by serologic testing to detect HAV-specific immunoglobulin (IgM) antibodies in the blood. Additional testing can include reverse transcriptase-polymerase chain reaction to detect the viral RNA. Immunoglobulin G (IgG) anti-HAV emerges soon after infection and remains present for the person’s lifetime. Blood work will reveal a mild lymphocytosis and normal prothrombin time. If the prothrombin time is elevated, it should raise suspicion of severe liver damage including risk for encephalopathy. Hepatitis A is associated with an elevation in aspartate aminotransferase, which returns to normal in 4-6 months. Bilirubin levels are also elevated and if they persist one should suspect cholestatic liver disease. Ultrasound is not done in routine cases of HAV. Complications Prolonged cholestasis Acute renal failure Autoimmune hepatitis Treatment No specific treatment is needed for most patients with acute, uncomplicated HAV infection beyond supportive care. Complete recovery from symptoms may take several weeks to months. In the rare case of fulminant hepatitis from HAV infection, liver transplantation may be a life-saving measure. Extrahepatic complications are managed routinely.