Hepatitis

7.9 Hepatitis

Introduction1–5

Hepatitis is defined as inflammation of the liver due to a number of possible causes. Jaundice or icterus implies a yellow discolouration of skin, sclera and mucous membranes due to hyperbilirubinaemia which may or may not be caused by hepatitis.

In children, the presentation of hepatitis includes a diverse number of viral and non-viral causes. Viral hepatitis continues to be a major health problem in developing and developed countries and can present as an acute or chronic illness.

Aetiology

• Drug and toxin related liver injury (Table 7.9.1).

• Chronic hepatitis.

• Persistent viral infection (hepatitis B, C, D).

• Autoimmune hepatitis.

• Sclerosing cholangitis.

• Metabolic diseases, e.g. Wilson’s disease, α₁-antitrypsin deficiency, cystic fibrosis.

• Systemic illnesses, e.g. inflammatory bowel disease, cardiac disease, total parenteral nutrition.

Table 7.9.1 Patterns of hepatic drug injury
Centrilobar necrosis	Paracetamol Halothane
Microvesicular steatosis	Valproic acid
Acute hepatitis	Isoniacid
General hypersensitivity	Sulfonamide Phenytoin
Fibrosis	Methotrexate
Cholestasis	Chlorpromazine Erythromycin Oestrogens
Veno-occlusive disease	Cyclophosphamide
Portal and hepatic vein thrombosis	Oestrogens Androgens
Biliary sludge	Ceftriaxone
Hepatic adenoma or carcinoma	Oral contraceptives Anabolic steroids

Viral hepatitis in children can present with various manifestations, ranging from asymptomatic seroconversions especially in infants, mildly symptomatic and anicteric presentations with symptoms of a flu-like or gastroenteritis-like illness, to fulminant hepatic failure as well as chronic hepatitis leading to cirrhosis and hepatocellular carcinoma. In adults, chronic hepatitis is defined as biochemical or histological changes that persist for more than 6 months. This definition in children would inappropriately delay the diagnosis of several childhood causes of non-viral chronic hepatitis which respond to specific medical therapy. Persistence of abnormal serum aminotransferase tests beyond 3 months warrants aggressive evaluation to define the aetiology of the liver injury. A child with clinical evidence of chronic liver disease should be referred to a paediatric gastroenterologist for further evaluation without the 3 month observation period.

History

Acute symptomatic viral hepatitis classically presents with a 1-week prodromal phase with non-specific symptoms of nausea, vomiting, malaise, anorexia and low-grade fever, followed by an icteric phase with dark urine followed by jaundice and pale stools. Prodromal symptoms fade with the onset of jaundice but anorexia and malaise may persist, and localised hepatic pain or tenderness and pruritus may develop. Important historical clues indicating an infectious aetiology are attendance of child care and possible disease among peers and childcare workers, exposure to highly endemic communities in Australia (e.g. remote Aboriginal communities) or overseas, attendance of schools and residential facilities for the disabled, exposure to blood products, injection drug use and high risk sexual activity (men who have sex with men). A history of acute drug or toxin ingestion or ongoing therapeutic use of potentially hepatotoxic agents should be elicited. The history should also explore the possibility of acute or chronic presentations of metabolic and systemic illnesses associated with liver disease e.g. neurological complaints in Wilson’s disease, respiratory difficulties in cystic fibrosis, or a history of cardiac disease.

Examination

Although jaundice is the hallmark of hepatitis, many children will present anicteric. Carotenaemia, which also causes a yellow-orange tinge of the skin due to high intake of carotenoids in carrots and other vegetables, can be differentiated from jaundice by the lack of scleral involvement. In addition to jaundice, physical examination in acute hepatitis may show tender hepatomegaly and mild splenomegaly. Arthralgias or arthritis and rashes can occur with hepatitis B. Signs of chronic liver disease should be specifically looked for including clubbing, leukonychia, palmar erythema, spider naevi, bruising, scratch marks, asterixis, ascites, prominent abdominal veins, oedema and signs of fat-soluble vitamin deficiency.

Investigations

Laboratory tests for hepatitis can be expensive and many may not be clinically useful in the emergency setting. Initial studies should include a full blood count, total and fractionated serum bilirubins, aspartate aminotransferase (AST), alanine aminotransferase (ALT), gamma glutamyl transferase (GGT) and prothrombin time (PT). A serum alkaline phosphatase level may be difficult to interpret in growing children because levels increase with bone growth. Serum AST, ALT and GGT are indicative of hepatocellular damage rather than ‘liver function tests’. Slight elevations of AST and ALT do not always predict mild disease and both can fall with end-stage liver disease. PT is the most useful indicator of synthetic function. If the aetiology of the hepatitis is unknown, anti-hepatitis A immunoglobulin M (IgM), hepatitis B surface antigen (HBsAg), IgM anti-hepatitis B core (HBc) and anti-hepatitis C virus (HCV) antibody should be obtained. If these tests are negative, other viral causes such as EBV and CMV should be considered. If no viral cause can be identified, metabolic and systemic causes of acute and chronic hepatitis should be excluded. Wilson’s disease can be detected by measuring serum coeruloplasmin levels and 24-hour urinary copper excretion, cystic fibrosis by measuring sweat electrolytes, α-antitrypsin deficiency by measuring serum α₁-antitrypsin levels.

Viral hepatitis1–4

Over the past decades the knowledge about the viruses that cause hepatitis has increased and is still evolving. The agents identified to cause hepatitis as their primary disease manifestation include hepatitis A virus (HAV), hepatitis B virus (HBV), hepatitis D virus (HDV) and formerly non-A, non-B designated viruses, hepatitis C (parenteral transmission) and hepatitis E (enteral transmission). HBV is a DNA virus whereas the other hepatotropic agents are RNA viruses. HAV and HEV are not known to cause chronic disease whereas the others can develop chronic infection. All five viruses can cause fulminant hepatitis with acute liver failure. A child with evidence of synthetic dysfunction (prolonged prothrombin time, hypoglycaemia, hyperammonaemia, lactic acidosis) with or without positive viral serology should be urgently referred to a paediatric gastroenterologist. Patients with severe hepatitis should be transferred early before intensive care therapy is required.

There are a number of other hepatotropic viruses which play a less well defined role in the pathogenesis of acute and chronic liver disease such as hepatitis G virus and TT virus. It is virtually impossible to clinically distinguish an acute infection due to one agent from another. Diagnosis is therefore dependent on the use of serologic and nucleic acid based assays. Many other viruses can cause hepatitis as part of their clinical spectrum, such as EBV and CMV.

Hepatitis A ¹^–³^,⁶^–⁹

Aetiology

HAV is an RNA virus classified as a member of the picorna virus group.

Epidemiology

The most common mode of transmission is person to person by the faecal–oral route. In developing countries, and also in certain Aboriginal communities, where infection is endemic, most persons are infected in the first decade of life. In developed countries, including much of Australia, infection may occur at an older age when susceptible adults travel to endemic areas. In Australia, the main patterns of hepatitis A are large, slowly evolving community outbreaks involving childcare centres, residential facilities, communities of intravenous drug users and male homosexuals, sporadic cases due to travel to endemic areas and point source outbreaks from contaminated food, water or an infected food handler. Faecal–oral transmission from asymptomatic infections, particularly in young children, likely accounts for many of the approximately 50% cases where the source cannot be determined.

The incubation period is 15–50 days (mean 30 days). The highest titres of HAV in stool occur during 1 to 2 weeks before the onset of illness, when patients are most likely to transmit HAV.

Clinical course

Hepatitis A is an acute self limited illness associated with fever, malaise, jaundice, anorexia and nausea. In children under 6 years of age symptomatic hepatitis occurs in only 30% and few will have jaundice. In older children and adults infection is usually symptomatic, typically lasting several weeks, and 70% will have jaundice. Prolonged or relapsing disease can occur though no chronic infection occurs. Fulminant hepatitis is rare but is more frequent with underlying liver disease.

Laboratory tests

HAV specific IgM and IgG antibody tests are available. IgM is invariably present by the time the patient presents and indicates current or recent infection and usually persists for 3 to 6 months. Anti-HAV IgG is detectable shortly after the appearance of IgM. The presence of anti-HAV IgG indicates past infection (or possibly immunisation) and immunity.

Management

There is no specific treatment for hepatitis A. Most patients can be managed at home. Hepatotoxic agents should be avoided. No specific dietary restrictions are required. Pruritus associated with cholestasis, which develops in 5–10%, may be treated with cholestyramine, an H₁-receptor blocker or local therapy.

Children and adults with acute HAV infection who are food handlers or work in child-care settings should be excluded for 1 week after the onset of illness. Hospitalised patients require contact precautions for 1 week after the onset of illness if they are incontinent or in nappies. Patients should be admitted if warning signs of acute liver failure develop (repeated vomiting, deepening jaundice and increasing prothrombin time), and transfer to a liver transplant centre is indicated at the onset of acute liver failure (increased prothrombin time and clouding of consciousness).

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Tags: Textbook of Paediatric Emergency Medicine

Sep 7, 2016 | Posted by admin in EMERGENCY MEDICINE | Comments Off

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