Viral Hepatitis

Viral Hepatitis: Excerpt from The 5-Minute Pediatric Consult

Jeremy King, DO

Vani V. Gopalareddy, MD

Viral Hepatitis - BASICS

Viral Hepatitis - description

Viral hepatitis is defined as a systemic viral infection in which the predominant manifestation is that of hepatic injury and dysfunction. It is usually caused by hepatotropic viruses, which include hepatitis A to E, but 10% of cases are caused by other viruses, such as Epstein–Barr virus (EBV), cytomegalovirus (CMV), herpes simplex virus (HSV), varicella-zoster virus (VZV), rubella, parvovirus, adenovirus, or enteroviruses such as Coxsackie B, and others. In the United States, hepatitis B accounts for 40% of acute viral hepatitis cases, whereas hepatitis A and C account for 30% and 20%, respectively.

Viral Hepatitis - general prevention

• Good sanitation, hygiene, screening blood products, condom use, safe disposal of needles
• Hepatitis A:
  • Vaccine (Havrix, Vaqta): 0.5-mL dose IM and 2nd dose 6–12 months later
  • Recent guidelines recommend that all children between the age of 1 and 18 years should be vaccinated
  • Use for travelers to endemic regions, daycare workers, children with other liver diseases, and during outbreaks
  • Avoid return to daycare center for 2 weeks after illness subsides.
  • Hepatitis A immunoglobulin for close contacts of infected individuals.
• Hepatitis B:
  • Screen all pregnant women.
  • Hepatitis B vaccine to all infants at birth; complete 3 vaccine series 0.5-mL dose IM during infancy
  • Vaccine and hepatitis B immunoglobulin to high risk infants

Viral Hepatitis - epidemiology

Viral Hepatitis - incidence

• Hepatitis A: 125,000–200,000 infections per year worldwide. ~30,000 US cases per year. 10% occur in daycare centers that care for children who are not toilet-trained.
• Hepatitis B: 140,000–320,000 infections per year worldwide. ~78,000 US cases per year. Since the 1991 implementation of universal vaccination of infants, the incidence of acute hepatitis B virus (HBV) cases in US children has declined from 3.03 per 100,000 in 1990 to 0.34 in 2002.
• Hepatitis C: 40,000 infections per year in the US
• Hepatitis E: Common in poorly developed countries but rare in the US

Viral Hepatitis - prevalence

• Hepatitis B: US has a low prevalence with <1% of the population infected. Higher rates in certain subgroups such as immigrants from endemic areas, homosexuals, and parenteral drug users
• Hepatitis C: US has prevalence of 1.8%, representing ~3.9 million people (85% chronically infected)

Viral Hepatitis - risk factors

• Hepatitis A (transmission: Fecal-oral):
  • Daycare attendance, household exposure, travel to endemic areas
  • Maximum infectivity 2 weeks before jaundice
• Hepatitis B and C (transmission: Blood, body fluids, and sexual contact):
  • Recipients of blood or blood products
  • IV drug users
  • Multiple sexual partners
  • Homosexual males
  • Body piercing and tattoos
  • HIV-positive status
  • Infants born to a mother with hepatitis B or C
  • Household contacts with hepatitis B or C

Viral Hepatitis - pathophysiology

• Acute viral hepatitis tends to affect the liver parenchyma, whereas chronic viral hepatitis affects portal and periportal areas.
  • In acute hepatitis, there is spotty necrosis, panlobular disarray, increased cellularity, pleomorphism of hepatocytes, and focal parenchymal necrosis.
  • Chronic viral hepatitis is continuing inflammation of the liver for >6 months and affects the portal tracts predominantly but also extends into the parenchyma (interface hepatitis).
  • Worsening injury leads to extensive fibrosis that occurs between portal tracts (portal bridging), nodular changes and, finally, cirrhosis.

Viral Hepatitis - DIAGNOSIS

Viral Hepatitis - signs & symptoms

• Fever
• Malaise and fatigue
• Nausea and vomiting, anorexia
• Jaundice: In hepatitis A, seen in 88% adults but only 65% children
• Hepatomegaly
• Right upper quadrant (RUQ) abdominal pain
• Dark urine and pale stools
• Arthralgias/Arthritis
• The vast majority are minimally symptomatic or asymptomatic, especially with chronic infection.

Viral Hepatitis - history

History should focus on risk factors for viral exposure, sick contacts, travel history, and high-risk behaviors. Family history of liver or autoimmune disease, medications, or drug and alcohol use should also be explored.

Viral Hepatitis - physical exam

Jaundice, hepatomegaly, or tenderness over the liver may or may not be present.

Viral Hepatitis - tests

Viral Hepatitis - lab

• Liver function tests:
  • Marked elevation of aspartate aminotransferase/alanine aminotranferease (AST/ALT) during acute infection. May be normal to mildly elevated in chronically infected individuals
  • Bilirubin from mild to marked elevation
• In severe hepatitis, monitor PT/PTT, albumin, electrolytes, glucose, and CBC
• Biochemical markers for each virus for diagnosis, management, and monitoring:
  • Anti-hepatitis A virus (HAV) IgM: Recent infection
  • Anti-HAV IgG: Past exposure or immunization acquired
  • Hepatitis B surface antigen (HBsAg): Current infection, acute or chronic
  • Hepatitis B surface antibody (HBsAb): Immunized or resolved infection
  • Hepatitis B “e” antigen (HBeAg): Significant infectivity, viral replication
  • Hepatitis B “e” antibody (HBeAb): End of severe infectivity (except in precore mutants)
  • Hepatitis B virus core antigen (HBcore) IgM: Early phase of acute infection, not present in chronic HBV
  • HBcore Total Ab: Exposed to HBV
  • HBV DNA: Quantification useful to assess viral load
  • HBV mutations: Useful to assess resistance to treatment with lamivudine
  • HDV Ab: Exposure to hepatitis D
  • HCV Ab: Exposure to HCV
  • HCV RNA: Quantitative, assess viral load; qualitative, assess presence/absence of virus
  • HCV genotype: Useful to determine duration of treatment and likelihood of response

Viral Hepatitis - imaging

Ultrasound may demonstrate portal hypertension, biliary obstruction or ascites.

Viral Hepatitis - diag proced-surgery

Liver biopsy is usually needed to determine type and extent of liver damage. It is almost always indicated prior to initiation of antiviral therapy in children because risk of treatment may sometimes outweigh the benefit.

Viral Hepatitis - pathological findings

A wide array of histological features is possible on liver biopsy, including inflammation, necrosis, and fibrosis based on the severity and chronicity of disease.

Viral Hepatitis - differencial diagnosis

• Many disorders give rise to elevated transaminases, and clues to a viral origin are based on the history, serology, and histologic findings.
• One often invokes the diagnosis of non-A, non-B, non-C hepatitis when the cause is almost certainly viral but no virus is isolated.
• Other possibilities include drug-induced, ischemic, alcoholic, or autoimmune hepatitis, as well as Wilson disease or α-1 antitrypsin deficiency.

Viral Hepatitis - TREATMENT

Viral Hepatitis - general measures

• Severe cases need inpatient care; acute liver failure needs intensive care.
• Monitor and correct coagulation defects, fluid, electrolyte, and acid–base imbalances.
• Report acute cases to public health department.
• Patients with acute liver failure should be transferred to a pediatric transplant center.

Viral Hepatitis - medication

Hepatitis A:

• No specific therapy is available.
• Postexposure prophylaxis with pooled human serum globulin at dose of 0.02 mL/kg for household contacts, intimate exposure contacts, and children and staff in nursery or daycare centers with outbreaks

Hepatitis B:

• Postexposure prophylaxis with hepatitis B vaccine and hepatitis B immunoglobulin (HBIG) is indicated for neonates born to mothers who are hepatitis B carriers, after sexual contact with carriers, and after accidental exposure to infected blood products.
• There is no treatment for acute hepatitis B, though lamivudine is reported to be effective in fulminant hepatitis due to HBV.
• Chronic hepatitis B is treated with the antiviral agents interferon, lamivudine, adefovir, or entecavir when ALT is elevated.
• The most successful treatment is still interferon with 33% success rate in meta-analysis of adult studies.
  • Interferon α: 10 MU/m² given three times a week for 6 months (not recommended for use in infants and very young children <2 years).
• Response rates may be slightly lower for lamivudine, adefovir, and entecavir although they have fewer side effects. End point to stop treatment is not clear.
  • Lamivudine (Epivir HBV) (tablets 100 mg, suspension 5 mg/mL). Pediatric dose for >2 years age is 3 mg/kg/d.
  • Adefovir dipivoxil (Hepsera) and Entecavir (Baraclude) is approved for the treatment of HBV in adults only at this time. The dose for adefovir is 10 mg/d and Entecavir is 0.5–1 mg daily.
  • Adefovir often works well in patients with lamivudine-resistant disease.
  • Newer medications: Telbivudine, emtricitabine, clevudine under trial.
• The factor most predictive of treatment response in children with chronic hepatitis B is an elevated pretreatment ALT. Low viral DNA, young age, and female sex imply favorable response.
• Each year, 5–10% of children spontaneously clear hepatitis Be antigen (HBeAg), at which point the disease usually becomes inactive, although a few will later reactivate.
• Some pediatric studies suggest that antiviral therapy hastens but does not increase the rate of HbeAg seroconversion.

Hepatitis C:

• Antiviral therapy with interferon is indicated for active liver disease.
• Peg-interferon + ribavirin is the treatment of choice for chronic hepatitis C (after it is approved for use in children).
• Treatment duration depends on genotype:
  • Genotype 1 and 4: 1 year (type 1 most common in US)
  • Genotypes 2 and 3: 6 months (types more likely to respond to therapy)
• Maintaining higher doses is possible by balancing side effects with erythropoietin and granulocyte-macrophage–colony-stimulating factor (GM-CSF) to counter hemolytic complications and leukopenia.

Viral Hepatitis - FOLLOW UP

• Serial measurement of serum AST/ALT, viral markers, α fetoprotein, and ultrasound of the liver
• Liver biopsy pretreatment and for evaluation of disease progression

Viral Hepatitis - prognosis

• Hepatitis A:
  • Mild disease usual
  • Rarely results in relapsing, fulminant, or cholestatic disease
  • No chronic liver disease
  • Mortality <1%
  • Protective antibodies develop in response to infection and persist for life.
• Hepatitis B:
  • Fulminant hepatitis 1–2%
  • Mortality 0.5–2%
  • Chronic sequelae: Carrier state 10–95%, chronic hepatitis 5–10% (but 90% if vertically acquired), cirrhosis <5%, hepatocellular carcinoma (more common in HBV to viral integration into the genome)
• Hepatitis C:
  • Fulminant hepatitis 1%
  • Chronic sequelae: Carrier state 10–20%, chronic hepatitis 10–50%, cirrhosis 10–20%, hepatocellular carcinoma 5–10%
    • In adult studies, sustained virologic response to therapy may decrease HCV-related hepatocellular carcinoma.

Viral Hepatitis - complications

• Patients with advanced liver disease due to chronic Hepatitis B or C are at risk of complications associated with cirrhosis and portal hypertension.
• Patients with chronic Hepatitis B or with cirrhosis due to Hepatitis C are at increased risk of hepatocellular carcinoma
• Hepatitis B
  • Hepatitis D co-infection: Acute hepatitis B and D virus infection occur simultaneously.
    • Mortality rate of 1–10%
  • Hepatitis D superinfection: Acute hepatitis D occurs in a chronic carrier of hepatitis B.
    • Mortality rate of 5–20%
    • Acute liver failure occurs more frequently, chronic hepatitis 75%
    • Chronic HDV causes cirrhosis in 70–80% of patients and is a rapidly progressive disease compared with chronic hepatitis B alone. Cirrhosis has been noted to occur in as little as 2–10 years.

Viral Hepatitis - patient monitoring

Hepatitis E: Mortality of 20% caused by acute liver failure in pregnant women.

Viral Hepatitis - bibliography

1. Hochman JA, Balistreri WF. Chronic viral hepatitis: always be current! Pediatr Rev. 2003;24(12):399–409.
2. Koff RS. Hepatitis vaccines. Infect Dis Clin North Am. 2001;15(1):83–95.
3. Laurer GM, Walker BD. Hepatitis C virus infection. N Engl J Med. 2001;345(1):41–52.
4. Lok AS, McMahon BJ. Chronic hepatitis B. Hepatology. 2007;45(7):507–539.
5. O’Connor JA. Acute and chronic viral hepatitis. Adolesc Med. 2000;11(2):279–292.
6. Popper H, Schaffner F. The vocabulary of chronic hepatitis. N Engl J Med. 1997;284:1154–1156.
7. Shneider BL, Gonzalez-Peralta R, Roberts EA. Controversies in the management of pediatric liver disease: hepatitis B, C and NAFLD: summary of a single-topic conference. Hepatology. 2006;44(5):1344–1354.
8. Strader DB, Wright T, Thomas DL, et al. Diagnosis, management and treatment of hepatitis C. Hepatology. 2004;39(4):1147–1171.

Viral Hepatitis - CODES

Viral Hepatitis - icd9

• Hepatitis A 070.1
• Hepatitis B 070.30
• Hepatitis C 070.51
• Hepatitis D 070.52
• Hepatitis E 070.53

Viral Hepatitis - FAQ

• Q: Why do infants who acquire HBV at birth have a higher incidence of chronicity?
• A: The immaturity of the neonatal immune system contributes to the higher incidence of chronicity in this population. Furthermore, prenatal exposure to HBeAg may result in immune tolerance to the virus.
• Q: Should a mother with HCV positivity breastfeed?
• A: Transmission of HCV via breast milk is unlikely.

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Book Source Details

• Book Title: The 5-Minute Pediatric Consult
• Author(s): M. William Schwartz MD; et al.
• Year of Publication: 2008
• Copyright Details: The 5-Minute Pediatric Consult, Copyright © 2008 Lippincott Williams & Wilkins.

More About Hepatitis A

• Back to disease: Hepatitis A: Introduction
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Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.

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More About This Book: Title: The 5-Minute Pediatric Consult Authors: M. William Schwartz MD; et al. Publisher: Lippincott Williams & Wilkins Copyright: 2008 ISBN: 0-7817-7577-9

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