Viral hepatitis

(Redirected from Viral Hepatitis)


  • Hepatocellular pattern of injury, where AST and ALT are higher than Tbili and Alk Phos; likely to have significantly elevated ALT and AST (20x normal or higher)
  • Of note, transmission of Hepatitis B and Hepatitis C through donated blood, blood products, and organs is rare in the US since blood screening became available in 1992

Overview of Common Viral Hepatitis Agents

  • Hepatitis A
    • Fecal-oral transmission
    • Associated with epidemics linked to a common source (water)
    • Most common risk factor is travel outside of the US [1]
    • Not associated with chronic carrier state; incubation period is approximately 30 days, and infectivity usually resolved prior to symptom onset
    • Most common form of transmission occurs from asymptomatic children to adults
      • Approximately only 5% of infected children symptomatic
      • Whereas ~75% of adults are symptomatic
    • Incubation period: 15-50d
    • Prodrome: nausea/vomiting, malaise, fever, abdominal pain
      • 1wk later: clay-colored stool, jaundice
    • Death from hepatic failure is rare
  • Hepatitis B
    • Transmitted parenterally, blood contact, and unprotected sex
    • 90% of exposed infants progress to chronic hepatitis; 10% of exposed adults progress to chronic hepatitis
    • Serology[2]
    • Incubation period: 1-3 months
    • Presentation is similar to hep A
    • Lab tests:
      • HBsAg: + implies infection
      • Anti-HBs: implies clearance or vaccination
      • Anti-HBc: Implies prior infection; IgM = acute & in flares; only marker in window period; IgG always present
      • HBe-Ag: Implies active viral replication & infectivity
      • Anti-HBe: low infectivity
      • HBV DNA: Similar to HBe-Ag but more sensitive
  • Hepatitis C
    • Blood-borne, in US, most commonly transmitted through IV drug use. Infrequently transmitted through sexual contact
    • 90% of HCV infections progress to chronic hepatitis[3]
    • Unlike Hep A and B, most often asymptomatic in acute phase of infection
    • >75% of patients advance to chronic stage
    • Active disease identified by reactive HCV ab and positive HCV RNA
  • Hepatitis D
    • Transmission similar to Hepatitis B
    • Can only co-infect patients with Hepatitis B (actively producing HBsAg)
    • Presentation can range from acute self-limited disease to fulminant hepatitis or chronic infection
    • Only occurs with comorbid hepatitis B
    • High incidence of cirrhosis
  • Hepatitis E
    • Fecal-oral transmission
    • Usually results in mild illness, but can cause fulminant hepatitis in pregnant women[4]
    • Fecal-oral transmission
    • No carrier state
    • High associated mortality
    • Common in Southeast Asia, but different genotypes found globally across Asia, Africa, Latin America[5]
    • Mortality in pregnancy dependent on trimester[6]
      • 1.5% in first trimester
      • 8.5% in second trimester
      • 21% in third trimester

Clinical Features

Acute Hepatitis Features

Jaundice of the skin
Pediatric jaundice with icterus of sclera.

Differential Diagnosis

Causes of acute hepatitis


  • LFTs
  • INR
  • Acute hepatitis panel
    • Hep A Ab IgM
    • Hep B cAb IgM
    • Hep B sAg
    • Hep B sAb
    • Hep C Ab

Interpreting Acute Hepatitis Panel Results

Anti-hepatitis A, IgM Hepatitis B surface antigen Anti-hepatitis B core, IgM Anti-hepatitis C Interpretation
Positive Negative Negative Negative Acute hepatitis A
Negative Positive Positive Negative Acute hepatitis B
Negative Positive Negative Negative Chronic hepatitis B infection
Negative Negative Positive Negative Acute hepatitis B; quantity of hepatitis B surface antigen is too low to detect
Negative Negative Negative Positive Acute or chronic hepatitis C; additional tests are required to make the determination



  • Admit
    • INR >2
    • Unable to tolerate PO
    • Intractable pain
    • Bilirubin >30
    • Hypoglycemia
    • Significant comorbidity/immunocompromised
    • Age >50 years

See Also


  1. Oyama, LC: Disorders of the Liver and Biliary Tractin Marx JA, Hockberger RS, Walls RM, et al (eds): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 8. St. Louis, Mosby, Inc., 2014, (Ch) 107: p 1186-1204.
  3. Oyama, LC: Disorders of the Liver and Biliary Tractin Marx JA, Hockberger RS, Walls RM, et al (eds): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 8. St. Louis, Mosby, Inc., 2014, (Ch) 107: p 1186-1204
  4. Rein DB, Stevens GA, Theaker J, Wittenborn JS, Wiersma ST. The Global Burden of Hepatitis E Virus Genotypes 1 and 2 in 2005. Hepatology, Vol. 55, No. 4, 2012: 988-997
  5. Chaudhry SA et al. Hepatitis E infection during pregnancy. Can Fam Physician. 2015 Jul; 61(7): 607–608.
  6. Ranger-Rogez S, Alain S, Denis F. Hepatitis viruses: mother to child transmission [article in French] Pathol Biol (Paris) 2002;50(9):568–75.
  7. Ostapowicz G, Fontana RJ, Schiodt FV, et al. Results of a prospective study of acute liver failure at 17 tertiary care centers in the United States. Ann Intern Med. 2002 Dec 17; 137(12): 947-54.