Viral hepatitis
(Redirected from HBV)
Background
- 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
- Nausea/Vomiting
- RUQ pain
- Enlarged, tender liver
- Fever
- Jaundice
- Bilirubinuria
Differential Diagnosis
Causes of acute hepatitis
- Acetaminophen toxicity (most common cause of acute liver failure in the US[7])
- Viral hepatitis
- Toxoplasmosis
- Acute alcoholic hepatitis
- Toxins
- Ischemic hepatitis
- Autoimmune hepatitis
- Wilson's disease
Evaluation
- LFTs
- INR
- Coagulopathy correlates w/more severe liver dysfunction
- 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 |
Management
- Supportive care
- Symptomatic management; antiemetics, pain control, rehydration
- Manage any complications of liver dysfunction and/or cirrhosis
- Avoid hepatotoxic meds
- HepA: Household or close contacts may require IM HepA Ig if within 14 days of exposure
- See also Hepatitis B post-exposure prophylaxis
- Outpatient treatments for HCV include Interferon-α, [ribavirin]], and newer direct acting antivirals (e.g. Harvoni)
Disposition
- Admit
- INR >2
- Unable to tolerate PO
- Intractable pain
- Bilirubin >30
- Hypoglycemia
- Significant comorbidity/immunocompromised
- Age >50 years
See Also
References
- ↑ 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.
- ↑ www.cdc.gov/hepatitis
- ↑ 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
- ↑ 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
- ↑ Chaudhry SA et al. Hepatitis E infection during pregnancy. Can Fam Physician. 2015 Jul; 61(7): 607–608.
- ↑ Ranger-Rogez S, Alain S, Denis F. Hepatitis viruses: mother to child transmission [article in French] Pathol Biol (Paris) 2002;50(9):568–75.
- ↑ 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.