Acute Hepatitis B

Gastroenterology

Clinicals - History

Fact Explanation
Asymptomatic Some patients may remain asymptomatic. Usually symptoms appear within 6 weeks to 6 months after the exposure. Asymptomatic
Some patients may remain asymptomatic. Usually symptoms appear within 6 weeks to 6 months after the exposure.
Fever Cell death and release of pyrogens due to the inflammation results in fever. Fever is usually mild and may be absent. Fever
Cell death and release of pyrogens due to the inflammation results in fever. Fever is usually mild and may be absent.
Fatigue and malaise Due to systemic viral infection. Fatigue and malaise
Due to systemic viral infection.
Anorexia This is very significant and appear in the prodromal period. Often people dislike the smell of food. Anorexia
This is very significant and appear in the prodromal period. Often people dislike the smell of food.
Right upper quad-rant discomfort Inflammation and congestion of the liver causes stretching of the liver capsule. Right upper quad-rant discomfort
Inflammation and congestion of the liver causes stretching of the liver capsule.
Flu-like symptoms Coryza, photophobia, headache, and myalgia may be the presenting complaint. Flu-like symptoms
Coryza, photophobia, headache, and myalgia may be the presenting complaint.
Yellow discoloration of eyes and skin Jaundice appares wthin 10 days of the symptom onset. Yellow discoloration of eyes and skin
Jaundice appares wthin 10 days of the symptom onset.
Serum sickness like illness This is a relatively rare presentation. Fever, skin rash and polyarthritis precede the appearance of jaundice. Serum sickness like illness
This is a relatively rare presentation. Fever, skin rash and polyarthritis precede the appearance of jaundice.
Polyarteritis nodosa Patients present with high fever, arthralgia, gastrointestinal disturbances and skin manifestations. Polyarteritis nodosa
Patients present with high fever, arthralgia, gastrointestinal disturbances and skin manifestations.
Arthralgia This is a relatively rare presentation. Arthralgia
This is a relatively rare presentation.
Symptoms of fulminant hepatitis Rarely acute HBV infection may cause fulminant hepatitis and acute liver failure. Features of coagulopathy (Spontaneous gum bleeding,cannula site bleeding), encephalopathy and cerebral edema develops. Once patients develop hepatic encephalopathy they have altered sleep wake cycle, somnolence, confusion and in extreme they develop coma. Symptoms of fulminant hepatitis
Rarely acute HBV infection may cause fulminant hepatitis and acute liver failure. Features of coagulopathy (Spontaneous gum bleeding,cannula site bleeding), encephalopathy and cerebral edema develops. Once patients develop hepatic encephalopathy they have altered sleep wake cycle, somnolence, confusion and in extreme they develop coma.
Dark urine and pale stools Acute hepatitis B sometimes result in cholestasis, resulting dark urine and pale stools. Dark urine and pale stools
Acute hepatitis B sometimes result in cholestasis, resulting dark urine and pale stools.
Features of Gianotti-Crosti syndrome This occurs in acute anicteric hepatitis. Infectious exanthema and lymphadenopathy occurs. Features of Gianotti-Crosti syndrome
This occurs in acute anicteric hepatitis. Infectious exanthema and lymphadenopathy occurs.
Features of Guillain-Barre syndrome Causes tingling, muscle weakness, and ascending paralysis. Features of Guillain-Barre syndrome
Causes tingling, muscle weakness, and ascending paralysis.
Aplastic anemia This is an extremely uncommon presentation. Aplastic anemia
This is an extremely uncommon presentation.
History of accidental needle prick injury Hepatitis B is spread by contact with infected blood. History of accidental needle prick injury
Hepatitis B is spread by contact with infected blood.
History of unprotected sexual exposure The body fluids (semen, vaginal fluids) also contain hepatitis B virus. This is a main mode of transmission in countries with low prevalence of hepatitis B. History of unprotected sexual exposure
The body fluids (semen, vaginal fluids) also contain hepatitis B virus. This is a main mode of transmission in countries with low prevalence of hepatitis B.
History of parenteral drug use When the needles are shared among infected and non-infected persons there is risk of infection. This mode of transmission is common in countries with low prevalance of the disease. History of parenteral drug use
When the needles are shared among infected and non-infected persons there is risk of infection. This mode of transmission is common in countries with low prevalance of the disease.
Infants born to Hepatitis B Virus (HBV) infected mothers. Hepatitis B virus is vertically transmitted to the fetus across the placenta and also during the process the labor. Infants born to Hepatitis B Virus (HBV) infected mothers.
Hepatitis B virus is vertically transmitted to the fetus across the placenta and also during the process the labor.
History of blood transfusion Although there are donor selection criteria and donor blood is screened before transfusion there is risk of hepatitis B infection after blood transfusion. History of blood transfusion
Although there are donor selection criteria and donor blood is screened before transfusion there is risk of hepatitis B infection after blood transfusion.
History of hemodialysis Hepatitis can transmit via poorly sterilized equipment. History of hemodialysis
Hepatitis can transmit via poorly sterilized equipment.
History of hepatitis B vaccination There is a small risk of development of hepatitis B infection after hepatitis B vaccination. History of hepatitis B vaccination
There is a small risk of development of hepatitis B infection after hepatitis B vaccination.

Clinicals - Examination

Fact Explanation
Icterus Jaundice develops due to reduced hepatic metabolism of bilirubin. Patients with anicteric or subclinical hepatitis may not have icterus. This is commoner in children. Patients develop jaundice after about 10 days of prodromal period and may last for months. Icterus
Jaundice develops due to reduced hepatic metabolism of bilirubin. Patients with anicteric or subclinical hepatitis may not have icterus. This is commoner in children. Patients develop jaundice after about 10 days of prodromal period and may last for months.
Mildly tender hepatomegaly Stretching of the liver capsule due to inflammation. Mildly tender hepatomegaly
Stretching of the liver capsule due to inflammation.
Splenomegaly Splenomegaly occurs secondary to hepatic congestion. Splenomegaly
Splenomegaly occurs secondary to hepatic congestion.
Palmar erythema Relatively rare finding. Occurs due to reduced hepatic metabolism of nitric oxide, a vasodilator. Palmar erythema
Relatively rare finding. Occurs due to reduced hepatic metabolism of nitric oxide, a vasodilator.

Investigations - Diagnosis

Fact Explanation
Liver transaminases Both ALT and AST are markedly elevated. Hepatocyte necrosis releases the enzymes to the circulation. Liver transaminases
Both ALT and AST are markedly elevated. Hepatocyte necrosis releases the enzymes to the circulation.
Serum bilirubin Bilirubin levels are raised. Usually the bilirubin rise is preceded by the rise of ALT. Serum bilirubin
Bilirubin levels are raised. Usually the bilirubin rise is preceded by the rise of ALT.
Prothrombin time (PT) and International Normalised Ratio (INR) PT is prolonged due to reduced synthesis of coagulation factors by the liver. Prothrombin time (PT) and International Normalised Ratio (INR)
PT is prolonged due to reduced synthesis of coagulation factors by the liver.
Hepatitis B Surface Antigen During the window period the HBSAg may not be detected. However this rises very early in the course of illness and aids early diagnosis. Hepatitis B Surface Antigen
During the window period the HBSAg may not be detected. However this rises very early in the course of illness and aids early diagnosis.
Hepatitis B DNA This is an early marker of HBV infection. DNA may be very low during the window period due to the rapid clearance of the viral load. Hepatitis B DNA
This is an early marker of HBV infection. DNA may be very low during the window period due to the rapid clearance of the viral load.
Hepatitis B e Antigen A marker of disease activity and infectivity. Higher the HBeAg levels higher the infectivity. Hepatitis B e Antigen
A marker of disease activity and infectivity. Higher the HBeAg levels higher the infectivity.
Anti-Hepatitis B core Antibody IgM type of antibodies indicate an acute infection. IgM antibodies are detected even during the window period of the illness. Anti-Hepatitis B core Antibody
IgM type of antibodies indicate an acute infection. IgM antibodies are detected even during the window period of the illness.

Investigations - Management

Fact Explanation
Hepatitis B Surface antigen (HBSAg) Hepatitis B tend to follow a chronic course if acquired during the neonatal period or during childhood rather than acquired during adulthood. If HBSAg persists in serum for more than 6 months, chronic hepatitis B is diagnosed. Hepatitis B Surface antigen (HBSAg)
Hepatitis B tend to follow a chronic course if acquired during the neonatal period or during childhood rather than acquired during adulthood. If HBSAg persists in serum for more than 6 months, chronic hepatitis B is diagnosed.
Hepatitis B Virus (HBV)-DNA Clearance indicates successful treatment. Persistent HBV-DNA indicates the risk of chronic hepatitis B. Around 15% to 40% of patients with chronic hepatitis B develop cirrhosis and subsequently hepatocellular carcinoma. Hepatitis B Virus (HBV)-DNA
Clearance indicates successful treatment. Persistent HBV-DNA indicates the risk of chronic hepatitis B. Around 15% to 40% of patients with chronic hepatitis B develop cirrhosis and subsequently hepatocellular carcinoma.
Anti-HBs Antibodies Development of anti- HBs antibodies indicates immunity and recovery from the infection. Anti-HBs Antibodies
Development of anti- HBs antibodies indicates immunity and recovery from the infection.
Hepatitis B e Antibody Indicates that the viral load and the infectivity is less. Hepatitis B e Antibody
Indicates that the viral load and the infectivity is less.
Ultra-sound scan of the abdomen If the patient develops chronic hepatitis ultrasound scan of the abdomen detects the development of cirrhosis. It is about 60% sensitive in detection of cirrhosis and done 6 months to 12months intervals. Ultra-sound scan of the abdomen
If the patient develops chronic hepatitis ultrasound scan of the abdomen detects the development of cirrhosis. It is about 60% sensitive in detection of cirrhosis and done 6 months to 12months intervals.
Serum alpha-feto protein. (AFP) AFP is a tumor marker. It is combined with the ultrasound assessment for the surveillance of hepatocellular carcinoma. Serum alpha-feto protein. (AFP)
AFP is a tumor marker. It is combined with the ultrasound assessment for the surveillance of hepatocellular carcinoma.
Hepatic transaminases In severe acute hepatitis B infection ALT rises more than 10times of the upper limit of the normal value. Hepatic transaminases
In severe acute hepatitis B infection ALT rises more than 10times of the upper limit of the normal value.
Serum bilirubin Serum bilirubin of more than 85 μm indicates acute severe hepatitis B infection. Serum bilirubin
Serum bilirubin of more than 85 μm indicates acute severe hepatitis B infection.
Prothrombin time and INR If prothrombin time increases more than 50% it indicates severe infection. Prothrombin time and INR
If prothrombin time increases more than 50% it indicates severe infection.
Hepatitis B Surface antigen (HBSAg) This is used in screening of high risk population. Hepatitis B Surface antigen (HBSAg)
This is used in screening of high risk population.

Management - Supportive

Fact Explanation
Rest Physical rest will quicken the recovery. Rest
Physical rest will quicken the recovery.
Adequate nutrition Since the oral intake was poor due to severe anorexia nutritional status of the patient should be optimized. Adequate nutrition
Since the oral intake was poor due to severe anorexia nutritional status of the patient should be optimized.
Adequate fluids Patient has lost significant amount of body fluids due to vomiting and poor oral intake. Adequate fluids
Patient has lost significant amount of body fluids due to vomiting and poor oral intake.
Vaccination High risk individuals can be vaccinated for the primary prevention of the infection. Vaccination
High risk individuals can be vaccinated for the primary prevention of the infection.

Management - Specific

Fact Explanation
Conservative managment In majority of patients no treatment is necessary and patients recover spontaneously. Antiviral therapy is proven to reduce the appearance of anti-HBs Antibodies and may dilute the immune response. Conservative managment
In majority of patients no treatment is necessary and patients recover spontaneously. Antiviral therapy is proven to reduce the appearance of anti-HBs Antibodies and may dilute the immune response.
Vaccination Hepatitis B vaccine if taken within 24 hours provides post-exposure prophylaxis. Vaccination
Hepatitis B vaccine if taken within 24 hours provides post-exposure prophylaxis.
Hepatitis B immune globulin This is also effective in post-exposure prophylaxis if taken within 24 hours of exposure. Protective effect lasts for about three months. This is also used in in neonates born to hepatitis B infected mothers. Hepatitis B immune globulin
This is also effective in post-exposure prophylaxis if taken within 24 hours of exposure. Protective effect lasts for about three months. This is also used in in neonates born to hepatitis B infected mothers.
Emergency liver transplantation This is the best possible treatment option in fulminant hepatitis and acute liver failure. Emergency liver transplantation
This is the best possible treatment option in fulminant hepatitis and acute liver failure.
Entecavir Entecavir is the commonly used first line therapy. It is a guanosine analogue and inhibits viral polymerase enzyme. Entecavir
Entecavir is the commonly used first line therapy. It is a guanosine analogue and inhibits viral polymerase enzyme.
Lamivudine Acts and clears the viral load very rapidly. Recently lamivudine resistance is detected. Lamivudine is proven to prevent the development of acute fulminant hepatic failure if started early in the illness. Lamivudine
Acts and clears the viral load very rapidly. Recently lamivudine resistance is detected. Lamivudine is proven to prevent the development of acute fulminant hepatic failure if started early in the illness.
Adefovir Nephrotoxicity is a possible side effect. However this is used as a second line treatment. Adefovir
Nephrotoxicity is a possible side effect. However this is used as a second line treatment.
Tenofovir Tenofovir has risk of nephrotoxicity however it is one of the first line treatment options. Tenofovir
Tenofovir has risk of nephrotoxicity however it is one of the first line treatment options.
Telbivudine This is also an antiviral drug. The antiviral drugs are continued for 3 months after the appearance of Anti-HBS antibodies . However some guidelines recommend that continuation of antiviral therapy until the clearance of HBs antigen is adequate. ( no need to continue for three months) Telbivudine
This is also an antiviral drug. The antiviral drugs are continued for 3 months after the appearance of Anti-HBS antibodies . However some guidelines recommend that continuation of antiviral therapy until the clearance of HBs antigen is adequate. ( no need to continue for three months)
Pegylated interferon alfa This is one of the first line treatment options. It has antiviral, antiproliferative, and immunomodulatory effects. Pegylated interferon alfa
This is one of the first line treatment options. It has antiviral, antiproliferative, and immunomodulatory effects.

Concise, fact-based medical articles to refresh your knowledge

Access a wealth of content and skim through a smartly presented catalog of diseases and conditions.

  1. ANDREA LISOTTI, FRANCESCO AZZAROLI, FEDERICA BUONFIGLIOLI, MARCO MONTAGNANI, FLAVIO ALESSANDRELLI, GIUSEPPE MAZZELLA. Lamivudine treatment for severe acute HBV hepatitis. Int J Med Sci [online] 2008; 5(6):309-312. [viewed 4 April 2014] Available from: doi:10.7150/ijms.5.309.
  2. ANTONIU E, LUCA V. Features of clinical evolution of severe acute viral hepatitis. Series of 72 cases. Rev Med Chir Soc Med Nat Iasi. [online] 2010;114:95–100. [viewed 4 April 2014] Available from:http://www.ncbi.nlm.nih.gov/pubmed/20509283
  3. CACOUB P, SAADOUN D, BOURLIÈRE M, et al.. Hepatitis B virus genotypes and extrahepatic manifestations. J Hepatol [online] 2005;43:764–770.
  4. CHISARI FV, FERRARI C. Viral Hepatitis. ed: Nathanson N et al., Viral Pathogenesis, Philadelphia, Lippincott - Raven, 1997:745-778.
  5. DAVID E J. All patients with acute hepatitis must be observed until the acute liver injury resolves. West J Med. [online] Jan 2000; 172(1): 32–33. [viewed 4 April 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1070719/
  6. DE SOCIO GV, MERCURI A, DI CANDILO F, BALDELLI F. Entecavir to treat severe acute hepatitis B. Scand J Infect Dis. [online] 2009;41:703–704. [viewed 4 April 2014] Available from: doi: 10.1080/00365540903062705.
  7. EASL Clinical Practice Guidelines: management of chronic hepatitis B. European Association For The Study Of The Liver. J Hepatol. [online] 2009;50:227–42. [viewed 4 April 2014] Available from: doi: 10.1016/j.jhep.2008.10.001.
  8. GIUSEPPE VITTORIO LUIGI DE SOCIO, ALESSIO SGRELLI, FRANCO BALDELLI. Severe Acute Hepatitis B Treated With Entecavir. Mediterr J Hematol Infect Dis. [online] 2011; 3(1): e2011010. [viewed 4 April 2014] Available from: doi: 10.4084/MJHID.2011.010
  9. GIUSEPPE VITTORIO LUIGI DE SOCIO, ALESSIO SGRELLI, FRANCO BALDELLI. Severe Acute Hepatitis B Treated With Entecavir. Mediterr J Hematol Infect Dis. [online] 2011; 3(1): e2011010. [viewed 4 April 2014] Available from: doi: 10.4084/MJHID.2011.010
  10. GIUSEPPE VITTORIO LUIGI DE SOCIO, ALESSIO SGRELLI, ANDREA TOSTI, FRANCO BALDELLI. Severe acute hepatitis b treated with entecavir. Mediterr J Hematol Infect Dis [online] 2011: 3(1). [viewed 4 April 2014] Available from: http://www.mjhid.org/article/view/7536
  11. HESHAM M. ELGOUHARI, TAREK I. ABU-RAJAB TAMIMI, WILLIAM D. CAREY. Hepatitis B virus infection: Understanding its epidemiology, course, and diagnosis [online] Journal of Medicine December 2008 vol. 75 12 881-889. [viewed 4 April 2014] Available from: doi: 10.3949/ccjm.75a.07019
  12. HOLLINGER FB, LIANG TJ. Hepatitis B Virus. ed: Knipe DM et al. Fields Virology, 4th ed. Philadelphia, Lippincott Williams & Wilkins, 2001:2971-3036.
  13. HOOFNAGLE JH, DOO E, LIANG TJ, FLEISCHER R LOK AS. Management of hepatitis B: summary of a clinical research workshop. Hepatology. [online] 2007;45:1056-75. [viewed 4 April 2014]
  14. Hepatitis B FAQs for the Public. [online] [viewed 4 April 2014] Available from: http://www.cdc.gov/hepatitis/b/bfaq.htm
  15. Hepatitis B FAQs for the Public. [online] [viewed 4 April 2014] Available from: http://www.cdc.gov/hepatitis/b/bfaq.htm
  16. Hepatitis B. World health organization. [online] [viewed 4 April 2014] Available from: http://www.who.int/mediacentre/factsheets/fs204/en/
  17. J. WIEGAND, H. WEDEMEYER, A. FRANKE, S. ROBLER, S. ZEUZEM, at el. Treatment of severe, nonfulminant acute hepatitis B with lamivudine vs placebo: a prospective randomized double-blinded multicentre trial. Journal of Viral Hepatitis. [online] 2013: 21(4). [viewed 4 April 2014] Available from: DOI: 10.1111/jvh.12210
  18. JOCHUM C, GIESELER RK, GAWLISTA I, FIEDLER A, MANKA P, SANER FH, ROGGENDORF M, GERKEN G, CANBAY A. Hepatitis B-associated acute liver failure: immediate treatment with entecavir inhibits hepatitis B virus replication and potentially its sequelae. Digestion. [online] 2009;80:235–40. [viewed 4 April 2014] Available from: doi: 10.1159/000236009
  19. KUO A, GISH R. Chronic hepatitis B infection. Clin Liver Dis. [online] May 2012;16(2):347-69. [viewed 4 April 2014]
  20. LOK ASF, MCMAHON BJ. Chronic Hepatitis B: Update 2009. AASLD practice guideline update. Hepatology. [online] 2009;50:661–662. [viewed 4 April 2014] Available from: doi: 10.1002/hep.23190.
  21. MEL KRAJDEN, GAIL MCNABB, MARTIN P. The laboratory diagnosis of hepatitis B virus. Can J Infect Dis Med Microbiol. [online] 2005 Mar-Apr; 16(2): 65–72. [viewed 4 April 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2095015/
  22. N. NISHINO, T. NISHIKAWA, M. UEDE, I. YATAKA, K. KUSUI. A clinical significance of vascular spider and palmar erythema in liver diseases. Gastroenterologia Japonica. [online] 1967: 2 (2), 142. [viewed 4 April 2014] Available from: DOI: 10.1007/BF02801516
  23. PAULG. M., JANEN. ZUCKERMAN, ARIEJ. Z. , SHEILA M. B., PAMELA J. at el. Acute hepatitis B infection after vaccination. The Lancet, [online] 28 January 1995: 345 (8944), 261 – 263. [viewed 4 April 2014] Available from: doi:10.1016/S0140-6736(95)90259-7
  24. PODDAR U, THAPA BR, PRASAD A, SINGH K. Changing spectrum of sporadic acute viral hepatitis in Indian children. J Trop Pediatr. [online] 2002 Aug;48(4):210-3. [viewed 4 April 2014] Available from:http://www.ncbi.nlm.nih.gov/pubmed/12200981
  25. ROBINSON WS. Hepatitis B virus and hepatitis D virus. ed: Mandell GL, Bennett JE, Dolin R,. Principles and Practice of Infectious Diseases, 4th ed. New York, Churchill Livingstone, 1995:1406-1439.
  26. RYDER S D, BECKINGHAM I J, Acute hepatitis. BMJ [online] 2001; 322 [viewed 4 April 2014] Available from: doi: http://dx.doi.org/10.1136/bmj.322.7279.151
  27. SINGAL A., VOLK M.L., WALJEE A., SALGIA R., HIGGINS P., ROGERS M.A., et al. (2009) Meta-analysis: surveillance with ultrasound for early-stage hepatocellular carcinoma in patients with cirrhosis. Aliment Pharmacol Ther [online] 2009: 30 (1): 37–47. [viewed 4 April 2014] Available from: doi: 10.1111/j.1365-2036.2009.04014.x
  28. SOLDAN K, RAMSAY M, COLLINS M. Acute hepatitis B infection associated with blood transfusion in England and Wales, 1991-7: review of database. BMJ. [online] Jan 9, 1999; 318(7176): 95. [viewed 4 April 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC27683/
  29. STANLEY PLOTKIN, ELKE LEURIDAN, PIERRE VAN DAMME. Hepatitis B and the Need for a Booster Dose. Clin Infect Dis. [online] (2011) 53 (1): 68-75. [viewed 4 April 2014] Available from: doi: 10.1093/cid/cir270
  30. TAÏEB A, PATRICE PLANTIN, DU PASQUIER P, GUILLET G, MALEVILLE J. Gianotti-Crosti syndrome: a study of 26 cases. British Journal of Dermatology. [online] July 1986 115 (1): 49–59. [viewed 4 April 2014] Available from: DOI: 10.1111/j.1365-2133.1986.tb06219.x
  31. WIEGAND J, WEDEMEYER H, FRANKE A, ROBLER S, ZEUZEM S, at el. Treatment of severe, nonfulminant acute hepatitis B with lamivudine vs placebo: a prospective randomized double-blinded multicentre trial. Journal of Viral Hepatitis. [online] 2013: 21(4). [viewed 4 April 2014] Available from: DOI: 10.1111/jvh.12210
  32. WRIGHT TL, LAU JY. Clinical aspects of hepatitis B virus infection. Lancet. 1993;342:1340–1344. [viewed 4 April 2014] Available from: doi: 10.1016/0140-6736(93)92250-W.
  33. YU JW, SUN LJ, ZHAO YH, KANG P, LI SC. The study of efficacy of lamivudine in patients with severe acute hepatitis B. Dig Dis Sci. [online] 2010;55:775–783. [viewed 4 April 2014] Available from: doi: 10.1007/s10620-009-1060-5.