History

Fact Explanation
Low grade fever Inflammation in the liver release cytokines which reset the temperature set point in the hypothalamus at a higher level causing fever.[1]
Yellowish discoloration of skin, sclera and mucous membranes Yellowish staining of the skin, sclera, and mucous membranes by bilirubin, a yellow-orange bile pigment due to dysfunction of the intra hepatic phase of bilirubin metabolism. Often manifest when the serum bilirubin level is greater than 2.5 to 3 mg per dL.[2]
Dark colored urine Due to excessive passage of conjugated bilirubin and urobilinogen in urine which makes urine dark.[1,2]
Pale stools Due to intra hepatic cholestasis which decreases the passage of bile into the gastrointestinal tract and which in turn reduces the level of stercobilin which is necessary to give normal color to the stools.[1,2]
Pruritus Elevated levels of bile salts in the skin act as pruritogens.[1,2,3]
Anorexia Associated viremia and action of cytokines make the patient anorexic. (Characteristically smokers develops distaste for cigarettes).[1]
Fatigue/malaise The viremia causes the patient to feel unwell with non specific symptoms.[1]
Nausea and vomiting Inflammatory mediators stimulate vomiting center in brain. So patients feel nausea and also vomit.[1]
Right sided abdominal pain Inflammation of the liver will cause liver enlargement, which stretches the liver capsule generating pain.[1]
History of ingestion of food or water from an unsafe source. Hepatitis A virus is shed in the stool and is primarily spread by food or water contaminated with fecal matter.[1,4]
References
  1. SAMUEL C MATHONY. Joe E Kingery. Hepatitis A. American Family Physician. December 2012. vol 86(11):1027-1034. [viewed on 08.04.2014] Available at: http://www.aafp.org/afp/2012/1201/p1027.html
  2. SEAN P. ROCHE. REBECCA KOBOS. Jaundice in the adult patient. American Family Physician. 2004 January. vol 15;69(2):299-304.[viewed on 08.04.2014] Available at: http://www.aafp.org/afp/2004/0115/p299.html
  3. ANDREAS E KREWER. Ronald P J Oude Elferink. Ulrich Beuers. Pathophysiology and current management of pruritus in liver disease. Clinical and Research in Hepatology and Gastroenterology. 2011. 35, 89-97. [viewed on 08.04.2014] Available at: http://www.researchgate.net/publication/51540646_Pathophysiology_and_current_management_of_pruritus_in_liver_disease DOI:10.1016/j.clinre.2010.10.007
  4. FIORE AE. Hepatitis A transmitted by food. Clinical Infectious Diseases. March 2004. vol 38(5):705–715.[viewed on 08.04.2014] Available at: http://www.ncbi.nlm.nih.gov/pubmed/14986256

Examination

Fact Explanation
Increased body temperature Inflammation in the liver release cytokines which reset the temperature set point in the hypothalamus at a higher level causing increased body temperature.[1]
Jaundice/scleral icterus Due to deposition of bilirubin in the skin, sclera and mucous membranes.[1,2]
Tender hepatomegaly Diffuse inflammation of the liver causes moderate enlargement of the liver with smooth edges and stretching of the liver capsule producing tender hepatomegaly.[1]
Mild splenomegaly Because of the immune hyperplasia as a response to viral infection.[1]
References
  1. SAMUEL C MATHONY. Joe E Kingery. Hepatitis A. American Family Physician. December 2012. vol 86(11):1027-1034. [viewed on 08.04.2014] Available at: http://www.aafp.org/afp/2012/1201/p1027.html
  2. SEAN P. ROCHE. REBECCA KOBOS. Jaundice in the adult patient. American Family Physician. 2004 January. vol 15;69(2):299-304.[viewed on 08.04.2014] Available at: http://www.aafp.org/afp/2004/0115/p299.html

Differential Diagnoses

Fact Explanation
Acute hepatitis E virus infection Difficult to differentiate as both have a similar clinical presentation and same mode of transmission. But Hepatitis A virus infection is commoner than Hepatitis E virus infection. Serological investigations will help in diagnosis.[1,2,11]
Acute hepatitis B,C virus infection Unlike hepatitis A, hepatitis B and C mainly transmits hematogenously or sexually, therefore should consider in a patient with a history of risky exposure. Additionaly arthritis, skin rashes, arteritis and glomerulonephritis can be seen in hepatitis B infection.[1,2,10]
Alcoholic hepatitis Consider in a patient with a history of heavy alcohol consumption. Presence of signs of chronic alcohol use such as parotid swellings and other peripheral stigmata of chronic liver disease also point towards alcoholic hepatitis. Additionally unlike in acute hepatitis AST level is typically higher than ALT in alcoholic hepatitis.[1,2,9]
Infectious mononucleosis Consider in a patient with a preceding history of sore throat and if found to have palatal petechie, generalized lymphadenopathy on examination. Atypical lymphocytosis will be found in blood counts and film.[8]
Cytomegalovirus infection Suspect in patients who are immunocompromised.[7]
Acute HIV infection Occurs within the first 2-4 weeks after someone is infected with human immunodeficiency virus. Since the clinical features are nonspecific such as fatigue, malaise, arthralgia...etc, need high index of suspicion. Consider in a patient with risk factors for development of HIV infection (IV drug users, homosexual men )[5]
Acute drug induced liver injury Can be either dose dependent or idiosyncratic. Consider if there is a history of ingestion of causative drug and rapid onset of symptoms.[6,2]
Autoimmune hepatitis Suspect in a female with history of other autoimmune disorders.[4,2]
Leptospirosis Patient will have acute onset high grade fever with chills , rigors and severe myalgia and also there will be a history of predisposing event such as muddy water contact or travel into an endemic area.[3]
References
  1. SAMUEL C MATHONY. Joe E Kingery. Hepatitis A. American Family Physician. December 2012. vol 86(11):1027-1034. [viewed on 08.04.2014] Available at: http://www.aafp.org/afp/2012/1201/p1027.html
  2. SEAN P. ROCHE. REBECCA KOBOS. Jaundice in the adult patient. American Family Physician. 2004 January. vol 15;69(2):299-304.[viewed on 08.04.2014] Available at: http://www.aafp.org/afp/2004/0115/p299.html
  3. Leptospirosis. WHO Recommended standards and strategies for surveillance, prevention and control of communicable diseases. [viewed on 08.04.2014] Available at: http://www.who.int/zoonoses/diseases/Leptospirosissurveillance.pdf
  4. ALBERT J CZAJA. Autoimmune Hepatitis – Approach to Diagnosis. MedGenMed. 2006; 8(2): 55. [viewed on 08.04.2014] Available at: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1785222/
  5. CHU C, Selwyn PA. Diagnosis and initial management of acute HIV infection. American Family Physician. 2010 May. vol 15;81(10):1239-44. [viewed on 08.04.2014] Available at: http://www.ncbi.nlm.nih.gov/pubmed/20507048
  6. KAZUTO TAJIRI. Yukihiro Shimizu. Practical guidelines for diagnosis and early management of drug-induced liver injury. World J Gastroenterol. Nov 28, 2008; 14(44): 6774–6785. [viewed on 08.04.2014] Available at: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2773872/ doi: 10.3748/wjg.14.6774
  7. ROSS SA. Novak Z. Pati S. Boppana SB. Overview of the diagnosis of cytomegalovirus infection. Infect Disord Drug Targets. 2011 Oct;11(5):466-74. [viewed on 08.04.2014] Available at: http://www.ncbi.nlm.nih.gov/pubmed/21827433
  8. MARK H. EBELL. Epstein-Barr Virus Infectious Mononucleosis. American Family Physician. 2004 Oct 1;70(7):1279-1287. [viewed on 08.04.2014] Available at: http://www.aafp.org/afp/2004/1001/p1279.html
  9. Luis S. Marsano.Christian Mendez.Daniell Hill.et al. Diagnosis and Treatment of Alcoholic Liver Disease and Its Complications. Alcohol Research & Health.Vol. 27, No. 3, 2003.[viewed on 08.04.2014] Available at: http://pubs.niaaa.nih.gov/publications/arh27-3/247-256.pdf
  10. THAD WILKINS. DAVE ZIMMERMAN. ROBERT R. SCHADE. Hepatitis B: Diagnosis and Treatment. American Family Physician. 2010 April. vol 15;81(8):965-972. [viewed on 08.04.2014] Available at http://www.aafp.org/afp/2010/0415/p965.html
  11. Aggarwal R. Diagnosis of hepatitis E.Nat Rev Gastroenterol Hepatol. 2013 Jan;10(1):24-33. [viewed on 08.04.2014] Available at: http://www.ncbi.nlm.nih.gov/pubmed/23026902

Investigations - for Diagnosis

Fact Explanation
Serological tests - antibodies Anti hepatitis A virus IgM or four fold rise IgG in two different serum samples taken in the acute stage and convalescent phase of the illness will indicate presence of an acute hepatitis A virus infection.[2]
Liver enzymes - Aspartate transaminase (AST), Alanine transaminase (ALT), Alkaline phosphatase (ALP) Usually all these enzymes levels are elevated which indicates hepatocellular injury and precedes the appearance of jaundice. AST and ALT rise >500IU/L and ALT level will be higher than AST.[3,2]
Serum bilirubin, Bilirubin in urine and urinary urobilinogen Usually bilirubin levels are normal during prodomal stage. Then it start to increase producing hyperbilirubinaemia and bilirubinuria.[2]
Full Blood Count Will show leucopenia with relative lymphocytosis.[2]
Hepatitis A virus RNA in blood or faeces Hepatitis A virus is a 27nm picornavirus with single stranded RNA genome. It replicates in the liver, excreted in bile and found in feces thereafter. During initial viremic phase it can be found in blood. Though it is not done routinely it helps definitive diagnosis when there is diagnostic uncertainty.[1]
Liver biopsy Perform only when there is an uncertainty about the diagnosis.[2]
References
  1. NAINAN OV. Xia G. Vaughan G. Margolis HS. Diagnosis of Hepatitis A virus infection: a molecular approach. Clinical Microbiology Review. January 2006. vol 19(1):63-79. [viewed on 08.04.2014] Available at: http://www.ncbi.nlm.nih.gov/pubmed/16418523
  2. SAMUEL C MATHONY. Joe E Kingery. Hepatitis A. American Family Physician. December 2012. vol 86(11):1027-1034. [viewed on 08.04.2014] Available at: http://www.aafp.org/afp/2012/1201/p1027.html
  3. Johnston DE. Special considerations in interpreting liver function tests. Am Fam Physician. 1999;59(8):2223–2230. [viewed on 08.04.2014] Available at: http://www.aafp.org/afp/1999/0415/p2223.html

Investigations - Fitness for Management

Fact Explanation
Prothrombin time Prolonged in sever cases such as fulminant hepatic failure.[2,1]
References
  1. SAMUEL C MATHONY. Joe E Kingery. Hepatitis A. American Family Physician. December 2012. vol 86(11):1027-1034. [viewed on 08.04.2014] Available at: http://www.aafp.org/afp/2012/1201/p1027.html
  2. Johnston DE. Special considerations in interpreting liver function tests. Am Fam Physician. 1999;59(8):2223–2230. [viewed on 08.04.2014] Available at: http://www.aafp.org/afp/1999/0415/p2223.html

Management - General Measures

Fact Explanation
Bed rest Hepatitis A acute illness period usually doesnot last more than 2 months, therefore hospital admission is also not necessary but bed rest is usually advised. When the fever and jaundice have subsided patient can return to work or school.[2]
Antipyretics For fever. Paracetamol must use cautiously.[2]
Analgesics To relieve pain.[2]
Antiemetics - metoclopromide For nausea and vomiting.[2,3]
Cholestyramine For pruritus.[1]
References
  1. ANDREAS E KREWER. Ronald P J Oude Elferink. Ulrich Beuers. Pathophysiology and current management of pruritus in liver disease. Clinical and Research in Hepatology and Gastroenterology. 2011. 35, 89-97. [viewed on 08.04.2014] Available at: http://www.researchgate.net/publication/51540646_Pathophysiology_and_current_management_of_pruritus_in_liver_disease DOI:10.1016/j.clinre.2010.10.007
  2. SAMUEL C MATHONY. Joe E Kingery. Hepatitis A. American Family Physician. December 2012. vol 86(11):1027-1034. [viewed on 08.04.2014] Available at: http://www.aafp.org/afp/2012/1201/p1027.html
  3. JEONG SH. Lee HS. Hepatitis A: clinical manifestations and management. Intervirology. 2010;53(1):15–19 [viewed on 08.04.2014] Available at: http://www.ncbi.nlm.nih.gov/pubmed/20068336

Management - Specific Treatments

Fact Explanation
Prevention 1)Practice proper hand washing techniques and maintaining good personal hygeine to stop faeco-oral transmissoion of the virus.[3,2] 2) Using boiled water for drinking as the virus is killed by boiling water.[3,2] 3) Immunization - inactivated hepatitis A virus vaccine for high risk groups(eg: travelers to endemic areas)[1] 4) Post exposure prophylaxis - immunoglobulins within 2 weeks of exposure to household and institutional contacts.[1] 5) Notification and contact tracing to prevent the spread of the disease.[1]
Liver transplantation For patients who have developed fulminant hepatic failure.[2,4]
References
  1. FIORE AE. Wasley A. Bell BP. Prevention of Hepatitis A through active or passive immunization: recommendation of the Advisory Committee on Immunization Practices (ACIP). MMWR Recomm Rep. 2006; ss (RR - 7): 1-23. [viewed on 08.04.2014] Available at: http://www.ncbi.nlm.gov/pubmed/16708058
  2. SAMUEL C MATHONY. Joe E Kingery. Hepatitis A. American Family Physician. December 2012. vol 86(11):1027-1034. [viewed on 08.04.2014] Available at: http://www.aafp.org/afp/2012/1201/p1027.html
  3. FIORE AE. Hepatitis A transmitted by food. Clinical Infectious Diseases. March 2004. vol 38(5):705–715.[viewed on 08.04.2014] Available at: http://www.ncbi.nlm.nih.gov/pubmed/14986256
  4. JEONG SH. Lee HS. Hepatitis A: clinical manifestations and management. Intervirology. 2010;53(1):15–19 [viewed on 08.04.2014] Available at: http://www.ncbi.nlm.nih.gov/pubmed/20068336