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ACUTE VIRAL HEPATITIS

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ACUTE VIRAL HEPATITIS

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ACUTE VIRAL HEPATITIS

  1. 1. CHAIRPERSON: DR.SANTOSH VASTRAD STUDENT: DR.BASITH LATEEF
  2. 2. What is Viral Hepatitis ? Viral hepatitis is a systemic disease with primary inflammation of the liver by any one of a heterogenous group of hepatotropic viruses
  3. 3. Clinical Terms  Hepatitis: inflammation of liver  Acute Viral Hepatitis: symptoms last less than 6 months  Acute Hepatic Failure: is the appearance of severe complications rapidly after the first signs of liver disease (such as jaundice), & indicates that the liver has sustained severe damage (loss of function of 80-90% of liver cells).Massive hepatic necrosis with impaired consciousness within 8 weeks of onset of illness.  Chronic Hepatitis: Inflammation of liver for at least 6 months  Cirrhosis: Replacement of liver tissue fibrosis(scar tissue).These changes lead to loss of liver function.  Fulminant Hepatitis: severe impairment of hepatic functions or severe necrosis of hepatocytes in the absence of preexisting liver disease.
  4. 4. ACUTE VIRAL HEPATITIS Acute Viral Hepatitis is a systemic infection with mainly involvement of liver & rarely can cause extrahepatic manifestation.  Hepatitis A and E viruses commonly cause acute viral hepatitis.  Other infections like CMV ,EB virus, coxsackie virus and adeno virus can cause acute hepatitis.
  5. 5. • About 15 to 30% of acute cases in india are caused by HBV. • HDV is found in 10% of patients with HBV. • HCV is a rare cause of acute hepatitis. • Majority of AVH are self limiting. • Chances of fulminant liver failure varies from 0.01 to 1%
  6. 6. Hepatitis A  Hepatitis A (formerly known as ―infectious hepatitis or epidemic jaundice) is an acute infectious disease caused by Hepatitis A virus (HAV).  Originally called as enterovirus 72  The disease is benign with complete recovery in several weeks.  It is the only human hepatitis virus which can be cultivated in vitro.  M/C of hepatits in children. transmission by feco-oral route.  Virus is shed in feces during the late Incubation period & prodromal phase of illness.
  7. 7. EPIDEMIOLOGY • It has worldwide distribution and highly endemic in developing countries • India is hyperendemic. • Most of the cases occur in areas of poor hygeine and sanitation.
  8. 8. Geographic Distribution of HAV Infection Anti-HAV Prevalence High Intermediate Low Very Low Dr.T.V.Rao MD 13
  9. 9. Agent factors a) AGENT: The causative agent, the hepatitis A virus, is an enterovirus of the Picornaviridae family. It multiplies only in hepatocytes. STRUCTURE •Picorna virus •Single stranded RNA virus •Measures 27-28nm. •Icosahedral shape •Non enveloped. •Has one serotype & more than three genotypes.
  10. 10. b) RESISTANCE: The virus is fairly resistant to heat and chemicals. Withstands heating to 60 deg C for 1 hr. It is not affected by chlorine in doses usually employed for chlorination.  Formalin is stated to be an effective disinfectant. The virus is inactivated by ultraviolet rays and by boiling for 5 minutes or autoclaving. It survives exposure to ether and acid at pH 3. Inactivated by heat at 85 deg C for 1 min. Survives in sea water & dried feces for 4 weeks.
  11. 11. c) RESERVOIR OF INFECTION: The human cases are the only reservoir of infection. d) PERIOD OF INFECTIVITY : The risk of transmitting HAV is greatest from 2 weeks before to 1 week after the onset of jaundice. e) INFECTIVE MATERIAL : Mainly man’s faeces. f) VIRUS EXCRETION: HAV is excreted in the faeces for about 2 weeks before onset of jaundice and for up to 2 weeks thereafter.
  12. 12. Host factors a) AGE: Infection with HAV is more frequent among children than in adults. However, people from all ages may be infected if susceptible. b) SEX: Both sexes are equally susceptible. c) IMMUNITY: Immunity after attack probably lasts for life. Environmental factors • Cases may occur throughout the year. • In India the disease tends to be associated with periods of heavy rainfall.
  13. 13. Routes of transmission 1. Feaco-oral transmission 2. Intra familial sexual contact with an infected person 3. Rarely parenteral 4. Ingestion of contaminated food. Persons at risk 1. Travellers to endemic areas 2. Sexual contacts of infected persons 3. Household members 4. Men having sex with men 5. Drug abusers. INCUBATION PERIOD : 15-50 DAYS
  14. 14. Detetction and Infectivity of HAV
  15. 15. Replication cycle of HAV
  16. 16. CLINICAL FEATURES • CLINICAL PATTERNS. 1. Asymptomatic without jaundice 2. Symptomatic with jaundice and self limiting after 8 weeks. 3. Cholestatic with jaundice lasting 10 weeks or more. 4. Relapsing (10%) 5. Fulminant hepatic failure.
  17. 17. Nausea Loss of appetite Vomiting Fatigue Fever Liver enlargement Dark urine Pale stool Jaundice Stomach pain diarrhea Cervical lymphadenopathy A person may have all, some or none of these Symptoms
  18. 18. Approach to Diagnosis Hepatitis A (HAV) IgM anti-HAV Negative Positive Assay “total” anti-HAV as clinically indicated (-) Not immune to HAV Acute HAV infection (+) Immune to HAV
  19. 19. DIAGNOSIS 1. Demonstration of Virus in feces, blood, bile: By: Immunoelectron microscopy 2. Virus Isolation: 3. Detection of Antibody :By ELISA 4. Biochemical tests: i) Alanine aminotransferase (ALT) ii) Bilirubin iii) Protein 5. Molecular Diagnosis : RT PCR of feces
  20. 20. INVESTIGATIONS URINE AND FEACES • Bilirubin appears in urine before jaundice. • Urobilnogen is found in late pre icteric phase it disappears at the height of jaundice ,its reappearence indicates recovery.
  21. 21. LIVER BIOCHEMISTRY • Conjugated bilirubin rises early even before total bilirubin. • A raised serum AST or ALT, which can sometimes be very high, precedes the jaundice. • ALP level is usually < 3 times elevated. Serum albumin globulin are unchanged. • In the icteric stage the serum bilirubin reflects the level of jaundice. • Serum AST reaches a maximum 1-2 days after the appearance of jaundice, and may rise above 500 IU/L, the aminotransferases may remain elevated for some weeks and occasionally for up to 6 months.
  22. 22. HAEMATOLOGICAL CHANGES • Leucopenia,and neutropenia is seen in pre icteric phase. • Aplastic anemia is rare. • PT is prolonged. • An INR of >1.5 is considered severe acute hepatitis. • ESR is raised in preicteric phase falls to normal during jaundice and rises again during recovery & returns to normal after recovery.
  23. 23. VIRAL MARKERS : • IgM anti HAV indicates acute infection • IgG anti HAV suggests previous infection or vaccination. • HAV RNA can be detected in blood, stools and liver but it is not used. • IgG antibodies are common in the general population over the age of 50 years, but an anti- HAV IgM means an acute infection. • In areas of high prevalence most children have antibodies by the age of 3 years following asymptomatic infection.
  24. 24. • Treatment has little effect in altering the course. • It is wise to treat all attacks as fatal. • Bed rest is advised till jaundice disappears, a less strict regime if patient is young • Rest after each meal is advised. • The traditional low fat & high carb diet is advised. Treatment
  25. 25. • When appetite returns, high proteins are advised. • Corticosteroids are not indicated except occasionally in cholestatic hepatitis A. • Follow up is advised till three months. • Alcohol denied for 6 months preferably 1 year
  26. 26. Complications Acute fulminant hepatitis. Cholestatic hepatitis Nephrotic syndrome Chronic autoimmune hepatitis. Relapsing hepatitis. Extra hepatic manifestations are rare
  27. 27. Extra hepatic manifestations Rash Artharlgias Leucocytoclastic vasculitis Glomerulonephritis Cryoglobinemia TEN Renal failure Aplastic anemia Optic neuritis Red cell aplasia Thrombocytopenia
  28. 28. PREVENTION  Provision of clean drinking water  Proper sewage disposal  Public education about hygeine  Highly effective active and passive immunisation are available.
  29. 29. PROPHYLAXIS 1. IMMUNE SERUM GLOBULIN o ISG is being replaced by vaccine o ISG is still used in those with acutely exposed o It is ineffective in hyperendemic areas or in interrupting common source outbreaks. 2. VACCINATION o Pre exposure prophylaxis with inactivated vaccines can give protection till 20 years o Passive immunisation is used in post exposure prophylaxis-0.02ml/kg BW on deltoid within two weeks along with active immunisation.
  30. 30. Immunization against HAV in chronic illnesses Pre-exposure prophylaxis recommended : • Chronic liver disease (risk of HAV-related morbidity & mortality) • Patients awaiting liver transplantation • Patients already undergone liver transplantation. • HIV patients (response to vaccination may be reduced because of a blunted immune system)
  31. 31. OUTCOME Recovery in > 99% Clinical relapse in 4-20% Rarely need to hospitalize or transplant Fulminant hepatitis <0.35%
  32. 32. HEPATITIS E Also known as enterically transmitted non-A non- B(NANB) virus or epidemic NANB.  Classified in the genus HERPES virus under the family CALIVIRIDAE.  Single stranded +sense RNA virus.  The viral particles in stool are spherical, 27 to 34 nm in diameter with icosahedral symmetry, and unenveloped, and they exhibit spikes on their surface.
  33. 33.  A unique feature is the clinical severity and high case fatality rate of 15-25% in pregnant women, especially in the last trimester of pregnancy.  Highest attack rates among young adults 15-40 years with relative sparing of children.  Characteristically associated with cholestasis  There are 4 Genotypes in india.  Genotype 1 is common in india.  It is highly endemic  Faecoral transmission is common.  Rarely parentrally transmitted.
  34. 34. SIMILARITIES IN HAV & HEV: 1. Both have acute onset with mild illness. 2. Both are transmitted by feco-oral route. DIFFERENCES IN HAV & HEV: 1. HAV is more common in children. While HEV is more common in young adult. 2. HEV can cause fulminant hepatitis in pregnant women ( not HAV). 3. Secondary attack rate of HEV is very low (2-3%) as against 10-20% in HAV.
  35. 35. DR.T.V.RAO MD 46
  36. 36. • Travellers to endemic areas • Sexual contacts of infected persons • Household members • Men having sex with men • Drug abusers. No potential for chronicity. ANIMAL RESEVOIRS : Pigs INCUBATION PERIOD : 2-9 WEEKS PERSONS AT RISK
  37. 37. Clinical features Varying clinical manifestations. 1. Anicteric 2. Icteric hepatitis 3. Fulminant hepatic failure. 4. Asymptomatic infection
  38. 38. Pathogenesis
  39. 39. Treatment and prevention • Acute hepatitis E is self limiting. • Supportive care and no specific intervention • Isolation of infected persons is not indicated. • Patients with fulminant hepatitis require anti edema measures and liver transplantation is to be considered. • In pregnant women no proven evidence of terminating pregnancy is documented.
  40. 40. • A vaccine using a recombinant truncated form of HEV capsid protein, produced in Spodoptera frugiperda cells infected with a recombinant baculovirus and adsorbed on aluminium hydroxide, has undergone phase 2 trails. • Vaccine showed 95.5% protective efficacy against hepatitis E disease among those who received three doses and 88.5% efficacy in an intention-to-treat analysis among those who had received only the first dose.
  41. 41. • The vaccine may be useful for travelers to HEV-endemic regions and for pregnant women and persons with chronic liver disease who reside in such regions. • Finally, cost considerations will determine whether this new and promising vaccine can be used
  42. 42. 1. Maintaining quality standards for public water supplies 2. Establishing proper disposal systems to eliminate sanitary waste. 3. Maintaining hygienic practices such as hand washing with safe water, particularly before handling food; 4. Avoiding drinking water and/or ice of unknown purity; 5. Avoiding eating uncooked shellfish, and uncooked fruits or vegetables that are not peeled or that are prepared by people living in or travelling in highly endemic countries Prevention Dr.T.V.Rao MD 55
  43. 43. FULMINANT HEPATITIS Trey and Davidson define ALF as occurrence of encephalopathy with or without coagulopathy within 8 weeks of onset of symptoms of acute hepatitis in an individual without any history of pre-existing liver disease. Rapid development of severe acute liver injury with impaired function and encephalopathy in previously normal liver(8 weeks) or (2 weeks)with underlying liver dysfunction.
  44. 44. • Fulminanat hepatitis is associated with A,B and E. • Pyrexia is more frequent with type A • The duration of illness before encephalopathy is more with non A non B non C. • Prothombin time is greatest with type B.
  45. 45. Clinical features • It occurs within 10 days • Disease can be confused with psychosis and meningoencephalitis • Patient becomes deeply jaundiced, has repeated vomiting, fetor hepaticus, confusion and drowsiness • Flapping tremor is transient but rigidity is usual • Coma superveins • Widespread haemorrhages may develop
  46. 46. • Leucocytosis can occur in contrast to leucopenia of viral hepatitis. • The rise of bilirubin and transaminases are poor indicators of prognosis. • Transaminases may fall when patients condition deteriorates. • Blood coagulation is grossly deranged • Prothrombin time is best indicator of prognosis.
  47. 47. • Hepatic encephalopathy • Cerebral edema • Sepsis • Renal failure(30-70%) • Cardiovasular dysfunction :arrythmias, hyperdynamic circulation. • Coagulopathy • Gastrointestinal bleeding • Pulmonary complication:ARDS ,pulmonary edema, aspiration. • Metabolic disturbance : metabolic acidosis, hypoglycemia, hypophosphatemia,hypokalemia. FHF complication
  48. 48. KING’S COLLEGE CRITERIA FOR PROGNOSIS
  49. 49. MANAGEMENT OF COMPLICATION CEREBRAL EDEMA: • Positioning of head and trunk at 35° to 40° angle above horizontal, • Avoiding unnecessary motions of the head and • Avoiding hypoxaemia, hypercapnoea, fluid overload and acidbase imbalance. • Rapid infusion of mannitol (20%) at a dose of 100 ml is the first step. • Induction of barbiturate coma may be used as a rescue therapy, if mannitol fails.
  50. 50. Sepsis: • Sepsis is the second major cause of death among Indian patients with ALF. • Gram-negative bacteria are the major cause of sepsis in these patients. • Prophylactic parenteral antibiotics using third generation cephalosporins. Renal Failure : low dose dopamine (2 µg/kg/hr to 2.5 µg/kg/hr) may be beneficial. • The mainstay of management of renal failure in patients with ALF however is haemodialysis.
  51. 51. Coagulopathy: • Coagulopathy associated with ALF is currently not preventable. • Prophylactic use of fresh frozen plasma (FFP) and vitamin K has not been shown to prevent bleeding.
  52. 52. LIVER TRANSPLANTATION • Urgent OLT is now the standard therapy for ALF in individuals who, on clinical and laboratory criteria, have a less than 20% chance of survival. Contraindications to OLT include 1. Irreversible brain damage, 2. Uncontrolled bacteraemia, 3. HIV 4. concurrent malignant disease • Auxiliary liver transplantation is another treatment option for ALF.
  53. 53. Acute hepatitis in HBV and HCV Clinical features and management are similar as acute hepatitis caused by HAV. The course may be anicteric. Sub-clinical episodes are extremely frequent. The non-icteric case is more liable to become chronic than the icteric one. The usual acute clinical attack, diagnosed in the adult , tends to be more severe than for HAV infections.
  54. 54. Benign course is marked by increased serum transaminase values for more than 100 days. Relapses are rare. Cholestatic hepatitis with prolonged deep jaundice is unusual. Acute hepatitis B is self-limited in 95–99% while hepatitis C is self-limited in only 15%
  55. 55. Treatment • SELF LIMITING • Does not require any specific treatment. • Patients should be followed up to detect chronicity particularly in children. • Treatment with lamivudine,telbivudine or entacavir is indicated in patients with fulminant hepatitis, proctracted severe infection.
  56. 56. Extra hepatic manifetations • Polyarteritis. This involves largely medium and small arteries and appears early in the course of the disease.  Plasmapheresis and adenine arabinoside have been used for treatment • Glomerulonephritis. This has been associated with HBV infection, largely in children . • Essential mixed cryoglobulinaemia is a rare association of HBV infection although very frequent in HCV • The Guillain–Barré syndrome has been reported with HBsAg-containing immune complexes in serum and cerebrospinal fluid.
  57. 57. Hepatitis D •DELTA agent is single stranded , circular, antisense RNA •HDV is considered to be a subviral satellite because it can propagate only in the presence of the hepatitis B virus (HBV). • It is highly infectious
  58. 58. VIRION: spherical, 36-38 nm particle with an outer coat composed of the HBsAg surrounding ssRNA genome. Satellite virus : replicates only in the presence of HBV
  59. 59. Incubation Period : 2-12 weeks Mode of Transmission: The primary route of Transmission are believed to be similar to those of HBV, though HDV does not appear to be sexually transmitted disease.
  60. 60. Risk factors  Intravenous drug abuse (strongly associated )  Homosexual men (infrequent)  Health-care workers  Transfusion recipients  Haemophiliacs  Immigrants  Developmentally disabled .  HDV can spread heterosexually .  Intrafamily spread has been noted in southern Italy .  Children can be affected.  HDV infection may be reactivated by HIV infection
  61. 61. CLINICAL FEATURES Infection is dependent on HBV replication, as HBV provides an HBsAg envelop for HDV. Two types of infection are recognised: coinfection and superinfection. In Coinfection, delta and HBV are transmitted together at the same time. In Superinfection, delta infection occurs in a person already harbouring HBV.
  62. 62. DIAGNOSIS Delta antigen is primarily expressed in liver cell nuclei, where it can be demonstrated by immunofluorescence.  Anti-delta antibodies appear in serum and can be identified by ELISA. IgM antibody appears 2-3 weeks after infection and is soon replaced by the IgG antibody in acute delta infection.
  63. 63. Co-infection  It is diagnosed by finding serum IgM anti-HDV in the presence of high-titre IgM anti-HBc.  These markers appear at 1 week, and IgM anti-HDV is gone by 5– 6 weeks but may last for up to 12 weeks  Self limited as HDV cannot outlive the transient HBs antigenemia. Superinfection  It is marked by the early presence of serum IgM anti-HDV, usually at the same time as early IgG anti-HDV and both antibodies persist.  IgM anti-HBc negative  the acute attack may be severe and even fulminant, or may be marked only by a rise in serum transaminase levels
  64. 64. Prevention • Vaccination against hepatitis B makes the recipient immune to HBV infection and protects against HDV infection. Treatment • Treatment is unsatisfactory. • High doses of interferon given for long periods result in reductions of AST but recurrence is usual
  65. 65. Hepatitis G virus • GB virus C (GBV-C) • HPgV • It is a virus in the Flaviviridae family and a member of the Pegivirus genus, is known to infect humans, but is not known to cause human disease. • HGV RNA has been found in patients with acute, chronic and fulminant hepatitis, hemophiliacs, patients with multiple transfusions and hemodialysis, intravenous drug addicts and blood donors.
  66. 66. Yellow fever • This acute infection is due to a group B arbovirus transmitted to man by the bite of infected mosquitoes. • The virus cycle is a direct human one in urban yellow fever, or may involve wild monkeys in the jungle variety
  67. 67. Clinical features • Incubation period of 3–6 days • Onset is sudden with fever, chills, headache, backache, prostration and vomiting, often of altered blood. • The blood pressure falls, haemorrhages become widespread • Jaundice and albuminuria are conspicuous • Delirium proceeds to coma • Death may occur within 9 days.
  68. 68. Diagnosis • Demonstrating specific IgM antibodies to yellow fever virus. • Prothrombin deficiency parallels the severity of the liver lesion. • The serum cholesterol and glucose levels fall in the fatal case. • Serum transaminases are increased relative to severity.
  69. 69. Treatment • There is no specific treatment. • Death results principally from renal damage. • The hepatic lesion is self-limited and short- lived and does not demand special treatment.
  70. 70. Epstein barr virus • Primary infection in children is usually asymptomatic. • In adolescents and young people, it causes a hepatitis which may mimic HAV, HBV or HCV hepatitis. • Presentation, particularly in adults, may be as fever with right, upper quadrant, abdominal discomfort. Pharyngitis and lymphadenopathy may be absent. • It can cause fulminant hepatitis in elderly people • It may be a trigger autoimmune hepatitis in susceptible people such as the immunosuppressed. • EBV infection may be associated with lymphoproliferative disorders.
  71. 71. Diagnosis • The serum albumin level may be slightly decreased and the serum globulin value slightly elevated. • Hyperbilirubinaemia is present in about one-half of patients. • Serum transaminase values are raised to about 20 times the normal in 80% of patients. • In about one-third the serum alkaline phosphatase value is increased, often more so than that of bilirubin. • The monospot reaction is positive. • The disease is diagnosed conclusively by an increase in serum IgM antibodies against EBV capsid antigens.
  72. 72. CMV: • The picture may simulate type A, B or C hepatitis, having a similar onset but with failure of the pyrexia to subside with the onset of jaundice. • Icterus lasts 2–3 weeks and even up to 3 months. Occasionally, massive hepatic necrosis may be fatal. • Granulomatous hepatitis can develop in a previously normal adult. • Cholangitis, papillary stenosis and sclerosing cholangitis can accompany cytomegalovirus infections in patients with AIDS • Rarely cause posttransfusion hepatitis. • Causes real problem in adult and paediatric recipients of kidneys and liver transplants
  73. 73. • Diagnosis is by isolation of virus from urine or saliva. • Complement-fixing antibodies rise and cytomegalovirus IgM antibodies can be found. • The virus cannot usually be shown in liver biopsy but direct hepatic involvement has been confirmed by demonstrating nuclear and cytoplasmic inclusions in hepatocytes
  74. 74. HERPES SIMPLEX. • Human herpes virus types I and II affect all humans at some time during their lives. • In infants, herpes hepatitis may be part of generalized herpetic disease. • In adults, disseminated herpes simplex is very rare. • It can affect those with underlying diseases e.g. ulcerative colitis , AIDS , those receiving immunosuppressive treatment or having organ transplants.
  75. 75. • Fulminant hepatic failure can also affect the previously normal and immunocompetent . • The onset is with fever, prostration, marked elevation of transaminases and leucopenia. • Jaundice is absent. • Fulminant liver failure with fatal coagulopathy can develop.
  76. 76. HEPATITIS DUE TO EXOTIC VIRUSES • These very dangerous viruses have the liver as the primary target . • They include Marburg, Lassa and Ebola viruses. Lassa fever • It is due to an arenavirus transmitted from rodents to man or from man to man. • It is largely found in West Africa. The case fatality rate is 36–67%. • Diagnosis is made by demonstrating virus in the blood during the first few days and by IgM antibodies from the fifth day. • It has been successfully treated with ribavirin
  77. 77. Marburg virus disease • It is due to an RNA virus transmitted by Vervet monkeys. • After an incubation period of 4–7 days the patients present with headache, pyrexia, vomiting, a characteristic rash, a haemorrhagic diathesis and central nervous system involvement. • Serum transaminase levels are very high Ebola virus infection • It resembles Marburg in clinical course, hepatic histology and electron microscopy • It has been reported from Zaïre and the Sudan and has been transmitted to biologists working with it.
  78. 78. Treatment : • There is no specific treatment for these exotic virus infections. • Symptomatic measures are used and very strict precautions are necessary to avoid spread to contacts

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