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Acute hepatitis
1. Acute viral hepatitis is defined as inflammation of the liver caused by viral infection, resulting in elevated liver enzymes for less than 6 months. The most common causes are hepatitis A, B, C, D, E viruses. 2. The document discusses the pathogenesis, clinical features, investigations, management, and prevention of different viral hepatitis types. Hepatitis A and E are usually self-limiting while hepatitis B, C and D can sometimes lead to chronic liver disease. 3. Supportive care is the main treatment approach for most cases of acute viral hepatitis. Specific antiviral therapy may be used for severe hepatitis B cases to prevent progression to liver failure. Vaccines exist to prevent hepatitis A and B infection
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Acute hepatitis
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- 3. INTRODUCTION Definition: • Acute ViralHepatitis is defined as inflammation of liver and sudden onset of aminotransferase elevation as a consequence of diffuse necro-inflammatory liver injury which lasts for < 6 months. Acute liver disease encompasses a wide range of disorders from asymptomatic transaminitis to ALF Viral hepatitis and DILI are the most frequent causes. Acute viral hepatitis is a self-limiting disease with chance of ALF in a small percentage of patients. M.C cause: Hepatitis A and E
- 4. Etiology of Acutehepatitis Infectious 1) Viral: Hepatitis A – E, EBV, CMV, Dengue, Yellow fever 1) Bacterial: Weil’s disease, MTB, Enteric fever 2) Protozoal: Malaria, Toxoplasmosis 3) Helminth: E. histolytica Non-infectious 1) Toxin: Mushroom, CCl4 2) Alcohol 3) Acute fatty liver of pregnancy 4) Acute budd chairi syndrome 5) Metabolic: Wilson’s disease 6) Autoimmune hepatitis 7) Ischemic hepatitis 8) Drugs: PCM, ATT, Phenytoin
- 5. Pathogenesis HAV: Survivesthe acidic digestion by gastric juice and reaches the portal circulation Multiplies in the hepatocytes and damages hepatocytes by immunological mechanism Excreted in feces HBV: Damages hepatocytes by immune mediated injury HCV: Binds to receptors on the hepatocyte surface Enters the cell by endocytosis Rarely causes immune mediated injury in acute phase and thus most of acute HCV infections are asymptomatic except for mild transaminesemia HDV: Causes infection only in the presence of HBV infection either as superimposed or co-infection CMV: Primary infection or as a reactivation of latent infection HSV: Neonates, Pregnancy, Immunocompromised patients a/w genital herpes infection
- 6. Headache, Myalgia, Arthralgia, Anorexia,Nausea, Vomiting, Fatigue, Pharyngitis, Cough, Coryza precedes the onset of jaundice by 1-2 weeks. Alteration in olfaction & distaste for cigarettes. Fever (100 - 102°F) Dark urine & clay colored stools 1 – 5 days before clinical jaundice. Jaundice Tender hepatomegaly Splenomegaly Cervical lymphadenopathy Infrequently cholestatic picture • Jaundice deepens • Stool becomes paler • Urine becomes darker • More hepatomegaly Appetite improves gradually Symptoms subside Some liver enlargement with deranged LFT Complete clinical & biochemical recovery • 1-2 months in HAV & HEV • 3-4 months in HBV & HCV • HBV self limited in 95-99% cases • HCV self limited in 15% cases PRODROMAL PHASE CLINICAL JAUNDICE RECOVERY PHASE
- 7. Hepatotropic virus-general characters HAVHBV HCV HDV HEV VIRUS Group NA Entero/Pi corna RNA Hepadna DNA Flavi RNA RNA Calci RNA Incubation period 15-45 days 30-180 days 15-160 days 30-180 days 15-60 days Spread Faeco-oral Parenteral Sexual Vertical Faeco-oral Chronicity Yes Yes Yes Prevention Active Passive Vaccine Immune serum globulin Vaccine Hyperimm une serum globulin No No HBV vaccine No No
- 8. Enterically (HAV & HEV) Parenterally (HBV,HCV, & HDV) Non-enveloped Shed in faeces Survive intact when exposed to bile Do not cause chronicity Do not have prolonged viremia Do not have carrier state M.C: HEV >> HAV Enveloped viruses Cause chronicity a/w persistent viremia Have a carrier state M.C: HBV + HDV HCV rarely causes AVH
- 9. HAV HBV HCVHDV HEV CMV HSV Age Any, mostly children Any age Usually adults Any age Any, Usually adults Immuno compro mised Sexually active adults Sympto ms Asympto matic in children Sympto matic with jaundice Cholesta tic with jaundice lasting > 10 weeks Relapsin g with 2 bouts over 6-8 wks Fulmina nt: 0.5% Prodrome fever Arthralgia Myalgia Jaundice (30%) Maculopa pular utricarial rash (10%) Acute hepatiti s (20%) Fatigue N/V Asympt omatic in children Self limiting acute hepatitis mimickin g flares of chronic HBV Anicteric hepatitis Icteric hepatitis FHF(20% ) in pregnan cy Asympto matic Subclinic al in most Mononu cleosis like illness Rarely cholesta tic May be seen as neonatal hepatitis
- 10. HAV HBV HCVHDV HEV CMV HSV Clinical Signs Tender hepato megaly (85%) Spleno megaly (15%) Cervical LN (15%) Hepatom egaly Rashes Jaundice Fluctuati ng transami nases Double peak transami nases if co- infected with HBV Jaundice Hepato megaly Splenom egaly Jaundice Hepato megaly Splenom egaly Jaundice Hepato megaly Splenom egaly Signs of DIC Duration Of Disease Recover y in 60% within 2 months & 100% in 6 months 95-99% resolve in 6 months Others progress to chronicity Usually resolves in 1 month (15%) Resolves in 4-8 weeks Self limiting Resolve in 6 weeks Resolves in 6-8 weeks
- 11. HAV HBV HCVHDV HEV CMV HSV Fulmina nt hepatitis Mostly in adults 55% in 1st week & 90% within 4 weeks < 0.5% overall In < 1% Within 4 weeks High mortality (80%) HBV+HDV > 50% cases Very rare 5-10% 20% in pregnan cy Occurs with MODS in immuno compro mised patient May develop in neonate as adrenal insufficie ncy In pregnan cy as well Extra- hepatic manifest ations Rash Arthralg ia Nephriti s Cutane ous vasculiti s Rash Arthritis Hematuria Proteinuria PAN GN Nephrotic syndrome Cryoglobulin emia Cryoglo bulinem ia GN Lichen planus Sicca syndro me PCT None Arthralgi a Pancreat itis Acalculo us cholecys titis Rash DIC
- 12. Investigations • Complete bloodcount ▫ Neutropenia & lymphopenia ▫ Relative lymphocytosis ▫ Pancytopenia (aplastic anemia) • Renal function tests • Liver function tests ▫ ↑Serum bilirubin: 5-20 mg/dL (both UB & CB equally) ▫ ↑AST/ALT (ALT >> AST): 400 – 4000 in icteric phase ▫ Diminishes gradually in recovery phase ▫ Anicteric hepatitis ( N bilirubin but ↑AST/ALT ) ▫ ALP: Increased but < 3 x UNL ▫ Albumin: Normal ▫ PT/INR: usually normal; poor prognosis if increased
- 13. • Viral serology: ▫HAV IgM, HAV RNA ▫ HBsAg, IgM anti-HBc, HBV DNA, HBeAg ▫ Anti-HCV(4-6 weeks), HCV RNA (1-2 weeks), HCV genotyping ▫ HDV RNA, anti-HDV antibodies ▫ HEV IgM ▫ EBV Capsid antigen, CMV DNA, HSV, VZV serology ▫ Dengue serology and NS1 antigen • Leptospirosis: ▫ Microscopic agglutination test (MAT): Gold standard ▫ ELISA, PCR : confirmatory • Enteric fever: ▫ Blood C/S, Typhi dot IgM • Malaria: ▫ MP antigen, Thick and Thin smear
- 14. • Alcoholic hepatitis: ▫↑AST/ALT – 2:1; calculate DF ▫ ↑γGGT • Acute fatty liver of pregnancy: ▫ USG abdomen • Acute budd-chiari syndrome: ▫ Doppler USG & Hepatic venography • Wilson’s disease: ▫ Serum ceruloplasmin, 24 hr urinary copper ▫ Slit lamp exam for KF rings • Autoimmune hepatitis: ▫ ANA, Anti-LKM Ab, ASMA, Anti SLA, serum IgG levels • Ischemic hepatitis: ▫ Rapid rise & fall in AST.ALT (>1000) and LDH within 1-3 days of insult • Drugs: ▫ Serum APAP & plot in Rumack-Matthew nomogram ▫ Treat Hypophosphatemia ▫ Modified ATT regimen if ATT induced liver injury
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- 16. N- acetylcysteine isadministered within 8 – 10 hours of ingestion as per toxicity line on Rumack-Matthew nomogram. ORAL • Loading dose: 140mg/kg • Maintenance dose: 70mg/kg every 4 hours for a total of 17 doses. INTRAVENOUS • Loading dose: 150mg/kg over 1 hour • Maintenance dose: 14mg/kg/hr for 4 hours and then 7mg/kg/hr for 16 hours • For late presenters(>8hrs) • LD: 140mg/kg over 1 hr • MD: 14mg/kg/hr for 44 hrs
- 17. Hepatitis A: Relapsing hepatitis Cholestatic hepatitis Hepatitis B: Serum sickness Hepatitis C: Porphyria cutanea tarda (PCT) Lichen planus Essential mixed cryoglobulinemia Fulminant hepatitis HBV + HDV > 50% cases HEV – 20% in pregnancy Drug induced Chronic hepatitis Aplastic anemia
- 18. Management- Hepatitis A Pre-exposureprohylaxis Post-exposure prohylaxis • Inactivated HAV vaccines containing single HAV antigen given IM into deltoid in a 2 dose regimen ( 0, 6-18 months) • Combination vaccines (HAV >720 ELISA unit + 20μg HBsAg) given in a 3 dose regimen (0, 1, & 6 months) • Given in chronic hepatitis B and C infections • Immune serum globulin 0.02 ml/kg/dose given on deltoid within 14 days of exposure • Effective in outbreak of hepatitis in school or nursery.
- 19. Management- Hepatitis B •Supportive with monitoring for ALF (<1% cases) • In adults, 90 -95% (99%) resolve with the development of anti HBs antibody --- thus, no role of antiviral therapy • The remaining 5 -10% develop chronic hepatitis B • Vertical transmission leads to chronic hepatitis B in 90 % of children & recovery is rare. • Role of antiviral proven in severe acute hepatitis B that may progress to ALF. • Entecavir or Tenofovir until 3 months after HBsAg seroconversion or 6 monhs after HBeAg seroconversion.
- 20. Management- Hepatitis B Pre-exposureprophylaxis Post-exposure prophylaxis • HBV vaccine: prepared from HBsAg given IM at 0, 1, and 6 months • Response is measured by anti-HBs levels ≥ 10 mIU/ml • Protected antibody response is > 90% after 3rd dose. • Infants born to HBsAg + mother: ▫ HBV vaccine & HBIg 0.5 ml within 12 hours of birth at two separate sites • Sexual partners + Needlestick injury: ▫ HBIg (0.04 – 0.07 ml/kg) + 1st dose of HBV vaccine at different sites within 48 hours but no more than 7 days ▫ 2nd dose HBIg after 30 days and complete the vaccination schedule
- 21. Management- Hepatitis C •In typical acute hepatitis C, recovery is rare. • Progression to chronicity is the rule. • 50-85%: develop chronicity ▫ 60-70%: Chronic hepatitis after 10 years ▫ 30%: Cirrhosis after 20-30 years ▫ 15%: HCC after 40 years • Interferon α 3 million units SC three times a week + Ribavarine
- 22. *HDV, HEV: supportive *HSV:IV acyclovir *CMV: Ganciclovir, Cidofovir, Foscarnet *Leptospirosis: Ceftriaxone, Doxycycline *Enteric fever: Ceftriaxone, Azithromycin, Ofloxacin *Malaria: Artesunate, Artemether *Acute budd-chiari syndrome: *Anticoagulation, surgical shunts, liver transplantaion *Wilson’s disease: D-penicillamine, Trientene *Autoimmune hepatitis: Steroids, Azathioprine *Ischemic hepatitis: correction of underlying cause that caused circulatory collapse *APAP toxicity: N-acetylcysteine
- 23. General Measures • ?Bed rest • ?Physical isolation to a single room & bathroom ▫ Fecal incontinence for hepatitis A and E ▫ Uncontrolled, voluminous bleeding for hepatitis B and C • Universal precaution for HBV & HCV ▫ Avoiding direct, ungloved hand contact with blood & other body fluids • High calorie diet – mainly in morning as nausea predominant during evening • Avoid hepatotoxic drugs • Cholestyramine for pruritis • Maintain proper sanitation, hygeine & avoidance of overcrowding in hepatitis A and E
- 24. Prevention • HAV: ▫ Cleandrinking water, proper sewage disposal ▫ Public education about the hygiene ▫ Active & passive immunization • HBV: ▫ Screening the transfused blood & blood products for HBsAg ▫ Using disposable syringes & needles ▫ Using safety precautions & practicing safe sex ▫ Active & passive immunization • HCV: ▫ Screening for anti-HCV • No active & Passive immunization available • HDV: ▫ Same as HBV but vertical transmission is extremely rare • HEV: ▫ Same as HAV ▫ HEV vaccine has been recently shown to be effective and is awaiting commercial availability
- 25. Points not tobe forgotten • Viral hepatitis (HAV & HEV) and DILI (PCM & ATT) are the most frequent causes of AVH. • M.C cause of parenterally mediated AVH: HBV + HDV • Hepatocyte injury is mainly via immune mediated injury. • 3 stages of clinical features. • Rate of fulminancy is least in isolated HAV, HBV, & HCV. • Rate of fulminancy is high with combined HBV + HDV & HEV in pregnancy (both 20%). • Acute hepatitis is rare in HCV & Chronic hepatitis is rare in PCM overdose. • HAV is associated with relapsing & cholestatic variant. • 95-99% of acute hepatits B resolve spontaneously but 90% of vertically transmitted children develop chronic hepatitis. • Progression to chronicity is the rule in acute hepatitis C; only 15% undergo spontaneous remission. • HDV is always co-infected with HBV as it uses HBsAg as its envelope. • Use Rumack-Matthew nomogram for APAP toxicity as a guide to treatment. • Both active & passive immunization are available for HAV & HBV. HBV vaccine is given in HDV infection. • Avoid hepatotoxic drugs