Acute Hepatitisi

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Acute Hepatitisi

  1. 1. Acute Hepatitis By Dr Osman Bukhari
  2. 2. <ul><li>Causes </li></ul><ul><li>1- Viral : HAV, HBV, HCV, HDV, HEV, EBV, CMV, HIV, Yellow fever </li></ul><ul><li>2- Non viral : Toxoplasmosis, Q fever & Leptospira iclerohaemorrhagua </li></ul><ul><li>3- Alcohol </li></ul><ul><li>4- Drugs & poisons : Paracetamol, Halothane, A.T.T, CCLY, Aspirin (Reyes) </li></ul><ul><li>5- Metabolic : Wilson's, alpha- one anti- trypsin deficiency </li></ul><ul><li>6- Ischemic : shock, Budd- chiari </li></ul>
  3. 3. <ul><li>Pathology </li></ul><ul><li>1- Depends on the cause </li></ul><ul><li>2- In viral & drug hepatitis : </li></ul><ul><li>- Pathology throughout the liver, specially centrilobular. Lobules affected variably </li></ul><ul><li>- Damaged hepatocyte are swollen & granular, while dead ones are shrunken & deeply stained acidophilic </li></ul><ul><li>- Mononuclear cell infiltration </li></ul><ul><li>- Polymorph infiltration & fatty change in some cases of tetracycline & CCL4 poisoning </li></ul>
  4. 4. <ul><li>- Severe damage collapse of reticulin frame work ,particularly between central </li></ul><ul><li>veins & portal tract linking them together (briding). Very severe damage massive necrosis & FHF </li></ul><ul><li>- Cholestasis +_ </li></ul>
  5. 5. <ul><li>Viral Hepatitis </li></ul><ul><li>Hepatitis A (HAV) </li></ul><ul><li>1- RNA- pecorna virus (27nm) </li></ul><ul><li>2- Secreted through the bile to the stools </li></ul><ul><li>3- Most common type of viral hepatitis </li></ul><ul><li>4- Faecal- oral spread </li></ul><ul><li>5- Over crowding & poor sanitation facilitate spread </li></ul>
  6. 6. <ul><li>6- No vertical spread </li></ul><ul><li>7- parental & sexual transmission is a rare possibility during the transient viraemia in the I.P </li></ul><ul><li>8- Patients are most infectious 2-3 weeks before the onset of jaundice & 1-2 weeks after . </li></ul><ul><li>9- I.P 2-4 weeks & mainly affect youngs </li></ul><ul><li>10- No carrier state or chronic sequelae </li></ul><ul><li>11- Mortality < 0.5% from FHF </li></ul><ul><li>12- Passive immunization of contact with 1g (0.04 - 0.06 units/kg I.M) protects for 3-4 months </li></ul>
  7. 7. <ul><li>13-Vaccin for people traveling to endemic areas & those with chronic liver disease. Single dose with booster one year after protects for 10year </li></ul><ul><li>14- Diagnosis : IgM anti HAV indicate acute infection (within 3months) & IgG anti HAV is persistent & used for epidemiology 15- The virus is cultured for research purposes </li></ul>
  8. 8. <ul><li>Hepatitis B (HBV) </li></ul><ul><li>1- DNA hepadna virus (42nm) </li></ul><ul><li>2- Has nucleocapsid core & envelope (capsule) </li></ul><ul><li>3- Contains HBsAg, HBeAg, HBcAg, DNA & DNA polymerase </li></ul><ul><li>4- Parental, sexual & vertical transmission </li></ul><ul><li>5- I.P 1-5 M </li></ul><ul><li>6- Individual incubating or with clinical attack are highly infections as long as HBsAg is positive </li></ul>
  9. 9. <ul><li>7- Carrier rate 0.5-15% </li></ul><ul><li>8- Chronic sequelae (chronic hepatitis, Cirrhosis & HCC) can follow infection. </li></ul><ul><li>9- Patients with chronic HBV infections are most infectious when markers of cont. replication are present in the blood:( HBeAg, DNA & DNA polymerase) & least infectious when they are absent & anti HBe is positive </li></ul><ul><li>10- Mortality 1% with FHF </li></ul><ul><li>11- Passive immunization with HBIG (500units for adult, 200units for neonates) </li></ul>
  10. 10. <ul><li>12- Active immunization with vaccine containing HBsAg for those at risk & who are anti HBsAg negative gives 90% protection. (day 0,1month , 6months & booster every 3-5 years) </li></ul><ul><li>13- People at risk include: I.V drugs abusers, homosexual, newborn of infected mother, regular sexual partener of infected person, dentists, surgeon, causality personale, in ICU, patients & staff in haemodialysis units, endoscopy units, liver units, oncology units & labs staff </li></ul>
  11. 11. <ul><li>14- Viral markers </li></ul><ul><li>- HBsAg: acute or chronic hepatitis or carrier state </li></ul><ul><li>- HBeAg: Persistant replication (highly infectious) </li></ul><ul><li>- HBV DNA: viral replication </li></ul><ul><li>- Anti HBsAg: immunity from previous exposure or vaccine </li></ul><ul><li>- Anti HBeAg: seroconversion </li></ul><ul><li>- Anti HBc IgM: acute infection </li></ul><ul><li>- Anti HBc IgG: previous exposure </li></ul>
  12. 12. <ul><li>Hepatitis D (HDV) </li></ul><ul><li>1- Incomplete RNA virus (35nm) </li></ul><ul><li>2- Can not replicate by it's own & has no independent existance </li></ul><ul><li>3- It occur either as super infection to HBV or as </li></ul><ul><li>co-infection </li></ul><ul><li>4- Similar mode of transmission to HBV specially in I.V drug abusers </li></ul><ul><li>5- I.P (6-9W) </li></ul><ul><li>6- Diagnosed by detecting IgM anti HDV or by HDV RNA in the serum </li></ul>
  13. 13. <ul><li>7-Fulminant hepatitis & chronic liver disease can follow </li></ul><ul><li>Hepatitis C (HCV) </li></ul><ul><li>1- RNA flaviurus (30-38nm) </li></ul><ul><li>2- Causes chronic liver disease & HCC </li></ul><ul><li>3- Most pts never suffer acute infection </li></ul><ul><li>4- Parental mode of transmission specially in I.V abusers (90%) & sexual transmission is possible but uncommon. Vertical transmission can occur </li></ul>
  14. 14. <ul><li>5- I.P (2-26weeks) </li></ul><ul><li>6- Diagnosis by detection of HCV RNA by PCR & detection of HCV antibodies </li></ul><ul><li>7- Mortality < 1% </li></ul><ul><li>8- Carrier rate varies from 0.2% in Europe , 6% in Africa & 19% in Egypt </li></ul>
  15. 15. <ul><li>Hepatitis E(HEV) </li></ul><ul><li>1- Prevalent in countries with poor sanitation and causes water born epidemics </li></ul><ul><li>2- RNA calici virus(27nm) </li></ul><ul><li>3- transmission is faecal oral </li></ul><ul><li>4- Similar clinical picture to HAV </li></ul><ul><li>5- No carrier state & no chronic sequelae </li></ul><ul><li>6- Diagnosis by detection of HEV RNA by PCR & by detection of IgG & IgM anti HEV by Eliza </li></ul>
  16. 16. <ul><li>Hepatitis G (HGV) </li></ul><ul><li>1- Parental mode of transmission </li></ul><ul><li>2-No evidence that it causes liver disease </li></ul>
  17. 17. <ul><li>Clinical picture of viral hepatitis </li></ul><ul><li>1- Prodromal symptoms preceed clinical </li></ul><ul><li>Jaundice by 1-2 W </li></ul><ul><li>2- Hepatomegaly which is tender </li></ul><ul><li>3- Rarely spleenomegaly & lymphoadenopathy </li></ul><ul><li>in children </li></ul><ul><li>4- Arthralgia, vasculitis, rash, myocarditis and G.N specially with HBV </li></ul><ul><li>5- Yellow sclerae & dark urine. 6- Pale stool with cholastasis </li></ul>
  18. 19. <ul><li>7- Most (95%) recover in 3-6 W </li></ul><ul><li>8- Few relapse </li></ul><ul><li>9- An icteric hepatitis occur in 65% </li></ul><ul><li>10- Massive hepatic necrosis occur in 1% causing F.H.F </li></ul><ul><li>Investigations </li></ul><ul><li>1- High ALT & AST(> 400U/L) </li></ul><ul><li>2- High Serum bilirubin </li></ul><ul><li>3- ALP rarely > 250U/L except in cholastasis </li></ul><ul><li>4- Normal serum alb </li></ul>
  19. 21. <ul><li>5- Prolong PT </li></ul><ul><li>6- Bilirubinuria. </li></ul><ul><li>7- Normal or low TWC with lymphsytosis </li></ul><ul><li>8- Viral markers </li></ul><ul><li>9- Mild proteinuria </li></ul><ul><li>Complications </li></ul><ul><li>1- F.H.F </li></ul><ul><li>2- Relapsing hepatitis (biochem. OR clinical) </li></ul><ul><li>3- Cholestasis </li></ul>
  20. 22. <ul><li>4- Post-hepatic syndrome </li></ul><ul><li>5- Unconjugated hyperbilirubinaemia (Gilbert) </li></ul><ul><li>6- A plastic anaemia (HAV, HCV, HEV) </li></ul><ul><li>7- Connective tissue disease </li></ul><ul><li>8- G.N & renal failure </li></ul><ul><li>9- H.Sch. purpura </li></ul><ul><li>10- Papular acrodermatitis </li></ul><ul><li>11- Chronic hepatitis, liver cirrhosis and HCC wz HBV &HCV. </li></ul>
  21. 23. <ul><li>Management </li></ul><ul><li>1- No specific treatment for acute hepatitis </li></ul><ul><li>2- Bed rest for elderly patients, pregnant ladies and patient with chronic liver disease </li></ul><ul><li>3- Good diet with vitamins supplements </li></ul><ul><li>4- Admit severe cases to guard against FHF </li></ul><ul><li>5- Avoid alcohol & sedatives </li></ul><ul><li>6- Avoid fatty meals </li></ul><ul><li>7- Antiviral (Ribavirin) and alpha interferon </li></ul><ul><li>8- Reassurance for post-hepatic syndrome </li></ul>
  22. 24. <ul><li>Prognosis </li></ul><ul><li>1- Mortality 0.5% in patients under 40 years and up to 3% in those over 60% </li></ul><ul><li>2- Mortality more with co-existing serous disease </li></ul><ul><li>3- 90-95% will have full recovery & 5-10% develop chronic infection </li></ul><ul><li>4- Maternal to child infection at birth lead to chronic infection in 95% & recovery is rare </li></ul><ul><li>5- Chronic infection is common with immuno-deficiency </li></ul>
  23. 26. <ul><li>6- Recovery in HBV occur in 6M. with appearance of anti-bodies to viral agents </li></ul><ul><li>7- Persistence of HBc Ag beyond 6M indicate chronic infection </li></ul><ul><li>8- 80% of HCV infection are chronic </li></ul><ul><li>9- Chronic HBV & HCV remain asymptomatic for years, however many patients eventually develop cirrhosis & some progress to HCC </li></ul><ul><li>10- Combined HBV, HDV cause more aggressive disease </li></ul>
  24. 27. <ul><li>Prevention </li></ul><ul><li>1- Improve over crowding & sanitation (HAV) </li></ul><ul><li>2- Active immunization & Ig. for immediate protection after exposure for HAV.to those at close contacts, elderly, pregnant & other major diseases </li></ul><ul><li>3- HBV vaccine to those at special risk who are not already immune (Anti HBs Ag negative). </li></ul><ul><li>Hyper immune serum glob within 7days.after exposure to infected blood </li></ul><ul><li>4- No vaccine for HCV </li></ul>
  25. 28. <ul><li>5- Sterilization of instruments & screening of blood & blood products for transfusion. </li></ul><ul><li>6- Moral vaccine. </li></ul>
  26. 29. <ul><li>Acute (Fulminat) hepatic failure </li></ul><ul><li>1- Rare condition in which encephalopathy result from sudden severe impairment of hepatic function occurring within 2W of onset of precipitating illness in the absence of pre-existing liver disease </li></ul><ul><li>2- If it occur 2-12W = sub acute FHF </li></ul><ul><li>3- Rare but 90% mortality following acute hepatitis from any cause </li></ul>
  27. 30. <ul><li>4- Causes include - viral infection (HAV , HBV , HDV) - drugs (pracetamol , aspirin , halothane , ATT) - poisons (mushroom , CCL4) - acute fatty liver of pregnancy - shock & cardiac failure - bud- chiari syndrome - leptospirosis - Wilson's disease </li></ul>
  28. 31. <ul><li>5-Pathologically </li></ul><ul><li>- There is extensive liver cell necrosis with severe fatty degeneration being characteristic of tetracycline , pregnancy & Reyes </li></ul><ul><li>- There is cerebral aedema & disruption of BBB </li></ul><ul><li>6- Clinically </li></ul><ul><li>Low alertness , poor conc. , restlessness , aggression, drowsiness , disorientation , change of sleep rhythm & coma </li></ul>
  29. 32. <ul><li>-Slurred speech , yawning , hiccough and seizures. - Asterixis (Flapping tremers) & foeter hepaticus are other features </li></ul><ul><li>- Myoclonus , spalicity , decorticate rigidity may be seen </li></ul><ul><li>- Papilla edema is very late (high I.C.P) </li></ul><ul><li>- Fever , vomiting , hypotension and hypoglythemia may occur </li></ul><ul><li>- Jaundice & small liver size </li></ul><ul><li>- Fluid retention & spleenomegaly are uncommon </li></ul>
  30. 33. <ul><li>7- Investigation </li></ul><ul><li>Markedly deranged LFT , ECG ,CBC , BUN & electrolytes , U/S ,viral markers , toxicity , screening , Auto-antibodies , CXR , se cu & caeruloplasmin </li></ul><ul><li>8- Management </li></ul><ul><li>1- No specific treatment except liver transplant </li></ul><ul><li>2- Support life & monitor </li></ul><ul><li>3- Ranitol , vitK , H2RA ,antibiotics </li></ul><ul><li>4-Treatment of cardio-respiratory arrest & fail. </li></ul><ul><li>5- Exchange transfusion , plasmapheres & charcoal haemoperfusion </li></ul>

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