Viral hepatitis by Dr. JohnPresentation Transcript
What is Hepatitis?‘hepa’ = liver‘titis’ = inflammation
Infectious (ie, viral, bacterial, fungal, and parasitic organisms) noninfectious (eg, alcohol, drugs, autoimmune diseases, and metabolic diseases)
Liver inflammation due to a viral infection. acute (recent infection, relatively rapid onset) or chronic forms. Hepatitis A, Hepatitis B, Hepatitis C, Hepatitis D, and Hepatitis E Herpes Simplex, Cytomegalovirus, Epstein- Barr virus, or Yellow Fever viral hepatitis does not include aforementioned virus except Hepatitis viruses A to E
Hepatitis A,E: Fecal–oral route Close contact Food or water that has been contaminated with infected faeces. (Commonest in children) Oral-anal sex
Blood + Body Fluid Blood products IV drug abusers Sexual intercourse Direct contact Vertical transmission (mother-to-child transmission)
Will you get infected though kissing?
The chance of contracting hepatitis from kissing is very small because the viruses that cause hepatitis are basically spread through blood and bodily fluids (hepatitis B, hepatitis C, hepatitis D) and fecal-oral contact (hepatitis A, hepatitis E). Concentration of virus in saliva is very low(Hep B,C) . Unless, there are faeces in his/her mouth(Hep A, D,E)!
Features of the Hepatotropic virusesVirology HAV RNA HBV DNA HCV RNA HDV RNA HEV RNAIncubation (days) 15-19 60-180 14-160 21-42 21-63TransmissionParenteral Rare Yes Yes Yes NoFecal-oral Yes No No No YesSexual No Yes Yes Yes NoPerinatal No Yes Rare Yes NoChronic infection No Yes Yes Yes NoFulminant disease Rare Yes Rare Yes YesNelson Textbook of Pediatrics 19th edition
Acute (Inflammation <6mths) ViralHepatitis Chronic (Inflammation >6mths) Hepatitis B ,C, D may progress to chronic hepatitis, in which the liver remains inflamed for more than six months. This condition can lead to cirrhosis, liver cancer, and possibly death.
Acute Phase: fatigue, nausea, poor appetite, belly pain, a mild fever, or yellow skin or eyes (jaundice.) HepatitisB, C, and D may become chronic, they may cause no symptoms for years. By the time there are any warning signs, the liver may already be damaged.
Chronic phase: -Tiredness, anorexia, nausea -Intolerance to fatty foods -Abdominal discomfort (particularly in the right upper quadrant region). -Fevers and night sweats can also occur.
Diagnosis of viral hepatitis is based on symptoms, physical findings as well as blood tests for liver enzymes, viral antibodies, and viral genetic materials. Patients with chronic hepatitis due to hepatitis B , C, and D often have no symptoms or only mild nonspecific symptoms such as chronic fatigue. Typically, these patients do not have jaundice until the liver damage is far advanced. Therefore, these patients can remain undiagnosed for years to decades.
3 types of blood tests for evaluating patients with hepatitis: 1 liver enzymes 2 Antibodies to the hepatitis viruses 3 Viral proteins or genetic material (viral DNA or RNA).
Aminotransferases.: • Aspartate aminotransferase(AST or SGOT) • Alanine aminotransferase (ALT or SGPT). (Normal range: ALT: 3-35iu/L, AST:3-35iu/L) • These enzymes normally are contained within liver cells. If the liver is injured (as in viral hepatitis), the liver cells spill the enzymes into the blood, raising the enzyme levels in the blood and signaling that the liver is damaged.
Antibodies are proteins produced by white blood cells that attack invaders such as bacteria and viruses. Antibodies against the hepatitis A, B, and C viruses usually can be detected in the blood within weeks of infection, and the antibodies remain detectable in the blood for decades thereafter. Blood tests for the antibodies can be helpful in diagnosing both acute and chronic viral hepatitis.
Genetic material Viral ProteinHAV-Ag HAV-RNAHBs-Ag HBV-DNAHBe-Ag HCV-RNAHCV-Ag HDV-RNA HEV-RNA *HBc-Ag is undetectable in serum
HBsAg: person is potentially infectious Anti-HBc :HBV infection, current or past IgM Anti-HBc: present in high titre during acute infection IgG Anti-HBc detectable for a lifetime Anti-HBe decreased infectivity HBeAg: High infectivity
Treatment of acute viral hepatitis and chronic viral hepatitis are different. Acute viral hepatitis : relieving symptoms and maintaining adequate intake of fluids. Chronic viral hepatitis eradicate the virus and taking measures to prevent further liver damage.
Relieve symptoms of nausea, vomiting, and abdominal pain. Sedatives and "tranquilizers" are avoided because they may accentuate the effects of liver failure. Avoid alcohol. Control fluid imbalance caused by vomiting.
Bleeding Cirrhosis Encephalopathy: • Liver disease that causes confusion and excessive sleepiness Hepatocellular Carcinoma Liver Failure Malnutrition
Hep A Hep B Hep C Hep D Hep E Hep GIncubation 15-30 days 60-180 days 2-24wk Co infection 3-8wks Unknownperiod (2-6 weeks) (2-6 months) ( 2wk-6m) with HBVTransmission Fecal-oral •Congenital •Blood Similar to Fecal-oral Parenteral •Blood •Sexual HBV Blood More in •Sexual (uncommon) More in children •Body secretion •Congenital adolescents (rare) and adultsSerum Anti-HAV HBsAg (first Ag Anti-HCV Anti-HDV Anti-HEV RNA by RT-markers detectable after (IgG, IgM), RNA PCR(specific Recent exposure and PCR forinvestigation) infection: Rise persists until HCV RNA in anti HAV recovery IgM antibody occurs) HbcAg, Immunity: IgG HBeAg, anti- antibodies HBs, anti-HBcFulminant Rare <1% unless co- uncommon 2-20% 20% Probably noliver failure infection with Most HDV complete recoverPersistent No •Carrier 85% but 2-70% No Persistentinfection •Chronic take longer infection hepatitis times (20-40 common, •5-10% but years) chronic faster (5-20yrs) disease rare 25
Hep A Hep B Hep C Hep D Hep ECompli Usually mild. Sometimes severe 1 Usually (80%) Super/ co- Usually mildcations Very low -2% mortality asymptomatic infection with except in mortality Up to 4% mortality HBV - often pregnancy very severe Prolonged/ •Chronic carrier •Chronic hepatitis (70-80%) with high Severe relapsing illness •Chronic hepatitis •Chronic carrier mortality rate infection in lasting 6-9 •Cirrhosis •Cirrhosis pregnancy months in 15% •HCC •HCC •Chronic (15-20% carrier mortality) •Cirrhosis •HCC Fulminant hepatic failureManage No specific Acute 1. IFN-alfa 2b Supportive Supportivement treatment •Largely supportive •Better compliance and fewer side effects Control and Supportive Chronic treat HBV •IV hydration Goal: cessation of 2. Ribavirin infection •Anti-pruritic active replications agents •Interferon alfa 2b S/E immunomodulator: •Fat soluble and lamivudine for •Anemia vitamins 4-6 months •Neutropenia •Serial •Recombinant •Influenza like symptoms monitoring for interferons - signs of ALF immunomodulatory Pt screen yearly with U/S and antiviral effects and serum AFP for HCC •Lamivudine – and vaccination against inhibits viral enzyme HAV and HBV to prevent reverse transcriptase super infection 26
Hep A Hep B Hep C Hep D Hep E Hep GPrevention Highly Vaccine: Screen Hep B Recombinant Screen blood contagious Hep B donated blood immunization Hep E for elevated (contagious immunoglobul for elevated vaccine hepatic for 2 weeks in hepatic Screen transaminase before and transaminase donated blood Good hygiene about 7 days Screen and anti-HCV for elevated after onset of donated blood (appears 4 hepatic jaundice) and for elevated months post transaminase should be hepatic infection, 6 and HBsAg excluded from transaminase months post- school, child and HBsAg transfusion) care during this period Vaccine: Immune serum globulin Good hygiene Hand washing 27
Fulminant hepetic failure (HF) - hepatic dysfunction (hepatic encephalopathy and coagulopathy) within 8 weeks of evidence of symptoms of liver disease and absence of pre-existing liver disease.
Disease Duration of onset of encephalopathy after jaundiceHyperacute/ <2 weeksFulminant HFSubfulminant HF 2-12 weeksSubacute/ Late- 8weeks – 6monthsonset HF
Jaundice with impalpable liver / reduce liver size Encephalopathy - may worsen rapidly Bruising, petechiae or bleeding from Deranged cloting unresponsive to vitamin K. Failure to maintain normoglycaemia (which aggravates encephalopathy) or presence of hyperammonaemia Increased intracranial pressure
Supportive Treatment: nurse in quiet darkened room with head-end elevated at 20 with no neck flexion (to decrease ICP and minimize cerebral irritability). DO NOT SEDATE unless already ventilated (may precipitate respiratory failure and death.) Maintain blood glucose between 6-9 mmol/l using minimal fluid volume(40-60 ml/kg/day crystalloid) with high dextrose concentrations e.g. 10-20%. Add Potassium as necessary.
check dextrotix 2 - 4 hourly.strict monitoring of urine output and fluid balance.Catheterise if necessary.Check urinary electrolytes, serumurea, creatinine, electrolytes and osmolarity.Frequent neurological observations (1-4 hourly).Maintain oxygenation with facial oxygen.Give vitamin K to attempt to correct prolongedPT, if frank bleeding (GIT/oral)Occurs, consider prudent use of FFP or IVcryoprecipitate at 10 ml/kg.
Prophylactic ranitidine plus oral antacid to prevent gastric, duodenal ulceration.Full septic screen (excluding LP) on admission, CXR. Treat sepsis aggressively, monitoring levels of aminoglycosides frequently.Stop oral protein initially. Gradually reintroduce 0.5- 1g/kg/day.Lactulose to produce 3-4 loose stools per day.*strict fluid balance is essential - aim for urine output < than 0.5 ml/kg/hour.consider N-acetylcysteine.
In the presence of sudden coma: Consider intracranial bleed Request a CT Brain. Patients in Grade 3 or 4 coma require mechanical ventilation to maintain normal cerebral perfusion pressure.
References: Nelson Textbook 19th edition Oxford Handbook Paediatric Protocol http://www.who.int/csr/disease/hepatitisBy: JOHN HII