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Jaundice in Children

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Jaundice in Children

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  1. Jaundice in Children Abdulwahab Telmesani FRCPC,FFAP Faculty of Medicine and Medical Science Umm Al-Qura University

  2. An Approach to aChild With Direct Hyperbilirubinemia

  3. Classic Approach • Proper detailed history • Proper physical examination • Formalize an impression of prioritized DDx • Appropriate investigations

  4. Identify • Acute • Chronic (more than 6 months)

  5. In Children • Acute • Chronic (more than 6 months)

  6. Identify • Hepatocellular • Chlestatic

  7. In Children • Hepatocellular(ALT/AST more than twice of ALP) • Cholestatic (ALT/AST less than twice of ALP)

  8. Remember The prognostic value of • Albumin • Coagulation profile

  9. Etiology • Infection • Drugs • Specific Entities • Vascular

  10. Etiology • Infection • Drugs • Specific Entities • Vascular

  11. Infections • Viral • Bacterial • Parasitic

  12. Viral Hepatitis • Hepatotropic Virus’s (replicate in the liver and causes hepatitis) • Others

  13. Hepatotropic Viruses • HBV (10-20% Chronic active hepatitis) • HCV (70-80% Chronic active hepatitis)

  14. Hepatotropic Viruses Non B / C Viral Hepatitis • HAV • HEV • HFV • HGV • TTV • SEN

  15. Others • EBV • CMV • Herpes • Other

  16. Hepatitis A Virus Most common cause of community acquired hepatitis through out the world

  17. Hepatitis A Virus • RNA Picorna Virus (Rhinovirus, Enterovirus, Cocxackievirus) • Feco - oral transmission (Food – borne +/- Water – borne) • Day care centers account for 10% of cases

  18. Hepatitis A Virus Transmission in 50% of contacts

  19. Hepatitis A Virus Liver injury in HAV is secondary to immune response not to cytopathy

  20. Hepatitis A Virus Presentation • Incubation period 4 weeks • Prodrome 1 week • Jaundice 1 – 3 weeks • Hepatomegaly • Liver enzymes 20 – 100 time upper normal • Spontaneous resolution

  21. Hepatitis A Virus Presentation • Sporadic • Epidemic • Endemic

  22. Geographic Distribution of HAV Infection

  23. Hepatitis A Virus Clinical Presentation in Endemic areas • 10 % of children below 6 years • 40 % of children 6 – 14 years • 70 % of subjects older than 14 years • 70 – 100 % of children have been infected

  24. Hepatitis A Virus Epidemic • Tend to seasonal • Symptoms as in sporadic cases

  25. Hepatitis A Virus No Chronic Sequelae

  26. Hepatitis A Virus Variants • Relapsing course up to 1 year • Cholestatic up to 2 years • Immune-complex features ( vasculitis, arthritis…)

  27. Hepatitis A Virus Fatalities • Secondary to acute hepatic failure • Less than 2 % • More in older children and adults • When on top of chronic hepatitis

  28. Hepatitis A Virus In Shanghais HVA epidemic, mortality was 5 times higher among patients with chronic hepatitis B

  29. Hepatitis A Virus Prevention • Immunoglobulin • Vaccination ( 2 doses 6 months apart above 1 year of age)

  30. Hepatitis A Virus ? Atopy protect against enteric infection including HAV P N Black Allergy 2005

  31. Hepatitis B Virus Vaccination decreased the incidence of hepatic carcinoma in children (in adults in future)

  32. Hepatitis C Virus • Perinatal transmission about 6% • Elective C/S might lower the risk • No evidence of risk of breast feeding

  33. Hepatitis E Virus • Single Strand RNA • Feco – oral transmission • Endemic in Tropical and Subtropical countries • Mortalities 0.2 % but as high as 4 % in pregnant women

  34. Hepatitis E Virus • Incubation period 2 – 9 weeks • Presentation similar to Hepatitis A • Diagnosed by Anti HEV IGM serology • No chronic sequelae reported • It worsens chronic hepatitis • No vaccine available yet

  35. Hepatitis G Virus • Enveloped RNA virus • Parental transmission • Detected by PCR • 2-39% of non A-E hepatitis • 16-43% of Fulminant hepatitis • ? Hepatotropic • No established serology

  36. TTV • Single strand DNA • Isolated from patients post transfusion (100 %) • Isolated from patients with non A-E Hepatitis • Presents in health individuals 1 – 13% (89 %) • ? Feco – oral transmission • ? Normal human viral flora

  37. SEN Virus • Single strand DNA virus • Most recent cause of non A- E Hepatitis • Found in Blood donors 1- 13% • In 70% of transfused patients • ? Hepatotropic • ? Feco – oral transmission.

  38. Etiology • Infection • Drugs • Specific Entities • Vascular

  39. Paracetamol • Commonest cause of acute liver failure in USA • We all have it at home • Toxic dose is more than 150 mg /Kg

  40. Paracetamol • Need repeated serum drug level • Follow Rumack-Matthew nomogram • A point of irreversible liver damage (end stage liver disease) • N-cetylcysteine is the anti-dote (oral/intravenous) • Liver transplant when end stage liver disease

  41. Etiology • Infection • Drugs • Specific Entities • Vascular

  42. Specific Entities • Wilson’s Disease • A1 Antitrypsin deficiency • IBD Hepatitis • Auto-immune Hepatitis • Syndromatic Diseases • Metabolic • Progressive Familial Intrahepatic Cholestasis

  43. Wilson’s Disease • Autosomal Recessive Disease • Low cerulplasmin • Copper deposition in; liver, brain, kidneys, eyes, heart, Hemolysis

  44. Wilson’s Disease Presents in any of the following; • Acute liver disease • Chronic liver disease • Minimal neurological manifestations • Sever neurological manifestations • Psychiatric symptoms • Renal tubular acidosis • Bony deformities • Hemolytic anemia

  45. Wilson’s Disease An 18 years old male and 19 years female reportedwithSchizophrenic symptoms; • No Kayser -Fleischer ring • Normal physical examination • Low cerulplasmin, high serum copper and high 24 HR urine copper • Symptoms improved on D – Penicillamine Patrick Stiller J Psych. Neurosci 2002

  46. Wilson’s Disease Liver biopsy and determination of hepatic copper is the golden standard for diagnosis of Wilson’s Disease

  47. Wilson’s Disease Diagnosis can be made based on at least two of the following; • Low serum Cerulplasmin • High 24 HR urine copper • K.F Ring Ashish Bavdekar J Gastr & Hepat 2004

  48. Wilson’s Disease Treatment; • D- Penicillamine • Trientine • Zinc

  49. Etiology • Infection • Drugs • Specific Entities • Vascular