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Jaundice in
Children

Abdulwahab Telmesani
FRCPC,FFAP
Faculty of Medicine and
Medical Science
Umm Al-Qura University

An Approach to a
Child With Direct
Hyperbilirubinemi
a

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

Identify
• Acute
• Chronic (more than 6 months)

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

Identify • Hepatocellular • Chlestatic .

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

Remember The prognostic value of • Albumin • Coagulation profile .

Etiology • Infection • Drugs • Specific Entities • Vascular .

Etiology • Infection • Drugs • Specific Entities • Vascular .

Infections • Viral • Bacterial • Parasitic .

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

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

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

Others • EBV • CMV • Herpes • Other .

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

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

Hepatitis A Virus Transmission in 50% of contacts .

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

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 .

Hepatitis A Virus Presentation • Sporadic • Epidemic • Endemic .

Geographic Distribution of HAV Infection .

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 .

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

Hepatitis A Virus No Chronic Sequelae .

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

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

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

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

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

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

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

2 % but as high as 4 % in pregnant women .Hepatitis E Virus • Single Strand RNA • Feco – oral transmission • Endemic in Tropical and Subtropical countries • Mortalities 0.

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 .

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 .

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 .

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

Etiology • Infection • Drugs • Specific Entities • Vascular .

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

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 .

Etiology • Infection • Drugs • Specific Entities • Vascular .

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

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

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 .

Neurosci 2002 .Wilson’s Disease An 18 years old male and 19 years female reported with Schizophrenic 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.

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

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

• D.Wilson’s Disease Treatment.Penicillamine • Trientine • Zinc .

Etiology • Infection • Drugs • Specific Entities • Vascular .

occlusive disease seen with chemotherapy .Vascular • Sickle cell Disease • Budd .Chiari Syndrome • Constrictive Pericarditis • Veno .