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 Viruss
(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

Hepatitis A Virus
RNA Picorna Virus

(Rhinovirus, Enterovirus,

Cocxackievirus)

Feco - oral transmission

(Food borne

+/- Water borne)

Day care centers account for 10%

of cases

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

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

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

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

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

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

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

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.

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
Wilsons Disease
A1 Antitrypsin deficiency
IBD Hepatitis
Auto-immune Hepatitis
Syndromatic Diseases
Metabolic
Progressive Familial Intrahepatic
Cholestasis

Wilsons Disease
Autosomal Recessive Disease
Low cerulplasmin
Copper deposition in;
liver,
brain,
kidneys,
eyes,
heart,
Hemolysis

Wilsons 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

Wilsons 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.
Neurosci 2002

Wilsons Disease
Liver biopsy and determination of
hepatic copper is the golden
standard for diagnosis of Wilsons
Disease

Wilsons 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

Wilsons Disease
Treatment;
D- Penicillamine
Trientine
Zinc

Etiology
Infection
Drugs
Specific Entities

Vascular

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