PPT on acute viral hepatitis in children

2.  A major health problem in both developing and
developed countries
 An inflammatory disorder of the liver which is
usually associated with a complete clinical and
histological recovery within a period of4-6weeks
Definition:

3. Viruses affect liver in two ways
directly –
hepatotropic viruses
Hepatitis A,B, C,D,E,G.
as a part of systemic
disease
eg:Epstein Barr virus
Herpes simplex virus
Coxsackie B virus
Cytomegalo virus

4.  Hepatitis A : 40 - 60 % ( commonest)
 Hepatitis E : 7 – 17 %
 Hepatitis B : 7 -15 %

5. • In India, > 90% of children are naturally exposed to
HAV by the age of 10 years
• HAV :entero virus of Picorna viridae
• Causes 50-80% of acute sporadic hepatitis in India
• Relatively benign disease

6. • Transmission by faeco- oral route
• Reaches liver by portal vein
• Replicates in the liver and excreted in the bile
• Stool is the infective material
 (highest concentration in the stool 2 weeks prior
 to the onset of jaundice and decline rapidly after
 jaundice appears.)

7.  Faeco oral:
• Direct transmission (person to person) by
contaminated hands or eating utensils
• Through contaminated food or milk or water
• Water-borne : more in developing countries, related to
overcrowding, poor hygiene and poor sanitation
• Food borne : more in developed countries through
infected food handlers, uncooked foods
 Parenteral transmission ?
 very rare

8. • Incubation period : 2-7 weeks
• 85 % cases anicteric in children
• Prodromal period
• mild, characterized by anorexia, nausea, vomiting,
fever, abdominal pain, then jaundice.
• Icteric phase
• Convalescent phase
• Recovers in 7 – 14 days
• Chronicity less

9.  Liver function tests
• S. bilirubin : increased ( usually < 10 mg /dl)
• Enzymes : ALT AST elevated
 Alk. Phosphatase
 Prothrombin time :
 prolonged in severe liver damage


10.  appears during late incubation
period
 and reaches peak by 2-3 weeks ;
 disappears by after 3-4 months

11. • Cholestatic hepatitis
• more in older children and adolescents lasts for 40-110 days
with severe itching good prognosis
 Autoimmune Hepatitis
• Fulminant hepatitis
 rare ( < 0.1%)

12.  Relapsing hepatitis
 relapse 3-90 days later
 occurs in 10% cases
 second episode 1-4 months after the
initial one
 may last for several months
 ultimate recovery is the rule


13. • Neurological complications
 G B syndrome, transverse myelitis
• Renal
 nephritis,nephrotic syndrome
• Haematological
 red cell aplasia
• Acute pancreatitis

14. • No specific therapy ; disease self
limited
• Only supportive
• No specific dietary restriction needed
• Avoid hepatotoxic drugs
• Specific antiviral agents not available

15. • Excellent prognosis
• Full recovery
• Mortality less than 0.1%
• Does not cause chronic liver disease

16. • Isolation of the patient not very effective
as the virus is already disseminated even
before the diagnosis is made
• Safe drinking water and proper disposal
of sanitary waste


17. • Passive Immunization
 Immunoglobulin within 2 weeks of exposure is
85%
 effective (0.02 ml /kg I/M)
• Active Immunization ----- after 1 year age
 Hepatitis A vaccine
 Inactivated vaccine I/M
 recommended after 2 doses 6 months apart
 highly effective
 Live attenuated vaccine – one dose ( egg protien
allergy)

18. • Travellers to areas of high
endemicity
• Lab. Personal
• Patients with chronic liver disease
• Household contacts of patients with
acute hepatitis A within 10 days

19.  Not showing expected recovery
 Worsening in absence of features of ALF
 Fever persisting after appearance of jaundice
 Atypical clinical features

20.  Malaria
 Fever with chills, palor, splenomegaly
 Dengue hepatitis
 Severe body ache, petichae, fluid collection in 3rd
spaces
 Enteric Hepatitis
 Continued high grade fever, toxic look, poor general
condition, splenomegaly , leucopenia
 a/c exacerbation of CLD
 h/o CLD, symptoms of CLD

21.  Symptoms of CLD
 Ascitis, GI bleed, encephapathy
 Early symptoms of Hep encephalopathy
 Flapping tremor
 Altered sensorium
 Excessive irritability
 Inconsolable cry

22. • Global communicable disease
• Global prevalence is divided into 3 zones based
 on the carrier state
 low zone : < 2%
intermediate zone : 2-7%
 high zone : > 7 %

 India comes under intermediate zone(3-5%)

23. • Double stranded DNA hepadna virus
• Dane particle - 42 nm
• 3 antigens
 HBs Ag (surface Ag)
 HBc Ag (core Ag)
 HBe Ag ( precore)
 Ccc DNA – covalenlty closed circular DNA-
 May Persist inside body to rest of life.

25.  HBV present in blood and body fluids ( saliva, breast
milk,nasopharyngeal secretions) of infected persons

• Blood and blood products
• Contact with infected and body fluids through
scratches cuts, bites or rashes
 (infective dose extremely minute- just 0.00001 ml)
• Sexual activity
• Vertical transmission

26.  Perinatal transmission from HBs Ag carrier
mothers to their infants is the most important
route of transmission of hepatitis B in children
 Risk is greatest if mother is also HBeAg+ ve
 upto 90%

27.  HBV is a non cytopathogenic virus, causing immune
mediated liver injury
 Natural History:
Acute hepatitis Fulminant hepatitis
develops immunity persistent infn death
carrier cirrhosis/ HCC

28.  Incubation period 6 weeks -6 months

• Course may be
 acute
 fulminant
 chronic
• Acute hepatitis

 symptoms similar to hepatitis A fever, vomiting, jaundice,
anorexia etc



29. • Polyarteritis
• Glomerulonephritis
• Papular dermatitis
• Aplastic anemia
•Serum sickness
•Arthralgia
•Guillain Barre Syndrome

30. • Carrier state – risk of chronicity inversly proportionate
to the age of acquisition of the illness
 adults : 10%
 children : 20%
 new borns : 90%
• Chronic hepatitis
• Subacute hepatic failure
• Cirrhosis
• Hepatocellular carcinoma

31. • HBs Ag : appears by 6 weeks after infection(even before
the onset of symptoms)
 disappears by 3-6 months
 if persists > 6 months- carrier state
 (marker both in acute and chronic infection)
• Anti HBs : protective antibody appears shortly after
the disappearance of HBs Ag

32. • HBe Ag : marker of active viral replication
 appears soon after HBs Ag disappears
 by 6 weeks
 if persists after 6 weeks indicates progression
to chronicity
• Anti HBe antibody : appears after the disappearance
 of HBe Ag not a protective antibody

33. • HBc Ag ( core antigen) : not present in blood
• Ig M anti HBc antibody: appears 1-2 weeks after the
 appearance of HBsAg
 (first antibody to appear even before anti
 HBe or anti HBs)
• Ig G anti HBc antibody: appears after 6 months
• HBV DNA : marker of replication and infectivity


35.  Acute liver cell failure
 coagulopathy, encephalopathy, cerebral
odema
 more frequently seen with HBV infection than
with any other hepatotropic viruses
 mortality due to acute liver cell failure is 30%

36. • Only symptomatic and supportive
for acute hepatitis
• IFN- Alpha and Lamivudine
approved for chronic cases

37.  Active immunization (Hepatitis B
vaccine)
 Passive prophylaxis ( HBIG -hepatitis
B immunoglobulin)

38. • Universal immunization is now recommended
 by AAP & IAP. Newborn period is targeted.
• Recombinant vaccine
• 3 doses
• Dosage shedule
 0, 6 and 10 weeks
 or
 6, 10 and 14 weeks
 or
 0, 1 and 6 months
• No booster dose needed

39.  For providing immediate protection of
people acutely
 exposed to HBsAg +ve blood
 Dose :
 1000 – 2000 IU( adult)
 32 – 48 IU/kg ( children)

40.  For newborn of HBV infected women HBIG 0.5
ml I/M – 100 – 200 units to be given within 12
hours of birth concurrently with HBV - first
dose
 If not given ,give booster of vaccine at 12 mnts
 Combination of HBIG and HBVaccine prevent
transmission in 95% cases

41.  A defective virus which cannot produce infection
without a concurrent HBV infection
 Co- infection
 as acute hepatitis and more severe
 or
 Super infection in HBV carriers
 as chronic infection and more common

42. • Diagnosis :
 Ig M anti HDV antibodies
• Treatment :
 supportive only
• Prevention :
 by preventing HBV infection

43. • Previously known as transfusion related
Non A Non B hepatitis
• Single stranded RNA virus
• 6 major genotypes

• Type 3 common in India

44.  Commonest
mode of
transfusion is
through blood
and blood
products
 (more common
in patients with
thalassemia,
hemophilia etc)

45.  Incubation period 7-8 weeks
 Insidious onset and mild
 Often asymptomatic and jaundice seen only in 25% cases
 Progression to acute liver cell failure is rare
 Aminotransferase levels typically fluctuate during HCV
infection and donot correlate with the degree of liver cell
fibrosis
 Vertical transmission is rare

46. • Diagnosis
 Ig M Anti HCV antibodies
 or
 HCV RNA
• Treatment
 chronic cases require interferon and
ribavirin
• Prevention
 no vaccine available
 only screening of blood

47. • HEV virus - a single stranded RNA virus
transmitted from person to person via fecal- oral
route

 (often through contaminated drinking water)
• Causes acute sporadic and epidemic viral hepatitis
• Common in older children and young adults

48.  Clinical presentation
 incubation period : 3-8 weeks
 features similar to HAV infection
 increased risk of fulminant
 hepatitis in pregnant women

49.  Diagnosis
 Ig M Anti HEV antibodies
 No specific therapy
 Prevention
 no vaccine
 good personal hygiene

50.  HGV – flavi like virus
 related to post transufusion hepatitis,
chronic hepatitis and cirrhosis
 TTV (Transfusion transmitted
virus)
 new virus
 related to transfusion.

51. • Hep.A : commonest cause of viral hepatitis in
children.
• Hep.B,C,D : responsible for transfusion related
hepatitis
• Hep A & E are waterborne infections
• Hepatitis A is generally mild and associated with
few complications

52. • Hepatitis B is associated with chronicity and acute liver
all failure
• Hep.C is often asymptomatic and associated with
 Chronicity ( majority)
• Vaccine available for Hepatitis A and B
• Perinatal transmission from HBs Ag carrier mothers
 to their newborns can be prevented by combined HBIG
and HBvaccine

53. Suspected Hepatitis
Do HBsAg and IgM
HAV
HBsAg
POSITIVE
IgM anti HBc
positive
HBV
IgM anti HBc
Negative
c/c HBV
Do HDV Rna or
Ig M anti HDV
Igm HAV
POSITIVE
Hepatitis A
Both negative
Do Ig M anti HEV

54. Thank you