A 4-year-old girl presented with fever, nausea, abdominal pain and jaundice. On examination, she had hepatomegaly and jaundice. Laboratory tests showed elevated liver enzymes. This raised suspicion for acute hepatitis of infectious etiology such as viral hepatitis, malaria or enteric fever. Further tests found elevated IgM antibodies confirming hepatitis A infection. Hepatitis A is a picornavirus transmitted through the fecal-oral route. It typically causes a self-limited illness with jaundice and hepatomegaly in children. Treatment is supportive and vaccination provides effective prevention.

2. A story to begin with…
4 yrs old girl child, h/o
Nausea, poor appetite – 8-10 days
Fever – 5-6 days, high grade, with chills and
rigors, 2-3 spikes/day
2 episodes of vomiting – on the first day of fever.
Abdominal distension - 4 days, pain in right
upper quadrant
Passing high colored urine , yellowish
discoloration of eyes - 4 days

3. Clinical History
No h/o:
clay colored
stools,
pedal edema
itching
bleeding
altered sensorium
Mixed diet- deficient in
calories- 600Kcal and 4g
protein/day
Developmentally normal,
routine immunisation
given including hep B.
Hep A not given.
Poor sanitary hygiene,
use tap water for
drinking, no known case
of jaundice in locality .

4. On Examination
Conscious,
cooperative
Vitals stable
Icterus+
No edema or skin
bleeds, cyanosis,
lymphadenopathy
Height-97
cm (25th
centile)
Weight-
12 kgs
(25th
centile)

5. Systemic examination
Liver:
4 cm, palpable below right
SCM, tender, soft, span 11
cm, round borders,smooth
surface.
Spleen – not palpable
No shifting dullness
Bowel sounds present
Other systems- CVS,
RS, CNS-normal

6. Initial Impression
4 yrs old girl with Febrile illness with jaundice,
hepatomegaly; suggestive of acute hepatitis of
infective etiology
Differential diagnosis-
Acute
viral
hepatitis
Malaria/
leptospiral
infection Enteri
c
fever

7. • Fever, icterus, vomiting,
anorexia seen
• Hepatomegaly can be
present
Acute viral
hepatitis
• Fever, hepatomegaly
seen
• Anicteric illness mostly
Malaria /
leptospira
infection
• Fever , hepatomegaly
• Frank jaundice is
uncommon
Enteric fever

8. Investigations
CBC
Hb 8.1 g/dl
HCT 23.8%
WBC 10,500/ul
P/L/E 64/35/01
Plt 216,000/ul
MCV 48.3 fl
MCHC 34 g/dl
RDW 17.2 %
ESR 40
LFT
T. BILI 7.1
INDIRECT BILI 4.9
T. PROTEIN 5.7
ALBUMIN 2.9
SGOT/PT 122/380
Alk PO4 699
PT/INR 1.2

9. Investigations contd…
RFT
electrolytes
BUN 07
CRT 0.5
Na+ 134
K+ 4.1
Ca++ 8.0
PO4- 4.5

11. Hepatitis A infection in
children
Dr Arun George
Junior Resident, Paediatrics
Under Guidance of – Dr Cherryl Tryphena, Paediatrics consultant, CHAD

12. VIRAL HEPATITIS A
• Hepatitis A is a liver disease caused by the hepatitis A virus
• Picorna virus
• Single stranded RNA virus
• Measures 27-28nm.
• Icosahedral shape
• Non enveloped.
• Has one serotype & more than three genotypes

13. • Unlike hepatitis B and C, hepatitis A infection does not cause
chronic liver disease and is rarely fatal,
• But…….
but it can cause debilitating symptoms and fulminant hepatitis
(acute liver failure), which is associated with high mortality.

14. Epidemiology:
• Occurs worldwide
• India –hyperendemic
• Community, restaurant, and school outbreaks due to contaminated
water or food
• Incubation period for HAV - 15 to 50 days
• Declined substantially since vaccination was recommended
• Potential for "herd protection"

15. Transmission
• The hepatitis A virus is transmitted primarily by the
faecal-oral route
• The virus can also be transmitted through close
physical contact with an infectious person
• PERIOD OF INFECTIVITY : The risk of transmitting HAV
is greatest from 2 weeks before to 1 week after the
onset of jaundice.

17. • Biphasic process
1. Non-cytopathic stage, viral replication occurs exclusively within the
cytoplasm of the hepatocyte.
2. Cytopathic stage, with florid portal zone infiltration, necrosis, and
erosion of the limiting plate.

18. • Hepatocellular damage and destruction  not the result of a direct
cytopathic effect by HAV …
but a process mediated by HLA-restricted, HAV-specific, CD8
lymphocytes, and natural killer cells.
• Interferon gamma - promoting clearance of infected hepatocytes.
• Excessive host response marked reduction in HAV RNA during acute
infection associated with severe hepatitis and a possible fulminant
course

19. Symptoms
• Symptoms of hepatitis A range from mild to severe .
• Acute, self-limited illness associated with general,
nonspecific symptoms, such as fever, malaise,
anorexia, vomiting, nausea, abdominal pain or
discomfort, and diarrhea.

20. • Prodromal period- aminotransferases are typically elevated.
• Jaundice (conjugated hyperbilirubinemia) usually occurs one week after
onset of symptoms, along with choluria (bilirubin in the urine) and mild
hepatomegaly.
• Symptomatic hepatitis occurs in approximately 30 percent of infected
children younger than six years, some of whom become jaundiced.
• When it does occur, jaundice usually lasts for less than two weeks.
Conjugated bilirubin and aminotransferases return to normal within two to
three months.

21. • In contrast, older children and adults with HAV infection are usually
symptomatic for several weeks.
• Approximately 70 percent are jaundiced, 80 percent have
hepatomegaly, and 40 percent are hospitalized.
• Symptoms lasting for up to six months have been described.

22. Extrahepatic manifestations:
• evanescent rash (11 percent)
• arthralgias (14 percent)
• less common- vasculitis, arthritis, optic neuritis, transverse myelitis,
encephalitis and bone marrow suppression

24. Diagnosis
• Specific diagnosis is made by the detection of HAV-specific IgM and
IgG antibodies in the blood. .

25. 25
Fecal
HAV
Symptoms
0 1 2 3 4 5 6 1
2
2
4
IgG anti-HAV
Titre ALT
IgM anti-HAV
Months after exposure
Typical Serological Course

27. Treatment
• Supportive treatment :
• Adequate intravenous hydration
• Antipruritic agents
• Fat soluble vitamins.
• Serial monitoring for ALF.
• Referral to a transplantation center.

28. General measures:
• Fecal-oral route- improved sanitary conditions, adherence to sanitary
practices (eg, handwashing), heating foods appropriately
• Chlorination and certain disinfecting solutions (household bleach
1:100 dilution) are sufficient to inactivate the virus.
Prevention

29. • IM administration of Ig (0.02mL/kg)
1. Preexposure:
• Suceptible travellers
• Children younger than 12 months
• Allergic to a vaccine component
• Those who elect not to receive the vaccine.
• If travel is planned les than 2wk, both Ig and HAV vaccine is given.

30. 2. Post exposure :
• As soon as possible.
• For patients who cannot take the vaccine.

31. Vaccine
• 2 inactivated , highly immunogenic and safe HAV vaccines available.
• Approved for children older than 12 month old.
• Administration : 2 dose schedule 6-12 mo apart.
• Seroconversion 90% after the first dose and approaches 100% after
the second.
• Protective titre persists for longer than 10 years.

32. Hepatitis A vaccine
• Liposomal adjuvanted inactivated hepatitis A vaccine, derived from
RG-SB strain.
• First dose at 12 mon, second dose at 18 mon. intramuscular route.
0.5 ml.
• Live attenuated vaccine from human diploid cell also available.
• Live vaccine given subcutaneously.

33. CATCHUP
• Administer 2 doses at least 6 months apart to unvaccinated
persons.
• For catch-up vaccination, prevaccination screening for hepatitis A
antibody is recommended in children older than 10 years as at this
age the estimated seropositive rates exceed 50%.
• Combination of hepatitis B and hepatitis A may be used in 0, 1,
6 schedule.

34. OUTCOME
Recovery in > 99%
Clinical relapse in 4-20%
Rarely need to hospitalize or transplant
Fulminant hepatitis <0.35%

35. References:
• Nelson Textbook of PEDIATRICS (first south asia edition)
• Uptodate -https://www.uptodate.com/contents/overview-of-
hepatitis-a-virus-infection-in-children
• Hepatitis A, B, and C – Pediatrics in Review: John C. Christenson, MD,
John J. Manaloor, MD; Vol. 37 No. 10 OCTOBER 2016
• Acute Viral Hepatitis - IAP UG Teaching slides 2015-16
• IAP Guidebook on immunization 2013-14