1. What is Hepatitis?
‘hepa’ = liver
‘titis’ = inflammation

2.  Infectious (ie, viral, bacterial, fungal, and parasitic organisms)
 noninfectious (eg, alcohol, drugs, autoimmune diseases, and
metabolic diseases)

3.  Liver inflammation due to a viral infection.
 acute (recent infection, relatively rapid
onset) or chronic forms.
 Hepatitis A, Hepatitis B, Hepatitis
C, Hepatitis D, and Hepatitis E
 Herpes Simplex, Cytomegalovirus, Epstein-
Barr virus, or Yellow Fever
 viral hepatitis does not include
aforementioned virus except Hepatitis
viruses A to E

4.  Hepatitis A,E:
 Fecal–oral route
 Close contact
 Food or water that has been contaminated with
infected faeces. (Commonest in children)
 Oral-anal sex

5.  Blood + Body Fluid
 Blood products
 IV drug abusers
 Sexual intercourse
 Direct contact
 Vertical transmission (mother-to-child
transmission)

6.  Will you get infected though kissing?

7.  The chance of contracting hepatitis from
kissing is very small because the viruses that
cause hepatitis are basically spread through
blood and bodily fluids (hepatitis B, hepatitis
C, hepatitis D) and fecal-oral contact
(hepatitis A, hepatitis E).
 Concentration of virus in saliva is very
low(Hep B,C) . Unless, there are faeces in
his/her mouth(Hep A, D,E)!

8. Features of the Hepatotropic viruses
Virology HAV RNA HBV DNA HCV RNA HDV RNA HEV RNA
Incubation (days) 15-19 60-180 14-160 21-42 21-63
Transmission
Parenteral Rare Yes Yes Yes No
Fecal-oral Yes No No No Yes
Sexual No Yes Yes Yes No
Perinatal No Yes Rare Yes No
Chronic infection No Yes Yes Yes No
Fulminant disease Rare Yes Rare Yes Yes
Nelson Textbook of Pediatrics 19th edition

9. Acute (Inflammation <6mths)
Viral
Hepatitis Chronic (Inflammation >6mths)
Hepatitis B ,C, D may progress to chronic
hepatitis, in which the liver remains inflamed for
more than six months. This condition can lead to
cirrhosis, liver cancer, and possibly death.

10.  Acute Phase: fatigue, nausea, poor
appetite, belly pain, a mild fever, or yellow
skin or eyes (jaundice.)
 HepatitisB, C, and D may become
chronic, they may cause no symptoms for
years. By the time there are any warning
signs, the liver may already be damaged.

11. Chronic phase:
-Tiredness, anorexia, nausea
-Intolerance to fatty foods
-Abdominal discomfort (particularly in the right
upper quadrant region).
-Fevers and night sweats can also occur.

12.  Diagnosis of viral hepatitis is based on symptoms,
physical findings as well as blood tests for liver
enzymes, viral antibodies, and viral genetic
materials.
 Patients with chronic hepatitis due to hepatitis B ,
C, and D often have no symptoms or only mild
nonspecific symptoms such as chronic fatigue.
 Typically, these patients do not have jaundice until
the liver damage is far advanced. Therefore, these
patients can remain undiagnosed for years to
decades.

13.  3 types of blood tests for evaluating
patients with hepatitis:
1 liver enzymes
2 Antibodies to the hepatitis viruses
3 Viral proteins or genetic material (viral
DNA or RNA).

14.  Aminotransferases.:
• Aspartate aminotransferase(AST or SGOT)
• Alanine aminotransferase (ALT or SGPT).
(Normal range: ALT: 3-35iu/L, AST:3-35iu/L)
• These enzymes normally are contained within
liver cells. If the liver is injured (as in viral
hepatitis), the liver cells spill the enzymes into the
blood, raising the enzyme levels in the blood and
signaling that the liver is damaged.

15.  Antibodies are proteins produced by white
blood cells that attack invaders such as
bacteria and viruses. Antibodies against the
hepatitis A, B, and C viruses usually can be
detected in the blood within weeks of
infection, and the antibodies remain
detectable in the blood for decades thereafter.
Blood tests for the antibodies can be helpful
in diagnosing both acute and chronic viral
hepatitis.

16.  Anti-HAV
 Anti-HBc
 Anti-HBs
 Anti-HBe
 Anti-HCV
 Anti-HDV
 Anti-HEV

17. Genetic material Viral Protein
HAV-Ag HAV-RNA
HBs-Ag HBV-DNA
HBe-Ag HCV-RNA
HCV-Ag HDV-RNA
HEV-RNA
*HBc-Ag is undetectable in serum

19.  HBsAg: person is potentially infectious
 Anti-HBc :HBV infection, current or past
 IgM Anti-HBc: present in high titre during
acute infection
 IgG Anti-HBc detectable for a lifetime
 Anti-HBe decreased infectivity
 HBeAg: High infectivity

20. 1 HBsAg(+), HBeAg(-), IgGAnti-HBs(-)
2 HBsAg(-), IgGAnti-HBs(+)
3 IgGAnti-HBc(+), HBsAg(-), IgGAnti-HBs(+)
4 IgGAnti-HBc(+), HBsAg(-), IgGAnti-HBs(-)
5 IgMAnti-HBc(+), HBsAg(-), IgGAnti-HBs(-)
(Acute hepatitis infection, Vaccinated, Past infection but
recovered, Window Period)

21.  Treatment of acute viral hepatitis and
chronic viral hepatitis are different.
 Acute viral hepatitis : relieving symptoms
and maintaining adequate intake of fluids.
 Chronic viral hepatitis eradicate the virus
and taking measures to prevent further
liver damage.

22.  Relieve symptoms of
nausea, vomiting, and abdominal pain.
 Sedatives and "tranquilizers" are avoided
because they may accentuate the effects
of liver failure.
 Avoid alcohol.
 Control fluid imbalance caused by
vomiting.

23.  Avoid alcohol.
 Smoking cessation.
 Drug: A DELETE
• Alpha interferon
• Adefovir
• Lamivudine
• Entecavir
• Tenofevir / Telbivudine

24.  Bleeding
 Cirrhosis
 Encephalopathy:
• Liver disease that causes confusion and
excessive sleepiness
 Hepatocellular Carcinoma
 Liver
Failure
 Malnutrition

25. Hep A Hep B Hep C Hep D Hep E Hep G
Incubation 15-30 days 60-180 days 2-24wk Co infection 3-8wks Unknown
period (2-6 weeks) (2-6 months) ( 2wk-6m) with HBV
Transmission Fecal-oral •Congenital •Blood Similar to Fecal-oral Parenteral
•Blood •Sexual HBV Blood
More in •Sexual (uncommon) More in
children •Body secretion •Congenital adolescents
(rare) and adults
Serum Anti-HAV HBsAg (first Ag Anti-HCV Anti-HDV Anti-HEV RNA by RT-
markers detectable after (IgG, IgM), RNA PCR
(specific Recent exposure and PCR for
investigation) infection: Rise persists until HCV RNA
in anti HAV recovery
IgM antibody occurs)
HbcAg,
Immunity: IgG HBeAg, anti-
antibodies HBs, anti-HBc
Fulminant Rare <1% unless co- uncommon 2-20% 20% Probably no
liver failure infection with
Most HDV
complete
recover
Persistent No •Carrier 85% but 2-70% No Persistent
infection •Chronic take longer infection
hepatitis times (20-40 common,
•5-10% but years) chronic
faster (5-20yrs) disease rare
25

26. Hep A Hep B Hep C Hep D Hep E
Compli Usually mild. Sometimes severe 1 Usually (80%) Super/ co- Usually mild
cations Very low -2% mortality asymptomatic infection with except in
mortality Up to 4% mortality HBV - often pregnancy
very severe
Prolonged/ •Chronic carrier •Chronic hepatitis (70-80%) with high Severe
relapsing illness •Chronic hepatitis •Chronic carrier mortality rate infection in
lasting 6-9 •Cirrhosis •Cirrhosis pregnancy
months in 15% •HCC •HCC •Chronic (15-20%
carrier mortality)
•Cirrhosis
•HCC
Fulminant
hepatic
failure
Manage No specific Acute 1. IFN-alfa 2b Supportive Supportive
ment treatment •Largely supportive •Better compliance and
fewer side effects Control and
Supportive Chronic treat HBV
•IV hydration Goal: cessation of 2. Ribavirin infection
•Anti-pruritic active replications
agents •Interferon alfa 2b S/E immunomodulator:
•Fat soluble and lamivudine for •Anemia
vitamins 4-6 months •Neutropenia
•Serial •Recombinant •Influenza like symptoms
monitoring for interferons -
signs of ALF immunomodulatory Pt screen yearly with U/S
and antiviral effects and serum AFP for HCC
•Lamivudine – and vaccination against
inhibits viral enzyme HAV and HBV to prevent
reverse transcriptase super infection 26

27. Hep A Hep B Hep C Hep D Hep E Hep G
Prevention Highly Vaccine: Screen Hep B Recombinant Screen blood
contagious Hep B donated blood immunization Hep E for elevated
(contagious immunoglobul for elevated vaccine hepatic
for 2 weeks in hepatic Screen transaminase
before and transaminase donated blood Good hygiene
about 7 days Screen and anti-HCV for elevated
after onset of donated blood (appears 4 hepatic
jaundice) and for elevated months post transaminase
should be hepatic infection, 6 and HBsAg
excluded from transaminase months post-
school, child and HBsAg transfusion)
care during
this period
Vaccine:
Immune
serum
globulin
Good hygiene
Hand
washing
27

29.  Fulminant hepetic failure (HF) - hepatic
dysfunction (hepatic encephalopathy and
coagulopathy) within 8 weeks of evidence
of symptoms of liver disease and absence
of pre-existing liver disease.

30. Disease Duration of onset of encephalopathy after jaundice
Hyperacute/ <2 weeks
Fulminant HF
Subfulminant HF 2-12 weeks
Subacute/ Late- 8weeks – 6months
onset HF

31.  Jaundice with impalpable liver / reduce liver
size
 Encephalopathy - may worsen rapidly
 Bruising, petechiae or bleeding from
 Deranged cloting unresponsive to vitamin K.
 Failure to maintain normoglycaemia (which
aggravates encephalopathy) or presence of
hyperammonaemia
 Increased intracranial pressure

32. Supportive Treatment:
nurse in quiet darkened room with head-end
elevated at 20 with no neck flexion (to decrease
ICP and minimize cerebral irritability).
DO NOT SEDATE unless already ventilated (may
precipitate respiratory failure and death.)
Maintain blood glucose between 6-9 mmol/l
using minimal fluid volume(40-60 ml/kg/day
crystalloid) with high dextrose concentrations
e.g. 10-20%. Add Potassium as necessary.

33. check dextrotix 2 - 4 hourly.
strict monitoring of urine output and fluid balance.
Catheterise if necessary.
Check urinary electrolytes, serum
urea, creatinine, electrolytes and osmolarity.
Frequent neurological observations (1-4 hourly).
Maintain oxygenation with facial oxygen.
Give vitamin K to attempt to correct prolonged
PT, if frank bleeding (GIT/oral)
Occurs, consider prudent use of FFP or IV
cryoprecipitate at 10 ml/kg.

34. Prophylactic ranitidine plus oral antacid to prevent
gastric, duodenal ulceration.
Full septic screen (excluding LP) on admission,
CXR. Treat sepsis aggressively, monitoring levels
of aminoglycosides frequently.
Stop oral protein initially. Gradually reintroduce 0.5-
1g/kg/day.
Lactulose to produce 3-4 loose stools per day.
*strict fluid balance is essential - aim for urine
output < than 0.5 ml/kg/hour.
consider N-acetylcysteine.

35. In the presence of sudden coma:
Consider intracranial bleed
Request a CT Brain.
Patients in Grade 3 or 4 coma require
mechanical ventilation to maintain normal
cerebral perfusion pressure.

36. References: Nelson Textbook 19th edition
Oxford Handbook
Paediatric Protocol
http://www.who.int/csr/disease/hepatitis
By: JOHN HII