1. Acute viral hepatitis is defined as inflammation of the liver caused by viral infection, resulting in elevated liver enzymes for less than 6 months. The most common causes are hepatitis A, B, C, D, E viruses. 2. The document discusses the pathogenesis, clinical features, investigations, management, and prevention of different viral hepatitis types. Hepatitis A and E are usually self-limiting while hepatitis B, C and D can sometimes lead to chronic liver disease. 3. Supportive care is the main treatment approach for most cases of acute viral hepatitis. Specific antiviral therapy may be used for severe hepatitis B cases to prevent progression to liver failure. Vaccines exist to prevent hepatitis A and B infection

1. Dr.VijayYadav
Lecturer
Internal Medicine

2. 80%
90% of the
remaining
20%
10%

3. INTRODUCTION
Definition:
• Acute Viral Hepatitis is defined as inflammation of liver and sudden
onset of aminotransferase elevation as a consequence of diffuse
necro-inflammatory liver injury which lasts for < 6 months.
Acute liver disease encompasses a wide range of disorders from
asymptomatic transaminitis to ALF
Viral hepatitis and DILI are the most frequent causes.
Acute viral hepatitis is a self-limiting disease with chance of ALF
in a small percentage of patients.
M.C cause: Hepatitis A and E

4. Etiology of Acute hepatitis
Infectious
1) Viral: Hepatitis A – E,
EBV, CMV, Dengue,
Yellow fever
1) Bacterial: Weil’s
disease, MTB, Enteric
fever
2) Protozoal: Malaria,
Toxoplasmosis
3) Helminth: E. histolytica
Non-infectious
1) Toxin: Mushroom, CCl4
2) Alcohol
3) Acute fatty liver of
pregnancy
4) Acute budd chairi
syndrome
5) Metabolic: Wilson’s
disease
6) Autoimmune hepatitis
7) Ischemic hepatitis
8) Drugs: PCM, ATT,
Phenytoin

5. Pathogenesis
 HAV:
 Survives the acidic digestion by gastric juice and reaches the portal circulation
 Multiplies in the hepatocytes and damages hepatocytes by immunological
mechanism
 Excreted in feces
 HBV:
 Damages hepatocytes by immune mediated injury
 HCV:
 Binds to receptors on the hepatocyte surface
 Enters the cell by endocytosis
 Rarely causes immune mediated injury in acute phase and thus most of acute
HCV infections are asymptomatic except for mild transaminesemia
 HDV:
 Causes infection only in the presence of HBV infection either as superimposed
or co-infection
 CMV:
 Primary infection or as a reactivation of latent infection
 HSV:
 Neonates, Pregnancy, Immunocompromised patients
 a/w genital herpes infection

6. Headache, Myalgia, Arthralgia,
Anorexia, Nausea, Vomiting, Fatigue,
Pharyngitis, Cough, Coryza precedes
the onset of jaundice by 1-2 weeks.
Alteration in olfaction & distaste for
cigarettes.
Fever (100 - 102°F)
Dark urine & clay colored stools 1 – 5
days before clinical jaundice.
Jaundice
Tender hepatomegaly
Splenomegaly
Cervical lymphadenopathy
Infrequently cholestatic
picture
• Jaundice deepens
• Stool becomes paler
• Urine becomes darker
• More hepatomegaly
Appetite improves
gradually
Symptoms subside
Some liver enlargement
with deranged LFT
Complete clinical &
biochemical recovery
• 1-2 months in HAV & HEV
• 3-4 months in HBV & HCV
• HBV self limited in 95-99% cases
• HCV self limited in 15% cases
PRODROMAL PHASE CLINICAL JAUNDICE RECOVERY PHASE

7. Hepatotropic virus-general characters
HAV HBV HCV HDV HEV
VIRUS
Group
NA
Entero/Pi
corna
RNA
Hepadna
DNA
Flavi
RNA RNA
Calci
RNA
Incubation
period
15-45
days
30-180
days
15-160
days
30-180
days
15-60
days
Spread Faeco-oral Parenteral Sexual Vertical Faeco-oral
Chronicity Yes Yes Yes
Prevention
Active
Passive
Vaccine
Immune
serum
globulin
Vaccine
Hyperimm
une serum
globulin
No
No
HBV
vaccine
No
No

8. Enterically
(HAV & HEV)
Parenterally
(HBV, HCV, & HDV)
 Non-enveloped
 Shed in faeces
 Survive intact when exposed
to bile
 Do not cause chronicity
 Do not have prolonged
viremia
 Do not have carrier state
 M.C: HEV >> HAV
 Enveloped viruses
 Cause chronicity
 a/w persistent viremia
 Have a carrier state
 M.C: HBV + HDV
 HCV rarely causes AVH

9. HAV HBV HCV HDV HEV CMV HSV
Age Any,
mostly
children
Any age Usually
adults
Any age Any,
Usually
adults
Immuno
compro
mised
Sexually
active
adults
Sympto
ms
Asympto
matic in
children
Sympto
matic
with
jaundice
Cholesta
tic with
jaundice
lasting >
10
weeks
Relapsin
g with 2
bouts
over 6-8
wks
Fulmina
nt: 0.5%
Prodrome
fever
Arthralgia
Myalgia
Jaundice
(30%)
Maculopa
pular
utricarial
rash
(10%)
Acute
hepatiti
s (20%)
Fatigue
N/V
Asympt
omatic
in
children
Self
limiting
acute
hepatitis
mimickin
g flares
of
chronic
HBV
Anicteric
hepatitis
Icteric
hepatitis
FHF(20%
) in
pregnan
cy
Asympto
matic
Subclinic
al in
most
Mononu
cleosis
like
illness
Rarely
cholesta
tic
May be
seen as
neonatal
hepatitis

10. HAV HBV HCV HDV HEV CMV HSV
Clinical
Signs
Tender
hepato
megaly
(85%)
Spleno
megaly
(15%)
Cervical
LN
(15%)
Hepatom
egaly
Rashes
Jaundice
Fluctuati
ng
transami
nases
Double
peak
transami
nases if
co-
infected
with
HBV
Jaundice
Hepato
megaly
Splenom
egaly
Jaundice
Hepato
megaly
Splenom
egaly
Jaundice
Hepato
megaly
Splenom
egaly
Signs of
DIC
Duration
Of
Disease
Recover
y in
60%
within 2
months
& 100%
in 6
months
95-99%
resolve in
6 months
Others
progress
to
chronicity
Usually
resolves
in 1
month
(15%)
Resolves
in 4-8
weeks
Self
limiting
Resolve
in 6
weeks
Resolves
in 6-8
weeks

11. HAV HBV HCV HDV HEV CMV HSV
Fulmina
nt
hepatitis
Mostly
in
adults
55% in
1st
week &
90%
within 4
weeks
< 0.5%
overall
In < 1%
Within 4
weeks
High
mortality
(80%)
HBV+HDV
> 50%
cases
Very
rare
5-10% 20% in
pregnan
cy
Occurs
with
MODS in
immuno
compro
mised
patient
May
develop
in
neonate
as
adrenal
insufficie
ncy
In
pregnan
cy as
well
Extra-
hepatic
manifest
ations
Rash
Arthralg
ia
Nephriti
s
Cutane
ous
vasculiti
s
Rash
Arthritis
Hematuria
Proteinuria
PAN
GN
Nephrotic
syndrome
Cryoglobulin
emia
Cryoglo
bulinem
ia
GN
Lichen
planus
Sicca
syndro
me
PCT
None Arthralgi
a
Pancreat
itis
Acalculo
us
cholecys
titis
Rash
DIC

12. Investigations
• Complete blood count
▫ Neutropenia & lymphopenia
▫ Relative lymphocytosis
▫ Pancytopenia (aplastic anemia)
• Renal function tests
• Liver function tests
▫ ↑Serum bilirubin: 5-20 mg/dL (both UB & CB equally)
▫ ↑AST/ALT (ALT >> AST): 400 – 4000 in icteric phase
▫ Diminishes gradually in recovery phase
▫ Anicteric hepatitis ( N bilirubin but ↑AST/ALT )
▫ ALP: Increased but < 3 x UNL
▫ Albumin: Normal
▫ PT/INR: usually normal; poor prognosis if increased

13. • Viral serology:
▫ HAV IgM, HAV RNA
▫ HBsAg, IgM anti-HBc, HBV DNA, HBeAg
▫ Anti-HCV(4-6 weeks), HCV RNA (1-2 weeks), HCV
genotyping
▫ HDV RNA, anti-HDV antibodies
▫ HEV IgM
▫ EBV Capsid antigen, CMV DNA, HSV, VZV serology
▫ Dengue serology and NS1 antigen
• Leptospirosis:
▫ Microscopic agglutination test (MAT): Gold standard
▫ ELISA, PCR : confirmatory
• Enteric fever:
▫ Blood C/S, Typhi dot IgM
• Malaria:
▫ MP antigen, Thick and Thin smear

14. • Alcoholic hepatitis:
▫ ↑AST/ALT – 2:1; calculate DF
▫ ↑γGGT
• Acute fatty liver of pregnancy:
▫ USG abdomen
• Acute budd-chiari syndrome:
▫ Doppler USG & Hepatic venography
• Wilson’s disease:
▫ Serum ceruloplasmin, 24 hr urinary copper
▫ Slit lamp exam for KF rings
• Autoimmune hepatitis:
▫ ANA, Anti-LKM Ab, ASMA, Anti SLA, serum IgG levels
• Ischemic hepatitis:
▫ Rapid rise & fall in AST.ALT (>1000) and LDH within 1-3 days of
insult
• Drugs:
▫ Serum APAP & plot in Rumack-Matthew nomogram
▫ Treat Hypophosphatemia
▫ Modified ATT regimen if ATT induced liver injury

15. Rumack-Matthew nomogram

16. N- acetylcysteine is administered within 8 – 10 hours of ingestion
as per toxicity line on Rumack-Matthew nomogram.
ORAL
• Loading dose: 140mg/kg
• Maintenance dose:
70mg/kg every 4 hours for
a total of 17 doses.
INTRAVENOUS
• Loading dose: 150mg/kg
over 1 hour
• Maintenance dose:
14mg/kg/hr for 4 hours
and then 7mg/kg/hr for 16
hours
• For late
presenters(>8hrs)
• LD: 140mg/kg over 1 hr
• MD: 14mg/kg/hr for 44 hrs

17.  Hepatitis A:
 Relapsing hepatitis
 Cholestatic hepatitis
 Hepatitis B:
 Serum sickness
 Hepatitis C:
 Porphyria cutanea tarda (PCT)
 Lichen planus
 Essential mixed cryoglobulinemia
 Fulminant hepatitis
 HBV + HDV > 50% cases
 HEV – 20% in pregnancy
 Drug induced
 Chronic hepatitis
 Aplastic anemia

18. Management- Hepatitis A
Pre-exposure prohylaxis Post-exposure prohylaxis
• Inactivated HAV vaccines
containing single HAV antigen
given IM into deltoid in a 2
dose regimen ( 0, 6-18
months)
• Combination vaccines (HAV
>720 ELISA unit + 20μg
HBsAg) given in a 3 dose
regimen (0, 1, & 6 months)
• Given in chronic hepatitis B
and C infections
• Immune serum globulin 0.02
ml/kg/dose given on deltoid
within 14 days of exposure
• Effective in outbreak of
hepatitis in school or nursery.

19. Management- Hepatitis B
• Supportive with monitoring for ALF (<1% cases)
• In adults, 90 -95% (99%) resolve with the development
of anti HBs antibody --- thus, no role of antiviral therapy
• The remaining 5 -10% develop chronic hepatitis B
• Vertical transmission leads to chronic hepatitis B in 90
% of children & recovery is rare.
• Role of antiviral proven in severe acute hepatitis B that
may progress to ALF.
• Entecavir or Tenofovir until 3 months after HBsAg
seroconversion or 6 monhs after HBeAg seroconversion.

20. Management- Hepatitis B
Pre-exposure prophylaxis Post-exposure prophylaxis
• HBV vaccine: prepared from
HBsAg given IM at 0, 1, and 6
months
• Response is measured by
anti-HBs levels ≥ 10 mIU/ml
• Protected antibody response is
> 90% after 3rd dose.
• Infants born to HBsAg +
mother:
▫ HBV vaccine & HBIg 0.5
ml within 12 hours of birth at
two separate sites
• Sexual partners +
Needlestick injury:
▫ HBIg (0.04 – 0.07 ml/kg) +
1st dose of HBV vaccine at
different sites within 48
hours but no more than 7
days
▫ 2nd dose HBIg after 30 days
and complete the vaccination
schedule

21. Management- Hepatitis C
• In typical acute hepatitis C, recovery is rare.
• Progression to chronicity is the rule.
• 50-85%: develop chronicity
▫ 60-70%: Chronic hepatitis after 10 years
▫ 30%: Cirrhosis after 20-30 years
▫ 15%: HCC after 40 years
• Interferon α 3 million units SC three times a
week + Ribavarine

22. *HDV, HEV: supportive
*HSV: IV acyclovir
*CMV: Ganciclovir, Cidofovir, Foscarnet
*Leptospirosis: Ceftriaxone, Doxycycline
*Enteric fever: Ceftriaxone, Azithromycin, Ofloxacin
*Malaria: Artesunate, Artemether
*Acute budd-chiari syndrome:
*Anticoagulation, surgical shunts, liver transplantaion
*Wilson’s disease: D-penicillamine, Trientene
*Autoimmune hepatitis: Steroids, Azathioprine
*Ischemic hepatitis: correction of underlying cause that caused
circulatory collapse
*APAP toxicity: N-acetylcysteine

23. General Measures
• ? Bed rest
• ?Physical isolation to a single room & bathroom
▫ Fecal incontinence for hepatitis A and E
▫ Uncontrolled, voluminous bleeding for hepatitis B and
C
• Universal precaution for HBV & HCV
▫ Avoiding direct, ungloved hand contact with blood &
other body fluids
• High calorie diet – mainly in morning as nausea
predominant during evening
• Avoid hepatotoxic drugs
• Cholestyramine for pruritis
• Maintain proper sanitation, hygeine & avoidance of
overcrowding in hepatitis A and E

24. Prevention
• HAV:
▫ Clean drinking water, proper sewage disposal
▫ Public education about the hygiene
▫ Active & passive immunization
• HBV:
▫ Screening the transfused blood & blood products for HBsAg
▫ Using disposable syringes & needles
▫ Using safety precautions & practicing safe sex
▫ Active & passive immunization
• HCV:
▫ Screening for anti-HCV
• No active & Passive immunization available
• HDV:
▫ Same as HBV but vertical transmission is extremely rare
• HEV:
▫ Same as HAV
▫ HEV vaccine has been recently shown to be effective and is
awaiting commercial availability

25. Points not to be forgotten
• Viral hepatitis (HAV & HEV) and DILI (PCM & ATT) are the most frequent
causes of AVH.
• M.C cause of parenterally mediated AVH: HBV + HDV
• Hepatocyte injury is mainly via immune mediated injury.
• 3 stages of clinical features.
• Rate of fulminancy is least in isolated HAV, HBV, & HCV.
• Rate of fulminancy is high with combined HBV + HDV & HEV in pregnancy
(both 20%).
• Acute hepatitis is rare in HCV & Chronic hepatitis is rare in PCM overdose.
• HAV is associated with relapsing & cholestatic variant.
• 95-99% of acute hepatits B resolve spontaneously but 90% of vertically
transmitted children develop chronic hepatitis.
• Progression to chronicity is the rule in acute hepatitis C; only 15% undergo
spontaneous remission.
• HDV is always co-infected with HBV as it uses HBsAg as its envelope.
• Use Rumack-Matthew nomogram for APAP toxicity as a guide to treatment.
• Both active & passive immunization are available for HAV & HBV. HBV
vaccine is given in HDV infection.
• Avoid hepatotoxic drugs