ACUTE HEPATITIS

General Considerations
Hepatitis can be caused by :
- drugs
- toxic agents

- viruses (HAV, HBV, HCV, Hepatitis D

virus, Hepatitis E virus)
Clinical manifestation of which maybe quite
similar
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Hepatitis A

HAV is a 27-nm RNA hepatovirus causing epidemics or

sporading cases of hepatitis.
Transmission is by the fecal oral route, and spread is favored
by crowding and poor sanitation.
Common source outbreaks result from contaminated water or
food.
The incubation period avarages 30 days
The mortality rates is low.
Fulminant type is uncommon
Chronic Hepatitis A doesnt occur and there is no carrier state.

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Jaundice
Symptoms

ALT
H AV in serum
Titer

IgM anti HAV

IgG
Anti HAV

Fecal
HAV

12

16

Weeks after exposure

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The typical course of acute type A hepatitis

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Hepatitis B

HBV is a 42-nm hepadnavirus

- double stranded DNA genome,
- inner core protein (HBcAg)
- outer surface code (HBsAg)
Transmitted by :
- inogulation of infected blood or blood products
- sexual contact
- present in saliva, sement, and vaginal secretion.
HBsAg positive mothers may transmit HBV at delivery, the risk of
chronic infection in the infant is as high as 90%.
HBV prevalent in homosexuals and IV drugs user.

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Hepatitis B

The greatest number of cases result from

heterosexual transmission.
Group at risk included patients and staff at HD center,
physicians, dentists, nurses, and personnel working
in clinical and patology laboratories and blood banks.
The onset of HBV is more insidious and the
aminotransferase levels higher than in HAV
infections.
Fulminant type is less than 1 %

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HBsAg

The apearance is the first evidance of infection

Apearing before biochemical evidance of liver
disease, persists throughout the clinical illness.
Persistance after the acute illness may be
associated with clinical and laboratory evidance
of chronic hepatitis.
The detection of HBsAg is established infection
with HBV and implies infectivity.

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Anti HBs
Spesific antibody to HBsAg, appears in most
individuals after clearance of HBsAg and
after successful vaccination against hepatitis
B.
Disappearance of HBsAg and the
appearance of anti HBs signals recovery
from HBV infection, non infectivity and
immunity.

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IgM Anti HBc

IgM anti HBc appers shortly after HBsAg is

detected.
Its presence in the setting of acute hepatitis
indicates a diagnosis of acute Hepatitis B
It fills the serologic gap in patients who have
cleared HBsAg but do not yet have the detectable
anti HBs
IgM anti HBC can perssist for 3-6 months or more
May also reappear during flares of previously in
active chronic Hepatitis B

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IgG Anti HBc

IgG anti HBc also appears during acute Hepatitis

B but persist in definitely, whether the patient
recovers ( anti HBs in serum) or develops
chorinc Hepatitis B (persistance of HBsAg)
In asymptommatic blood donor, an isolated anti
HBc with no other positive HBV results may
represent a fasley positive results or laten
infection in which HBV DNA is detectable only
by polymerase chain reaction testing.

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HBeAg
A soluble protein found only in HBsAg
positive serum
Indicated viral replication and infectivity
Persistence in serum beyond 3 months
indicated an increased likelihood of chornic
Hepatitis B
Its disappearance is often followed by the
apreance anti HBe, signifying diminished
viral replication and decreased infectivity

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HBV DNA
The presence in serum generally parallels
the presence of HBeAg
HBV DNA is more sensitive and precise
marker viral replication and infectivity
In some patients with chronic Hepatitris B,
HBV DNA is present at high levels results
HBeAg in serum because of a mutation
that prevents synthetis of HBeAg in
infected hepatocytes

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Jaundice
Symptoms

ALT
Titer

HBeAg

Anti-Hbe

HBV DNA

HBsAg
IgG anti-HBc

Anti-HBs

IgM anti-HBc

12

16

20

24

28

32

36

40

Weeks after exposure

The Typical course of acute type B hepatitis

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Clinical Findings of Acute Hepatitis

The

Cilinical picture of viral hepatitis

is extremely variable,
Ranging from asymptomatic infection
without jaundice to a fulminating
disease and death in few days

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A. Symptoms
1. Prodromal

Phase
The onset may be abrupt or insidious,
with:
a. general malaise
b. myalgia, arthralgia
c. easy fatigability
d. upper repiratory symptoms
e. anorexia.
f. distaste for smoking
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A. Symptoms
g.

paralleling anorexia may occur early

h. nausea and vomiting are frequent
i. diarrhea or constipation may occur
j. fever is generally present but is low
grade
k.abdominal pain is usually mild and
constant in the right upper quadant or
epigastrum
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2. Icteric Phase
Jaundice occurs after 5-10 days
With the onset of jaundice, there
is often worsening of the
prodromal symptoms, followed by
progressive clinical improvement.

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3. Convalescent Phase
There is an increasing sense of well being,
return of appetite,
Disappearance of :
a. Jaundice
b. abdominal pain and tenderness
c. fatigability.

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4. Course and Complications

The acute illness usually subsides over 2-3
weeks.
Complete clinical and laboratory recovery by 9
weeks (hepatitis A) and by 16 weeks (hepatitis
B)
Less than 1% will have a fulminant course.
In some cases of acute hapatitis A, clinical,
biochemical and serelogic recovery may be
followed by one or two relapses.
Hepatitis B, D and C (and G) may become
chronic.
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B. Signs
Hepatomegaly-rarely

marked-is
present in over half of cases.
Liver tenderness is usually present.
Splenomegaly is reported in 15% of
patients and soft, enlarged lymph
nodes-especially in cervical or
epitochlear areas may occur.

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C. Laboratory Findings

The white blood cell count is normal to low,

especially in the preicteric phase.
Large atypical lymphocytes may occasionally be
seen.
Mild proteinuria is common and bilirubinia often
precedes the appreance of jaundice.
Acholic stools are often present during the icteric
phase.
Strikingly elevated AST or ALT occurs early
followed by elevations of bilirubin and alkaline
phosphatase
Cholestatis is occasionally marked in acute
hepatitis A.

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Differential Diagnosis
The

prodromal phase of viral hepatitis

must be distinguished from other
infectious disease such as influenza,
upper respiratory infections, and the
prodromal
stages
of
the
exanthematous diseases.

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Prevention
Strict isolation of patients is not necessary.
Hand washing after bowel movements is
required.
Hand washing by medical staff who has
contacted contaminated materials
Careful handling of disposable needlesincluding not recapping used needles-is
routine for medical personel.

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Prevention
Screening of donated blood for HBsAg, and HBc, and antiHCV has reduced the risk of transfusion-associated hepatitis
markedly.
All pregnant women should undergo testing for HBsAg. HBV-and HCV-infected persons should practice safe sex, but there
is little evidence that HCV is spread easily by sexual contact.

Vaccination against HAV (after fit screening for prior

immunity) and HBV is recommended for patients with chronic
hepatitis C, and vaccination against HAV is recommended for
patient with chronic hepatitis B.

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HEPATITIS A

Immune globulin should be given to all close (eg,

household) personal contacts of patients with hepatitis
A. The recommended dose of 0.02 ml/kg
intramucularly is protective if administered during
incubation Two effective inactivated hepatitis A
Vaccines are available and recommended for persons
living in or traveling to endemic areas (including
military personnel), homosexual and bisexual men,
animal handlers, illicit drug users, sewage workers,
food handlers, and children and caregivers in day care
centers and institutions.

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HEPATITIS A

Routine vaccination of all children has been

recommended in states with a high incidence of
hepatitis A. HAV vaccine is also effective in the
prevention of secondary spread to household contacts
of primary cases. The recommended dose for adults is
1
ml
(1440
ELISA units)
of
Havrix
(GlaxoSmithKline) or 0.5 ml (50 units) of Vaqta
(Merck) intramuscularly, followed by a booster dose
at 6-12 months. A combined hepatitis A and B vaccine
(Twinrix, GlaxoSmithKline) is available.

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HEPATITIS B
Hepatitis B immune globulin (HBIG) may be protective
or may attenuate the severity of illnessif given in large
doses within 7 days after exposure (adult dose is 0.06
ml/kg body weight) followed by initiation of the HBV
vaccine series.
This approach is currently recommended for individuals
exposed to hepatitis B surface antigen-contaminated
material via mucous membranes or through breaks in
the skin and for individuals who have had sexual contact
with persons with HBV infection. HBIG is also indicated
for newborn infants of HBsAg-positive mothers followed
by initiation of the vaccine series.

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HEPATITIS B
The currently used vaccines are recombinantderived. Initially, the vaccine was targeted to
persons at high risk, including renal dialysis
patients and attending personnel, patients
requiring repeated transfusions, HBsAg-positive
individuals, men who have sex with men,
intravenous drug users, new-borns of HBsAgpositive mothers, beginning medical and nursing
students, and all medical technologists.

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Treatment

Bed rest is recommended only if symptoms are marked.

If nausea and vomiting are pronounced or if oral intake is
substantially decreased, intravenous 10% glucose is
indicated.
Dietary management consists of palatable meals as
tolerated, without overfeeding; breakfast is usually best
tolerated.
Corticosteroids have no benefit in patients with viral
hepatitis, including those with fulminant disease.
Treatment of acute hepatitis C patients with interferon
alfa for 6-24 weeks appreciably decreases the risk of
chronic hepatitis.

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Prognosis

In the majority, clinical recovery is complete in 36 weeks.

Laboratory evidence of liver dysfunction may persist for a
longer period, but most patients recover completely. The
overall mortality rate is less than 1%, but the rate is
reportedly higher in older people.
Hepatitis A does not cause chronic liver disease, though it
may persist for up to 1 year, and clinical and biochemical
relapses may occur before full recovery. The mortality rate is
less than 0.2%. The mortality rate for acute hepatitis B is 0.11%, but higher with superimposed hepatitis D. Fulminant
hepatitis C is rare in the United States. For unknown
reasons, the mortality rate for hepatitis E is especially high in
pregnant women (10-20%).

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Chronic hepatitis, characterized by elevated aminotransferase levels for more than 6 months, develops in 12% of immunocompetent adults with acute hepatitis B but
in as many as 90% of infected neonates and infants and a
substantial proportion of immunocompromised adults. As
many as 80% of all persons with acute hepatitis C develop
chronic hepatitis, which in many cases progresses very
slowly. Ultimately, cirrhosis develops in up to 30% of those
with chronic hepatitis C and 40% of those with chronic
hepatitis B; the risk of cirrhosis is even higher in patients
coin-fected with both viruses or with HIV. Patients with
cirrhosis are at risk of hepatocellular carcinoma at a rate of
3-5% per year. Even in the absence of cirrhosis, patients
with chronic hepatitis B particularly those with active viral
replicationare at increased risk.

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