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HEPATITIS &

PREGNANCY

DR shams rehan

THREE PATHOLOGICAL
PROCEDURES LEADS TO JAUNDICE
HAEMOLYSIS
CONGENITAL HYPERBILIRUBINEMIA

CONJUGATED
UNCONJUGATED

CHOLESTASIS
INTRAHEPATIC
EXTRAHEPATIC

VIRAL HEPATITIS
HEPATITIS A VIRUS

MEMBER OF PICORNAVIRIDAE FAMILY


NON ENVELOPED
RESISTANT TO ORGANIC SOLVENTS
RELATIVELY STABLE IN ENVIRONMENT ,
RESISTANT TO HEAT & INACTIVATION BY
DRYING FOR UP TO ONE MONTH
AUTOCLAVING , HEATING FOOD TO ABOUT
185F FOR ONE MINUTE , OR DISINFECTING
SURFACES
WITH
DILUTE
CHLORIDE
BLEACH WILL INACTIVATE THE VIRUS

HEPATITIS A VIRUS
Global distribution
Outbreaks in areas with crowded
conditions , inadequate water supply,
poor hygiene & sanitation
Highly contagious virus with fecal-oral
route of transmission& exposure to
contaminated food & water
Parenteral transmission is rare b/c
virus is present only transiently in
serum

HEPATITIS A VIRUS
DIAGNOSIS
INITIAL CLINICAL SYMPTOMS
Fatigue , malaise, fever , nausea , anorexia
Significant weight loss may be presenting
symptom in pregnant women
THE CLASSICAL ICTERIC ILLNESS become
apparent with in 10 days of generalized
symptoms & is usually preceded by
palpable hepatosplenomegaly
FULMINANT HEPATITIS resulting in death in
<1% of cases

HEPATITIS A VIRUS
MATERNAL & FETAL EFFECTS

Self limiting illness


No increased risk of adverse outcome
Supportive care is essential
Nutritional needs should be addressed
Infected women may need hospitalization
with strict contact isolation
Administration of Immunoglobulins is
recommended for neonates born to within
2 weeks acute maternal illness with HAV
conferring protection up to 3 months

HEPATITIS A VIRUS
MANAGEMENT OPTIONS

Both preventive vaccination & post


exposure
prophylaxis
with
immunoglobulin are available
As an inactivated virus vaccine ,
there is no contraindication to the
use of HAV vaccine during pregnancy
Administration of immunoglobulin is
still recommended for neonates born
to mothers with recent HAV infection

HEPATITIS B IN GENERAL
HBV , a major global health problem with
600,000 ANNUAL DEATHS attributable to
consequences of HBV infection
IN AREAS OF ASIA, 8-10 % of the adult
population is chronically infected with HBV
The earlier in life a person is infected, the
higher the risk of being a chronic carrier,
so the risk of chronic HBV infection for a
child infected in the newborn period, in the
absence of prophylactic therapy is 70-90 %

TRANSMISSION OF HBV
1. BLOOD & BLOOD PRODUCTS are the most
thoroughly established sources of HBV
infection
2. BODY FLIUDS like Serum ,saliva & semen
have been associated consistently with
transmission
3. PER-CUTANEOUS TRANSFER of the virus is the
most obvious route of transmission in the
medical settings , through needle stick
injuries
4. Contact of infectious material with BROKEN
SKIN or mucous membranes

TRANSMISSION OF HBV
HBV is fairly stable virus & remains
infectious on household surfaces up to 7
days
Although transmission in households is
more common through sexual contacts
NONSEXUAL HOUSEHOLD TRANSMISSION
(fomite contacts) has been established as a
route for HBV infection
Therefore , any surfaces potentially
contaminated with infectious blood should
be cleaned with 1:10 of bleach solution

TRANSMISSION OF HBV
Vertical transmission is a major
source & 40-50 % 0f HBsAg
carriers become infected in
perinatal period
Children born to carrier mothers
who escapes the neonatal period
without evidence of infection are
still
at
risk
of
childhood
acquisition of HBV

DIAGNOSIS

DISTINGUISHING FEATURES OF
HEPATITIS B VIRUS
LONG INCUBATION PERIOD ( 1-6
MONTHS)
By the presence of extra hepatic
symptoms in 20% of
patients( arthralgia , rash , myalgia)
Detection of HBV specific serum
markers
There are three distinct antigen-

HBV CONSISTS OF THREE STRUCTURAL


ANTIGENS
HEPATITIS SURFACE(S) ANTIGEN (Hb S Ag)

HEPATITIS SURFACE(e) ANTIGEN (Hbe Ag)

HEPATITIS SURFACE(S) ANTIBODY (Hb S Ab)

HEPATITIS SURFACE(e) ANTIBODY (Hbe Ab)

HEPATITIS CORE Ab ANTIBODY (Hb C Ab)

HEPATITIS SURFACE(S) ANTIGEN


(Hb S Ag)

HBS AG THE FIRST EVIDENCE OF INFECTION ,


appears before biochemical evidence of liver
disease & persists through out the clinical illness &
remains detectable for 1-6 weeks in most patients
In 90-95 % of the patients in whom chronic
infection does not develop, HBs Ag titer decreases
as symptoms diminishes
PERSISTENCE OF HBS AG

more than

months ( 20 weeks) after the acute illness


signifies CHRONIC HBV INFECTION

SPECIFIC ANTIBODY TO HbsAg


HEPATITIS SURFACE(S) ANTIBODY(Hb S Ab)

THE APPEARANCE OF HBsAb DEFINES


THE ABSENCE OF CARRIER STATE
HBsAb titer increases slowly during the
clinical recovery period & may continue
to increase up to 10-12 months after
HbsAg is no longer detectable
In most patients with self limited ,
acute HBV, Hb S Ab is detectable only
after Hb S Ag titers in serum
disappears.

HEPATITIS SURFACE(S) ANTIBODY


(Hb S Ab)

DISAAPEARANCE OF HB s Ag &
THE APPEARANCE OF
ANTI
HBsAb SIGNALS
1. RECOVERY FROM HBV
INFECTION
2. NONINFECTIVITY
3. IMMUNITY

WINDOW PERIOD
A WINDOW OF TIME has been described
In which a patient still with clinical hepatitis
is negative for both HB s Ag & HBsAb.
During this time ,HBV infection still can be
diagnosed by the detection of hepatitis B core
antibody ( HBcAb), which begins to appear 3-5
weeks after HBsAg does
HBcAb titers may drop off in the first 1-2 years
after infection , although the antibody is still
detectable years after acute disease in most
patients

Anti Hbc
HBcAg alone doest appear in serum
IgM anti-HBc appears shortly after HBsAg is detected
IgM anti-HBc indicates a diagnosis of acute hepatitis
B, and it fills the serologic gap in rare patients who
have cleared HBsAg but dot yet have detectable
antiHBs.
IgM anti-HBc may also reappear during flares of
previously inactive chronic heptitis B
IgG antiHBc also appear during acute hepatitis B but
persits
indefinitely;
whether
the
patient
recovers( with appearance of anti HBs) or chronic
HBV develop( with persistence of HBsAg)

HEPATITIS CORE ANTIGEN &


ANTIBODY( HBcAb)
HBc Ab titers may drop off in the first
1-2 years after infection , although
the antibody is still detectable years
after acute disease in most patients
HBc Ab is detectable in serum of
carriers at levels higher than those
seen in either acute or recovering
self limited infections

HBeAg
It appears in serum during the incubation
period shortly after detection of Hb s Ag
IT INDICATES VIRAL REPLICATION &
INFECTIVITY
Persistence of Hbe Ag beyond three months
indicates increased likely hood of chronic
hepatitis B
Its disappearance is often followed by the
appearance of anti Hbe, signifying diminished
viral replication & decreased infectivity

HB Anti- Anti HBeA Ant interpretation


sAg HBs g
i
HBc
HB
e

Ig +
M
IgG +
*
IgG -

ACUTE HEPATITIS B

CHRONIC HEPATITIS B WITH


ACTIVE VIRAL REPLICATION

IgG +
or
_

+
-

0r

CHRONIC HEPATITIS B WITH


LOW VIRAL REPLICATION

CHRONIC HEPATITIS B WITH


HETEROTYPIC ANTI-HBS ( IN
10 % OF CASES)

MATERNAL & FETAL RISK


RISK DURING PREGNANCY

ACUTE HBV INFECTION DURING


PREGNANCY: IS USUALLY MILD
NAUSEA & VOMITTING
JAUNDICE
UP
TO 30 % OF PATIENTS
RUQ PAIN
FULMINANT HEPATIC FAILURE is
seen in 0.5- 1.5% of infective
individuals

PREGNANCY & HBS


The presence of HBS Ag does not
appear to increase the risk of
adverse pregnancy outcome.
In addition, pregnancy does not
exacerbate chronic HBV infection
or alter HBV viral levels

MANAGEMENT
TREATMENT DURING PREGNANCY IS MAINLY
SUPPORTIVE AS IN NON-PREGNANT STATE
HOSPITALIZATION SHOULD BE CONSIDERED
FOR PREGNANT WOMEN WITH ACUTE HBV
INFECTION IF
ENCEPHALOPATHY
COAGULOPATHY
SEVERE NUTRITIONAL & FLUID IMBALANCE
NO TERATOGENIC ASSOCIATION HAS BEEN
ESTABLISHED

MANAGEMENT

1. MAINTAIN ADEQUATE NUTRITION


2. AVOID LIVER METABOLIZED DRUGS
OR MONITOR THROUGH BLOOD
LEVELS
3. APPROPRIATE
IMMUNOPROPHYLAXIS
OF
HOUSEHOLD & SEXUAL CONTACTS
4. ACUTE HBV DURING LATER STAGES
CAN BE DIFFERENTIATED FROM PE
OR
HELLP
SYNDROME
USING
NORMAL BP CRITERIA & PRESENCE
OF JAUNDICE

VERTICAL TRANMISSION
The rate of vertical transmission
during
acute
maternal
HBV
infections
depends
on
the
gestational age of fetus
DURING FIRST TRIMESTER --- up
to 10 % of neonates will be
infected
-DURING THIRD TRIMESTER -- up
to 80-90 % of neonates will be
HBs Ag positive.

HEPATITIS B SCREENING IN
PREGNANCY

The CDC Recommended routine prenatal


screening with HBsAg for all pregnant
women regardless of risk factors
The CDC also recommends that pregnant
women who are HBsAg- negative & at high
risk for HBV infection should be retested
upon admission to labour & delivery.
HIGH RISK WOMEN INCLUDES
Women with more than > I sex partner in
past 6 months
Evaluation & treatment for other STI
Recent or current injection drug use
Positive sex partners

INFANTS BORN TO HBSAG POSITIVE WOMEN SHOULD


RECEIVE WITH IN 12 HOURS OF BIRTH

HBIG ( 0.5 ml) intramuscularly ( IM)


CONCURRENT HBV VACCINE AT DIFFERENT SITE
( 0.5 ML IM)
THE TIMING OF HBIG APPEARS TO BE MORE
CRITICAL THAN THAT OF VACCINE IN ACHIEVING
MAXIMAL EFFECTIVENESS OF PASSIVE-ACTIVE
THERAPY
SUBSEQUENT VACCINATION IS PERFORMED ,ALSO
0.5 ML I/M, AT ONE MONTH & 6 MONTHS OF AGE
THE COMBINATION HBIG & VACCINE IN THE
NEWBORN PERIOD CONFERRED SIGNIFICANTLY
GREATER PROTECTION AGAINST PERINATALLY
TRANSMITTED HBV THEN EVEN THE VACCINE
ALONE

POST EXPOSURE
TREATMENT
Single dose of HBIG administered

as
temporally as possible immediate to the
exposure
A series of HBV vaccination should also be
initiated ,if the exposure was within a setting
of ongoing risk e.g health care.
The regimen consists of injections at 0,1,6
months
Administration
of
HBV
vaccine
simultaneously with HBIG doest diminish the
immunologic response to the vaccine

PREVENTION OF IN UTERO HBV


INFECTION
IN UTERO HBV INFECTION IS DETERMINED BY
MULTIPLE POTENTIAL FACTORS INCLUDING
1. HBV DNA LEVEL
2. GESTATIONAL AGE
3. PLACENTA INTEGRITY
4. GENETIC SUSCEPTIBILITY OF FETUS
5. SEVERAL PROPHYLACTIC THERAPIES ( HBV
vaccine, Immunoglobulins , lamivudine )
have been proposed to possibly reduce the
risk of in utero transmission

PREVENTING
TRANSMISSION

PERINATAL

There may be a theoretical risk of HBV


transmission, a lack of data exist
regarding risk of transmission with
fetal scalp monitoring & operative
vaginal delivery.
According to the CDC, an HBS positive
mother can breast feed even prior to
the infant receiving the HBV vaccine
& HBIG.
The route of delivery has not

HEPATITIS VACCINATION IN
PREGNANCY
PREGNANCY IS NOT A
CONTRAINDICATION TO VACCINATION.
Limited data suggest that developing
fetuses are not at risk for adverse
events when hepatitis B vaccine is
administered to pregnant women.
Available
vaccines
contain
noninfectious
HBsAg
and
should
cause no risk of
infection to the
fetus.

HEPATITIS B SEROLOGY
HBs
Ag
ACUTE

HBs Ab HBc Ig
M

HBc
IgG

HBeAg

HBeAb

HBV
DNA

+
RESOLVE
D ACUTE
INFECTIO
N
CH
CARRIER
STATE
CH
ACTIVE
HEPATITI
S
VACCINAT
ED

+/_

+
+

+/_

INTERPRETATION OF HEPATITIS B PANEL


TEST

RESULT

HBsAg
Anti- HBc
Anti- HBs
HBsAg
Anti- HBc
Anti- HBs
HBsAg
Anti- HBc
Anti- HBs

NEGATIVE
NEGATIVE
NEGATIVE
NEGATIVE
POSITIVE
POSITIVE
NEGATIVE
NEGATIVE

INTERPRETATIO
N

SUSCEPTIBLE
IMMUNE DUE
TO NATURAL
INFECTION
IMMUNE DUE
TO HEPATITIS
B
VACCINATION

POSITIVE

INTERPRETATION OF HEPATITIS B PANEL


TEST

RESULT

HBsAg
Anti- HBc
IgM Anti- HBc
Anti- HBs

POSITIVE
POSITIVE
POSITIVE
NEGATIVE

INTERPRETATIO
N

ACUTELY
INFECTED

CHRONICALLY HBsAg
POSITIVE
INFECTED
Anti- HBc
POSITIVE
IgM Anti- HBc NEGATIVE
Anti- HBs

NEGATIVE

INTERPRETATION NOT CLEAR


FOUR POSSIBILITIES
INTERPRETATI
ON NOT
CLEAR
1.RESOLVED
INFECTION( M
OST
COMMON)
2.FALSE
POSITIVE
ANTI-HBC,
THUS
SUSCEPTIBLE
3.LOW LEVEL
CHRONIC

TESTS
HBsAg
Anti- HBc
Anti- HBs

RESULTS

NEGATIVE
POSITIVE
NEGATIVE

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