1

SEMINAR
ON
HEPATITIS

SUBMITTED TO, SUBMITTED BY,

MRS SMITHA. M SOUMYA RAJ
HOD PEDIATRICS MSC NSG 2NDYEAR
VCON VCON

SUBMITTED ON: 19 /04/18

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I) INTRODUCTION

Hepatitis is a disease characterized by inflammation of an injury

to the liver. Hepatitis, inflammation of the liver, can be caused by viruses,

bacteria, and other microorganisms, toxic chemicals, alcohol, and other drugs,

but viral hepatitis is the most common cause of hepatitis. Viral hepatitis is a

systemic infection in which virus infects the liver cells, causing biochemical and

cellular changes and interfering with liver function

Hepatitis is an inflammation of the liver. The condition can be self-

limiting or can progress to fibrosis (scarring), cirrhosis or liver cancer. Hepatitis

viruses are the most common cause of hepatitis in the world but other

infections, toxic substances (e.g. alcohol, certain drugs), and autoimmune

diseases can also cause hepatitis.

There are 5 main hepatitis viruses, referred to as types A, B, C, D

and E. These 5 types are of greatest concern because of the burden of illness and

death they cause and the potential for outbreaks and epidemic spread. In

particular, types B and C lead to chronic disease in hundreds of millions of

people and, together, are the most common cause of liver cirrhosis and cancer.

Hepatitis A and E are typically caused by ingestion of contaminated

food or water. Hepatitis B, C and D usually occur as a result of parenteral contact

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with infected body fluids. Common modes of transmission for these viruses

include receipt of contaminated blood or blood products, invasive medical

procedures using contaminated equipment and for hepatitis B transmission from

mother to baby at birth, from family member to child, and also by sexual

contact.

Acute infection may occur with limited or no symptoms, or may include

symptoms such as jaundice (yellowing of the skin and eyes), dark urine, extreme

fatigue, nausea, vomiting and abdominal pain.

II) DEFINITION

Viral hepatitis may be defined as infection of the liver caused by any half
dozen viruses

[K.Park]
Hepatitis means injury to the liver with inflammation of liver cells
[medical news today]

Hepatitis is an acute or chronic inflammation of the liver that can result from
several different causes

[Wong’s essentials of pediatric nursing]

Hepatitis is an inflammation of the liver that is caused by a variety of agents,
including viral infections, bacterial invasion, metabolic disorders, chemical
toxicity and trauma.
[Parul Dutta, essentials of pediatric nursing]
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III) THE DIFFERENT HEPATITIS VIRUSES

Scientists have identified 5 unique hepatitis viruses, identified by the

letters A, B, C, D, and E. While all cause liver disease, they vary in important

ways.

Hepatitis A virus (HAV) is present in the faeces of infected persons and is

most often transmitted through consumption of contaminated water or food.

Certain sex practices can also spread HAV. Infections are in many cases mild, with

most people making a full recovery and remaining immune from further HAV

infections. However, HAV infections can also be severe and life threatening. Most

people in areas of the world with poor sanitation have been infected with this

virus. Safe and effective vaccines are available to prevent HAV.

Hepatitis B virus (HBV) is transmitted through exposure to infective blood,

semen, and other body fluids. HBV can be transmitted from infected mothers to

infants at the time of birth or from family member to infant in early childhood.

Transmission may also occur through transfusions of HBV-contaminated blood

and blood products, contaminated injections during medical procedures, and

through injection drug use. HBV also poses a risk to healthcare workers who

sustain accidental needle stick injuries while caring for infected-HBV patients.

Safe and effective vaccines are available to prevent HBV.

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Hepatitis C virus (HCV) is mostly transmitted through exposure to infective

blood. This may happen through transfusions of HCV-contaminated blood and

blood products, contaminated injections during medical procedures, and

through injection drug use. Sexual transmission is also possible, but is much less

common. There is no vaccine for HCV.

Hepatitis D virus (HDV) infections occur only in those who are infected

with HBV. The dual infection of HDV and HBV can result in a more serious

disease and worse outcome. Hepatitis B vaccines provide protection from HDV

infection.

Hepatitis E virus (HEV) is mostly transmitted through consumption of

contaminated water or food. HEV is a common cause of hepatitis outbreaks in

developing parts of the world and is increasingly recognized as an important

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cause of disease in developed countries. Safe and effective vaccines to prevent

HEV infection have been developed but are not widely available.

TYPES OF HEPATITIS

There are 6 types of hepatitis.

1. Hepatitis A

2. Hepatitis B

3. Hepatitis C

4. Hepatitis D

5. Hepatitis E

6. Hepaitis G

HEPATITIS A
I) INTRODUCTION

Hepatitis A, caused by an RNA virus of the Enterovirus family, is foodborne

hepatitis, spread by the fecal-oral route, most commonly from contaminated food,
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water, or shellfish, or through oral-anal sexual practices. Hepatitis A virus (HAV)

may cause individual infections or epidemics. Outbreaks have occurred in daycare

centers, probably from diaper contamination of surfaces, such as changing tables,

and facilities with people with developmental disabilities. Hepatitis A is the most

common form of acute viral hepatitis in most part of world.

Hepatitis A is a liver disease caused by the hepatitis A virus. The virus is

primarily spread when an uninfected (and unvaccinated) person ingests food or

water that is contaminated with the faeces of an infected person. The disease is

closely associated with unsafe water or food, inadequate sanitation and poor

personal hygiene.

Unlike hepatitis B and C, hepatitis A infection does not cause chronic liver

disease and is rarely fatal, but it can cause debilitating symptoms and fulminant

hepatitis (acute liver failure), which is often fatal.

Hepatitis A occurs sporadically and in epidemics worldwide, with a tendency for

cyclic recurrences. The hepatitis A virus is one of the most frequent causes of

foodborne infection. Epidemics related to contaminated food or water can erupt

explosively, such as the epidemic in Shanghai in 1988 that affected about 300

000 people1. Hepatitis A viruses persist in the environment and can withstand
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food-production processes routinely used to inactivate and/or control bacterial

pathogens.

The disease can lead to significant economic and social consequences in

communities. It can take weeks or months for people recovering from the illness

to return to work, school, or daily life. The impact on food establishments

identified with the virus, and local productivity in general, can be substantial.

II) DEFINITION

Hepatitia A is anacute infectious disease caused by hepatitis A virus.

111) EPIDEMIOLOGY

Epidemiological determinants

IV) FACTORS

AGENT FACTORS

a) AGENT: The causative agent , the hepatitis A virus, is an enterovirus of the

picornaviridae family

b) RESISTANCE: the virus is fairely resistant to heat and chemicals. It has been
shown to survive more than 10 weeks in well water.

It withstand heating to 60°C for one hour, and is not affected by chlorine in
closes usually employed for chlorination.

Formalin is stated to be an effective disinfectant

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The virus is inactivated by ultraviolet rays and by boiling for 5mts of or

autoclaving.

C) RESERVO IR OF INFECTION:- The human cases are the only reservoir of

infection.

d) PERIOD OF INFECTIVITY:- The risk of transmitting HAV is greatest from 2

weeks before to 1 week after the onset of jaundice. Infectivity falls rapidly with
the onset of jaundice.

e) INFECTIVE MATERIAL:- Mainly man’s faeces blood, serum and other fluids
are infective during the brief stage of viraemia.

f) VIRUS EXCRETION:- HAV is excreted in the faeces for about 2 weeks before
the onset of jaundice and for up to 2 weeks thereafter. The virus may also be
excreted in urine.

HOST FACTORS

a) AGE: infection with HAV is more frequent among children than in adults, in

young children, infections tend to be mild or sub clinical; the clinical severity
increases with age. However, faecal excretion of HAV antigen and RNA persists
longer in the young than in adults. In, India, by the age of 10 years, 90 percent
of healthy persons have serological evidence of HAV infection.

b) SEX: Both sexes are equally susceptible.

c) IMMUNITY: Immunity after attack probably lasts for life. Second attack have
been reported in about 5 percent of patients.
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ENVIRONMENTAL FACTORS

Cases may occur throughout the year. In India the disease tends to be
associated with periods of heavy rain fall. Poor sanitation and overcrowding favor
the spread of infection, giving rise to water-borne and food borne epidemics.

V) MODE OF TRANSMISSION

a) FAECAL-ORAL ROUTE: This is the major route of transmission, it may occur

by direct (person-to-person) contact or indirectly by way of contaminated water,
food or milk.

b) PARENTERAL ROUTE: Hepatitis A is rarely, if ever, transmitted by

parenteral route (i.e., by blood and blood products or by skin penetration through
contaminated needles).

V) PATHOLOGY AND PATHOGENESIS

Having entered the body through the oral route, viruses enter the circulation
resulting in viremia. After circulating for some time, the viruses mainly affect
liver. Often they affect kidney, small intestine and spleen.

Essential pathology occurs in Liver.

 There is degeneration and necrosis of the hepatocytes. It is slight and is seen

in the central zone of the lobule.
 Degeneration is followed by regeneration following the production of
antibodies. Thus recovery is the rule.
 Cell –cords are distributed but not the reticular frame work. Its only in
fulminant cases there in extensive necrosis of liver lobules, damaging even
the reticular frame-work resulting in hepatitis failure.
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 When there is degeneration of hepatocytes, liver function is affected

resulting in hyper bilirubinemia, giving rise to returns.
 Because of the inflammation of the liver, there is hepatomegalys, giving rise
to pressure effects mainly on stomach.
 In the kidney, there is only interstial edema but no inflammation.
 In the spleen, there is hyperplasia of lymphoid tissue
 In the small intestine, mucous membrane becomes edematous and there is
infiltration of mononuclear cells.

Incubation period: 15 to 50 days

VI) CLINICAL FEATURES

These occur in 3 stages

Preicteric stage (prodromal stage)

This is characterized by –

 sudden onset of fever

 Often associated with chills
 Fatigue
 Malaise
 Head ache
 Body ache

Within a day or two, the individual will develop gastro intestinal symptoms
due to presence effect of enlarged liver over stomach, such as anorexia,
nausea and even vomiting followed by high colored urine, light colored
stools lasting for about 3-5 days.

There will be discomfort or pain in the right upon quadrant of abdomen .

Icteric stage
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This is characterized by onset of jaundice (yellow coloration of sclera). With the

onset of jaundice, fever subsides sclera looks yellow and skin looks lemon
tinged. Severity of nausea and vomiting diseases.

 High colored urine continues for several days.

 Jaundice usually reaches maximum by 2 weeks and diseases steadily
thereafter.
 On examination the abdomen, liver is enlarged, soft and tends surface
smooth. Spleen may enlarge.
 This stage starts for 4 to 6 weeks.

Conrale scent stage (stage of Recovery)

After about 6 to 8 weeks, following the production of antibodies the

inflammatory process comes down, there is regeneration of lives cells, liver
regress in size, pressure effects are released, appetite improves, icterus
disappeares.

 Urine and stool become normal

 This stage starts for 2 to 6 weeks
 Only in fulminant cases, there will be hepatic coma and death.


RISK PERSONS
Anyone who has not been vaccinated or previously infected can get

infected with hepatitis A virus. In areas where the virus is widespread (high

endemicity), most hepatitis A infections occur during early childhood. Risk factors in

intermediate and high endemicity areas include:

 poor sanitation;
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 lack of safe water;

 use of recreational drugs;

 living in a household with an infected person;

 being a sexual partner of someone with acute hepatitis A infection; and

 travelling to areas of high endemicity without being immunized

VII) INVESTIGATIONS

Cases of hepatitis A are not clinically distinguishable from other types of acute viral
hepatitis.

 Increase in serum bilirubin level

 Demonstration of viral particles in the stools, by electron microscopy
 Demonstration of a rise in HAV antibody titer
 Demonstration of bile salts and bile pigments in the urine.
 Detection of HAV-specific Immunoglobulin G (IgM) antibodies in the
blood.
 Additional tests include
 Reverse transcriptase polymerase chain reaction (RT-PCR) to detect
the hepatitis A virus RNA, and may require specialised laboratory
facilities.

VIII) PREVENTION AND CONTROL

Elimination of reservoirs

This is difficult because of the following reasons:

 There is no treatment
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 The individual will have already spread the disease before clinical diagnosis is
made (because the cases will be shedding the virus in last 2 weeks of
incubation period and first week of illness).
 There will be existence of large number of subclinical cases acting as carriers.
Difficult to identify them.
 However, concurrent disinfection of patient’s excreta by using 0.5 percent
sodium hypochlorite must be carried out.

IX) MANAGEMENT

 Absolute bed rest is traditional. This prevents the patient from getting
fatigue, exhaustion,etc
 Avoiding fatty and oily foods will prevent the liver from secreting more
bile juice, there by liver gets rest.
 Energy requirement, have to be made up with carbohydrate rich diet.
 Symptomatic treatment is given with antipyretic and antiemetic
 Antibodies play no role. However, neomycin can be given in advanced
cases.
 Steroids play no role, except that they give symptomatic relief. They do
not alter the cause of disease. They are indicated only in advanced cases.
 Fluids and electrolyte balance will have to be maintained.

Breaking the channel of transmission

This is the important measure in the control of an outbreak of VHA. Since the
disease is transmitted by free-oral route, it can be broken by construction of
‘sanitation barrier’ which prevents the access of the pathogens from the feces
of the cases to the months of susceptible through 6 Fs.

Protection of susceptible
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Susceptible are protected by immunization and health education.

Immunization

Active immunization

Two types of HAV vaccines are now available namely inactivated vaccine and
live alternated vaccine.

i) Inactivated vaccine

 It is a cell – culture liquid vaccine.

 The Hepatitis virus of HM-175 strain (ice 7 -strain) is propagated on human
diploid cells, purified by and ultra filtration technique and

ii) Live vaccine: A live attenuated freeze dried vaccine, containing H2 strain of
Hepatitis A viruses, cultured an human diploid cells, has been developed in
china.

 The diluents is sterile distilled water

 Single dose of 0.5 ml is recommended to administer subcutaneously, in
the deltoid region, for all above one year age.
 This has been found to be safe, highly immunogenic with good tolerability
and minimal reactogenecity.
 Immunity lasts for 15 years.
 No boosts dose is required.
 Storage temperature is 20 c to 80 c
 This does not provide cross immunity against other hepatitis virus like B, C,
delta and E viruses.
 Passive immunization
 It is human normal immunoglobulin.
 It is prepared from the pooled plasma of multiple donors.
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 Since it is not a specific immunoglobulin, it may not protect the person

from getting the disease but it may prevent or modify the course of the
disease, resulting in subclinical infection.
 Inactivated by formaldehyde and adsorbed on aluminum hydroxide.
 Each 1 ml contains not less than 720 Elisa-units of viral antigens.
 Dose: 0.5 ml for children
 Route : deltoid region
 Infants are not given
 Primary course consists of 2 doses of with 4 to 6 weeks interval, followed
by a booster dose after 6 to 12 months.
 Immunity is type specific and lasts for about 15 to 20 years,
 There is no cross immunity against other hepatitis viruses.
 A combination of vaccine containing inactivated Hepatitis-A and
recombinant Hepatitis – B vaccine has been listened since 1966 for
children in several countries.
 The schedule of the combined vaccine is 0, 1 and 6 months.

Developing healthy habits

Measures to reduce the risk of getting hepatitis B, C and HIV

 Do not abuse drugs; do not inject drugs. Never ever share needles and
syringes.
 Sharing personal care items like razors, tooth brushes etc. should be
avoided since they might have infected blood.
 Health care professionals must have strict compliance to universal
precautions while handling blood or body fluids, safe handlings of
needles and other sharps is sought all time.
 Avoid risk products like tattooing, body piercing and acupuncture etc.
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 Persons who have recently been exposed to HBV should be administered

Hepatitis B immune globulin (HBIG) and vaccine preferably within 24
hours, but not later than 2 weeks of exposure.

Vaccination

The Hepatitis B offers brilliant protection against HBV. The vaccine is safe and
greatly effective. Vaccination consists of 3 doses of vaccine over the course of 6
months. It protects person for 20 years from Hepatitis B.

Hepatitis-B vaccine (rDNA) is a non infective recombinant DNA Hepatitis B vaccine.

Pediatric dose vaccine: 10 mg dose (in 0.5mlsuspension) is recommended for

neonates, infants, children up to 10 years of age.

Time schedule for injections

1st dose At selected date

2nd dose 4-10 weeks after

3rd dose 1-5 months after the 2nd dose

Route of administration : IM

Hepatitis B immunoglobulin

This is used for protecting those acutely exposed to HBIG like health care
professionals, newborn infants of carrier mothers, sexual contacts of acute
hepatitis B patients.
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Ideal to give within 6 hours, but not later than 48 hours. Simultaneously the
victim’s blood is tested for HBSAG testing. If it is negative, routine course of
hepatitis B vaccine is given.

Combined vaccine

Simultaneous administration of hepatitis B immunoglobulin(HBIG) and

hepatitis B is more efficacious than HBIG alone.

 HBIG: - 0.05-0.07 ML/Kg body weight within 24 hours.

 Hepatitis B vaccine- 1ml (20mg/1ml)- within 7 days of exposure, the next
dose after 1 month and third dose after 6 months of the 1 st dose.

Other measures

 Screening the blood donors.

 Hygienic measures like strict hand washing.
 Strict check an sterilization procedure.

HEPATITIS B

I)INTRODUCTION

Hepatitis B is a potentially life-threatening liver infection caused by the

hepatitis B virus (HBV). It is a major global health problem. It can cause chronic

infection and puts people at high risk of death from cirrhosis and liver cancer.
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A vaccine against hepatitis B has been available since 1982. The vaccine is 95%

effective in preventing infection and the development of chronic disease and liver

cancer due to hepatitis B.

II) DEFINITION

Hepatitis B is an acute systemic infection with major pathology in the

liver, caused by hepatitis B virus (HBV) and transmitted usually by the parentral

route.

III) INCIDENCE

 Hepatitis B prevalence is highest in the WHO Western Pacific Region and the

WHO African Region, where 6.2% and 6.1% respectively of the adult

population is infected.

 In the WHO Eastern Mediterranean Region, the WHO South-East Asia Region

and the WHO European Region, an estimated 3.3%, 2.0% and 1.6%% of the

general population is infected, respectively.

 0.7% of the population of the WHO Region of the Americas is infected.

IV)EPIDIMIOLOGY

Epidemiological determinats
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Agent factors

a) AGENT: Hepatitis B virus

b) RESEVOIR OF INFECTION: man is the only reservoir of infection which can be

spread either from carriers or from cases.

c) Infective material: contaminated blood is the main source of infection. Although

the virus can be seen in body secreations such as saliva , vaginal secreations and

semen of infected persons.

d) RESISTANCE: the virus is quiet stable and cpable of surviving for dayson

environmental surface. It can be readily destroyed by sodium hypochlorite as is

by heat sterilization in an autoclave for 30 to 60 mts.

e) PERIOD OF COMMUNICABILITY: The virus is present in the blood during

incubation period and acute phase of the disease. Period of communicability is

usually several months.

V) TRANSMISSION

Route of transmission

Contact with infectious blood, semen, and other body fluids primarily through:

• Birth to an infected mother

• Sexual contact with an infected person

• Sharing of contaminated needles, syringes, or other injection drug equipment

• Needle sticks or other sharp instrument injuries

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The hepatitis B virus can survive outside the body for at least 7 days. During

this time, the virus can still cause infection if it enters the body of a person who

is not protected by the vaccine.

The incubation period of the hepatitis B virus is 75 days on average, but can

vary from 30 to 180 days. The virus may be detected within 30 to 60 days after

infection and can persist and develop into chronic hepatitis B.

In highly endemic areas, hepatitis B is most commonly spread from mother to

child at birth (perinatal transmission), or through horizontal transmission

(exposure to infected blood), especially from an infected child to an uninfected

child during the first 5 years of life. The development of chronic infection is very

common in infants infected from their mothers or before the age of 5 years.

Hepatitis B is also spread by percutaneous or mucosal exposure to infected

blood and various body fluids, as well as through saliva, menstrual, vaginal, and

seminal fluids.

Sexual transmission of hepatitis B may occur, particularly in unvaccinated

men who have sex with men and heterosexual persons with multiple sex

partners or contact with sex workers. Infection in adulthood leads to chronic

hepatitis in less than 5% of cases.

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Transmission of the virus may also occur through the reuse of needles and

syringes either in health-care settings or among persons who inject drugs.

In addition, infection can occur during medical, surgical and dental

procedures, through tattooing, or through the use of razors and similar objects

that are contaminated with infected blood.

VI) SYMPTOMS

Most people do not experience any symptoms during the acute infection phase.

However, some people have acute illness with symptoms that last several weeks,

including

 Yellowing of the skin and eyes (jaundice)

 Dark urine

 Extreme fatigue

 Nausea

 Vomiting

 Abdominal pain.

 A small subset of persons with acute hepatitis can develop acute liver failure,

which can lead to death.

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 In some people, the hepatitis B virus can also cause a chronic liver infection

that can later develop into cirrhosis (a scarring of the liver) or liver cancer.

VII) RISK FACTORS

The likelihood that infection becomes chronic depends upon the age at which a

person becomes infected. Children less than 6 years of age who become infected

with the hepatitis B virus are the most likely to develop chronic infections.

In infants and children:

 80–90% of infants infected during the first year of life develop chronic

infections; and

 30–50% of children infected before the age of 6 years develop chronic

infections.

In adults:

 less than 5% of otherwise healthy persons who are infected as adults will

develop chronic infection; and

 20–30% of adults who are chronically infected will develop cirrhosis and/or

liver cancer.

HBV-HIV CO-INFECTION

About 1% of persons living with HBV infection (2.7 million people) are also

infected with HIV. Conversely, the global prevalence of HBV infection in HIV-infected
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persons is 7.4%. Since 2015, WHO has recommended treatment for everyone

diagnosed with HIV infection, regardless of the stage of disease. Tenofovir,

which is included in the treatment combinations recommended in first intention

against HIV infection, is also active against HBV.

VIII) DIAGNOSIS

HBV diagnosis is accomplished by testing for a series of serological markers of

HBV and by additional testing to exclude alternative etiological agents such as

hepatitis A and C viruses. Serological tests are used to distinguish acute, self-limited

infections from chronic HBV infections and to monitor vaccine-induced immunity.

1) HBsAg (Hepatitis B surface antigen): HBsAg is the first serological

marker after infection (HBV DNA is the first marker).

 The antigen is detectable even before the liver enzymes elevation

and onset of clinical illness. In the typical case it disappears at 2

months of start of clinical illness but sometimes it lasts for more than

6 months i.e. chronic infection. So if this test is positive it implies

that the patient is infectious and if it is negative chronic

2) Anti-HBs (Antibody to HBV surface antigen) This antibody appears

when HBsAg is no longer detectable.

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 It is a protective antibody and indicates immunity to HBV either

through past

 infection or through vaccination. The protective level of anti-HBs

antibodies is ≥ 10 mIU/ml.

3) Anti-HBc ( Antibody to HBV core antigen): The anti-HBc IgM is the

earliest antibody marker following infection

 The anti-HBc IgM appears in the serum a week or two after the

appearance of

 HBsAg and is therefore the earliest antibody marker to be seen in

blood. Figure 2: The typical clinical and laboratory features of

Hepatitis B 19 The anti-HBc IgG antibody possibly persists for life and

is therefore a useful

 indicator of prior infection with HBV. IgM anti-HBc is seen in acute

infections but after six months is replaced by IgG.

 Therefore total antibody to HBc denotes past or active infection.

IgG anti-HBc is a

 reliable marker for previous HBV infection as it even persists when

anti-HBs titers decline to undetectable levels many years following

recovery from HBV infection. infection is typically ruled out.

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Laboratory diagnosis of hepatitis B infection focuses on the detection of the

hepatitis B surface antigen HBsAg. WHO recommends that all blood donations be

tested for hepatitis B to ensure blood safety and avoid accidental transmission to

people who receive blood products.

 Acute HBV infection is characterized by the presence of HBsAg and

immunoglobulin M (IgM) antibody to the core antigen, HBcAg. During the initial

phase of infection, patients are also seropositive for hepatitis B e antigen (HBeAg).

HBeAg is usually a marker of high levels of replication of the virus. The presence of

HBeAg indicates that the blood and body fluids of the infected individual are highly

infectious.

 Chronic infection is characterized by the persistence of HBsAg for at least 6

months (with or without concurrent HBeAg). Persistence of HBsAg is the principal

marker of risk for developing chronic liver disease and liver cancer (hepatocellular

carcinoma) later in life.

IX) TREATMENT

There is no specific treatment for acute hepatitis B.

Aim of treatment

 Maintaining comfort and

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 Maintaining adequate nutritional balance, including replacement of fluids

lost from vomiting and diarrhoea.

Chronic hepatitis B infection can be treated with medicines, including oral antiviral

agents. Treatment can slow the progression of cirrhosis, reduce incidence of liver

cancer and improve long term survival.

WHO recommends the use of oral treatments - tenofovir or entecavir, because

these are the most potent drugs to suppress hepatitis B virus. They rarely lead to

drug resistance as compared with other drugs, are simple to take (1 pill a day), and

have few side effects so require only limited monitoring.

Entecavir is off-patent, but availability and costs vary widely.

In most people, however, the treatment does not cure hepatitis B infection, but

only suppresses the replication of the virus. Therefore, most people who start

hepatitis B treatment must continue it for life.

There is still limited access to diagnosis and treatment of hepatitis B in many

resource-constrained settings. In 2015, of the 257 million people living with HBV

infection, 9% (22 million) knew their diagnosis. Of those diagnosed, the global

treatment coverage was only 8% (1.7 million). Many people are diagnosed only

when they already have advanced liver disease.

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Among the long-term complications of HBV infections, cirrhosis and

hepatocellular carcinoma cause a large disease burden. Liver cancer progresses

rapidly, and since treatment options are limited, the outcome is in general poor.

In low-income settings, most people with liver cancer die within months of

diagnosis. In high-income countries, surgery and chemotherapy can prolong life

for up to a few years.

Liver transplantation is sometimes used in people with cirrhosis in high

income countries, with varying success.

X) PREVENTION

The hepatitis B vaccine is the mainstay of hepatitis B prevention. WHO

recommends that all infants receive the hepatitis B vaccine as soon as possible

after birth, preferably within 24 hours. The low incidence of chronic HBV

infection in children under 5 years of age at present can be attributed to the

widespread use of hepatitis B vaccine.

. The birth dose should be followed by 2 or 3 doses to complete the primary

series. In most cases, 1 of the following 2 options is considered appropriate:

 A 3-dose schedule of hepatitis B vaccine

 First dose (monovalent) being given at birth

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 Second and third (monovalent or combined vaccine) given at the same time

as the first and third doses of diphtheria, pertussis (whooping cough), and

tetanus – (DTP) vaccine.

 A 4-dose schedule, where a monovalent birth dose is followed by three

monovalent or combined vaccine doses, usually given with other routine infant

vaccines.

The complete vaccine series induces protective antibody levels in more than 95%

of infants, children and young adults. Protection lasts at least 20 years and is

probably lifelong. Thus, WHO does not recommend booster vaccination for persons

who have completed the 3 dose vaccination schedule.

All children and adolescents younger than 18 years-old and not previously

vaccinated should receive the vaccine if they live in countries where there is low or

intermediate endemicity. In those settings it is possible that more people in high-risk

groups may acquire the infection and they should also be vaccinated. They include:

 people who frequently require blood or blood products, dialysis patients,

recipients of solid organ transplantations;

 people interned in prisons;

 persons who inject drugs;

 household and sexual contacts of people with chronic HBV infection;

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 people with multiple sexual partners;

 healthcare workers and others who may be exposed to blood and blood

products through their work; and travellers who have not completed their

hepatitis B vaccination series, who should be offered the vaccine before leaving

for endemic areas.

The vaccine has an excellent record of safety and effectiveness. Since 1982, over 1

billion doses of hepatitis B vaccine have been used worldwide. In many countries

where between 8–15% of children used to become chronically infected with the

hepatitis B virus, vaccination has reduced the rate of chronic infection to less than

1% among immunized children.

In 2015, global coverage with the third dose of hepatitis B vaccine reached 84%,

and global coverage with the birth dose of hepatitis B vaccine was 39%.

In addition, implementation of blood safety strategies, including quality-assured

screening of all donated blood and blood components used for transfusion, can

prevent transmission of HBV.

Safe injection practices, eliminating unnecessary and unsafe injections, can be

effective strategies to protect against HBV transmission. Furthermore, safer sex

practices, including minimizing the number of partners and using barrier protective

measures (condoms), also protect against transmission.

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HEPATITIS C

I) DEFINITION

Hepatitis C is the infectious disease that is caused by Hepatitis C virus (HCV).

II) INCIDENCE

WHO estimates that 3 percent of world population is infected with HCV

and associated 170 million individuals are chronic carriers.

III) EPIDIMIOLOGY

Epidemiological determinants

 AGENT: hepatitis C virus (HCV)

 TRASMISSION: the virus is transmitted through transfusion of contaminated

blood or blood products. Traditional practices such as circumcision , tattoing

and scarification with contaminated instruments can spread HCV infections.

 INCUBATION PERIOD:
 6- 7 weeks
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IV) SCREANING AND DIAGNOSIS

i) Serological test for anti-HCV antibodies
ii) If the test is positive anti- HCV antibodies , a nucleic acid test for HCV-RNA

is needed to confirm chronic HCV infections because about 15- 45 percent

of infected people clear the infection spontaneously by a strong immune

response without the need for treatment.

iii) Liver biopsy is done to assess the degree of liver damage.

High risk group got HCV infection

 Injectable drug users

 Recipient of infected blood or blood products
 Recipients of invasive procedure in health care facilities within adequate

infection control practice.

 Sexual partners of infected persons
 People with HIV infection
 Prisoners and previously incarcerated persons
 People who have had tattoos or piercings

V) TREATMENT
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Treatment is always not necessary because majority recover spontaneously

following immune response and some with chronic infection do not develop

liver damage.

Until recently the treatment for hepatitis C was weekly injections with

interferons and ribavirin for 48 weeks giving 5o percent cure rate, with a risk of

life threatening adverse reactions.

Recently, more effective , safer and better tolerated new antiviral drugs has

been developed. There are called Direct anti viral agents. (DAA) . They are

Teleprevir or Beceprevir. It is given in combination with pegylated interferone

and ribavirin.

VI) PREVENTION

Primary prevention

This consists of prevention of exposure to the virus, in health care settings.

These measures are

Hand hygiene
Safe handling and disposal of sharpes and waste
Provision of sterile syringes and needles for injectable drug users.
Screening of blood for Hepatitis B, and C as well as for HIV and syphilis
Treating of health personal
Promotion of correct and consistent use of condoms
Restriction of alcohol intake if any
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Secondary and tertiary prevention

These measures are for HCV infected persons

Education and counselling on options for care and treatment

Immunization with Hepatiris A and Hepatitis B vaccines to prevent co-infections

of these viruses to protect the liver

Early and approptriate management with antiviral therapy
Regular monitoring for early diagnosis of chronic liver disease

HEPATITIS D

I)INTRODUCTION

Hepatitis D virus otherwise called delta hepatitis is caused by hepatitis delta

virus (HDV), a defective RNA virus

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Hepatitis D is a liver disease in both acute and chronic forms caused by the

hepatitis D virus (HDV) that requires HBV for its replication. Hepatitis D infection

cannot occur in the absence of hepatitis B virus. The co-infection or super

infection of HDV with HBV causes a more severe disease than HBV mono

infection.

A vaccine against hepatitis B is the only method to prevent HDV infection.

III) INCIDENCE

It is estimated that globally, 5% of HBsAg positive people are coinfected with

HDV and the distribution is worldwide. High-prevalence areas include the

Mediterranean, Middle East, Pakistan, Central and Northern Asia, Japan, Taiwan,

Greenland and parts of Africa (mainly the horn of Africa and West Africa), the

Amazon Basin and certain areas of the Pacific. Prevalence is low in North

America and Northern Europe, South Africa, and Eastern Asia.

III) TRANSMISSION

HDV can be transmitted percutaneously or sexual contact through contact

with infected blood or blood products. Bllod is infectious through all phases of

active hepatitis D infection. Infectivity is at highest level before the onset of acute

disease. Chronic HBV carries are at risk for infection with HDV.
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IV) SYMPTOMS

Acute hepatitis:

Simultaneous infection with HBV and HDV can lead to a mild-to-severe or

even fulminant hepatitis, but recovery is usually complete and development of

chronic hepatitis D is rare (less than 5% of acute hepatitis).

Super infection:

HDV can infect a person already chronically infected with HBV. The

superinfection of HDV on chronic hepatitis B accelerates progression to a more

severe disease in all ages and in 70‒90% of persons. HDV superinfection

accelerates progression to cirrhosis almost a decade earlier than HBV

monoinfected persons, although HDV suppresses HBV replication. The

mechanism in which HDV causes more severe hepatitis and a faster progression

of fibrosis than HBV alone remains unclear.

V) RISK PERSONS

 Chronic HBV carriers are at risk for infection with HDV.

 People who are not immune to HBV (either by natural disease or

immunization with the hepatitis B vaccine) are at risk of infection with HBV

which puts them at risk of HDV infection.

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VI)SCREENING AND DIAGNOSIS

HDV infection is diagnosed by high titres of Immunoglobulin G (IgG) and

Immunoglobulin M (IgM) anti-HDV, and confirmed by detection of HDV RNA in

serum.

However, HDV diagnostics are not widely available and there is no

standardization for HDV RNA assays, which are used for monitoring response to

antiviral therapy.

VII)TREATMENT

There is no effective antiviral therapy available currently for hepatitis D.

The only alternative measure is to prefer liver transplantation for cases of

fulminate acute and end-stage chronic hepatitis D.

VIII)PREVENTION

Prevention and control of HDV infection requires prevention of HBV

transmission through hepatitis B immunization, blood safety, injection safety,

and harm reduction services. Hepatitis B immunization does not provide

protection against HDV for those already HBV infected.

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HEPATITIS E

I)INCIDENCE

Every year there are an estimated 20 million hepatitis E infections and 56,600

hepatitis E related deaths. Hepatitis E is found to be prevalent in east and South

Asia. Hepatitis E is caused by the Hepatitis E virus.

II)MODE OF TRASMISSION

1. Food borne transmission through ingestion of products of infected animals.

2. Water borne
3. Transferring infected blood products
4. Mother to child transmission from a pregnant women to her child

Incubation period

3 to 8 weeks or an average of 40 days

III)PREVENTION

 The transmission risk can be reduced by following quality standards for public

water supplies
 Proper disposal systems to dispose sanitary waste strict adherent on hygiene

practices like hand washing before handling food

 Avoiding drinking water and ice from unknown sources
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 Be complaint to WHO safe food practices

IV)NURSING MANAGEMENT

Nursing diagnosis

1. Imbalance nutrition less than body requirement related to

 Insufficient intake to meet metabolic demands
 Altered absorption and metabolism of ingested food
 Increased caloric needs
2. Deficient fluid volume related to
 Excessive losses through vomiting and diarhea

 Altered clotting process

3. Fatigue related to
 Decreased metabolic energy production
 States of discomfort
 Altered body chemistry
4. Impaired skin integrity
Risk factors may include
 Chemical substances , bile salt accumulation in the tissue
5. Knowledge deficit related to
 Lack of exposure or recall information
 Unfamiliarity with resources
6. Risk for infection related to
 Inadequate secondary defense
 Malnutrition
 Insufficient knowledge to avoid exposure to pathogense

WORLD HEPATITIS DAY

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IV) CONCLUSION

Hepatitis is an inflammation of the liver. The condition can be self-limiting or can

progress to fibrosis (scarring), cirrhosis or liver cancer. Hepatitis viruses are the most common

cause of hepatitis in the world but other infections, toxic substances (e.g. alcohol, certain

drugs), and autoimmune diseases can also cause hepatitis.

V) BIBLIOGRAPHY

1. Maryn J Hockenbery. Wong’s essentials of pediatric Nursing. 21sted. New Delhi: Elseveir

publication; 2001.
2. Marlow R Dorothy. Text book of pediatric Nursing. 20 th ed. New Delhi: Elseveir publication;

2003.
3. Hay W William. Current diagnosis and treatment: 1st ed. New Delhi: Elseveir publication;

2010.
4. Kyle Terri. Essentials of pediatric Nursing. 1st ed. Wolkers publishers; 2001.
5. Haffield T Nancy. Broadrbb’s introductory pediatric nursing. 7th ed. New Delhi: wolters

kluwer(India) pvt.Ltd; 2008.

VII) NET REFERENCES
1. http://www.who.int/features/qa/76/en/
2. http://www.who.int/mediacentre/factsheets/hepatitis-d/en/
3. http://www.ncdc.gov.in/writereaddata/linkimages/guideline_hep20158117187417.pdf
4. http://www.ncdc.gov.in/writereaddata/linkimages/guideline_hep20158117187417.pdf