hepatits

Nitha k
2nd year msc nursing
INTRODUCTIO
N
 Hepatitis

Infection of the liver caused by different viruses

 Acute hepatitis is defined as less than 6 months of
liver inflammation, and
chronic hepatitis indicates an inflammatory process
which has been present for 6 or more months.
 Etiology
It’s commonly caused by a viral infection, but there are
other possible causes of hepatitis. These include
autoimmune hepatitis and hepatitis that occurs as a
secondary result of medications, drugs, toxins, and
alcohol.
Viral
Hepatotropic viruses – HAV, HBV (serum virus), HCV,
HDV, HEV
Non hepatotropic viruses
• Cytomegalovirus (CMV)
 Epstein Barr (EBV)
 Adenovirus
 Herpex simplex (HSV)
 Dengue virus etc.
 Mumps
 Varicella zoster
 HIV

Non viral
 Leptospirosis,
 Enteric fever,
 TB,
 Histoplasmosis,
 Amebiasis.
Drug and toxin induced –
 Acetaminophen,
 Phenytoin
 INH
 Nitrofurantoin
 Methotrexate
 Alcohol.
 Autoimmune
 Autoimmune hepatitis, SLE, JRA
 Metabolic
 Tyrosinemia
Wilson disease
 Ischaemic hepatitis
 Shock,
CHF
 Non alcoholic fatty liver disease – Reye syndrome
 Viral hepatitis
 Most common cause worldwide
 Caused by 5 pathogenic hepatotropic viruses :
 Hepatitides A (HAV), B(HBV), C(HCV), D(HDV) and
E(HEV) viruses.
• HAV – most common in India , > 80% children • Although
the agents can be distinguished by their antigenic
properties, the 5 kinds of viruses may produce clinically
similar illness.
 Epidemiology
   70% to 80% of all new cases of viral hepatitis are related
to HAV,
 5% to 30% are related to HBV,
 5% to 15% are related to HCV.
 The major risk factors for HBV and HCV are injection
drug use, frequent exposure to blood products
(hemophilia, organ transplants, chronic renal failure), and
maternal infection.
 HBV and HCV cause chronic infection, which may lead to
cirrhosis and is a significant risk factor for hepatocellular
carcinoma and represents a persistent risk of transmission.
 Pathophysiology
 Viruses enter the blood stream and spread to the liver.

 They infect the hepatocytes and multiply. They change the

antigen structure on the virus site.
 The body begins to use self-mediated immune response
attempting to damage the hepatocytes.

 In Hep B and C, they can continue this process over and

over for years.
 Stage
P I C
r ct o
o e n
d ri v
r c al
o e
m s
al c
e
n
t
 In the prodromal stage, the virus is in the blood and
will release chemicals. These chemicals will create
symptoms such as fever, headache, fatigue, nausea,
vomiting, skin rashes and joint pains.
 In the icteric stage, conjugated bilirubin and
transaminases spills into the blood because of damage
of bile ducts and hepatocytes. The conjugated and
unconjugated bilirubin make the patient appear yellow
and present with dark urine. The liver may become
enlarged in this state as well which is termed
hepatomegaly.
In the convalescent stage, the symptoms become better
or the patient returns to normal
 Hepatitis A
 Most prevalent
 Infective hepatitis
 HAV – RNA virus, picornavirus family
 Host – human and other primates
 Transmission – Faeco oral route
 Faecal excretion of virus starts late in the incubation period
and reaches the peak just before the onset of symptoms and
resolves within 2 weeks after onset of jaundice
 Source of infection is Crowded conditions, poor personal
hygiene, Poor sanitation, Contaminated food, water,
shellfish, person with subclinical infections, infected food
handlers.
 More prevalent in underdeveloped countries.
 People who travel to developing countries more likely to
get Hep A.
 Clinical features
  The illness remain asymptomatic or can be seen as acute
or sub acute clinical hepatitis
 Illness is usually symptomatic in older children
 Onset usually with prodromal stage of illness for 1-2 week
 Moderate fever
 Severe malaise
 Nausea
 Anorexia
 Vomiting
 Headache , upper abdominal pain
Prodromal phase over
Pass dark urine
Clay coloured stool
Jaundice
Yellowish discoularation of sclera and skin
1- 4 week
 Hepatomegaly , regional lymph nodes and spleen may
be enlarged
 Acute pancreatitis, gastrointestinal ulcers ,
myocarditis, nephritis, arthritis – circulating immune
complexes
 Complication fullmilant hepatitis, liver failure
 Relapse occur
 Diagnosis
 History of illness and clinical examination
 Rise in serum transaminases, bilirubin and alkaline
phosphatase is universal and hence cannot distinguish
between other forms of hepatitis
Two kinds of antibodies to the virus. IgM antibodies
and IgG antibodies. IgM antibodies show acute
infection.
IgG antibodies show previous infection or
immunization
.
Detection of Anti-HAV Ig M antibodies – remains for
4-6 months with low or absent IgG antibody to HAV is
presumptive evidence of HAV. 
 Viral particles in faeces
 Ig G type is detected within 8 weeks of infection
 Management
o No specific treatment
o Bedrest
o Carbohydrate rich food , adequate protein
o Fat restricted according to patient tolerance
o Vitamin supplementation
o Fat soluble vitamins for prolonged cholestatic form.
o Serial monitoring for signs of acute liver failure
o Patients contagious 2 weeks before and 7 days after onset
of jaundice.
o Hand washing after toilet
Vitamin k
Anti emetic drug
Fluid and electrolyte
 Prevention
Safe water supply
Personal hygiene
Improving sanitation
Food hygiene
Sanitary disposal excreta
Water treatment and purification
Prevent contamination of food and milk
Disinfection of stool and fomitus of infected person
Passive immunization Anti HAV gamma globulin to
the close contact hepatitis B
Efficacy 6 month
Active immunization inactivated or live attenauted
vaccines
Inacivated vacccines are only available
 Post exposure prophylaxis with Ig –
 Not effective 2 weeks after exposure.
 For exposure less than 2 weeks: < 1 y.o. child - 0.02 ml/kg.
For immuno compromised host and those with chronic
liver disease – give HAV as well. > 1 year – HAV vaccine.
Ig is optional.
 Vaccine : - Inactivated vaccine ( Haverix) 0.5 ml I.M in
deltoid, 2 doses > 1 year of age 6 months apart. • Live
vaccine is also available in India (Biovac A) – Single dose
of H2 strain.
 Intravenous immunoglobulin – ‘Pre exposure prophylaxis’
for travellers to endemic regions. Provides protection up to
3 months

 AGE EXPECTED EXPOSURE DURATION DOSE < 1

year <3 months 3-5 months > 5 months 0.02 ml/kg 0.06
ml/kg 0.06 ml/kg , repeated every 5 months ≥ 1 year
Healthy Immunocompromised / chronic liver disease HAV
vaccine HAV vaccine + 0.02 ml/kg
 Hepatitis B
 DNA virus, Hepadnaviridae family.
 Discovered in 1966.
 Also known as Dane Particle.
 HBV is present in high concentrations in blood , serum and
serous exudates and moderate concentrations in semen,
vaginal fluid and saliva
 Modes of Transmission:
 Perinatal – Vertical transmission from mother to baby
 Parentral – Transfusion of infected blood and its products,
using non sterile syringes,needles and medical instruments.
 Sexual
 Risk of transmission increases with the level of HBV DNA
in serum and HBeAg positive
In children, most important mode is vertical
transmission. 90% of these infants remain chronically
infected if untreated
 Intrauterine infection occurs in 2.5 %
HBsAg is inconsistently recovered from human milk
of infected mothers.
 Breastfeeding of non immunized infant by an infected
mother does not confer a greater risk of hepatitis than
formula feeding.
 Hepatitis B virus can cause acute and chronic
infection. Acute hepatitis B infection may last up to 6
months (with or without symptom) and infected
persons are able to pass these virus during these time.
Chronic hepatitis B is defined as persistence of HBsAg
for 6 months or more after acute infection with HBV.
 Hepatitis B virus is a complex structure with 3 distinct
antigens:
1. HBcAg- Hepatitis B core antigen.
2. HBsAg- Hepatitis B surface antigen.
 3. HBeAg- An independent protein circulating in the
blood.
Clinical features
Similar to viral hepatitis
Onset is insidious
Nausea and vomiting are uncommon, anorexia mild
Illness may be asymptamatic with minimal liver
damage in carrier state
It may be found as acute or chronic atate
Acute hepatitis B presented as Hepatitis A
Jaundice may be absent
Fulminant hepatitis common
Extra hepatic manifestations are characteristics
Rashes, Urticarai, Purpura, Arthralgia,
Polyarthritis,Nodosa, Glomerular nephritis, severe
aplastic anemia, pleural effusion , myocarditis,
Pericarditis.
Chronic hepatitis B
 CHRONIC PERSISTANT
 CHRONIC ACTIVE
o about 70%
o manifested without clinical jaundice and general
condition remains good.
o Benign in nature
o Elevated transaminase
o Recover completly
About30%
o Chronic jaundice
o Increased liver enzyme
o Liver cirrhosis and hepatic failure
Fulminant hepatitis and subfulminant hepatitis
Hepatic failure and encephalopathy

Chronic carrier hepatocellular carcinoma

Diagnosis
 History and clinical examination
 Wbc, SGPT, alkaline phosphate,
 LFT’s - Elevations of ALT and AST levels are hallmarks of
acute hepatitis. Values as high as 1000-2000 IU/L are
typical, with ALT values higher than AST values.
 Blood tests: AST, ALT, ALP,GGT, Serum proteins, PT,
Urinary bilirubin, Urinary Urobilinogen, Total serum
bilirubin.
 Serological tests: HBsAg, Anti-HBs, HBeAg, Anti-Hbe,
Anti-HBe IgM, Anti- Hbe IgG, HBV genotyping.
 Liver ultrasound: Transient elastography can show the
amount of liver damage
 Liver biopsy.
 Fibro tests
 HBsAg (also known as the Australia antigen) is the surface
antigen of the hepatitis B virus (HBV). Its presence
indicates current hepatitis B infection.
 Definitive diagnosis depends on serologic testing for HBV
infection.
 Serological Diagnosis in Hepatitis B
 Patients with signs of chronic disease may require a liver
biopsy - extent of histologic involvement and response to
therapeutic protocols.
 Pathognomonic ground glass hepatocyte inclusions
(arrows) distributed singly in a haphazard fashion with no
zoning preference.
Management
 No special treatment
 Bed rest
 General supportive measures
 Chronic persistant hepatitis no specific treatment
 Chronic active hepatitis
  Nucleoside and Nucleotide analog such as Tenofovir,
adenofovir, lamivudine.
 Interferon: Standard interferon( Intron A), Pegylated
interferon ( Peglntron,) 
 alpha interferons
 adenosine, arabinoside, acyclovir
 Fulminant hepatitis
 Antibiotic
 Ampicillin Neomycin
 Protein free diet
 Carbohydrate rich foods
 Lactulose
 Intravenous 10%glucose
 Exchange blood transfusion
 Plasmaphresis
Prevention
Active immunization
The dose of Hep B Child below 10 years 10
microgram in 0.5 ml intramuscular for recombinant
vaccine
2nd dose after one month
3rd dose after 6 month
Passive immunization
Hepatitis B immunoglobulin in post exposure
conditions like needle stick injury, mucocutaneous
exposure, neonates with hepatitis B mother
 Neonate o HBsAg positive carriers mother should receive
HBIg and HB vaccine
 IM at separate site 12-24hrs of birth followed by2nd and 3rd
dose of vaccine at one month and 6 month of age
 HB vaccine can be administered to them within 7 days of
birth for first dose
 Prevention of hepatitis B
 Hepatitis B vaccine and hepatitis B immunoglobulin
(HBIG) are available for prevention of HBV infection.
Hepatitis B Immunoglobulin
 HBIG is indicated only for specific postexposure
circumstances and provides only temporary protection
(3-6 mo) .
It plays a pivotal role in preventing perinatal
transmission when administered within 12 h of birth.
 Two single antigen vaccines (Recombivax HB and
Engerix-B) are approved for children and are the only
preparations approved for infants <6 mo old.
 Three combination vaccines can be used for subsequent
immunization dosing and enable integration of the HBV
vaccine into the regular immunization schedule.
 Seropositivity is >95% with all vaccines, achieved after
the 2nd dose in most patients. The 3rd dose serves as a
booster and may have an effect on maintaining long- term
immunity.
Prevention
 Universal precaution
 Prevention of spread of infection
 Appropriate sterilization
 Public awareness of mode of transmission
 Promotion of HB vaccination
 Screening of donar cells
 Avoidance of commercial blood donation
 Precautions to carriers
HbsAg-positive mothers?
 To prevent perinatal transmission through improved maternal
screening and immunoprophylaxis of infants born to HbsAg-
positive mothers, infants born to HBsAg-positive women
should receive vaccine at birth, 1-2 mo, and 6 mo of age.
 The first dose should be accompanied by administration of
0.5 mL of HBIG as soon after delivery as possible (within 12
hr) because the effectiveness decreases rapidly with increased
time after birth.
Post-vaccination testing for HBsAg and anti-HBs should be
done at 9- 18 mo.
 If the result is positive for anti-HBs, the child is immune to
HBV.
If the result is positive for HBsAg only, the parent
should be counseled and the child evaluated by a
pediatric gastroenterologist.
 If the result is negative for both HBsAg and anti-HBs,
a 2nd complete hepatitis B vaccine series should be
administered, followed by testing for anti-HBs to
determine if subsequent doses are needed.
 Hepatitis c
 RNA
 Flaviviridae
 6 major phenotypes
 HCV is uncommon in the pediatric population
 Seroprevalence is 0.2 % in < 11 yrs and 0.4 % in ≥ 11 yrs
 Mode of transmission – Illegal drug abuse, sexual
transmission. Blood transfusion before 1992, occupational
exposure

 Vertical transmission in children – main – 20 %

 Incubation period 7-9 weeks.
Clinical features
 Acute HCV:
 Mild, insidious onset
 Nausea
 Vomiting
 Pain abdomen
 Icterus
 Dark urine
 Chronic HCV : Most likely to progress to chronic infection
Diagnosis
 Detection of antibodies to HCV antigen by EIA ( enzyme
immune assay)
 Detection of Viral RNA by PCR. Usually detectable within 1-2
weeks of exposure.
 Anti HCV is not a protective antibody and therefore does not
confer immunity
 Acute infection - The peak serum ALT level is less than 2000
IU/mL in most patients with acute HCV infection, and 50%
have a peak serum ALT level of less than 800 IU/mL. Overall,
this peak is generally less than that seen in hepatitis A or B
infections.
 Liver biopsy – assess presence and extent of hepatic fibrosis
 Seroconversion after HCV infection may occur 6 months
after infection.
 A positive result of HCV ELISA should be confirmed with
the more specific recombinant immunoblot assay, which
detects antibodies to multiple HCV antigens.
 Detection of HCV RNA by PCR is a sensitive marker for
active infection, and results of this test may be positive 3
days after inoculation.
Management
 Children has a higher spontaneous clearance rate than
adults (45% till 19 yrs).
 Peg interferon has been approved for those > 3 yrs
 Treatment considered for those with evidence of advanced
fibrosis or injury on liver biopsy
 Current recommendation – 48 weeks of peginterferon and
ribavirin
 Those with normal biochemical profile and mild
histological change – no specific treatment
 Screen yearly with liver ultrasound and alpha fetoprotein
for HCC No vaccine yet available
 In a patient with acute hepatitis C , treatment with
Pegylated interferon within the 12-24 weeks of
infection reduce the development of chronic hepatitis
C.
 Chronic HCV: Pegylated interferon, Ribavirin
Rebetol, Protease inhibitors such as incivek and
Boceprevir.
 Hepatitis D
RNA virus
Delta virus
Defective – only can cause infection along with HBV
as it is incapable of making its own coat proteins
Co-infection or superinfection, uncommon in children
Chronic asymptomatic carriers of HBV risk
Incubation period 2-8 week
Clinical manifestations
Symptoms similar to infection with other hepatitis
viruses, but more severe.
In co infection, acute hepatitis is much more severe
than for HBV alone
In super infection, acute illness is rare, but chronic
hepatitis is common. Risk of acute liver failure is
highest
DIAGNOSIS
HDV – not yet isolated
IgM antibody to HDV – 2-4 weeks after co infection,
10 weeks after super infection
COMPLICATIONS
HDV to be considered in all cases of acute liver failure
 Hepatitis E
RNA virus
 Epidemic form of what was formerly called as non A
non B hepatitis
Transmission – faecal-oral route
Clinical features
Similar to that of HAV but more severe. Chronic
illness does not occur
Major pathogen in pregnant women – acute liver
failure with higher fatality incidence
Diagnosis
  HEV-RNA can be detected in stool from 1 week prior to
the onset of symptoms and for more than 2 weeks after the
onset.
 Detection of IgM antibody 1 week after illness
Management
 No specific HDV or HEV targeted treatments yet
 Control and treat HBV infection without which HDV
cannot induce hepatitis.
 Ongoing trials – Interferons •
 No vaccine available for both Once chronic infection is
identified,
Prevention
Safe drinking Water
Appropriate sewage disposal
General hygenic practice
 Complications
 A protracted or relapsing course may develop in 10%
to 15% of cases of HAV in adults, lasting for 6 months
with an undulating course before eventual clinical
resolution.
Fulminant hepatitis with hepatic encephalopathy,
gastrointestinal bleeding from esophageal varices or
coagulopathy, and profound jaundice is uncommon,
but is associated with a high mortality rate.
 Prognosis
• Most cases of acute viral hepatitis resolve without specific
therapy, with less than 0.1% of cases progressing to
fulminant hepatic necrosis.
• HBV, HCV, and HDV may persist as chronic infection with
chronic inflammation, fibrosis, and cirrhosis and the
associated risk of hepatocellular carcinoma.
• Five percent to 10% of adults with HBV develop persistent
infection, defined by persistence of HBsAg in the blood for
more than 6 months compared with 90% of children who
acquire HBV by perinatal transmission.
• Approximately 85% of persons infected with HCV remain
chronically infected, which is characterized by fluctuating
transaminase levels.
• Approximately 20% of persons with chronic infection
develop cirrhosis, and approximately 25% of those develop
hepatocellular carcinoma.
 In immunosuppressed patients and infants <2,000
g birthweight, a 4th dose is recommended, as is
checking for seroconversion.
Nursing management
 Imbalanced Nutrition: Less Than Body
Requirements
Insufficient intake to meet metabolic demands:
anorexia, nausea/vomiting
Altered absorption and metabolism of ingested foods:
reduced peristalsis (visceral reflexes), bile stasis
Increased calorie needs/hypermetabolic state
Monitor dietary intake and caloric count.
Encourage mouth care before
Recommend eating in upright
Encourage intake of fruit juices, carbonated beverages, and hard
candy throughout the day.
Consult with dietitian, nutritional support team to provide diet
according to patient’s needs, with fat and protein intake as tolerated.
Protein restriction may be indicated in severe disease (fulminant
hepatitis) because the accumulation of the end products of protein
metabolism can potentiate hepatic encephalopathy.
Monitor serum glucose as indicated.
Administer medications as indicated:Antiemetics: metoclopramide
(Reglan), trimethobenzamide (Tigan)
 Risk for Deficient Fluid Volume
Excessive losses through vomiting and diarrhea, third-
space shift
Altered clotting process
Monitor I&O, compare with periodic weight. Note
enteric losses: vomiting and diarrhea.
Assess vital signs, peripheral pulses, capillary refill,
skin turgor, and mucous
Check for ascites or edema formation.
Measure abdominal girth as indicated.
Use small-gauge needles for injections, applying
pressure for longer than usual after venipuncture.
Provide IV fluids (usually glucose), electrolytes.
Protein hydrolysates.
 Fatigue
Decreased metabolic energy production
States of discomfort
Altered body chemistry (e.g., changes in liver
function, effect on target organs)
 Institute bed red or chair rest during toxic state. Provide quiet
environment; limit visitors as needed.
 Recommend changing position frequently.
 Provide and instruct caregiver in good skin care.
 Do necessary tasks quickly and at one time as tolerated.
 Determine and prioritize role responsibilities and alternative
providers and possible community resources available
 Promotes problem solving of most pressing needs of individual
and family.
 Identify energy-conserving techniques: sitting to shower and
brush teeth, planning steps of activity so that all needed materials
are at hand, scheduling rest periods.
 Risk for Impaired Skin Integrity
 Chemical substance: bile salt accumulation in the tissues
 Deficient Knowledge
 Lack of exposure/recall; information misinterpretation
 Unfamiliarity with resources
 Situational Low Self-Esteem
 Annoying/debilitating symptoms, confinement/isolation,
length of illness/recovery period
 Risk for Infection
Inadequate secondary defenses (e.g., leukopenia,
suppressed inflammatory response) and
immunosuppression
Malnutrition
Insufficient knowledge to avoid exposure to pathogens
Related article
Treatment of chronic hepatitis B in children
Flavia Bortolotti
Only IFN-α has been approved for the treatment of
children with CHB. A 6-month course of IFN at a dose
of 5–6 MU/m2 thrice weekly is efficient in children
with high ALT and low viremia levels. Lamivudine
monotherapy is well tolerated, but its efficacy is also
limited to children with high ALT levels, and the
development of resistant HBV mutants has to be
weighed cautiously.
There are currently no drugs to treat children with
normal ALT and high viremia levels who are expected
to maintain long-lasting virus replication. Studies
investigating different regimens of combination of
lamivudine and IFN are under way in adults and
children. Other nucleoside analogues are currently
being investigated in adult patients