Hepatitis B (Serum Hepatitis)

Hepatitis B is the inflammation of the liver caused by hepatitis B virus.

This is considered to be more serious than hepatitis A due to the possibility of
severe complications such as massive damage and hepatocarcinoma of the
liver.
Hepatitis B is a viral infection that attacks the liver and can cause both acute
and chronic disease.About 2 billion people worldwide have been infected with
the virus and about 350 million live with chronic infection.
An estimated 600 000 persons die each year due to the acute or chronic
consequences of hepatitis B.
About 25% of adults who become chronically infected during childhood later
die from liver cancer or cirrhosis (scarring of the liver) caused by the chronic
infection.
The hepatitis B virus is 50 to 100 times more infectious than HIV.
Hepatitis B virus is an important occupational hazard for health workers.
Hepatitis B is preventable with a safe and effective vaccine.
Etiologic Agent:
The disease is caused by Hepatitis B virus
1. This virus has very limited tissue tropism
2. HBV infects the liver and possibly the pancreas.
3. HbsAg appears in the blood 30 to 60 days after exposure and
persists for variable periods of time.
Incubation Period:
The incubation period is 50 to 189 days or two to five months with a mean
equal to 90 days.
Period of Communicability:
The patient is capable of transmitting the virus during the latter part of the
incubation period and during the acute phase. The virus may persist in the
blood for many years.
Mode of Transmission:
1. Hepatitis B can be directly transmitted by person to person contact via
infected body fluids.
2. It can be transmitted though contaminated needles and syringes.
3. Transmission can occur through infected blood or body fluids introduced at
birth.
4. It can also be transmitted through sexual contact.
HBV transmission does not occur.
1. by fecal-oral route
2. by food-borne or water-borne transmission
3. by arthropod (mosquito) transmission.
Pathogenesis:
1. HBV can cause acute or chronic hepatitis.
2. Production of virus and high level of HbsAg is continuous and the particles are
found in the blood until the infections is resolved.
3. The virus must be delivered into the liver to establish infection.
4. The virus replicates and large amount of HbsAg is released into the blood.
5. Initiation of virus replication may be as short as three days from acquisition,
but symptoms may not be observed for 45 days or much longer.
6. Replication of the virus is not cytopathic and proceeds to relatively long
periods without causing liver damage.
7. During the acute phase of infection, the liver parenchyma shows degenerative
changes consisting of cellular swelling and necrosis, especially in hepatocytes.
Clinical Manifestations:
1. Prodormal period
Fever, malaise, and anorexia.
Nausea, vomiting, abdominal discomfort, fever and chills.
Jaundice, dark urine, and pale stools.
Recovery is indicated by a decline of fever and improved appetite.
2. Fulminant hepatitis may be fatal and manifested by severe symptoms like
ascitis and bleeding.
Diagnostics Procedures:
1. Compliment fixation test
2. Radio-immunoassay-hemaglutinin test
3. Liver function test
4. Bile examination in blood and urine
5. Blood count
6. Serum transaminase SGOT, SGPT, ALT
7. HbsAg
Prevention:
1. Blood donors must be screened to exclude
carriers.
2. Caution must be observed in giving care to
patients with known HBV.
3. Hands and other skin areas must be washed
immediately and thoroughly after contact
with body fluids.
4. Avoid injury with sharp objects or instruments.
5. Use disposable needles and syringes only once and discard properly.
6. Avoid sharing of toothbrush, razor, and other instruments that may be
contaminated with blood.
7. Observe safe sex.
8. Have adequate rest, sleep, and exercise and eat nutritious food.
9. Hepatitis B vaccine is recommended for pre-exposure.
10. Hepatitis Immune Globulin (HBIg) should be administered within 72 hours to
those exposed directly to hepatitis B virus either by ingestion, by prick or by
inoculation.




Viral Hepatitis
Is a viral infectionof the liver associated with a broad spectrum of clinical
manifestations from asymptomatic infection through icteric hepatitis to hepatic
necrosis.
Five forms of viral hepatits:
Type A Hepatitis (HAV)
Is caused by an RNA virus of the enterovirus family.
It spreads primarily by fecal-oral route, usually through the ingestion of
infected food or liquids.
It may also spread from person-to-person contact and, rarely, by blood
transfusion.
Type A hepatitis occurs worldwide, especially in areas with overcrowding and
poor sanitation.
Type B Hepatitis (HBW)
Is caused by a double-shelled virus containing DNA.
It spreads primarily through blood (percutaneous and permucosal route).
It can also spread by way of saliva, breast feeding, or sexual activity (blood,
semen, saliva, or vaginal secretions.
Male homosexuals are at high risk for infection.
After acute infection, 10% of patients progress on to carrier status or develop
chronic hepatitis.
HBV is the main cause of cirrhosis and hepatocellular carcinoma.
Type C Hepatitis (HCV)
Formerly called non-A, non-B hepatitis, usually spreads through blood or
blood product transfusion, usually from asymptomatic blood donors.
It may also be transmitted through unsterile piercing or tattooing tools or dyes.
It commonly affects I.V. drug users and renal dialysis patients and personnel.
HCV is the most common form of postransfusion hepatitis.
Type D Hepatitis (HDV)
Also known as Delta hepatitis.
Is caused by a defective RNA virus that requires the presence of hepatitis B-
specifically, hepatitis B surface antigen (HBsAg) to replicate.
HDV occurs along with HBV or may superinfect a chronic HBV carrier, and
cannot outlast a hepatitis B infection.
It occurs primarily in I.V. drug abusers or those who have had multiple blood
transfusions, but the highest incidence is in the Mediterranean, Middle East,
and South America.
Type E Hepatitis (HEV)
Is caused by a nonenveloped, single-strand RNA virus.
It transmitted by the fecal-oral route but is hard to detect because it is
inconsistently shed in the feces.
Its occurence is primarily in India, Africa, Asia, or Central America.
Fulminant Hepatitis
Is a rare but severe complication of hepatitis, which may require liver
transplantation.
Assessment:
Type A hepatitis
Incubation period, 3 to 5 weeks.
Prodromal symptoms: fatigue, anorexia, malaise, headache, low-grade fever,
nausea, vomiting. Highly contagious at this time, usually 2 weeks before onset
of jaundice.
Icteric phase: jaundice, tea-colored urine, clay0colored stools, right upper
quadrant pain and tenderness.
Symptoms often milder in children.
Type B hepatitis
Incubation period, 2 to 3 months.
Prodronal symptoms (insidious onset): fatigue, anorexia, transient fever,
abdominal discomfort, nausea, vomiting, headache.
May also have myalgias, photophobia, arthritis, angioedema, urticaria,
maculopapular rash, vasculitis.
Icteric phase occurs 1 week to 2 months after onset of symptoms.
Type C hepatitis
Incubation period, 6 weeks to several months.
Similar to HBV but less severe.
Type D hepatitis
Unclear incubation period.
Similar to HBV but more severe.
Applicable to all type:
Obtain a patient history. Ask about I.V. drug use, blood transfusions, contact
with infected persons (including sexual activity), travel to endemic areas, and
ingestion of possible contaminated food or water to help determine cause of
hepatitis.
Diagnostic Evaluation:
1. All forms of hepatitis; elevated serum transferase levels (aspartate
aminotransferase, lanine aminotransferase); may have abnormal clotting tests.
2. HAV: radioimmunoassay detects immunoglobulin M (IgM) antibodies to
hepatitis A virus in the acute phase.
3. HBV: radioimmunoassays detect hepatitis B surface antigen (HBsAg),
antibody to hepatitis B core antigen (anti-HBc), anti-HBsAg in various stages
of hepatitis B infection.
4. HCV: hepatitis C antibody may not be detected for 3 to 6 months after onset of
illness (used for screening); polymerase chain reactiontesting evaluates viral
activity.
5. HDV: anti-delta antibodies in the presence of HBsAg, or detection of IgM in
acute disease and IgG in chronic disease.
6. Hepatitis E antigen (with HCV ruled out).
7. If indicated, prepare the patient for liver biopsy to detect chronic active
disease, track progression, and evaluate response to therapy.
Pharmacologic Interventions:
1. Vitamin K injected subcutaneously (S.C.) if prothrombin time is prolonged.
2. I.V. fluid and electrolyte replacements as indicated.
3. Antiemetic for nausea.
4. Long-term interferon therapy in combination with oral ribavirin may produce
remission inHCV patients. Peginterferon alfa-2b is a long-acting preparation
given S.C., once per week, and ribavirin is taken twice daily.
5. Antiviral treatment is being investigated for HBV.
Nursing Interventions:
1. Monitor hydration through intake and output.
2. Monitor prothrombin time and for signs of bleeding.
3. Encourage the patient to eat meals in a sitting position to reduce pressure on
the liver.
4. Encourage pleasing meals in an environment with minimal noxious stimuli
(odors, noise, and interruptions).
5. Teach self-administration of antiemetics as prescribed.
6. Encourage rest during symptomatic phase, according to level of fatigue.
7. Encourage diversional activities when recovery and convalescence are
prolonged.
8. Encourage gradual resumption of activities and mild exercise during
convalescent period.
9. Stress importance of proper public and home sanitation and proper preparation
and dispensation of foods.
10. Encourage specific protection for close contacts.
11. Explain precautions about transmission and prevention of transmission to
others to the patient and family.
12. Warn the patient to avoid trauma that may cause bruising.
13. Stress the need to follow precautions with blood and secretions until the
patient is deemed free of HBsAg.
14. Emphasize that most hepatitis is self-limiting, but follow up is needed for liver
function tests.