Hepatitis Nursing management

June 4, 2024
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Hepatitis Nursing management

Hepatitis is an umbrella term for a variety of viral, bacterial, and noninfectious causes of widespread inflammation that results iecrosis and scaring of liver cells. Inflammation of the liver can be due to viral or bacterial invasion. Noninfectious causes include physical or toxic chemical agents (e.g., drugs, alcohol, industrial chemicals) and nonalcoholic or autoimmune hepatitis.

Viral infections can be transmitted by blood and body fluids and/or food. These viruses are designated by letters of the alphabet, (A, B, C, D, E, G) and variously used (e.g., B is known as HBV, or HepB). HCV is responsible for about 30% of viral hepatitis cases. Other causes of hepatitis include cytomegalovirus (CMV), Epstein-Barr virus (EBV), Mycobacterium avium complex (MAC), toxoplasmosis, and histoplasmosis. Studies have shown that almost 25% of persons with human immunodeficiency virus (HIV) infection also have hepatitis.

 


Hepatitis can be acute or chronic. Although most cases of hepatitis are self-limiting, approximately 5%–10% of clients with hepatitis B and 80%–85% of clients with hepatitis C progress to a chronic state. Chronic inflammation can lead to fibrotic scarring (cirrhosis) and can be fatal.

Client Assessment Database
   Data depend on the cause (type of hepatitis) and severity of liver involvement/damage.
Activity/Rest
May report: Fatigue, weakness, general malaise, muscle aches

Circulation
May exhibit: Bradycardia (severe hyperbilirubinemia)
Jaundiced sclera, skin, mucous membranes

Elimination
May report: Dark urine
Diarrhea/constipation, clay-colored stools
Current/recent hemodialysis

Food/Fluid
May report: Loss of appetite (anorexia), weight loss or gain (edema)
Nausea/vomiting
May exhibit: Ascites

Neurosensory
May exhibit: Irritability, drowsiness, lethargy, asterixis, headache

Pain/Discomfort
May report: Abdominal cramping, right upper quadrant (RUQ) tenderness
Myalgias, arthralgias; headache
Itching (pruritus)
May exhibit: Muscle guarding, restlessness

Respiration
May report: Distaste for/aversion to cigarettes (smokers)
Recent flu-like URI signs and symptoms

Safety
May report: Transfusion of blood/blood products in the past
May exhibit: Fever
Urticaria, maculopapular lesions, irregular patches of erythema
Exacerbation of acne
Spider angiomas, palmar erythema, gynecomastia in men (sometimes present in alcoholic hepatitis)
Splenomegaly, posterior cervical node enlargement

Sexuality
May report: Lifestyle/behaviors increasing risk of exposure (e.g., sexual promiscuity, sexually active homosexual/bisexual male)

Teaching/Learning
May report: History of known/possible exposure to virus, bacteria, or toxins (contaminated food, water, needles, surgical equipment or blood), carriers (symptomatic or asymptomatic), recent surgical procedure with halothane anesthesia, exposure to toxic chemicals (e.g., carbon tetrachloride, vinyl chloride)
History of known/possible exposure to hepatotoxic prescription (e.g., sulfonamides, phenothiazines, isoniazid) or OTC drug use (e.g., acetaminophen)
Use of herbal supplements associated with heptotoxicity, (e.g., chaparral, JinBuHuan, germander, comfrey, mistletoe, skullcap, margosa oil, pennyroral)
Use of street injection drugs or alcohol
Travel to/immigration from China, Africa, Southeast Asia, Middle East (hepatitis B [HBV] and C (HVC) are endemic in these areas)
Concurrent diabetes, HF, malignancy, or renal disease

Discharge plan
considerations: May require assistance at home with maintenance tasks
Refer to section at end of plan for postdischarge considerations.

Diagnostic Studies
Liver enzymes/isoenzymes: Abnormal (4–10 times normal values). However, of limited value in differentiating viral from nonviral hepatitis.
AST/ALT: Initially elevated. May rise 1–2 weeks before jaundice is apparent, then decline.
Alkaline phosphatase (ALP): Slight elevation (unless severe cholestasis present).
Hepatitis A, B, C, D, E panels (antibody/antigen tests): Specify type and stage of disease and determine possible carriers.
CBC: Red blood cells (RBCs) decreased because of shortened lifespan of RBCs (liver enzyme alterations) or hemorrhage.
WBC count and differential: Leukopenia, leukocytosis, monocytosis, atypical lymphocytes, and plasma cells may be present.
Serum albumin: Decreased.
Blood glucose: Transient hyperglycemia/hypoglycemia (altered liver function).
Prothrombin time: May be prolonged (liver dysfunction).
Serum bilirubin: Above 2.5 mg/100 mL. (If above 200 mg/100 mL, poor prognosis is probable because of increased cellular necrosis.)
Stools: Clay-colored, steatorrhea (decreased hepatic function).
Bromsulphalein (BSP) excretion test: Blood level elevated.
Liver biopsy: Usually not needed, but should be considered if diagnosis is uncertain, or if clinical course is atypical or unduly prolonged.
Liver scan: Aids in estimation of severity of parenchymal damage.
Urinalysis: Elevated bilirubin levels; protein/hematuria may occur.
Nursing Care
Nursing Priorities

1. Reduce demands on liver while promoting physical well-being.
2. Prevent complications.
3. Enhance self-concept, acceptance of situation.
4. Provide information about disease process, prognosis, and treatment needs.

Discharge Goals

1. Meeting basic self-care needs.
2. Complications prevented/minimized.
3. Dealing with reality of current situation.
4. Disease process, prognosis, transmission, and therapeutic regimen understood.
5. Plan in place to meet needs after discharge.

NURSING DIAGNOSIS: Fatigue
May be related to

Decreased metabolic energy production
States of discomfort
Altered body chemistry (e.g., changes in liver function, effect on target organs)

Possibly evidenced by

Reports of lack of energy/inability to maintain usual routines
Decreased performance
Increase in physical complaints

DESIRED OUTCOMES/EVALUATION CRITERIA—CLIENT WILL:
Endurance (NOC)

Report improved sense of energy.
Perform ADLs and participate in desired activities at level of ability.


NURSING DIAGNOSIS: imbalanced Nutrition: less than body requirements
May be related to

Insufficient intake to meet metabolic demands: anorexia, nausea/vomiting
Altered absorption and metabolism of ingested foods: reduced peristalsis (visceral reflexes), bile stasis
Increased caloric needs/hypermetabolic state

Possibly evidenced by

Aversion to eating/lack of interest in food; altered taste sensation
Abdominal pain/cramping
Loss of weight; poor muscle tone

DESIRED OUTCOMES/EVALUATION CRITERIA—CLIENT WILL:

Treatment Behavior: Illness or Injury (NOC)
Initiate behaviors, lifestyle changes to regain/maintain appropriate weight.
Nutritional Status (NOC)
Demonstrate progressive weight gain toward goal with normalization of laboratory values and no signs of malnutrition.

NURSING DIAGNOSIS: risk for deficient Fluid Volume

Risk factors may include

Excessive losses through vomiting and diarrhea, third-space shift
Altered clotting process
Possibly evidenced by
[Not applicable; presence of signs and symptoms establishes an actual diagnosis.]

DESIRED OUTCOMES/EVALUATION CRITERIA—CLIENT WILL:

Hydration (NOC)

Maintain adequate hydration, as evidenced by stable vital signs, good skin turgor, capillary refill, strong peripheral pulses, and individually appropriate urinary output.
Coagulation Status (NOC)
Be free of signs of hemorrhage with clotting times WNL.

NURSING DIAGNOSIS: situational low Self-Esteem

May be related to
Annoying/debilitating symptoms, confinement/isolation, length of illness/recovery period
Possibly evidenced by

Verbalization of change in lifestyle, fear of rejection/reaction of others, negative feelings about body, feelings of helplessness
Depression, lack of follow-through, self-destructive behavior

DESIRED OUTCOMES/EVALUATION CRITERIA—CLIENT WILL:

Self-Esteem (NOC)

Verbalize feelings.
Identify methods for coping with negative perception of self.
Verbalize acceptance of self in situation, including length of recovery/need for isolation.
Acknowledge self as worthwhile; be responsible for self

NURSING DIAGNOSIS: risk for Infection

Risk factors may include

Inadequate secondary defenses (e.g., leukopenia, suppressed inflammatory response) and immunosuppression
Malnutrition
Insufficient knowledge to avoid exposure to pathogens

Possibly evidenced by

[Not applicable; presence of signs and symptoms establishes an actual diagnosis.]

DESIRED OUTCOMES/EVALUATION CRITERIA—CLIENT WILL:

Risk Control (NOC)

Verbalize understanding of individual causative/risk factor(s).
Demonstrate techniques; initiate lifestyle changes to avoid reinfection/transmission to others.

NURSING DIAGNOSIS: risk for impaired Skin/Tissue Integrity

Risk factors may include
Chemical substance: bile salt accumulation in the tissues
Possibly evidenced by
[Not applicable; presence of signs and symptoms establishes an actual diagnosis.]

DESIRED OUTCOMES/EVALUATION CRITERIA—CLIENT WILL:

Tissue Integrity: Skin and Mucous Membranes (NOC)

Display intact skin/tissues free of excoriation.
Report absence/decrease of pruritus/scratching.

NURSING DIAGNOSIS: deficient Knowledge [Learning Need] regarding condition, prognosis, treatment, self-care, and discharge needs

May be related to

Lack of exposure/recall; information misinterpretation
Unfamiliarity with resources
Possibly evidenced by

Questions or statements of misconception, request for information
Inaccurate follow-through of instructions, development of preventable complications

DESIRED OUTCOMES/EVALUATION CRITERIA—CLIENT WILL:

Knowledge: Illness Care (NOC)

Verbalize understanding of disease process, prognosis, and potential complications.
Identify relationship of signs/symptoms to the disease and correlate symptoms with causative factors.
Verbalize understanding of therapeutic needs.
Initiate necessary lifestyle changes and participate in treatment regimen.

POTENTIAL CONSIDERATIONS following acute hospitalization (dependent on client’s age, physical condition/presence of complications, personal resources, and life responsibilities)

Fatigue—generalized weakness, decreased strength/endurance, pain, imposed activity restrictions, depression.
impaired Home Maintenance—prolonged recovery/chronic condition, insufficient finances, inadequate support systems, unfamiliarity with neighborhood resources.
imbalanced Nutrition: less than body requirements—insufficient intake to meet metabolic demands: anorexia, nausea/vomiting; altered absorption and metabolism of ingested foods; increased calorie needs/hypermetabolic state.
risk for Infection—inadequate secondary defenses; malnutrition; insufficient knowledge to avoid exposure to pathogens.

 

 

Definition:

Hepatitis A is a liver disease caused by the hepatitis A virus. This is an inflammation of the liver that is not really very severe and runs an acute course. This generally starts within two to six weeks after contact with the virus, and lasts no longer than two months. It is known as infectious hepatitis because it spreads relatively easy from those infected to close contact.

Incubation Period:

The incubation period for hepatitis A ranges from 15-60 days or three to five weeks; with a mean incubation period of 30 days.

Period of Communicability:

The infected patient is capable of transmitting the organism a week before and a week after the appearance of symptoms.

Mode of Transmission:

  1. hepatitiscarrier thumb Hepatitis AHepatitis A virus is transmitted by ingestion of contaminated drinking water or ice, uncooked fruits and vegetable, and fruits and vegetables grown in or washed with contaminated water.

  2. It is also transmitted through fecal-oral pathway.

  3. The virus is transmitted also by infected food handlers.

Groups who are at risk for Hepatitis A Virus:

  1. Children in Day Care Centers can transmit the infection through diapers and toys.

  2. Troops living under crowded conditions at military camps or in the field are at great risk.

  3. Homosexual men are increasingly at risk of HAV infection from oral-anal sexual contact.

  4. People who live in areas with breakdown sanitary conditions, such as after flood and other natural disaster.

Clinical Manifestations:

  1. Flu-like illness with chills and high fever

  2. Diarrhea, fatigue and abdominal pain
  3. Loss of appetite
  4. Nausea, diarrhea and fever
  5. Jaundice and dark-colored urine.

  6. The infection in young children is often mild and asymptomatic.

Complications:

  1. Progressive encephalopathy characterized by drowsiness and cerebral edema

  2. GIT bleeding progressing to stupor and later coma. Bleeding is not responsive to parenteral Vitamin K administration.

  3. Clonus and hyperflexia are later replaced by loss of deep tendon reflexes.

  4. Edema and ascitis
  5. Aplastic anemia.
  6. In late course of the disease, loss of corneal and papillary reflexes, elevated arterial blood, respiratory failure, to cerebrovascular collapse may be present.

Diagnostic Procedure:

  1. HAV and HBV – complement fixation rate

  2. Liver function test – to determine the presence and extent of liver damage and to check the progress of the liver

  3. Bile examination in stool and urine

  4. SGOT – serum glutamix oxaloacetic transaminase
  5. SGPT – serum glutamic pyruvic transaminase
  6. ALT – serum alanine transaminase
  7. IgM level

Treatment Modalities:

  1. There is no specific treatment, although bed rest is essential.

  2. Diet must be high in carbohydrate, low in fat, and low in protein.

  3. Patient must take vitamin supplement especially the B complex group.

  4. Intravenous therapy is occasionally necessary.

  5. Isoprinosine (methisoprenol) may enhance the cell-mediated immunity of the T-lymphocytes.

  6. Alkalies, belladonna and anti-emetics should be administered to control dyspepsia and malaise.

Nursing Management:

  1. The patient must be isolated (enteric isolation).

  2. Patient should be encouraged to rest during acute or symptomatic phase.

  3. Improve nutritional status.
  4. Utilize appropriate measures to minimize spread of the disease.

  5. Observe the patient for melena and check stool for the presence of blood.

  6. Provide optimum skin and oral care.

  7. Increase in ability to carry out activities.

    1. Encourage the patient to limit activity when fatigued.

    2. Assist the client in planning periods of rest and activity.

    3. Encouraged gradual resumption of activities and mild exercise during recovery.

Prevention Control:

  1. Hands should be washed thoroughly every after use of toilet.

  2. Travelers should avoid water and ice if unsure of their purity.

  3. Food handlers should carefully be screened.

  4. Safe preparation and serving of food must be practiced.

  5. The public should be educated on the mode of transmission of the disease.

Hepatitis A Vaccines:

  • vaccines thumb Hepatitis AThe vaccine protects against the virus in more than 95% of cases for 10 years.

  • It contains inactivated Hepatitis A virus providing active immunity against a future infection.

  • The vaccine was first phased in 1996 for children in high-risk areas, and in 1999 it was spread to areas with elevating levels of infection.

  • The vaccine is given in two doses in the muscle of the upper arm. The first dose provides protection two to four weeks after initial vaccination; the second booster dose, given six to twelve months later, provides protection for up to twenty years.

Nursing Care Plan – Hepatitis A
More About Hepatitis

What Are the Occupational Risks of Hepatitis B?

Christine M. Kukka
HBV Project Manager;

Many people infected with the hepatitis B virus (HBV) wonder if their bloodborne infection poses a health risk to others in workplace settings, such as offices, factories, health care facilities, schools or daycare centers. They wonder if it is necessary to disclose their infection to protect coworkers, students or patients.

Federal and state laws in the United States have examined this topic in-depth and have overwhelmingly concluded that any workers who might conceivably come into contact with blood or body fluids in the course of their jobs be immunized against hepatitis B and trained in standard precautions.

Standard precautions, mandated by the Occupational Safety and Health Administration (OSHA), require every worker to keep a barrier between them and anyone’s blood or body fluids. This practice must be applied to everyone, not just to those who have a diagnosed bloodborne infection such as hepatitis B or C or HIV.

Why must they be used with everyone?

Because one out of every four people infected with HIV doesn’t know s/he is infected, and only 30 percent of adults with hepatitis C know they are infected. There are many adults and children with hepatitis B who are also unaware of their infections.

With so many undiagnosed infections around, health officials require standard precautions to be used with everyone at all times. Employers must also design blood and body fluid exposure policies as if everyone was infected with HIV or hepatitis.

Because all employers, supervisors, police, teachers and daycare providers must practice standard precautions, the Centers for Disease Control and Prevention (CDC) and other agencies have stated that neither adults nor students have to disclose their infections in most workplaces, schools or daycare centers.

Standard precautions have been very successful in safeguarding everyone’s health. For example, one CDC study of police, firefighters and prison guards found their HBV infection rate was no higher than the general population, despite their increased chances of exposure to blood through accidents, fights and bites.

But what about medical settings, where accidental needle sticks and surgery and other procedures involving sharp instruments increase the odds that a patient might be exposed to the blood of an HBV-infected doctor or nurse? Does this mean HBV-infected people can’t become doctors or nurses?

Can Hepatitis B Sideline a Health Care Career?

Hepatitis B is 100-times more transmissible than HIV or hepatitis C because of the high volume of hepatitis B viruses in the blood of infected people, compared to the lower viral load in people infected with HIV or hepatitis C. A safe and effective vaccine does exist that prevents HBV infection, but unfortunately, not all patients have been immunized.

Even when health care workers practice standard precautions and are as careful as possible, there is still a chance that a doctor or nurse could cut him or herself during an “exposure-prone” medical procedure, such as surgery, and infect a patient who has not been vaccinated.

While there is no clear national policy on this topic, many medical organizations and hospitals require health care workers who perform exposure-prone procedures to be tested for HIV and hepatitis B and C. HBV-infected people who have high viral loads and the “e” antigen (HBeAg) have been restricted from performing surgery and other high-risk procedures.

But these policies vary widely between hospitals, creating much confusion and anxiety among infected health care workers. The ethics of these regulations, and their varying interpretations, continue to be hotly debated.

The CDC currently recommends that healthcare workers who are infected with HIV or HBV (and are “HBeAg” positive with high viral loads) not perform exposure-prone procedures unless they have sought “counsel from an expert review panel.”

To avoid discrimination and invasion of healthcare providers’ privacy, a number of medical ethicists have made alternate recommendations that are now under consideration. They propose that:

• Hospitals should provide hepatitis B vaccination to patients undergoing elective procedures to reduce HBV transmission risk.

• HBV-infected health care workers should practice without restrictions on patients who have already been infected with, or have been vaccinated against hepatitis B. This would avoid discrimination against infected health care workers.

• If health care workers had the option to disclose their HBV infections to susceptible patients, this could provide an opportunity for patients to choose what risks they were willing to accept in the course of their health care. Doctors and nurses could educate their patients about infectious diseases, such as HBV. Infected health care workers could then perform more exposure-prone procedures if patients agreed.

However, these policies may be of limited help to HBV-infected medical students. It would be difficult to keep their infection confidential as they rotate frequently through different departments during their training. A large number of people would need to know their practice restrictions in order to avoid putting non-immune patients at risk of contracting hepatitis B, which would violate the medical student’s privacy.

Disclosure opportunities to patients would be more difficult, because students are often requested to assist in procedures with minimal advance notice, and students do not have the same type of relationship with patients as doctors and nurses on staff.

Ironically, this same dilemma confronts medical personnel and health care students who fail to respond to a hepatitis B immunization. A small percentage of people fail to create sufficient antibodies to protect them against hepatitis B, even after two rounds of vaccination. These people remain vulnerable to infection from HBV-infected patients. In some cases, these people are discouraged from practicing medicine because of their risk.

Debate on this issue will continue, and many hope the CDC will re-examine this ethical dilemma and issue new guidelines.

 

About hepatitis C

Hepatitis C is the most common cause of chronic viral hepatitis in the United States, affecting more than 4 million patients and contributing to liver diseases such as fibrosis, cirrhosis, liver failure, and liver cancer.1,2 Up to 85% of people infected with hepatitis C virus (HCV) eventually develop chronic liver disease.1 The rest clear the virus without treatment and remain free from chronic disease.

Because HCV has at least six major genotypes with 50 known subtypes, researchers haven’t been able to develop a vaccine.1,3 Genotype 1 is the most prevalent, followed by genotypes 2 and 3 (more on genotyping later). The virus is spread via blood and body fluids; I.V. drug abuse is now the most common mode of transmission, accounting for about 60% of new cases. Before 1992, when HCV screening of donated blood was instituted, blood transfusions were a major source of HCV transmission.3,4

Unlike hepatitis B, HCV is rarely transmitted sexually. Sexual transmissions account for less than 5% of cases with an increase in incidence in individuals who participate in risky sexual practices.1 Other sources of transmission include maternal-fetal transmission.4 Currently, the prevalence of HCV is highest in adults ages 25 to 40 and in African-Americans and Mexican-Americans.3

The good news is that since testing blood for HCV began in 1992, the annual incidence of HCV has decreased more than tenfold. In the 1980s, almost a quarter-millioew cases of HCV were diagnosed each year in the United States; by 2006, that figure had declined dramatically to 19,000 new cases.5

The incubation period for HCV can be lengthy, with a mean of 50 days and a range of 15 to 120 days. In up to 80% of patients, the acute disease is asymptomatic or only mildly symptomatic, so most people don’t realize they have HCV. Symptoms of acute or chronic disease include nausea, loss of appetite, right upper quadrant abdominal pain, fatigue, muscle and joint pain, dark urine, and jaundice.

When HCV goes chronic

Chronic liver disease can take up to 20 or more years to develop, as was the case with Mr. Carleton. The virus attacks the hepatocytes, which stimulates release of inflammatory mediators. Iormal, healthy patients, repair and replacement of hepatocytes is in balance; in patients with HCV, the repairing process can overwhelm the replacing process, leading to abundant scar tissue (fibrosis). This fibrosis interferes with normal liver function.

If fibrosis continues to develop, cirrhosis (severe scarring) occurs. Fibrosis, depending upon the extent, may be reversible; cirrhosis isn’t. Besides interfering with normal hepatic functioning, cirrhosis also impedes circulation through the liver and causes portal hypertension, which further impairs liver function.

An estimated 70% of patients with chronic HCV infection eventually develop chronic liver disease, such as fibrosis. About 20% of those develop cirrhosis and about 3% of patients with cirrhosis develop hepatocellular carcinoma or liver cancer. In the United States, HCV is the most common indication for liver transplantation. Of patients with chronic HCV, between 1% and 5% die each year.1,3,5,6

Determining disease extent

To confirm HCV and determine the extent of the disease, various diagnostic tests may be ordered. (For information on screening, see Screening: For high-risk patients only.)

* Testing for HCV antibodies is the first step for a patient suspected of having HCV. Presence of the anti-HCV antibody (via enzyme immunoassay technology) indicates past exposure; this result stays positive even in the 15% of patients who eventually clear the virus from their bodies, so this screening tool doesn’t confirm chronic infection.1,4 The new Prism HCV test is the first fully automated test for HCV antibodies.

In general, all patients with a positive anti-HCV test should have additional testing to confirm HCV infection and to determine if the disease is chronic.

* Confirming HCV infection and determining viral load is the next step. A positive Western blot test confirms that the patient has been infected with the virus but doesn’t confirm if the infection is cleared, dormant, or active. The HCV RNA polymerase chain reaction (PCR) test can help determine if the infection is past or current. However, a single PCR reading is of little value because some people can display intermittent viremia, or presence of the virus in the blood.

Quantitative testing via PCR measures viral load, or how much of the virus is in the body. (This same test can assess treatment progress, as treatment should reduce the viral load.) A high viral load is considered a value equal to or greater than 800,000 IU/mL. Viral load also can be quantified by branched-chain DNA. The patient’s initial viral load levels don’t indicate disease severity or prognosis.

* HCV genotyping helps determine the viability of antiviral therapy. Of the six genotypes identified to date, genotype 1 accounts for about 75% of cases, but it’s the genotype least likely to respond to antiviral therapy. Patients with genotypes 2 and 3 are two to three times more likely to respond to interferon-based therapy than those with genotype 1.4

* Testing for hepatocellular carcinoma is done by assessing serum levels of alpha-fetoprotein and performing regular abdominal ultrasounds or computed tomography scans.1

* Hepatitis B and HIV often are also present in patients with HCV, so testing for each of these diseases is also indicated.

* Liver biopsy isn’t necessary for diagnosis, but the healthcare provider may order it if he’s unsure whether treatment is feasible or when alanine aminotransferase (ALT) levels remain elevated after treatment.4 Biopsy results also are used to grade the severity of disease and stage the degree of fibrosis and cirrhosis and to confirm cancer. Liver biopsy may also help the provider to evaluate treatment progress and decide whether to stop or continue treatment.

Rare complications of liver biopsy include hemorrhage, infection, and puncture of other organs. Administer analgesics as prescribed to manage pain during and after the procedure.

* Fibrosis tests, although still experimental, eventually may be an intermediate alternative for patients who aren’t good candidates for liver biopsy.6 One of these tests is elastrography, a noninvasive measurement of liver stiffness. Sound or magnetic waves are passed through the liver; measuring the speed at which they return determines the liver’s elasticity or stiffness, an indirect measurement of fibrosis.

In patients whose disease has become active, aspartate aminotransferase and ALT measurements may be double or triple the normal levels. Even if your patient has a minimal rise in ALT values, HCV testing may be ordered because up to 40% of patients with chronic HCV have normal serum ALT levels, even when tested on multiple occasions.6

Treating HCV

A hepatologist or other practitioner specializing in treating hepatitis or liver diseases is best qualified to treat HCV. Treatment carries potential complications, and patients may have risk factors that might interfere with a positive outcome, such as continued I.V. drug abuse. However, treatment is recommended for all patients who have fibrosis or moderate to severe inflammation and necrosis on liver biopsy. Patients with less severe disease should be offered treatment on an individual basis.

If the patient has cirrhosis, therapy isn’t likely to improve survival or quality of life. Because HCV seems to be more rapidly progressive than HIV, patients coinfected with HIV should be treated for HCV if there are no contraindications.7 Patients coinfected with hepatitis B virus also should be treated for HCV.

Treatment is most likely to succeed in patients with HCV genotypes 2 or 3, women, patients under age 40, and those who don’t use alcohol or have cirrhosis.3 Because there’s no cure, the goal is to manage viral levels.

A combination regimen of ribavirin, an oral antiviral agent, and pegylated interferon (peginterferon) is used to treat HCV. Peginterferon is produced by adding a large inert molecule of polyethylene glycol to alfa interferon, prolonging the drug’s half-life and making it more active.7

Contraindications to peginterferon treatment include severe depression or other psychiatric states that may put the patient at risk for worsening psychiatric problems or suicide, continuing alcohol or drug abuse, and poorly controlled autoimmune disease. Contraindications to ribavirin treatment include significant anemia, renal disease, and cardiovascular disease. Both drugs are contraindicated in patients at risk for pregnancy secondary to unreliable contraception because of the risk of birth defects.7

All patients receive weekly subcutaneous doses of peginterferon alfa-2a in a fixed dose or alfa-2b in a weight-based dose.7 Patients with HCV genotype 1 receive a daily oral dose of ribavirin along with the peginterferon for 48 weeks. Progress (determined by the level of HCV RNA in the blood) is checked at 12 weeks; if no progress is being made, the patient and practitioner may elect to stop treatment.

Patients with genotypes 2 or 3 receive ribavirin along with the peginterferon for 24 weeks. The difference in length of treatment and dosing is consistent with the greater difficulty of achieving viral suppression in genotype 1.5

A complete course of treatment will result in a negative HCV RNA in 50% of patients with genotype 1 and 80% of those with genotype 2 or 3.5 Treatment success is defined as no detectable HCV RNA in the serum for 6 to 12 months after treatment is completed.3,7

Coping with adverse reactions

In general, the use of peginterferon and ribavirin is much like the use of chemotherapy in cancer, with many similar mental and physiologic adverse reactions.

Treatment with peginterferon can be difficult. After each treatment, the patient may experience flulike symptoms for the first 48 hours, transient gastrointestinal symptoms (such as nausea and vomiting), central nervous system symptoms (such as headache, irritability, and depression), rashes, and alopecia. Other possible adverse reactions include bone marrow suppression and worsening depression and anxiety. The most common adverse reaction to ribavirin is hemolytic anemia, but neutropenia may also occur.

Some adverse reactions may be handled symptomatically; for example, antiemetics for nausea or antidepressants for depression or anxiety. Ibuprofen can be given for fever or pain. If your patient develops anemia, he may need to discontinue ribavirin. Teach him about adjunct medications for symptom control and to eat small, frequent meals to help reduce nausea.

Dealing with refractory disease

A patient whose HCV viral load doesn’t decrease with drug therapy should work with his healthcare provider to determine whether to consider treatment a failure or to continue therapy indefinitely. If he’s tolerated peginterferon well, for example, he may elect to continue treatment with peginterferon indefinitely.

Cost may be a factor for a patient considering indefinite therapy: Peginterferon costs more than $20,000 for the first 48 weeks of treatment. Multiplying this out over a lifetime is a huge expense that’s unlikely to be covered by insurance.8 Long-term outcomes of this approach aren’t known at this time.7

Often, treatment for HCV isn’t well tolerated. Up to 40% of patients need additional medications to combat adverse reactions. If the dosage has to be reduced because of adverse reactions, the likelihood of eradicating the virus also decreases. In addition, the virus resurfaces in about 20% of patients for whom initial therapy was effective. Research is continuing into more effective and better-tolerated treatments.2

Helping your patient

Mr. Carleton is diagnosed with HCV genotype 2 and early signs of fibrosis. Reassure him that this genotype is one of the most treatable and teach him and his family about HCV therapy.

Mr. Carleton has been prescribed a course of treatment with peginterferon and ribavirin. Teach him about his medications, including adverse reactions. Encourage him to keep all of his clinic and lab appointments to monitor his response to treatment as indicated by liver function and HCV viral load. While Mr. Carleton is on HCV therapy, monitor for coagulopathies, anemia, and nutritional deficiencies.

Refer the Carletons to psychological counseling. Because of his history of PTSD and substance abuse, Mr. Carleton is at risk for a relapse of destructive behaviors and depression. Enlist the help of social services to find support groups and other help for him and his family.

Teach him about preventing the spread of HCV. For example, he shouldn’t share items that may carry his blood, such as toothbrushes and razors. Tell him to keep cuts and scrapes clean of blood and covered, and to dispose of bloody first-aid materials properly (for example, in a lidded container or by double bagging) to avoid contaminating another person. Because of his HCV, he won’t be permitted to donate blood or tissue. Let him know that the risk of sexual transmission of HCV in monogamous relationships is very low, but he should still use a condom.9

To prevent worsening liver disease, teach Mr. Carleton to avoid alcohol and medications that are metabolized through the liver, such as acetaminophen. Tell him to talk with his healthcare provider before taking any medication, including nonprescription and herbal products. The healthcare provider can weigh risks and benefits of medications that are metabolized by the liver or that could impair liver function. If the healthcare provider approves the use of a medication, he’ll monitor the patient’s liver function tests closely.

Provide information about appropriate nutrition and weight control. Although no specific diet has been shown to be beneficial in treating HCV, encourage a balanced diet that includes protein, fruits, and vegetables and is low in cholesterol, fats, carbohydrates, and simple sugars. Tell your patient to avoid alcohol and limit caffeine to no more than 2 cups a day. (Limiting caffeine has been shown to reduce hospitalization and mortality in patients with chronic liver disease.) Encourage him to drink adequate fluids.

Tell your patient to practice immune-boosting activities such as using good hygiene; getting exercise, enough rest, and adequate nutrition; avoiding stress; and getting the influenza and pneumonia immunizations. Because Mr. Carleton tested negative for hepatitis B, encourage him to get that vaccine.9 (Patients with cirrhosis also should have an annual influenza vaccination and vaccinations against pneumococcal pneumonia and hepatitis A and B.)

Encourage any patient to stop drinking and avoid risky behaviors that may lead to transmission of HCV and other pathogens, such as recreational use of I.V. drugs or intranasal cocaine and unsafe sexual practices. If a patient continues to use illicit drugs, urge him not to share needles and other equipment. Also tell patients not to obtain tattoos or body piercing from anyone who doesn’t use disposable instruments or an appropriate sterilization unit.

To protect yourself, use standard precautions with every patient, perform frequent hand hygiene, appropriately handle and dispose of sharps, and appropriately contain and clean up blood and body fluid spills. Remind other healthcare professionals to do the same.

A brighter future

Mr. Carleton and his wife sought counseling about hepatitis and depression. Working with his healthcare team, his HCV went into remission. By understanding HCV and how it’s managed, you can help your patient take an active part in coping with this chronic condition.

For high-risk patients only

Screening for HCV isn’t routine and isn’t recommended by the U.S. Preventive Services Task Force because data haven’t shown that it improves long-term health outcomes.5 However, patients in these higher-risk categories should be considered for screening:

* history of I.V. drug abuse

 

Figure. No caption available.

* chronic hemodialysis

* history of a blood transfusion before June 1992

* living in the same household with a patient with HCV

* sexual partner of a person with HCV who’s ionmonogamous relationships

* history of sharing intranasal devices for cocaine

* history of liver disease

* healthcare providers who received a needle-stick injury from a person with HCV.5

Screening for exposure to blood or body fluids from a person known to have HCV begins at baseline (immediately after exposure) and is repeated again at 4 to 6 months if the first test result is negative. The HCV RNA test can be used at 4 to 6 weeks for earlier screening.5

 

Hepatitis D and E

Authors: Craig V. Towers, M.D., Patricia D. Hastings, RN, BSN, MSN

Objectives: Upon the completion of this CNE article, the reader will be able to:

  1. Discuss the potential clinical impact of Hepatitis D and Hepatitis E infections and how patients are diagnosed.

  2. Describe how Hepatitis D and Hepatitis E are transmitted and discuss the effects of these viral infections on pregnancy and the risk of vertical transmission.

  3. Discuss the current treatment options for Hepatitis D and Hepatitis E infected individuals, the limitations of treatment, and the potential for future prevention.

Background and Significance of Hepatitis D

The first virus identified that caused hepatitis, was Hepatitis B, discovered in 1965. This was followed a few years later by the discovery of Hepatitis A in 1973. The Hepatitis D virus (HDV) or delta agent was the third hepatitis virus discovered. The first report on HDV was by Rizzetto and colleagues in Italy in 1977. The virus was identified within the liver cell of a patient who had hepatitis B, but it was distinct from the hepatitis B viral DNA (deoxyribonucleic acid). The viral particle was eventually found to be a defective RNA (ribonucleic acid) virus that was 35 to 37 nanometers in diameter but was encapsulated by the hepatitis B surface antigen protein coating. It is considered to be a defective virus because it requires a co-infection with hepatitis B in order to support its replication. It is not seen in the presence of anti-HBsAg (the antibody to the surface antigen of hepatitis B) or as an infection by itself.

Three distinct genotypes have been cloned. Genotype I is the most common and has been found worldwide. Genotype II has primarily been found in Japan and other Asian countries, whereas genotype III is primarily found in South America.

An infection with Hepatitis D can develop in 3 separate ways. It can occur as an acute infection simultaneously with an acute hepatitis B infection; or it can present as an acute infection superimposed upon a chronic hepatitis B infection; and lastly it can be a chronic hepatitis D infection superimposed upon a chronic hepatitis B infection. Hepatitis D appears to compete somewhat with Hepatitis B in these co-infections, because the HBV-DNA titer often decreases when an individual becomes infected with HDV.

Even though this virus has been known for nearly 25 years, the significance of its impact on healthcare is still relatively undefined. One of the reasons for this issue is that the virus cannot exist without a co-infection with Hepatitis B. Therefore, the majority of research has focused on Hepatitis B. However, a combined acute Hepatitis B / Hepatitis D infection will often take on a more fulminant course when compared to an acute hepatitis B virus infection alone. In addition, in patients who have a chronic Hepatitis B / Hepatitis D infection, about 75% will ultimately develop cirrhosis and up to 25% of these will eventually die from hepatic failure.

Patients with chronic Hepatitis B infections are at risk for developing hepatocellular carcinoma in the future. Surprisingly, the patients with hepatocellular carcinoma are usually HDV negative. One explanation for this finding is that HDV may somehow inhibit the development of hepatocellular cancer. However, because patients with chronic HBV / HDV infections often progress to cirrhosis quicker than those who are only HBV infected, another explanation may be that the time needed for developing hepatocellular carcinoma is lacking.

Diagnosis of Hepatitis D

Originally, the diagnosis of an acute Hepatitis D infection required the detection of the delta antigen in hepatic tissue obtained by liver biopsy. Today, reverse transcription polymerase chain reaction testing or RT-PCR-HDV can be used to detect the presence of the virus. Antibody testing can also be obtained and both IgM anti-HDV and IgG anti-HDV tests are available. For HDV, one of the difficulties is that the IgM antibody can remain positive for years. Therefore, a positive IgM antibody does not always signify a new infection. It must also be stated that the patient has to be HBsAg positive.

Another interesting finding is that an IgG antibody does not develop in every case. For example, if a person is infected acutely with Hepatitis B and Hepatitis D, they will be positive for HDV by the RT-PCR test and will also have a positive IgM antibody. However, if the infected individual develops immunity to the acute Hepatitis B infection by producing anti-HBsAg and their HBsAg becomes negative, the person’s RT-PCR-HDV and IgM for HDV will also become negative (because HDV cannot exist without HBsAg). In some of these cases, an IgG antibody has not formed and therefore, no serologic marker for a prior HDV infection remains. When the IgG antibody does develop, it will usually remain positive in patients who become chronically infected and can persist for years in cases where the patient has become immune.

Diagnosing an acute HDV infection on top of a chronic HBV infection can be difficult, because the IgM antibody can remain positive for years in some patients. However, an acute HDV infection (in a chronic HBV infected individual) is assumed if the patient shows an elevation in their liver function tests in conjunction with a positive RT-PCR-HDV and a positive IgM anti-HDV test. Some researchers suggest obtaining serial titers of anti-HDV antibodies to better differentiate acute from chronic infections. If the patient has a positive RT-PCR-HDV test for more than 6 months, they are assumed to have a chronic HDV infection.

Transmission of Hepatitis D

Transmission of Hepatitis D is similar to that of Hepatitis B. In areas of high concentration, such as the Mediterranean and northern parts of South America, it appears that transmission involves both the percutaneous route (illicit IV drug usage and blood products) as well as the permucosal route (through intimate contact, etc). In areas where HDV is not endemic, the primary route of transmission is percutaneous.

Blood and blood products in the United States are not tested for HDV because the virus cannot live without the presence of HBsAg. Blood is always tested for Hepatitis B and if absent, there is essentially no risk of transmitting HDV.

Vertical Transmission of Hepatitis D

Vertical transmission of the Hepatitis D virus from a mother to her child has also been documented; however, the complete significance of this is unknown. Very few pregnant women with an ongoing HDV infection have been studied. Therefore, the true incidence of transmission in pregnant women with a dual infection is not known. However, as stated several times before, HDV requires an infection with HBV. Therefore, if the child does not become HBV infected, then perinatal HDV infection cannot occur. Unfortunately, because a dual infection in adults is usually more severe than an HBV infection alone, likewise, a dual infection in a child is usually more severe.

In the cases where vertical transmission has occurred, there is no evidence of in utero passage of the virus. Like Hepatitis B, if perinatal transmission occurs, it probably occurs at the time of delivery. Therefore, appropriate immunization of the newborn in cases where a mother is HBsAg positive will also minimize the potential for HDV transmission.

Treatment of Hepatitis D

Unfortunately, for patients with an active HDV infection, no specific treatment has been found that greatly impacts the disease course. Currently, most specialists use interferon alpha therapy. However, as seen with Hepatitis B, relapse is common when treatment is discontinued. In addition, several researchers have studies the potential benefit of using Lamivudine, a treatment that has be used for Hepatitis B. In these cases, the HBV-DNA titers fell when Lamivudine was administered. Unfortunately, it did not appear to affect the viral load of HDV.

Therefore, the best treatment against HDV is prevention. If children and adults are vaccinated with the Hepatitis B vaccine and become immune, they cannot become infected with Hepatitis D. If a person is acutely exposed to Hepatitis B, the treatment involves the use of hepatitis B immunoglobulin (HBIG) followed by the vaccine series. Therefore, if an individual is susceptible, and is exposed to someone with a dual infection, the acute treatment is still HBIG; no hepatitis D immunoglobulin is available.

Background and Significance of Hepatitis E

The first report on this new virus actually occurred in 1957 when approximately 30,000 cases of hepatitis developed in Delhi, India in the winter of 1955-56 following a sewage contamination of the city water. The virus appeared to have an oral-fecal spread and did not have an apparent chronic disease state. The pattern and course of the infection were very similar to Hepatitis A but testing that was performed later revealed that it was something different. The disease was eventually called epidemic enterically transmitted Non-A, Non-B hepatitis.

Between 1984 and 1988, several researchers described the detection of virus-like particles by immune electron microscopy in fecal specimens of patients with enterically transmitted Non-A, Non-B hepatitis. In 1989, the detection of a viral antigen in liver tissue using an immunofluorescent method was described. Reyes et al eventually reported the isolation of the virus in 1990. It was found to be a 32 to 34 nanometer, single stranded, non-enveloped RNA virus that was distinct from the other hepatitis viruses and was labeled Hepatitis E (HEV).

The majority of literature on this viral infection in the early 1990’s came from epidemics and sporadic cases seen in Asia, North Africa, and Mexico. In addition, the only cases seen in the United States occurred in individuals who had contracted the virus while traveling in countries where the virus was endemic. However, in the past 5 years, numerous sporadic cases have been reported in Europe, the United Kingdom, South America, and the United States in people who have not traveled and have no explanation for developing the infection. Because of the explosion in viral study and DNA / RNA sequencing, it has now been suggested that several genotypes of HEV may exist due to significant differences between isolates. The first two and most prevalent genotypes are the Asian/Burmese (genotype 1) and the Mexican (genotype 2). The United States genotype is 3 and there may be up to 6 others from China, Argentina, Europe, and North Africa. In addition, recently an HEV-like virus was isolated from swine in Iowa, which could represent a potential for human exposure in and around farm operations.

Hepatitis E has a relatively short incubation of 4 to 10 weeks with a mean of 40 to 45 days. Initially, the knowledge of this virus came from studies involving acute infections and it was assumed that the majority of individuals who contracted the virus had clinical symptoms. However, prevalence studies are now occurring and evidence of past infection in groups of individuals from endemic countries is as high as 50% to 60%, many of which had no symptoms. In addition, seroprevalence rates ion-endemic countries ranges from 1% to 10% (again, most individuals reporting no symptoms). Therefore, many infections are probably sub-clinical, similar to Hepatitis A.

In endemic countries, such as India, Hepatitis E is responsible for nearly half of the acute cases of hepatitis. One has to question why infection with this virus seems to be on the rise or is now playing a major role in cases of acute hepatitis. Some of this is due to the fact that healthcare providers and researchers are now testing for this virus; however, it is also possible that something genetically has changed and the virus has become more pathologic over time.

Diagnosis of Hepatitis E

The diagnosis of an HEV infection is by clinical presentation in conjunction with positive serology. Usually, Hepatitis A, B and C are ruled out first. An anti-HEV by fluorescent antibody blocking assay or by enzyme-linked immunosorbent assay (ELISA) can detect IgG and IgM antibodies. A positive IgM antibody is indicative of acute infection and this antibody usually disappears within 3 to 6 months. The IgG antibody will usually stay positive and current research shows that it remains for years.

The virus can also be detected in the blood by polymerase chain reaction (PCR) testing; however, this test is usually only performed in research laboratories. The presence of the virus in blood and stool seems to occur about 1 to 2 weeks before the onset of clinical symptoms, if symptoms develop. Viral shedding in the stool on average only lasts for about 2 to 4 weeks; however, in rare cases, fecal shedding has been reported to last up to 7 weeks. Likewise, viremia is also relatively short and in most cases is no longer detected by the time of biochemical resolution. However, as seen with stool shedding, rare cases of viremia have been reported to last for up to 16 weeks.

Transmission of Hepatitis E

When large epidemics of acute HEV occur, the majority of these almost always trace the source to contaminated drinking water (an oral-fecal spread like Hepatitis A). However, unlike Hepatitis A, these studies do not appear to show much person-to-person transmission. Therefore, though not completely tested, transmission from saliva or through intimate contact during acute infections seems uncommon. How transmission occurs in sporadic cases is not completely understood. Because an HEV-like virus has been detected in some swine, it may be shown that some transmissions occur from an animal or insect vector. This possibility, however, has not been proven to date. Finally, because there is no known chronic carrier state, transmission through blood and blood products is minimal. The only potential for this avenue of transmission would be if blood were donated when an individual was viremic.

Based on clinically apparent infections, the highest attack rate seems to occur in young adults between the ages of 15 and 40. The mortality rate (in the non-pregnant population) is also low ranging from 0.05% to 0.5% overall and is basically only seen in cases that become fulminant.

Vertical Transmission of Hepatitis E

Hepatitis viral infections in general are not any more severe in women who are pregnant compared to the non-pregnant state; however, this virus acts differently. In the pregnant population in endemic countries, the attack rate is higher if a woman is pregnant and the mortality rate is increased, reaching as high as 25% in some studies. Whether this increase in severity seen in pregnancy is due to the pregnancy itself or the poor living conditions and malnutrition that is often seen in these populations is uncertain. In the case of pregnancy, the development of fulminant hepatitis needs to be closely observed.

Furthermore, vertical transmission of this virus has been reported though the true incidence is unknown due to small numbers. Khuroo et al described 10 women in India who developed acute HEV in the third trimester. Six of these women developed fulminant hepatic failure and 3 died (two of which were undelivered). In the evaluation of the 8 delivered infants, 5 (63%) showed strong evidence for transplacental infection with positive cord blood for HEV RNA by PCR (all 5), elevated liver enzymes at birth (all 5) and positive IgM antibody (3 of 5). Two of these neonates died and on autopsy, one showed massive hepatic necrosis. All 8 neonates were positive for IgG antibody, as would be expected since IgG antibodies can cross the placenta. The 3 surviving infected neonates remained IgG positive. Two apparently uninfected infants cleared antibody at 3 and 6 months. The final case was still IgG positive at 6 months. Other studies on pregnant women with fulminant Hepatitis E have fetal loss rates reaching 50%. Again, the reason for these high fetal loss rates may be partly due to the living conditions and nutritional status of these pregnant women.

Treatment of Hepatitis E

At the present time, no treatment has been described for an acute HEV infection other than supportive care. Standard immune globulin for household contacts is of little or no benefit because significant antibody levels to HEV have not been detected in immune globulin. Future treatment will probably require a separate HEV immune globulin that may need to be developed from plasma obtained in endemic areas where a high concentration of IgG antibody is detected.

The development of a vaccine will also be beneficial to travelers and could also prove useful in immunizing children who live in highly endemic areas. However, an effective vaccine is currently not available.

Some unanswered questions still exist for this virus. During acute infection, is the virus found in other body fluids such as saliva, semen, and vaginal secretions? Can the virus be transmitted between children in daycare settings like Hepatitis A? Can the virus be transmitted sexually during the acute phase of viremia? Is this infection more fulminant for pregnant women and their unborn babies if it develops in industrialized countries such as the United States?

What is becoming apparent is that the detection of this virus is occurring in all continents. In addition, there is some suggestion that there could be an animal or insect vector. Because of this, healthcare professionals should remain cognizant of this virus.

 

 

  • Is a viral infection of 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 reaction testing 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.

Related Nursing Articles

  1. Hepatitis D – Delta HepatitisHepatitis D is a defective RNA that appears to replicate only with the hepatitis B virus. It requires HbsAg to replicate. It occurs along with Hepatitis B or may superinfect a chronic HBV carrier. It…
  2. Hepatitis CHepatitis C (HCV) was formerly called non-A, non-B hepatitis and is an RNA virus. It is not related to any virus that cause hepatitis. Usual mode of transmission is through blood and blood products, including:…

  3. 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…

  4. Hepatitis EIt was in 1980 that hepatitis E was discovered to be distinct from other types of hepatitis. This type of hepatitis is caused by Hepatitis E virus. The Hepatitis E virus is described to be…
  5. Nursing Care Plan – Hepatitis AHepatitis A, (formerly known as infectious hepatitis), is an acute infectious disease of the liver caused by Hepatitis A virus, which is most commonly transmitted by the fecal-oral route via contaminated food or drinking water….

 

 

 

 

 

 

 

 

 

References or Suggested Reading:

  1. Rizzetto M, Canese MG, Arico S, et al. Immunofluorescence detection of a new antigen/antibody system (delta/anti-delta) associated with hepatitis B virus in liver and serum of HBsAg carriers. Gut 1977;18:997-1003.

  2. Rizzetto M. The Delta Agent. Hepatology 1983;3:729-37.

  3. Wu JC, Choo KB, Chen CM, et al. Genotyping of hepatitis D virus by restriction-fragment length polymorphism and relation to outcome of hepatitis D. Lancet 1995;346:939-41.

  4. Jacobson IM, Dienstag JL, Werner BG, et al. Epidemiology and clinical impact of hepatitis D virus (delta) infection. Hepatology 1985;5:188-91.

  5. Shattock AG, Irwin FM, Morgan BM, et al. Increased severity and morbidity of acute hepatitis in drug abusers with simultaneously acquired hepatitis B and hepatitis D virus infections. Br Med J 1985;290:1377-80.

  6. Caredda F, Rossi E, Monforte A, et al. Hepatitis B virus-associated co-infection and super-infection with delta agent: Indistinguishable disease with different outcome. J Infect Dis 1985;151:925-28.

  7. Farci P, Gerin JL, Aragona M, et al. Diagnostic and prognostic significance of the IgM antibody to the hepatitis delta virus. JAMA 1986;255:1443-6.

  8. Smedile A, Dentico P, Zanetti A, et al. Infection with the delta agent in chronic HBsAg carriers. Gastroenterology 1981;81:992-7.

  9. Bart PA, Jacquier P, Zuber PL, et al. Seroprevalence of HBV (anti-HBc, HBsAg and anti-HBs) and HDV infections among 9006 women at delivery. Liver 1996;16:110-6.

  10. Huang YH, Wu JC,
    Sheng WY

    , et al. Diagnostic value of anti-hepatitis D virus (HDV) antibodies revisited: a study of total and IgM anti-HDV compared with detection of HDV-RNA by polymerase chain reaction. J Gastroenterol Hepatol 1998;13:57-61.

  11. Lau DT, Doo E, Park Y, et al. Lamivudine for chronic delta virus. Hepatology 1999;30:579-81.

  12. Wolters LM, van Nunen AB, Honkoop P, et al. Lamivudine-high dose interferon combination therapy for chronic hepatitis B patients co-infected with the hepatitis D virus. J Viral Hepat 2000;7:428-34.

  13. Vashwanathan R. Infectious hepatitis in Delhi (1955-1956): a critical study: epidemiology. Indian J Med Res 1957;45(suppl):1-30.

  14. Enterically Transmitted Non-A, Non-B Hepatitis-Mexico. MMWR 1987;36:597-602.

  15. Enterically Transmitted Non-A, Non-B Hepatitis – East Africa. MMWR 1987;36:241-44.

  16. Hepatitis E Among U.S. Travelers, 1989-1992. MMWR 1993;42:1-4.

  17. Sreenivasan MA, Arankalle VA, Sehgal A, Pavri KM. Non-A, non-B epidemic hepatitis; visualization of virus-like particles in the stool by immune electron microscope. J Gen Virol 1984;65:1005-7.

  18. Arankalle VA, Ticehurst J, Sreenivasan MA, et al. Aetiological association of a virus-like particle with enterically transmitted non-A, non-B hepatitis. Lancet 1988;1:550-4.

  19. Bradley DW, Krawczynski K, Cook EH, et al. Enterically transmitted non-A, non-B hepatitis: serial passage of disease in cynomolgus macaques and tamarins and recovery of disease associated 27- to 34-nm virus-like particles. Proc Natl Acad Sci USA 1987;84:6277-81.

  20. Krawczynski K, Bradley DW. Enterically transmitted non-A, non-B hepatitis: identification of virus associated antigen in experimentally infected cynomolgus macaques. J Infect Dis 1989;159:1042-9.

  21. Reyes GR, Purdy MA, Kim JP, et al. Isolation of a cDNA from the virus responsible for enterically transmitted non-A, non-B hepatitis. Science 1990;24:1335-9.

  22. Goldsmith R, Yarbough PO, Reyes GR, Frey KE, et al. Enzyme-linked immunosorbent assay for diagnosis of acute sporadic hepatitis E in Egyptian children. Lancet 1992;339:328-31.

  23. Favorov MO, Fields HA, Purdy MA, et al. Serologic identification of hepatitis E virus infections in epidemic and endemic settings. J Med Virol 1992;36:246-50.

  24. Ecker JC, Desai SM, Schlauder GG, et al. A hepatitis E virus variant from the United States: molecular characterization and transmission in cynomolgus macaques. J Gen Virol 1999;80:681-90.

  25. Schlauder GG, Frider B, Sookoian S, et al. Identification of 2 novel isolates of hepatitis E virus in Argentina. J Infect Dis 2000;182:294-7.

  26. Karetnyi YV, Gilchrist MJ, Naides SJ, et al. Hepatitis E virus infection prevalence among selected populations in Iowa. J Clin Virol 1999;14:51-5.

  27. Li TC, Zhang J, Shinzawa H, et al. Empty virus-like particle-based enzyme-linked immunosorbent assay for antibodies to hepatitis E. J Med Virol 2000;62:327-33.

  28. Madan K, Gopalkrishna V, Kar P, et al. Detection of hepatitis C and E virus genomes in sera of patients with acute viral hepatitis and fulminant hepatitis by their simultaneous amplification in PCR. J Gastroenterol Hepatol 1998;13:125-30.

  29. Aggarwal R, Kini D, Sofat S, et al. Duration of viraemia and faecal excretion in acute hepatitis E. Lancet 2000;356:1081-2.

  30. Nanda SK, Ansari IH, Acharya SK, Jameel S, Panda SK. Protracted viremia during acute sporadic hepatitis E virus infection. Gastroenterology 1995;108:225-30.

  31. Rab MA, Bile MK, Mubarik MM, et al. Water-borne hepatitis E virus epidemic in Islamabad, Pakistan: a common sourse outbreak traced to the malfunciton of a modern water treatment plant. Am J Trop Med Hyg 1997;57:151-7.

  32. Singh V, Singh V, Raje M, et al. Routes of transmission in the hepatitis E epidemic of Saharanpur. Trop Gastroenterol 1998;19:107-9.

  33. Khuroo MS, Kamili S, Jameel S. Vertical transmission of hepatitis E virus. Lancet 345:1025-26, 1995.

  34. Hamid Ss, Jafri SM, Khan H, et al. Fulminant hepatic failure in pregnant women: acute fatty liver or acute viral hepatitis? J Hepatol 1996;25:20-7.

 

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