Hepatitis Nursing Management

 HEPATITIS

Hepatitis is a viral infection of the liver [associated with a broad spectrum of clinical manifestation from asymptomatic infection through icteric hepatitis to hepatic necrosis]

Classification and Causes

1. Type A Hepatitis (HAV) caused by hepatitis A virus (RNA virus of enterovirus family)
2. Type B Hepatitis (HBV) caused by hepatitis B Virus (Double shelled particle containing DNA)
3. Type C Hepatitis (HCV)/Non-A, Non-B hepatitis an RNA virus.
4. Type D Hepatitis (HDV, Delta Hepatitis) - Hep: D virus.
5. Type E Hepatitis (HEV) - Non enveloped singie-strand RNA virus.

Mode of Transmission

• Hep A fecal oral route, through ingestion of contaminated food and liquids, overcrowding, poor sanitation infected food handlers/person to person contact and rarely blood transfusion.
• Hep B Parenterally or by intimate contact with carriers or those with acute disease; male homosexuals. [Vertical, transmission] from mothers to infants, contaminated instruments, syringes, needles; renal dialysis.
• Hep C-Through blood or blood product transmission, sexual intercourse, contaminated piercing and tattooing tools [Found among IV drug use's and renal dialysis patients and personnel].
• Hep D-same as HBV.
• Hep E - Fecal oral route [This virus is inconsistently shed in feces, detection is-difficult]

Incubation Period:

1. A-3-5 weeks (with an average of 4 weeks]
2. B-2-5 months
3. C-1 week-several months
4. D-same as HBV 2- CAPA
5. E-same as HAV 3-5

Clinical Manifestations:

Hep A: Prodromal symptoms fatigue, anorexia, malaise, headache, low-grade fever, nausea and vomiting. [Highly contagious during this period, usually 2 weeks before the onset of jaundice.]

Icteric phase, jaundice, ten-colored urine, clay-colored stools and right upper quadrant tenderness

Hep B: Onset-more insidious and prolonged compared to HAV.

1 week 2 months of prodromal symptoms fatigue, anorexia, transient fever, abdominal discomfort, nausea, vomiting and headache.

Extrahepatic manifestation myalgias, photophobia, arthritis, angioedema, uricaria, maculo-papular eruptions, skin rashes, vasculitis.

Jaundice in icteric phase.

Hep C: Parallel to 1IBV but often less severe

Hep D: Parallel to HBV but more severe.

Diagnostic Evaluation

1. Elevated serum transferase levels [aspartate transaminase [AST], alanine transaminase [ALT] [for all hepatitis).
2. Radioimmunoassays-reveal IgM Abs to hep virus in the acute phase of HAV
3. Radioimmunoassays to include HbsAg, anti-HBc, 'anti HbsAg detected in various stages of HBV. Hep. B Synce Antigen
4. Hep C Ab-may not be detected for 3-6 months after onset of HCV illness, Ag tests for HCV are being developed that will confirm diagnosis sooner.
5. Antidelta Abs of HbsAg for HDV or the detection of IgM in acute disease and IgG in chronic disease.
6. Hep E Ag (with HCV ruled out).
7. Liver biopsy to detect chronic active disease, progression and response to therapy.

Management All types of hepatitis:

• Rest
• Hospitalization
• Eat small, high-calorie, high protein meals (Protein intake should be reduced if signs of precomalethargy, confusion, mental changes develop) [Large meals are batter tolerated in the morning because many patients experience nausea late in the day]. Proteins are restricted when the liver cannot metabolize protein by-products. 
•  IV fluid and e replacement [if vomiting persists and if unable to maintain oral intake]as indicated.
• Vitamin K injected S/C if prothrombin time is prolonged.
• Antiemetics [(trimethobenzamide or benzquinamide)] may be given a 14 hour before meals to relieve nausea and prevent vomiting.
• For severe pruritis, the resin cholestyramine, which sequesters bile salts, may be given.

For HCV patients

• Long-term interferon (Betaseron) therapy may produce at least temporary remission.
• Combination interferon and ribaviron (AZT) treatment

Complications

1. Dehydration, hypokalemia
2. Chronic "carrier" hepatitis or chronic active hepatitis
3. Cholestatic hepatitis.
4. Fulminant hepatitis
5. HBV and HCV carriers have a higher risk of developing hepatocellular carcinoma.

Nursing Care

1. Encourage frequent small feedings of high-calorie, low-fat diet. Avoid large quantities of protein during acute phase of illness,
2. Encourage eating meals in a sitting position to decrease pressure on liver
3. Encourage taking meals in an environment with minimal noxious stimuli (odors, noise, interruptions).
4. Administer anti-emetics as prescribed. [Avoid phenothiazines, such as chlorpromazine (Thorazine), which have a cholestatic effect and may cause/worsen jaundice.]Provide frequent oral fluids as tolerated.
5. Administer IVF for patients with inability to maintain oral fluids.
6. Monitor Intake/Output.
7. Promote rest during symptomatic phase, according to the level of fatigue.
8. Administer analgesics as prescribed for comfort.
9. Provide emotional support and divertional activities (when recovery and convalescence are prolonged].
10. Encourage gradual resumption of activities and mild exercise during convalescent period.
11. Educate patient about disease and its transmission.
12. Explain need for follow-up of LFT.
13. Stress on proper public and home sanitation and preparation and dispensation of foods
14. Encourage special protection for close contacts [a. Immunoglobulin (Gammar) as soon as possible to household contacts of HAV patients, b. Hep B immune globulin as soon as possible to blood or body fluid contacts of HBV patients, followed by HBV vaccinie series]
15. Explain precautions to patient and family about transmission and prevention of transmission to others. [a.Good handwashing and hygiene after using bathroom. b. Avoidance of sexual activity (especially for HBV) until free of HbsAg, c. Avoidance of sharing needles, eating utensils and toothbrushes to prevent blood or body fluid contact (especially for HBV)]
16. Avoid trauma that may cause bruising if possible.
17. Report all causes of hepatitis to public health officials.
18. Monitor prothrombin tine and administer vitamin K as ordered.
19. Encourage vaccination for HBV with series of 3 shots (at 0, 1 & 6 months) for high-risk patients health care workers or institutionalized persons, as well as vaccination of all children from birth or at adolescence.
20. Instruct all patients who have received a blood transfusion to refrain from donating blood for 6 months (the IP of HBV). After hepatitis infection, blood should never be given if patient is a hepatitis B carrier or was infected with hepatitis C.

Hep B vaccine: For prevention of hep. B.

• Recommended for those at high risk of develop hep В
• Health care workers exposed to blood, haemodialysis and oncology patients and staff, homosexually active males, and users of illicit injectable drugs. Produces active immunity.
• Does not provide protection to those already exposed
• Most common post-injection complaint-soreness and redness at the injection site.

Hep B Immune Globulin:

• Recommended for unprotected people exposed to hep. B virus through accidental contamination of mucous membranes or breaks in the skin.
• Prepared from pooled venous plasma of donors with a high titer of anti-HBs Abs.
• Provides passive immunity.
• Given IM as soon as possible, but no later than 7 days after exposure
• 2 dose-given-25-30 days after the 1".
• LFTs serum bilirubin, direct; serum bilirubin total, urine bilirubin; urine urobilinogen; fecal urobilinogen - Measures ability to liver to conjugate and excrete bilirubin.
• Dye clearances Indocyamine green dye extracted from blood and excreted by liver. Bromsulphalein excretion (BSP test) BSP binds to albumin in blood. Liver cells unbind BSP, conjugate it and excrete it in bile.
• Protein studies Total serum pilotein, serum albumin, serum globulin, serum protein electro phoresis; Albumina, globulin, az globulin, ẞ globulin, globulin; A/G ratio Proteins are manufactured by the liver.
• Serum alkaline phosphatase manufactured in bones, liver, kidneys and intestine and excreted through biliary tract.
• Serum transaminase studies- SGOT (AST), SGPT (ALT)Based on release of enzyme from damaged liver cells.
• Blood ammonia - Liver converts ammonia to urea. Increases in liver failure.
• Cholesterol - Increased in biliary obstruction and decreased in parenchymal liver disease.