Lola Oyedele MSN, RN, CTN

1
Liver
and
Biliary
Pancreatic Problems
NRS 108

• Lola Oyedele MSN, RN, CTN
• Majuvy L. Sulse MSN, RN, CCRN

2
LIVER

• Largest organ excluding skin located RUQ
• Lobule is functional unit
• Fat, CHO, Protein metabolism
• Clotting
• Drug metabolism detoxification
• Liver enzymes
• Alamine Aminotransferase
• ALT, SGPT-5-35U/L
• Aspartate Aminotransferase
• AST, SGOT 0-35U/L
• Alkaline Phosphatase
• ALP 20-90U/L

3
Liver

• Aminotransferases
• Found in hepatocytes
• Markers of liver cell injury
• Detected within hours of injury to liver
• AST used in conjunction with ALT
• AST elevated in cardiac/skeletal muscle
• Laboratory tests
• PT/PTT
• Se Albumin
• Se Ammonia
• Se Bilirubin
• Conjugated-Direct, post hepatic, glucoronic acid
• Unconjugated- indirect, pre hepatic,albumin bound
• Urobilinogen-sensitive test for hepatic damage

4
Liver Biopsy

• Pre procedure
• Needle between 6-7 or 8-9th intercostals
• Check coagulation
• Type X-match
• Baseline VS
• Sustained exhalations- prevent lung injury
• consent
• Post procedure
• VS
• Lie on R side for 2 hours
• Flat 12-14 hours
• Watch for complications-shock, R pneumothorax,
  Biliary peritonitis (rigid abdomen, high temp)

5
Jaundice

• Yellowish discoloration from bilirubin
  breakdown of Hgb
• Normal 2-3MG/DL (jaundice 3-4x normal value)
• Sclera skin, palm of hands/feet
• Hemolytic
• Increased RBC breakdown
• Increased unconjugated bilirubin
• Hemolytic anemia, ABO incompatibility
• Hepatocellular
• Liver unable to take up bilirubin
• Conjugated excreted
• Cirrhosis
• Obstructive
• Impeded or obstructive
• Intrahepatic- swelling, fibrosis, tumors,
  cirrhosis, hepatitis
• Extrahepatic-CBD stones, Ca pancreas

6
CIRRHOSIS

• DESCRIPTION
• A chronic, progressive disease of the liver,
  characterized by diffuse damage to cells with
  fibrosis and nodular regeneration
• Repeated destruction of hepatic cells causes the
  formation of scar tissue-nodular
• ASSESSMENT
• Anorexia and weight loss
• Early morning nausea and vomiting (presence of
  blood in vomitus)
• Dyspepsia
• Flatulence and changes in bowel habits
• Emaciation
• Fatigue

7
CIRRHOSIS

• Hepatomegaly
• Protruding umbilicus
• Dilated abdominal veins
• Fetor hepaticus the fruity, musty breath odor of
  chronic liver disease
• Asterixis (liver flap) A course tremor
  characterized by rapid, nonrhythmic extension and
  flexions in the wrist and fingers
• Delirium

• ASSESSMENT
• Jaundice
• Abdominal pain or tenderness
• Ascites
• Peripheral edema
• Dry skin and rashes
• Petechiae or ecchymosis
• Spider angiomas on the nose, cheeks, upper
  thorax, and shoulders

8
TYPES OF CIRRHOSIS

• LAENNEC'S CIRRHOSIS
• Alcohol-induced, nutritional, or portal cirrhosis
• Cellular necrosis causes eventual widespread scar
  tissue, with fibrotic infiltration of the liver
• POSTNECROTIC CIRRHOSIS
• Occurs after massive liver necrosis
• Results as a complication of acute viral
  hepatitis or exposure to hepatotoxins
• Scar tissue causes destruction of liver lobules
  and entire lobes

9
TYPES OF CIRRHOSIS

• BILIARY CIRRHOSIS
• Develops from chronic biliary obstruction
  (secondary), bile stasis (Primary), and
  inflammation resulting in severe obstructive
  jaundice
• CARDIAC CIRRHOSIS
• Associated with severe, right-sided congestive
  heart failure (CHF) and results in an enlarged,
  edematous, congested liver
• The liver becomes anoxic, resulting in liver cell
  necrosis and fibrosis

10
COMPLICATIONS OF CIRRHOSIS

• PORTAL HYPERTENSION
• A persistent increase in pressure within the
  portal vein that develops as a result of
  obstruction to flow of blood
• Causes splenomegaly as blood backs up
• Also results in ascites, esophageal varices
  hemorrhoids

11
COMPLICATIONS OF CIRRHOSIS

• ASCITES
• The accumulation of fluid (plasma)within the
  peritoneal cavity that results in venous
  congestion of the hepatic capillaries
• Increased hydrostatic pressure leads to plasma
  leaking directly from the liver surface and
  portal vein
• Increased hepatic lymph formation present
• Renal vasoconstriction-triggers RAS-causes water
  Na reabsorption

12
ASCITES

• Treatment
• Non surgical management
• Diet
• Drug
• Comfort measures
• Paracentesis
• Surgical management
• Shunt
• Peritoneovenous(LeVeen shunt)
• Denver shunt

13
COMPLICATIONS OF CIRRHOSIS

• BLEEDING ESOPHAGEAL VARICES
• Fragile, thin-walled, distended esophageal veins
  that become irritated and rupture
• Caused by-chemical irritant, mechanical trauma,
  increased pressure from esophagus stomach
• Treatment-
• Esophageal tamponade
• Gastric decompression lavage
• Vasopressin
• Endoscopic sclerotherapy or ligation
• TIPS

14
COMPLICATIONS OF CIRRHOSIS

• JAUNDICE
• Occurs because the liver is unable to metabolize
  bilirubin and because the edema, fibrosis, and
  scarring of the hepatic bile ducts interfere with
  normal bile and bilirubin secretion
• PORTAL SYSTEMIC ENCEPHALOPATHY
• End stage hepatic failure and cirrhosis,
  characterized by altered LOC, neurological
  symptoms, impaired thinking, and neuromuscular
  disturbances

15
Encephalopathy

• Stages of encephalopathy
• Stage 1-
• mild confusion, forgetfulness, mood changes,
  irritability, sleep disturbance
• Stage 2
• lethargy
• Aberrant behavior
• Liver flaps
• Stage 3
• Severe confusion-violent behavior
• Speech mumbling, asterixis
• hyperventilation
• Stage 4
• Comatose
• Abnormal posturing
• EEg abnormal

16
Management of Encephalopathy

• Identify treat cause
• GI bleed, systemic infection, drugs, alkalosis,
  dehydration
• Eliminate or reduce generation of Ammonia toxins
• Control intakelt0.5G/Kg/Day
• Calories 35-40KCAL/Kg/Day ltTyrosine/Phenylalanine,
  gt Leucine/Valine
• Vit A,D,E, K
• Reduce amount of bacteria in bowel
• Stop Nitrogen containing drugs, give Neomycin,
  Lactulose, Magnesium Citrate, fiber, stool
  softener, enemas
• Hasten movement of ammonia in the bowel-3-5x
  stools/day
• Lactulose

17
COMPLICATIONS OF CIRRHOSIS

• HEPATORENAL SYNDROME
• Progressive renal failure associated with hepatic
  failure
• Characterized by a sudden decrease in urinary
  output, elevated blood urea nitrogen (BUN) and
  creatinine, decreased urine sodium excretion, and
  increased urine osmolarity
• COAGULATION DEFECTS
• Decreased synthesis of bile fats in the liver
  prevent the absorption of fat-soluble vitamins
• Without vitamin K and clotting factors II, VII,
  IX, and X, the client is prone to bleeding

18
CIRRHOSIS

• IMPLEMENTATION
• Elevate the head of the bed to minimize shortness
  of breath
• If ascites and edema is absent and the client
  does not exhibit signs of impending coma, a
  high-protein diet supplemented with vitamins is
  prescribed
• Provide supplemental vitamins (B complex, vitamin
  A, C, and K, folic acid, and thiamine) as
  prescribed
• Restrict sodium intake and fluid intake as
  prescribed
• Initiate enteral feedings or TPN as prescribed
• Administer diuretics as prescribed
• Monitor IO and electrolyte balance
• Weigh client and measure abdominal girth daily
• Monitor LOC assess for precoma state (tremors,
  delirium)

19
CIRRHOSIS

• IMPLEMENTATION
• Monitor for asterixis
• Maintain gastric intubation to assess bleeding
  and/or esophagogastric balloon tamponade to
  control bleeding varices if prescribed
• Administer blood products as prescribed
• Monitor coagulation laboratory results
  administer vitamin K if prescribed
• Administer low-sodium antacids as prescribed
• Administer Lactulose (Chronulac), which decreases
  the pH of the bowel, decreases production of
  ammonia by bacteria in the bowel, and facilitates
  the excretion of ammonia

20
CIRRHOSIS

• Administer neomycin (Mycifradin) as prescribed to
  inhibit protein synthesis in bacteria and
  decrease the production of ammonia
• Avoid medications such as narcotics, sedatives,
  and barbiturates, and any hepatotoxic medications
  or substances
• Instruct the client about the restriction of
  alcohol intake
• Prepare the client for paracentesis to remove
  abdominal fluid
• Prepare the client for surgical shunting
  procedures if prescribed

21
Fatty Liver

• Accumulations of triglycerides fats in hepatic
  cells
• Causes- alcoholism, malnutrition, DM, Obesity
  TPN, Pregnancy
• S/S-RUQ pain, edema, hepatomegaly, jaundice
• Dx-liver biopsy
• Tx-dietary restrictions

22
Hepatic Abcess

• Invasion of bacteria or protozoa-causing necrotic
  cavity filled with leukocytes infective agents.
• Causative agents- E Coli, Klebsiella, Salmonella,
  Enterococcus Staph
• Dx-liver scan
• Labs-blood culture to detect organism

23
LIVER Cancer

• Hepatocellular carcinoma- most common primary
  liver Ca
• Metastatic Ca is more common than primary Ca
• Malignant cells cause liver to be enlarged and
  mishapen
• Difficult to diagnose
• Clinical manifestations similar to cirrhosis
• Tests used-CT, MRI, ERCP, liver biopsy, AFP
  (elevated in 70 of hepatocellular Ca helps to
  distinguish primary from metastatic cancer
• Cryosurgery- cryoprobes directly in liver-liquid
  nitrogen used to freeze liver tissue
• Radiofrequency-electrical energy to create heat
  in specific location
• PEI-percutaneous ethanol injection-guided US
• chemotherapy
• Liver transplantation

24
CHOLECYSTITIS

• DESCRIPTION
• An inflammation of the gallbladder that may occur
  as an acute or chronic process
• Acute inflammation is associated with gallstones
  (cholelithiasis)
• Chronic cholecystitis results when inefficient
  bile emptying and gallbladder muscle wall disease
  cause a fibrotic and contracted gallbladder
• A calculus cholecystitis occurs in the absence of
  gallstones and is due to bacterial invasion via
  the lymphatic or vascular systems

25
CHOLECYSTITIS

• ASSESSMENT
• Nausea and vomiting
• Indigestion, Belching, Flatulence
• Epigastric pain that radiates to the scapula 2 to
  4 hours after eating fatty foods and may persist
  for 4 to 6 hours
• Pain localized in right upper quadrant
• Guarding, rigidity, and rebound tenderness
• Mass palpated in the right upper quadrant
• Murphys sign (cannot take a deep breath when the
  examiners fingers are passed below the hepatic
  margin)
• Elevated temperature, Tachycardia
• Signs of dehydration
• Jaundice, pruritus, dark orange and foamy urine
• Steatorrhea and clay-colored feces

26
CHOLECYSTITIS

• IMPLEMENTATION
• Maintain NPO status during nausea and vomiting
  episodes
• Maintain nasogastric decompression
• Administer antiemetics
• Administer analgesics as prescribed to relieve
  pain and reduce spasm (morphine sulfate or
  codeine sulfate may cause spasm of the sphincter
  of Oddi and increase pain)
• Administer antispasmodic (anticholinergics) as
  prescribed to relax smooth muscle
• Instruct the client with chronic cholecystitis to
  eat low-fat meals more frequently in small
  amounts
• Instruct the client to avoid gas-forming foods
• Prepare the client for nonsurgical and surgical
  procedures as prescribed

27
CHOLECYSTITISNONSURGICAL IMPLEMENTATION

• DISSOLUTION THERAPY
• To remove cholesterol stones
• Chenodeoxycholic acid (Chenodiol) or ursodiol
  (Actigall) is administered PO to decrease the
  size of the stones or to dissolve small stones
• Direct contact with repeated injections and
  aspirations of a dissolution agent via
  percutaneous catheter may be performed

28
CHOLECYSTITISNONSURGICAL IMPLEMENTATION

• EXTRACORPOREAL SHOCK WAVE LITHOTRIPSY
• Shock waves are administered that disintegrate
  stones in the biliary system
• Oral dissolution follows

29
CHOLECYSTITISSURGICAL IMPLEMENTATION

• CHOLECYSTECTOMY
• Removal of the gallbladder
• CHOLEDOCHOTOMY
• Incision into the common bile duct to remove the
  stone
• Surgical procedures may be performed by
  laparoscopy

30
CHOLECYSTITIS

• POSTOPERATIVE IMPLEMENTATION
• Monitor for respiratory complications secondary
  to pain at the incisional site
• Encourage coughing, deep breathing early
  ambulation
• Splinting the abdomen to prevent discomfort
  during coughing
• Administer antiemetics as prescribed for nausea
  and vomiting
• Administer analgesics as prescribed for pain
  relief
• Maintain NPO status and NG tube suction as
  prescribed
• Advance diet from clear liquids to solids when
  prescribed and as tolerated by the client
• Maintain and monitor drainage from the T-tube, if
  present

31
PANCREATITIS

• DESCRIPTION
• An acute or chronic inflammation of the pancreas
  with associated escape of pancreatic enzymes into
  surrounding tissue
• Acute pancreatitis occurs suddenly as one attack
  or can be recurrent, but resolves
• Chronic pancreatitis is a continual inflammation
  and destruction of the pancreas, with scar tissue
  replacing pancreatic tissue
• Precipitating factors
• trauma, alcohol, biliary tract disease, viral or
  bacterial disease, hyperlipedemia, hypercalcemia,
  cholelithiasis, hyperparathyroidism, ischemic
  vascular disease, and peptic ulcer disease

32
ACUTE PANCREATITIS

• ASSESSMENT
• Abdominal pain, including a sudden onset at the
  mid-epigastric or left upper quadrant location
  with radiation to the back
• Pain that is aggravated by a fatty meal, alcohol,
  or lying in a recumbent position
• Abdominal tenderness and guarding
• Nausea and vomiting
• Weight loss
• Cullens sign (discoloration of the abdomen and
  periumbilical area)
• Turners sign (bluish discoloration of the
  flanks)
• Absent or decreased bowel sounds
• Elevated WBC, glucose, bilirubin, alkaline
  phosphatase, urinary amylase
• Elevated lipase and amylase

33
CULLENS SIGN VS TURNERS
SIGN
34
ACUTE PANCREATITIS

• IMPLEMENTATION
• Maintain NPO status and maintain hydration with
  IV fluids as prescribed
• Administer TPN for severe nutritional depletion
• Administer supplemental preparations and vitamins
  and minerals to increase caloric intake if
  prescribed
• Maintain NG tube to decrease gastric distention
  and suppress pancreatic secretion
• Administer meperidine hydrochloride (Demerol) as
  prescribed for pain because it causes less
  incidence of smooth muscle spasm of the
  pancreatic ducts and sphincter of Oddi (avoid
  morphine sulfate or codeine sulfate, which may
  cause spasms)
• Administer antacids as prescribed to neutralize
  gastric secretions

35
ACUTE PANCREATITIS

• IMPLEMENTATION
• Administer histamine H2-receptor antagonists as
  prescribed to decrease hydrochloric acid
  production and prevent activation of pancreatic
  enzymes
• Administer anticholinergics as prescribed to
  decrease vagal stimulation, decrease GI motility,
  and inhibit pancreatic enzyme secretion

36
ACUTE PANCREATITIS

• CLIENT EDUCATION
• The importance of avoiding alcohol
• The importance of follow-up visits with the
  physician
• To notify the physician if acute abdominal pain,
  jaundice, clay-colored stools, or dark urine
  develops

37
CHRONIC PANCREATITIS

• ASSESSMENT
• Abdominal pain and tenderness
• Left upper quadrant mass
• Steatorrhea and foul-smelling stools that may
  increase in volume as pancreatic insufficiency
  increases
• Weight loss
• Muscle wasting
• Jaundice
• Signs and symptoms of diabetes mellitus

38
CHRONIC PANCREATITIS

• IMPLEMENTATION
• Provide supplemental preparations and vitamins
  and minerals to increase caloric intake
• Administer pancreatic enzymes as prescribed to
  aid in the digestion and absorption of fat and
  protein
• Administer insulin or oral hypoglycemic
  medications as prescribed to control diabetes
  mellitus, if present

39
CHRONIC PANCREATITIS

• CLIENT EDUCATION
• The prescribed dietary measures (fat and/or
  protein intake may be limited)
• Avoid heavy meals
• The importance of avoiding alcohol
• The use of pancreatic enzyme medications
• The treatment plan for glucose management
• To notify the physician if increased steatorrhea
  occurs or if abdominal distention or cramping,
  and skin breakdown develops
• The importance of follow-up visits

40
HEPATITIS

• DESCRIPTION
• An inflammation of the liver caused by a virus,
  bacteria, or exposure to medications or
  hepatotoxins
• The goals of treatment include resting the
  inflammed liver to reduce metabolic demands and
  increasing the blood supply, thus promoting
  cellular regeneration and preventing
  complications

41
STAGES OF VIRAL HEPATITIS

• PREICTERIC STAGE
• The first stage of hepatitis preceding the
  appearance of jaundice
• Flu-like symptoms malaise, fatigue
• Anorexia, nausea, vomiting, diarrhea
• Pain headache, muscle aches, polyarthritis
• Serum bilirubin and enzyme levels are elevated

42
STAGES OF VIRAL HEPATITIS

• ICTERIC STAGE
• The second stage of hepatitis, which includes the
  appearance of jaundice and associated symptoms
  such as elevated bilirubin levels, dark or
  tea-colored urine, and clay-colored stools
• Jaundice
• Pruritus
• Brown-colored urine
• Lighter-colored stools
• Decrease in preicteric phase symptoms

43
STAGES OF VIRAL HEPATITIS

• POSTICTERIC STAGE
• The convalescent stage in which the jaundice
  decreases and the color of the urine and stool
  return to normal
• Energy levels increase
• Pain subsides
• GI symptoms are minimal to absent
• Serum bilirubin and enzyme levels return to
  normal

44
VIRAL HEPATITISLABORATORY ASSESSMENT

• ALANINE AMINOTRANSFERASE (ALT)
• Elevated to more than 1000 mU/ml and may rise to
  as high as 4000 mU/ml
• Normal adult blood value 6 to 24 U/L
• ASPARTATE AMINOTRANSFERASE (AST)
• May rise to 1000 to 2000 mU/ml
• Normal adult blood value 8 to 26 U/L
• ALKALINE PHOSPHATASE LEVELS
• May be normal or mildly elevated
• Normal adult blood value 4.5 to 13
  King-Armstrong units/dl
• SERUM TOTAL BILIRUBIN LEVELS
• Elevated to greater than 2.5 mg/dl
• Normal less than 1.5 mg/dl
• Elevated levels of bilirubin in the urine

45
HEPATITIS A (HAV)

• DESCRIPTION
• Formerly known as infectious hepatitis
• Commonly seen during the fall and early winter
• INCREASED RISK INDIVIDUALS
• Commonly seen in young children
• Individuals in institutionalized settings
• Health care personnel

46
HEPATITIS A (HAV)

• TRANSMISSION
• Fecal-oral route
• Person-to-person contact
• Parenteral
• Contaminated fruits, vegetables, or uncooked
  shellfish
• Contaminated water or milk
• Poorly washed utensils
• INCUBATION PERIOD
• 2 to 6 weeks
• INFECTIOUS PERIOD
• 2 to 3 weeks prior to, and 1 week after,
  developing jaundice
• COMPLICATION
• Fulminant hepatitis

47
HEPATITIS A (HAV)

• PREVENTION
• Strict handwashing
• Stool and needle precautions
• Treatment of municipal water supplies
• Serologic screening of food handlers
• Hepatitis A vaccine (Havrix)
• Immune globulin (IG) For individuals exposed to
  HAV who have never received the hepatitis A
  vaccine administer during the period of
  incubation and within 2 weeks of exposure
• IG is recommended for household members and
  sexual contacts of individuals with Hepatitis A
• Pre-exposure prophylaxis with IG is recommended
  for individuals traveling to countries with poor
  or uncertain sanitation conditions

48
HEPATITIS B (HBV)

• DESCRIPTION
• Is nonseasonal in nature
• All age groups are affected
• INCREASED RISK INDIVIDUALS
• Drug addicts
• Clients undergoing long-term hemodialysis
• Health care personnel

49
HEPATITIS B (HBV)

• TRANSMISSION
• Blood or body fluid contact
• Infected blood products
• Infected saliva or semen
• Contaminated needles
• Sexual contact
• Parenteral
• Perinatal period
• Blood or body fluids contact at birth

50
HEPATITIS B (HBV)

• INCUBATION PERIOD
• 6 to 24 weeks
• COMPLICATIONS
• Fulminant hepatitis
• Chronic liver disease
• Cirrhosis
• Primary hepatocellular carcinoma

51
HEPATITIS B (HBV)

• TESTING
• Infection established by the presence of
  hepatitis B antigen-antibody systems in the blood
• Presence of hepatitis B surface antigens (HBsAG)
  is the serologic marker to establish the
  diagnosis of hepatitis B
• Hepatitis B early antigen (HBeAG) is detected in
  the blood about 1 week after the appearance of
  HBsAG and its presence determines the infective
  state of the client

52
HEPATITIS B (HBV)

• TESTING
• If the serologic marker (HBsAG) is present after
  6 months, it indicates a carrier state or chronic
  hepatitis
• Normally the serologic marker (HBsAG) level
  declines and disappears after the acute hepatitis
  B episode
• The presence of antibodies to HBsAG (anti-HBS)
  indicates recovery and immunity to hepatitis B

53
HEPATITIS B (HBV)

• PREVENTION
• Strict hand washing
• Screening blood donors
• Testing of all pregnant women
• Needle precautions
• Avoiding intimate sexual contact if hepatitis B
  surface antigen (HBsAG) is positive
• Hepatitis B vaccine Engerix-B, Recombivax HB
• Hepatitis B immune globulin (HBIG) For
  individuals exposed to HBV either through sexual
  contact or through the percutaneous or
  transmucosal routes, who have never had hepatitis
  B and have never received hepatitis B vaccine

54
HEPATITIS C (HCV)

• DESCRIPTION
• Occurs year-round
• Can occur in any age group
• Is common among drug abusers and is the major
  cause of post-transfusion hepatitis
• Risk factors are similar as HBV since hepatitis C
  is also parenterally transmitted
• INCREASED RISK INDIVIDUALS
• Parenteral drug users
• Clients receiving frequent transfusions
• Health care personnel

55
HEPATITIS C (HCV)

• TRANSMISSION
• Same as HBV primarily through blood
• INCUBATION PERIOD
• 5 to 10 weeks
• COMPLICATIONS
• Chronic liver disease
• Cirrhosis
• Primary hepatocellular carcinoma

56
HEPATITIS C (HCV)

• TESTING
• Anti-HCV is the antibody to HCV and is most
  accurate in detecting chronic states of hepatitis
  C
• PREVENTION
• Strict hand washing
• Needle precautions
• Screening of blood donors

57
HEPATITIS D (HDV)

• DESCRIPTION
• Common in the Mediterranean and Middle Eastern
  areas
• Seen with hepatitis B and may cause infection
  only in the presence of active HBV infection
• Coinfection with the delta-agent intensifies the
  acute symptoms of hepatitis B
• Transmission and risk of infection is the same as
  HBV, via contact with blood and blood products
• Prevention of HBV infection with vaccine also
  prevents HDV infection, since HDV is dependent on
  HBV for replication

58
HEPATITIS D (HDV)

• HIGH RISK INDIVIDUALS
• Drug users
• Clients receiving hemodialysis
• Clients receiving frequent blood transfusions
• TRANSMISSION
• Same as HBV
• INCUBATION PERIOD
• 7 to 8 weeks

59
HEPATITIS D (HDV)

• COMPLICATIONS
• Chronic liver disease
• Fulminant hepatitis
• TESTING
• Serologic hepatitis delta virus (HDV)
  determination is made by detection of the
  hepatitis D antigen (HDAg) early in the course of
  the infection and by detection of anti-HDV
  antibody in the later disease stages
• PREVENTION
• Because hepatitis D must coexist with hepatitis
  B, the precautions that help prevent hepatitis B
  are also useful in preventing delta hepatitis

60
HEPATITIS E (HEV)

• DESCRIPTION
• A water-borne virus
• Prevalent in areas where sewage disposal is
  inadequate or where communal bathing in
  contaminated rivers is practiced
• Risk of infection is the same as HAV
• Presents as a mild disease except in infected
  women in the third trimester of pregnancy, for
  whom the mortality rate is high

61
HEPATITIS E (HEV)

• TRANSMISSION-Same as HAV
• INCUBATION PERIOD-2 to 9 weeks
• COMPLICATIONS
• High mortality rate in pregnant women
• Fetal demise
• TESTING
• Specific serologic tests for hepatitis E virus
  (HEV) include detection of IgM and IgG antibodies
  to hepatitis E (anti-HEV)
• PREVENTION
• Strict hand washing
• Treatment of water supplies and sanitation
  measures

62
HEPATITIS G (HGV)

• DESCRIPTION
• Non-A, non-B, non-C hepatitis
• Autoantibodies are absent
• RISK FACTORS
• Similar to those for hepatitis C
• Hepatitis G (HGV) has been found in some blood
  donors, IV drug users, hemodialysis clients, and
  clients with hemophilia however, HGV does not
  appear to cause significant liver disease

63
CLIENT AND FAMILY EDUCATION FOR HEPATITIS

• Strict and frequent hand washing
• Do not share bathrooms unless the client strictly
  adheres to personal hygiene measures
• Individual washcloths, towels, drinking and
  eating utensils, as well as toothbrushes and
  razors, must be labeled and identified
• The client must not prepare food for other family
  members

64
CLIENT AND FAMILY EDUCATION FOR HEPATITIS

• The client should avoid alcohol and
  over-the-counter medications, particularly
  acetaminophen (Tylenol) and sedatives, because
  these medications are hepatotoxic
• The client should increase activity gradually to
  prevent fatigue
• The client should consume small, frequent,
  high-carbohydrate, low-fat foods
• The client is not to donate blood

65
CLIENT AND FAMILY EDUCATION FOR HEPATITIS

• The client may maintain normal contact with
  people as long as proper personal hygiene is
  maintained
• Close personal contact such as kissing should be
  discouraged until HBsAg test results are negative
  
• The client is to avoid sexual activity until
  hepatitis B surface antigen (HBsAg) results are
  negative