Transcript Hepatitis B (HBV)

NURSING MANAGEMENT
OF ADULTS WITH
DISORDERS OF THE LIVER
2009
TOPICS TO BE REVIEWED
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HEPATITIS
CIRRHOSIS
STEATOHEPATITIS (FATTY LIVER)
HEPATIC ABSCESS
LIVER TRAUMA
CANCER OF LIVER
LIVER TRANSPLANT
NORMAL FUNCTION OF
LIVER
MAIN FUNCTIONS OF THE LIVER: storage, protection,
metabolism
• Maintains normal serum glucose levels
• Ammonia conversion
• Protein metabolism
• Fat metabolism
• Vitamin and Iron storage
• Drug metabolism and detoxification
LIVER FUNCTION:
GLUCOSE METABOLISM
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What happens to glucose in the liver?
Where is it stored?
When is it released?
What is gluconeogenesis?
When does it take place?
LIVER FUNCTION:
AMMONIA CONVERSION
• When gluconeogenesis takes place
what is the byproduct of the process?
• What happens to the byproduct?
• What do the bacteria in the intestines
produce as a byproduct?
• How is this byproduct removed?
LIVER FUNCTION:
PROTEIN METABOLISM
• What is the liver’s job in terms of
synthesizing plasma proteins?
• What does the liver need to complete
it’s job?
LIVER FUNCTION:
FAT METABOLISM
• What is the liver’s job in terms of fat
metabolism?
• When does the liver do this?
• What are the results of this metabolism used
for?
LIVER FUNCTION:
VITAMIN & IRON STORAGE
• Stores which fat soluble vitamins?
• What other vitamins are stored in the
liver?
• What are these vitamins responsible
for?
• Which minerals are stored in the liver?
LIVER FUNCTION:
DRUG METABOLISM and
DETOXIFICATION
• THE FOLLOWING CLASSIFICATION
OF DRUGS ARE METABOLIZED BY
THE LIVER?
• What else is metabolized by the liver?
• What does the liver do in terms of
detoxification?
NORMAL FUNCTION: bile
secretion
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What is the liver’s job with Bile?
When is bile secreted?
Where is Bile collected and stored?
How is this related to Billirubin?
When do Billirubin levels increase?
LIVER FUNCTION:
PROTECTION
• What does the liver’s protection function
involve?
• What do the cells do?
LIVER FUNCTION
CONTINUED
• Inactivates Hormones
– Estrogen
– Testoterone
– Progesterone
– Aldosterone
– cortisol
• Sinusoids store blood (about 200-400
cc)
DISORDER OF THE LIVER
HEPATITIS
Hepatitis
Widespread viral inflammation of liver cells
• Hepatitis A (HAV)
• Hepatitis B (HBV)
• Hepatitis C (HCV)
• Hepatitis D (HDV)
• Hepatitis E (HEV)
• Hepatitis F and G are uncommon (HFV, HGV)
• DRUG INDUCED HEPATITIS
• Occurs as a secondary infection
Hepatitis A (HAV)
• Similar to that of a typical viral syndrome;
often goes unrecognized
• Spread via the fecal-oral route by oral
ingestion of fecal contaminants
• Contaminated water, shellfish from
contaminated water, food contaminated by
handlers infected with hepatitis A
• Also spread by oral-anal sexual activity
(Continued)
Hepatitis A (HAV)(Continued)
• Incubation period for hepatitis A is 15 to 50 days.
• Disease is usually not life threatening.
• Disease may be more severe in individuals older
than 40 years of age.
• Many people who have hepatitis A don’t know it;
symptoms are similar to a gastrointestinal illness.
Hepatitis B (HBV)
• Spread is via unprotected sexual
intercourse with an infected partner,
sharing needles, accidental needle
sticks, blood transfusions,
hemodialysis, maternal-fetal route.
• Symptoms occur in 25 to 180 days
after exposure; symptoms include
anorexia, nausea and vomiting, fever,
fatigue, right upper quadrant pain,
dark urine, light stool, joint pain, and
jaundice.
(Continued)
Hepatitis B (HBV) (Continued)
• Hepatitis carriers can infect others,
even if they are without symptoms.
Hepatitis C (HCV)
• Spread is by sharing needles, blood, blood
products, or organ transplants (prior to 1992),
needle stick injury, tattoos, intranasal cocaine
use.
• Incubation period is 21 to 140 days.
• Most individuals are asymptomatic; damage
occurs over decades.
• Hepatitis C is the leading indication for liver
transplantation in the U.S.
• NOT TRANSMITTED BY CAUSUAL OR INTIMATE
HOUSEHOLD CONTACT
Hepatitis D (HDV)
• Transmitted primarily by parenteral
routes
• Incubation period 14 to 56 days
• HDV coinfects with HBV and needs it
presence to replicate
Hepatitis E (HEV)
• Present in endemic areas where waterborne
epidemics occur and in travelers to those areas
(India, Asia, Africa, Middle East, Mexico, Central
America & South America)
• Also seen in travellers coming from these areas
• Transmitted via fecal-oral route
• Resembles hepatitis A
• Incubation period 15 to 64 days
Clinical Manifestations of all
Hepatitis
• Abdominal pain
• Changes in skin or
eye color
• Arthralgia (joint pain)
• Myalgia (muscle pain)
• Diarrhea/constipation
• Wgt loss
• Hepatomegaly
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Fever
Lethargy/Malaise
Nausea/vomiting
Intolerance to
fats/dyspepsia
• Pruritus
• CHANGES IN
COLOR OF URINE
AND STOOL
ASSESSMENT
HEALTH HISTORY
• Suspected exposure
• Medical history
SIGNS/SYMPTOMS
• Pre-icteric stage
• Icteric stage
• Post-icteric stage
SIGNS/SYMPTOMS
• PRE-ICTERIC STAGE
• Lasts about 1 week
SIGNS AND SYMPTOMS
• ICTERIC STAGE
• Lasts 2-6 weeks
• Jaundice appears
• Yellow skin, sclera,
mucous membranes
• Dark amber urine
• Clay colored stools
SIGNS AND SYMPTOMS
• POST-ICTERIC
STAGE
• Lasts 2-6 weeks
• Jaundice subsides
• Liver decreases in
size
• Good appetite
LABORATORY TESTS FOR
HEPATITIS
• There will be an increase of liver
enzymes and serologic markers
INDICATING A PRESENCE OF
HEPATITIS A, B, C
LABORATORY TESTS FOR
HEPATITIS A (HAV)
• Presence of hepatitis A in client: when hepatitis A
(HAV) antibodies (anti-HAV) are found in the blood
• Presence of immunoglobulin M(IgM) antibodies
means that ongoing inflammation of liver present
(persisits for 4-6 wks)
• Previous infection indicated by presence of
immunoglbulin G (IgG) antibodies which provides
permanent immunity to disease
LABORATORY TESTS FOR
HEPATITIS B (HBV)
Serologic markers which indicate client has Hepatitis B
(HBV) are:
• HBsAg (Hepatitis B surface Antigen)
• Anti-HBc IgM (IgM antibodies to hepatitis B core
antigen)
If these levels are elevated after 6 months: chronic or
carrier state
Presence of antibodies to HBsAb (hepatitis B surface
antibody): indicates recovery and immunity to
hepatitis B
Someone immunized will have a positive HBsAb
LABORATORY TESTS FOR
HEPATITIS C (HCV)
• ELISA (enzyme linked immunosorbent assay )
SCREENS INITIALLY & for HCV antibodies (antiHCV): can detect antibodies in 4 wks
• RIBA: (recumbent immunoblot assay): used to
confirm that client has been exposed and has
developed antibody
• HCV PCR (HCV polymerase chain reaction test):
confirms presence of circulating active virus
LABORATORY TEST FOR
HEPATITIS D (HDV)
• Presence of virus confirmed by
identification of intrahepatic delta
antigen
• Also by rise in hepatitis D virus
antibodies (anti-HDV) titer
• Found within a few days of infection
LBORATORY TESTS FOR
HEPATITIS E (HEV)
• VIRUS CANNOT BE DETECTED
• Presence of hepatitis E antibodies (antiHEV) is found in people infected with
virus
LABORATORY TESTS
CONTINUED
• A person having a previous infection is
indicated by immunoglobulin G (IgG)
antibodies. They persist in blood and
provide permanent immunity to HAV
LABORATORY TESTS
INDICATING HEPATITIS
TESTS WHICH ARE LOWERED:
• Leukocytes (leukopenia)
• Serum albumin
• Serum glucose (hypoglycemia)
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PT (prolonged)
TESTS WHICH ARE
ELEVATED:
• serum bilirubin
• Bilirubin in urine
• ALT
• AST
• Alkaline phosphatase
elevated or may be normal
Nonsurgical Management
• Physical rest
• Psychological rest
• Drug therapy includes:
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Antiemetics
Antiviral medications
Immunomodulators
Corticosteroids
• DECREASE # MEDS TO ALLOW LIVER TO
REST
DRUGS
• ANTIVIRALS:
– Lamivudine (Epivir-HBV)
– Adefovir dipivoxil (Hepsera)
• USED: to destroy Hepatitis B virus in
chronic disease
• SIDE EFFECTS: alters renal function;
granulocytopenia
DRUGS
IMMUNOMODULATING DRUGS:
– Interferon(peginterferon alfa-2a) (Pegasys)
– Oral ribavirin (Virazole)
NURSING CARE
Diet therapy
• Hydration
• No alcohol
• Low fat, moderate protein, high CHO
diet, high calorie
• Small frequent meals
• Vit B, C, K
PATIENT EDUCATION
• Prevention to health care
professionals
• Knowledge of transmission
routes
• Proper personal hygiene and
good sanitation
• Gamma Globulin
• Avoid sex until antibody
results (negative)
• Hepatitis A Vaccine
• Hepatitis B vaccine
• No vaccine for
Hepatitis E
• Hepatitis C mainly
spread through blood
transfusions: (screen
blood products)
CIRRHOSIS DEFINED
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Chronic
Degenerative
Causes liver enlargement
Causes loss of normal liver function
PATHOPHYSIOLOGY
• Fibrotic bands of connective tissue change
the structure of the liver
• Inflammation causes degeneration and
destruction of liver cells
• Tissue becomes nodular
• Nodules block bile ducts and normal blood
flow throughout the liver
• Blood flow changes occur from compression
by the fibrous tissue
TYPES OF CIRRHOSIS
• Laennec’s cirrhosis: chronic ETOH,
nutritional deficiencies
• Biliary
• Postnecrotic cirrhosis: hepatic necrosis
• Cardiac: congestion and tissue damage
due to heart failure
ETIOLOGY
• Known causes of liver disease include:
– Alcohol
– Viral hepatitis
– Autoimmune hepatitis
– Steatohepatitis
– Drugs and toxins
– Biliary disease
(Continued)
ETIOLOGY CONTINUED
– Metabolic/genetic causes
– Cardiovascular disease
EARLY SIGNS AND
SYMPTOMS CIRRHOSIS
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Same for all types regardless of the cause
Start out vague, like flu
General weakness, Fatigue
Anorexia, Indigestion
Abnormal bowel function (constipation, or diarrhea)
Abdominal pain/liver tenderness
LATE S & S
• Jaundice, pruritus, dry skin, warm bright red palms of hands
(palmar erythema), rashes
• Edema, ascites, significant wgt change, peripheral dependent
edema extremities and sacrum
• Bleeding tendencies/Anemia/petecchiae, echymosis
• Infections
• Menstrual irreg/gynecomastia/impotence
• Renal failure/dark amber urine
• Clay colored stools
ASSESSMENT
INSPECTION:
• Jaundice
• Caput medusae: dilated abd veins,
• striae,
• spider angiomas
• Contour of abdomen: Distension: massive ascites
• Everted umbilicus (umbilicus protrusion)
• HEPATOMEGALY, SPLENOMEGALY
Other Physical
Assessments
• Assess nasogastric drainage,
vomitus, and stool for presence of
blood
• Fetor hepaticus (breath odor)
• Amenorrhea
• Gynecomastia, testicular atrophy,
impotence
• Neurologic changes: changes in
LOC, leading to coma, Asterixis
HOW TO ELICIT ASTERIXIS
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Have client extend the arm,
dorsiflex the wrist
Extend the fingers
OBSERVE rapid non-rhythmic
extensions and flexions
Laboratory Assessment
• AST: Aminotransferase serum levels and LDH: lactate
dehydrogenase may be elevated from hepatic cell destruction.
• Alkaline phosphatase levels may increase from obstructive
jaundice.
• Total serum bilirubin from hepatic disease and urobilinogen
levels may rise from hepatocellular obstruction or liver
disease.
• decrease.
(Continued)
Laboratory Assessment
(Continued)
• Fecal urobilinogen is decreased due to
obstructive liver disease
• Total serum protein and albumin levels
decreased
• Prothrombin time prolonged; platelet
count low
• Decreased hemoglobin and hematocrit
values due to anemia and white blood cell
count
LABORATORY
ASSESSMENT CONTINUED
• Elevated ammonia levels: liver
cannot excrete ammonia
• BUN and Serum creatinine level
possibly elevated due to decreased
renal function
COMPLICATIONS:
PORTAL HYPERTENSION
• Increase pressure in portal vein
• Comes from obstruction of blood flow
from pressure by CT bands (see patho)
• New channels looked for
• Blood flows back to spleen
(splenomegaly)
• Veins become dilated (esophagus,
stomach, intestines, abdomen, rectum)
PORTAL HYPERTENSION
(CONTINUED)
• Results in:
– Ascites
– Esophageal varices
– Prominent abdominal veins (caput
medusae)
– hemorroids
COMPLICATION: ASCITES
DEFINED AS:
• Accumulation of free fluid within the
peritoneal cavity
• With increased hydrostatic pressure
from portal hypertension fluid leaks into
peritoneal cavity
• Albumin in fluid
hypoalbuminemia
ASCITES CONTINUED
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Hypovolemia renal vasoconstriction
Renin-angiotensin system triggered
Sodium and water retention
Leads to increased hydrostatic pressure
Perpetuates the cycle of ASCITES
COMPLICATIONS
ASCITES:
• Bed rest, HOB up 30 degrees or higher; or
sitting in chair
• Abdominal girth measurements
• bid wgts standing
• Strict fluid restriction; strict I & O, vitamin
supplements
• Salt free diet/diuretics/electrolyte replacement
Excess Fluid Volume
(Continued)
Paracentesis is insertion of trocar
catheter into abdomen to remove &
drain fluid from the peritoneal cavity.
– Observe for possibility of impending
shock, electrolyte imbalances: albumin
IV.
EXCESS FLUID SURGICAL
MANAGEMENT CONTINUED
– LAVEEN SHUNT (peritoneovenous shunt): surgical procedure,
tube placed in peritoneal cavity, drain fluid into superior vena
cava
– PORTACAVAL SHUNT: (See p 1378
fig 62.4) surgical shunting diverts portal venous blood flow
from the liver
TIPS (transjugular intrahepatic portalsystemic shunt): non
surgical procedure creating a connection within the liver
between the portal and systemic circulation to reduce portal
pressure
COMPLICATION: BLEEDING
ESOPHAGEAL VARICES
DEFINED: fragile thin walled esophageal
veins become distended from pressure
Portal hypertension blood backs up
from liver to esophageal and gastric
vessels
COMPLICATIONS
ESOPHAGEAL VARICES
MEDICAL EMERGENCY
LIFE THREATENING
S&S: hematemesis, melena, shock
Can occur spontaneously
Can be caused by any activity that
Abdominal pressure
TREATMENT OF BLEEDING
ESOPHAGEAL VARICES
• IV fluids/electrolytes/volume expander/
transfuse
• ESOPHAGOGASTRIC BALLOON
TAMPONADE: via SengstakenBlakemore tube
– Compressing bleeding vessels with this
tube
SENGSTAKEN-BLAKEMORE
TUBE
Used to control bleeding
• Esophageal balloon
• Gastric balloon
• 3 lumens
– 1 for gastric lavage
– 1 for inflating the esophageal balloon
– 1 for inflating the gastric balloon
SENGSTAKEN-BLAKEMORE
TUBE: NRSG CARE
• MD inserts tube with HOB 30-45 degrees
MOST SERIOUS COMPLICATION: ASPIRATION AND AIRWAY
OCCLUSION
SURGICAL SCISSORS AT BEDSIDE
• Monitor for respiratory distress
• Suction saliva from upper esophagus, nasopharynx
• Check nostrils frequently, cleanse and lubricate to prevent
ulceration
• Removed after bldg controlled
RUPTURE OF
ESOPHAGEAL VARICIES
• Vasopressin: constriction arterial bed
• Somatostatin: decreases bldg without
vasoconstrictive effects of Vasopressin
• Propranolol: beta blocker to decrease
portal pressure
COMPLICATION:
COAGULATION DEFECTS
• synthesis of bile in liver
• Prevents absorption of fat soluble
vitamins (vit K)
• Without vit K clotting factors are not
produced
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susceptible to bleeding
• Abnormal PT (prolonged or )
COMPLICATION:
SPLENOMEGALY
• Backup of blood into spleen
• Spleen destroys platelets
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thrombocytopenia (first sign of liver
dysfunction)
COMPLICATION: JAUNDICE
• Liver cells cannot excrete bilirubin
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circulating bilirubin levels
LABORATORY TESTS: changes with hepatocellular jaundice
Serum bilirubin (indirect and direct)
Urine bilirubin
Urobilinogen stool: normal to
Urobilinogen urine: normal to
COMPLICATIONS:
PORTAL SYSTEMIC
ENCEPHALOPATHY (PSE)
• Also called HEPATIC ENCEPHALOPATHY AND HEPATIC
COMA
SEE: neurologic symptoms
Impaired LOC
Impaired thinking
Impaired neuromuscular disturbances
ACUTE AND REVERSIBLE with early intervention
CAUSED BY: elevated ammonia levels
NURSING DIAGNOSIS
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Activity intolerance
Fluid volume deficit
Fluid volume excess
Ineffective breathing patterns
Risk for hemorrhage
Risk for infection
Altered nutrition
Pain
Sexual dysfunction
NURSING DIAGNOSIS
CONTINUED
• Altered thought processes
• Risk for violence
NURSING CARE
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Bed rest with controlled activity, prevent clots
Prevent infection (pneumonia)
Assess for bleeding
Treat dry itching skin: no soap, soft linens,
lotions, antihistamines
• Assess F & E status, bid wgts, abd girth once
shift, I&O, fluid restriction, amt of dietary
protein
• Assess neuro status q 2 hr
• Psychological support/abstinence of alcohol
Fatty Liver (Steatohepatitis)
• Fatty liver is caused by the
accumulation of fats in and around
the hepatic cells.
• Causes include:
– Diabetes mellitus
– Obesity
– Elevated lipid profile
• Many clients are asymptomatic.
Hepatic Abscess
• Liver invaded by bacteria or protozoa
causing abscess
• Pyrogenic liver abscess; amebic
hepatic abscess
• Treatment usually involves:
– Drainage with ultrasound guidance
– Antibiotic therapy
Liver Trauma
• The liver is the most common organ injured in
clients with penetrating trauma of the abdomen,
such as gunshot wounds and stab wounds.
• Clinical manifestations include abdominal
tenderness, distention, guarding, rigidity.
• Treatment involves surgery, multiple blood
products.
Cancer of the Liver
• One of the most common tumors in the
world
• LIVER BX: done in same day surgery,
local anesthetic, done through skin.
CRITICAL THAT COAGULATION TESTING
BE DONE. MAJOR SE: hemorrhage
• Most common c/o: abd discomfort
• Tx includes: Chemotherapy/Surgery
Liver Transplantation
• Used in the treatment of end-stage liver disease,
primary malignant neoplasm of the liver
• Donor livers obtained primarily from trauma
victims who have not had liver damage
• Donor liver transported to the surgery center in a
cooled saline solution that preserves the organ
for up to 8 hours
Complications
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Acute, chronic graft rejection
Infection
Hemorrhage
Hepatic artery thrombosis
Fluid and electrolyte imbalances
Pulmonary atelectasis
Acute renal failure
Psychological maladjustment