NURSING MANAGEMENT OF ADULTS WITH DISORDERS OF THE LIVER. 2009. TOPICS TO BE REVIEWED. 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
NURSING MANAGEMENT OF ADULTS WITH DISORDERS OF THE LIVER
STEATOHEPATITIS (FATTY LIVER)
CANCER OF LIVER
MAIN FUNCTIONS OF THE LIVER: storage, protection, metabolism
Maintains normal serum glucose levels
Vitamin and Iron storage
Drug metabolism and detoxification
What happens to glucose in the liver?
Where is it stored?
When is it released?
What is gluconeogenesis?
When does it take place?
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?
What is the liver’s job in terms of synthesizing plasma proteins?
What does the liver need to complete it’s job?
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?
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?
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?
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?
Sinusoids store blood (about 200-400 cc)
DISORDER OF THE LIVER
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
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
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.
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.
Hepatitis carriers can infect others, even if they are without symptoms.
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
Transmitted primarily by parenteral routes
Incubation period 14 to 56 days
HDV coinfects with HBV and needs it presence to replicate
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
Changes in skin or eye color
Arthralgia (joint pain)
Myalgia (muscle pain)
Intolerance to fats/dyspepsia
CHANGES IN COLOR OF URINE AND STOOL
Lasts about 1 week
Lasts 2-6 weeks
Yellow skin, sclera, mucous membranes
Dark amber urine
Clay colored stools
Lasts 2-6 weeks
Liver decreases in size
There will be an increase of liver enzymes and serologic markers INDICATING A PRESENCE OF HEPATITIS A, B, C
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
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
ELISA (enzyme linked immunosorbent assay ) SCREENS INITIALLY & for HCV antibodies (anti-HCV): 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
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
VIRUS CANNOT BE DETECTED
Presence of hepatitis E antibodies (anti-HEV) is found in people infected with virus
A person having a previous infection is indicated by immunoglobulin G (IgG) antibodies. They persist in blood and provide permanent immunity to HAV
TESTS WHICH ARE LOWERED:
Serum glucose (hypoglycemia)
TESTS WHICH ARE
Bilirubin in urine
Alkaline phosphatase elevated or may be normal
Drug therapy includes:
DECREASE # MEDS TO ALLOW LIVER TO REST
Adefovir dipivoxil (Hepsera)
USED: to destroy Hepatitis B virus in chronic disease
SIDE EFFECTS: alters renal function; granulocytopenia
Interferon(peginterferon alfa-2a) (Pegasys)
Oral ribavirin (Virazole)
Low fat, moderate protein, high CHO diet, high calorie
Small frequent meals
Vit B, C, K
Prevention to health care professionals
Knowledge of transmission routes
Proper personal hygiene and good sanitation
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)
Causes liver enlargement
Causes loss of normal liver function
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
Laennec’s cirrhosis: chronic ETOH, nutritional deficiencies
Postnecrotic cirrhosis: hepatic necrosis
Cardiac: congestion and tissue damage due to heart failure
Known causes of liver disease include:
Drugs and toxins
Same for all types regardless of the cause
Start out vague, like flu
General weakness, Fatigue
Abnormal bowel function (constipation, or diarrhea)
Abdominal pain/liver tenderness
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
Renal failure/dark amber urine
Clay colored stools
Caput medusae: dilated abd veins,
Contour of abdomen: Distension: massive ascites
Everted umbilicus (umbilicus protrusion)
Assess nasogastric drainage, vomitus, and stool for presence of blood
Fetor hepaticus (breath odor)
Gynecomastia, testicular atrophy, impotence
Neurologic changes: changes in LOC, leading to coma, Asterixis
Have client extend the arm,
dorsiflex the wrist
Extend the fingers
OBSERVE rapid non-rhythmic extensions and flexions
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.
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
Elevated ammonia levels: liver cannot excrete ammonia
BUN and Serum creatinine level possibly elevated due to decreased renal function
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)
Prominent abdominal veins (caput medusae)
Accumulation of free fluid within the peritoneal cavity
With increased hydrostatic pressure from portal hypertension fluid leaks into peritoneal cavity
Albumin in fluid hypoalbuminemia
Hypovolemia renal vasoconstriction
Renin-angiotensin system triggered
Sodium and water retention
Leads to increased hydrostatic pressure
Perpetuates the cycle of 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
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.
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
DEFINED: fragile thin walled esophageal veins become distended from pressure
Portal hypertension blood backs up from liver to esophageal and gastric vessels
S&S: hematemesis, melena, shock
Can occur spontaneously
Can be caused by any activity that
IV fluids/electrolytes/volume expander/ transfuse
ESOPHAGOGASTRIC BALLOON TAMPONADE: via Sengstaken-Blakemore tube
Compressing bleeding vessels with this tube
Used to control bleeding
1 for gastric lavage
1 for inflating the esophageal balloon
1 for inflating the gastric balloon
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
Vasopressin: constriction arterial bed
Somatostatin: decreases bldg without vasoconstrictive effects of Vasopressin
Propranolol: beta blocker to decrease portal pressure
synthesis of bile in liver
Prevents absorption of fat soluble vitamins (vit K)
Without vit K clotting factors are not produced
susceptible to bleeding
Abnormal PT (prolonged or )
Backup of blood into spleen
Spleen destroys platelets
thrombocytopenia (first sign of liver dysfunction)
Liver cells cannot excrete bilirubin
circulating bilirubin levels
LABORATORY TESTS: changes with hepatocellular jaundice
Serum bilirubin (indirect and direct)
Urobilinogen stool: normal to
Urobilinogen urine: normal to
Also called HEPATIC ENCEPHALOPATHY AND HEPATIC COMA
SEE: neurologic symptoms
Impaired neuromuscular disturbances
ACUTE AND REVERSIBLE with early intervention
CAUSED BY: elevated ammonia levels
Fluid volume deficit
Fluid volume excess
Ineffective breathing patterns
Risk for hemorrhage
Risk for infection
Altered thought processes
Risk for violence
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 is caused by the accumulation of fats in and around the hepatic cells.
Elevated lipid profile
Many clients are asymptomatic.
Liver invaded by bacteria or protozoa causing abscess
Pyrogenic liver abscess; amebic hepatic abscess
Treatment usually involves:
Drainage with ultrasound guidance
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.
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
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
Acute, chronic graft rejection
Hepatic artery thrombosis
Fluid and electrolyte imbalances
Acute renal failure