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Care of patients with liver impairment/FAILURE

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School of Nursing
Care of Patients with Impaired Liver Function
I. Bleeding
A. Due to:
1. Decreased in formation of plasma proteins-fibrinogen, prothrombin.
2. Portal hypertension can cause bleeding esophageal varices or varices
in upper part of the stomach and bleeding hemorrhoids.
3. Splenomegaly from portal hypertension can cause increase in platelet
destruction.
4. Conditions causing biliary obstruction cause lack of absorption of Vit.K.
Thus the liver cannot synthesize prothrombin from Vit. K.
B. Possible Nursing Diagnosis:
1. Potential for bleeding
2. Altered tissue perfusion; systemic related to hemorrhagic shock.
3. Activity intolerance; fatigue-weakness related to anemia from blood loss
C. Nursing Care
1. Goals: Prevent trauma and detect early bleeding.
2. Small gauge needles used for injections; prolonged pressure needed at
injection sites and venipuncture sites.
3. Soft bristled toothbrush and gentle mouth care.
4. Check stool for occult blood (guaiac)
5. Observe for bleeding from nose, urine, mouth, skin, emesis, gums.
6. Move and handle extremities at joints-not muscle belly.
7. Check on stool consistency. If hard, get order for stool softener. Hard
stools increase chance of bleeding from hemorrhoids.
8. Don’t blows nose hard or manipulate nose excessively.
9. If O2 is given, be sure it is well humidified.
10. Check V.S. for increased pulse, decreased BP. Do orthostatic BP and
pulse if bleeding is suspected or to monitor blood loss.
11. If varices are present, no coarse foods given (mechanical soft diet), avoid
straining, vomiting, lifting, coughing, retching—anything that would
increase intra-abdominal pressure.
12. Vit. K is sometimes given parenterally.
a. If bleeding is due to decreased absorption of Vit. K, the
prothrombin time should return to normal.
b. If liver is badly damaged, Vit. K will not help and little or no
change in pro time because liver cannot synthesize
prothrombin from Vit. K.
13. Check lab values of prothrombin tinme and INR
a. Pro time: the greater in seconds from normal, the greater the
chance for bleeding.
b. INR: the larger the number from 1.0, the greater the chance for
bleeding.
II. Problem of Edema
A. Can be due to:
1. Decreased plasma proteins decreased colloid osmotic pressure.
2. Portal hypertensionincreased hydrostatic pressure in portal system and
destruction of lymphaticsascites. Fluid high in protein. Increased
oncotic pressure of peritoneal fluid pulls fluid out from vascular
compartment.
3. Decreased renal perfusion due to decreased circulating blood
volumerenin-angiotensin-aldersterone mechanism
activatedincreased Na and water to restore blood volume.
B. Possible Nursing Diagnosis:
1. Alteration in fluid volume: excess
2. Alteration in body image or self-concept.
3. Ineffective breathing pattern.
4. Alteration in nutrition: less than body needs.
5. Alteration in skin integrity: decubiti
6. Alteration in tissue perfusion: peripheral & DVT
7. Alteration in comfort: abdominal pain.
8. Potential for injury: falls
9. Potential alteration in electrolyte balance.
C. Nursing Care
1. Edema usually generalized: ascities and hydrothorax often present
2. Review care for patients with CHF.
3. Skin care essential-total serum proteins also reduced, building and
repairing of tissue potentially decreased
4. I/O, daily weights
5. Know fluid goal: fluids restricted in some cases, esp. if Na+ is low.
6. If ascities is present:
a. self image altered
b. may be unsteady-center of gravity is off, safety factors; need help
with foot care and parts that are difficult to reach.
c. abdomen can be very taut, tense and painful.
d. may need to measure abd. girth daily. Do so at umbilicus
e. increased abdominal pressure may decrease volume return from
lower extremities. Thrombo-embolic events possible.
1) dorsiflexion exercises; avoid dependent position of legs
2) no pressure on veins; prevent injury to legs.
f. breathing difficulties-impingement on diaphragm; semi-Fowler’s
position most comfortable usually. Keep fluid in lower part
of peritoneal space; decreased activity and need for oxygen.
g. anorexia and difficulty eating due to congestion of abdominal
viscera and liver disease per se.
1) frequent small feedings
2) feed patients when they are hungry.
3) calorie count kept on these patients, if necessary.
4) must encourage patients to eat; diet is their medicine
5) usually salt restricted diet-not too appealing.
h. administer diuretics as ordered
1) watch I/O & daily weights. 1-2 lb.weight loss per day is good
2) observe for fluid and electrolyte imbalances esp. decreased K.
Remember decreased K can precipitate hepatic coma.
3) spironalactone is a diuretic frequently given. Causes K+ to
be spared. Check K+ levels frequently and urine output to be
sure K+ levels will not increase dangerously due to lack of urine
output.
7. Note blood chemistry teststotal serum protein and serum albumin.
8. Shunt surgery to decrease ascites.
III. Encephalopathy or Hepatic Coma
A. Mechanism involved which causes cerebral symptoms is: NH3 ties up glutamic acid
needed for brain tissue activity and functioning. NH3 interferes with oxidation
of glucose which brain needs for energy.
B. Signs and symptoms—characterized by progressive failure of all aspects of liver
function and associated with neurological manifestations. Symptoms include:
1. Mild apathy, lethargy, drowsiness, mental dullness (obtunded), loss of
memory, loss of neatness, sloppy in eating, distant stare.
2. Confusion, disorientation, irritability abusiveness, slurred speech.
3. Lethargy progresses to stupor and coma.
4. Fetor hepaticus—bad taste in mouth, sweet, musty odor of breath—
characteristic of diffuse liver necrosis; may be early sign of impending
coma.
5. Increased temperature.
6. Flapping tremor or liver flap called ASTERIXIS. Check for this daily.
7. Muscular twitching and poor muscle coordination. Unable to construct a
simple design, e.g. O or +, worsening or change in handwriting from day
to day (check this daily)
8. Unable to think clearly, e.g. subtract serial &’s, translate parables.
9. Increased blood NH3
C. Possible Nursing Diagnosis:
1. Potential for injury (falls and other injuries)
2. Alteration in communication: confusion, forgetfulness
3. Self care deficit: ADL’s
4. All of the diagnoses that deal with immobility if the person is comatose.
5. Alteration in mental status and thought processes
6. Alteration in respiratory function: potential airway obstruction (if comatose)
D. Treatment and Nursing Care:
1. Patient safety-patient is stuporous, lethargic or even comatose; does not use
good judgment and may have difficulty with muscular coordination.
2. Good oral hygiene (fetor hepaticus)
3. Don’t give sedatives for delirious or agitated behavior.
4. Do a mental test on patients daily-simple math, orientation—time, place,
person, who is the president of the US etc.
5. Patients can be difficult to deal with due to personality changes. Simple
directions, don’t argue with patients. Try to keep them oriented and safe.
6. If in a coma—keep airway open, safety factors, problems of immobility,
never leave unconscious patients on their backs unattended-may aspirate
fluid into the lung. Elevate HOB 23-30 degrees.
7. Observe patients frequently for even minor changes so that a coma can be
aborted by early treatment. Very important nursing function.
8. Carry out medical plan of care
a. Reduction of dietary protein—20 Gm/day
b. Enemas or laxatives to purge GI tract of any blood and by-products of
protein breakdown (blood is good source of protein on which gut
bacteria can act)
c. Administration of antibiotics to sterilize the bowel may be ordered
1) Neomycin may be ordered. Poorly absorbed and less toxic
2) Causes inhibition of bacterial action on protein substances in
the bowel. Destroys normal bacterial flora of gut so they
are no longer present to break down protein with
resultant production of NH3
3) With Neomycin therapy, dietary protein can often be
increased
d. Lactulose syrup (Cephulac or Duphaluc)
1) Dose 30-40 cc tid or qid po, NG or rectally.
2) Mechanism: acidifies colon contents. Colon retains NH3 as
NH4; blood NH3 migrates to colon. It also forms NH4
and is trapped in bowel; laxative action of lactulose
expels NH4 out of colon in stool.
3) Side effects: flatulence, belching, abd. cramps, diarrhea
(watch for > 6 stools/day)
9. Avoid conditions that can precipitate coma.
a. Excessive protein intake.
b. Massive bleeding in GI tract
c. Certain diuretics: thiazides
d. K+ depletion (check K+ levels—if on diuretics, extremely important)
e. Paracentesis—probable mechanism in increased NH3 formation by
kidneys or acid-base imbalance.
f. Acute infections and surgical procedures; increased demands on
already failing liver due to increased metabolic needs.
g. morphine (mechanism unknown)
h. AZOTEMIA (increased nitrogenous products in blood)
10. Know blood ammonia level and plan care accordingly. (The higher it is, the
greater the potential for coma or coma present). Patients do vary in
terms of NH3 levels and presence of S&S. Some tolerate high levels
without symptoms, others may be in a coma with lower levels.
IV. Problem of Drug Toxicity
1. Observe for S&S of drug toxicity or intensified action of drugs
2. Don’t give MSO4, barbiturates or Tylenol to these patients or only in very small
dosages.
3. Patients should take no medications unless ordered by doctor. Drugs that are
metabolized or detoxified by the liver are the greatest danger.
4. Further liver damage can result from effects of some drugs: Compazine family, birth
control pills, anesthetics such as Halothane and Tylenol, certain antibiotics such
as sulfa drugs.
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