Care of the Patient with Cirrhosis
Zach, a 47-year old male, has just been promoted to foreman of the nightshift for a building supply warehouse. He has
been sober for 2 years, supported by his wife and his Alcoholic Anonymous group. Unfortunately, his cirrhotic liver has
not recovered from 20 years of heavy drinking, and he has suffered residual effects. During the past 2 days he has had a
‘bad cough.’ This morning he coughed up bright red blood and came to the emergency department. His coughing and
bleeding have subsided for now. An IV of 5% dextrose and normal saline with 20mEq/L of KCl was initiated at
100ml/hour. Baseline laboratory tests are drawn. He is admitted to the GI unit for observation. You are the nurse
assigned to care for Zach. Shortly after you complete his admission assessment, you hear coughing while passing his
room. You enter his room and see bright red blood covering the front of his gown and bed linens. He looks very
frightened.
1. What is happening to Zach? He has bleeding esophageal varices. What is the underlying cause of the bleeding?
Cirrhosis…. Destruction of hepatocytes. Destruction of hepatic and portal veins obstruction of the normal
blood flow through the liver portal HTN development of collateral circulation in an attempt to decrease
high portal pressure and blood volume. Collateral circulation develops in the lower esophagus, anterior portion
of the abdominal wall, and rectum. These veins have very little elastic tissue and are very fragile, and easily
bleed. Bleeding varices is the most life-threatening complication. Coughing caused the varices to rupture.
Rupturing can also occur as a result of ulceration and irritation, alcohol ingestion, poorly chewed food,
swallowing course food, acid regurgitation from the stomach, increased abdominal pressure from vomiting,
straining to have a bowel movement, sneezing, or lifting heavy objects.
2. What would you, as the nurse, do to immediately intervene?
Assure the airway is open
Elevate HOB
Take VS
Assure patent IV line
Notify the physician
3. What can be done to stop the bleeding?
Octreotide (Sandostatin). Causes selective vasoconstriction by inhibiting glucagon release. Preferred b/c it lacks
the vasoconstrictive effects of vasopression.
Vasopressin (Pitressin) IV. Produces vasoconstriction of the arteries of the abdominal organs  decreased
portal blood flow decreased portal HTN. It also causes decreased coronary blood flow and increased heart
rate and increased BP. So Nitroglycerin (IV, SL, or transdermal) is given to decrease the detrimental effects of
vasopressin.
Sclerotherapy. Sclerosing agent introduced during endoscopy. It thrombosis and obliterates the distended vein.
Esophageal banding. A rubber band is slipped around the base of the bleeding varices via an endoscopic
procedure.
Balloon tamponade. Controls hemorrhage by mechanical compression of the bleeding varices. A
Minnesota or Blakemore tube is used. There are 2 balloons: a gastric balloon and an esophageal balloon. When
inflated, the balloons put pressure on any bleeding varices. The gastric balloon anchors the tube in place and
also applies pressure to any bleeding gastric varices. (Blakemore tube has a lumen for gastric suctioning; the
Minnesota tube has a lumen for esophageal suctioning.) Tube is inserted by physician. Inserted via nose or
mouth. Placement confirmed by x-ray. Sometimes patient wears a football-type helmet and tube is secured to
the mouth guard. Balloon is deflated every 8-12 hours to prevent necrosis. Lavage is done to remove blood from
the stomach (This prevents blood from breaking down to ammonia and leading to hepatic encephalopathy).
Possible complications from the tube: Aspiration pneumonia, erosion of esophagus, regurgitation and aspiration
of gastric contents (keep HOB elevated), occlusion of airway by the balloon (if gastric balloon breaks and
esophageal balloon moves upward, airway could be occluded: nurse must cut lumen to esophageal balloon to
deflate it, so scissors should be kept at bedside). Patient can’t swallow saliva R/T inflated balloons, so nurse
must provide emesis basin and oral care (Minnesota tube has esophageal suction to alleviate this problem.)
Vitamin K to correct clotting abnormalities.
H2 receptor blockers. Decreases gastric acidity (a cause of irritation and bleeding.)
Beta Blockers. Decreases portal HTN.
Also:
Patient most likely will need blood transfusion
Neomycin. Decreases bacterial flora and thus decreases ammonia production.
4. What lifestyle pattern do you think predisposed Zach to the pathological changes in his liver? Explain. Alcohol.
Alcohol causes fat to accumulate in the liver cells. If the patient stops drinking, these fatty changes are
potentially reversible. But continued alcohol causes scarring to occur. Scar tissue replaces liver cells. Hypoxia
occurs r/t inadequate blood flow thru the liver and scar tissue impaired liver functioning.
5. What other clinical manifestations would you expect to see in Zach related to his cirrhosis?
GI distrubances r/t liver’s altered metabolism of carbs, fats, and proteins: anorexia, N/V, flatulence, abdominal
pain (dull, heavy feeling in RUQ r/t swelling of liver), slight weight loss, fever, enlarged liver.
Jaundice. R/T liver cell damage and compression of bile ducts by connective tissue overgrowth as liver tries to
regenerate itself. Also r/t decreased ability of liver to conjugate and excrete bilirubin. Pruritis r/t accumulation of
bile salts under the skin. Urine often is cola colored and stool is gray or clay-colored.
Skin lesions. R/T liver’s decreased ability to metabolize hormones, resulting in increased circulating estrogen.
Spider angiomas- small, dilated blood vessels with a bright red center and spider-like branches on nose, cheeks,
trunk, neck, and shoulders.
Palmar erythema- red area on palms that blanches with pressure.
Hematologic problems.
Coagulation disorders r/t liver’s decreased ability to produce thrombin and other clothing factors. Assess for
epistaxis, petechiae, easy bruising, bleeding gums, and heavy menstrual bleeding.
Thrombocytopenia-Leukopenia-Anemia r/t splenomegaly. Results from a backup of blood from the portal vein
into the spleen overactivity of enlarged spleen increased removal of blood cells from circulation.
Peripheral neuropathy. Probably r/t dietary deficiency of thiamine, folic acid, vitamin B12. Results in sensory
deficits.
Endocrine disturbances. R/T liver’s inability to metabolize hormones (estrogen, testosterone).
Men: Loss of axillary and pubic hair, impotence
Women: Amenorrhea (younger), vaginal bleeding (older)
6. What other complications is Zach at risk for acquiring?
Peripheral edema. R/T decreased colloid osmotic pressure from impaired liver synthesis of albumin, and from
increased pressure from portal HTN.
Ascites. Accumulation of serous fluid in the abdominal cavity r/t HTN in the liver proteins move from blood to
lymph spaces. When lymphatic system is unable to carry off the excess proteins and water, they leak thru the
liver into the abdominal cavity. The osmotic pressure of the proteins pulls additional fluid into the abdominal
cavity. Ascites is also r/t hypoalbuminemia from the liver’s inability to synthesize albumin  decreased osmotic
colloid pressure.
Hepatic Encephalopathy (coma). Major source of ammonia is r/t the breakdown of bacteria in the intestine.
Normally, this goes to the liver via the portal blood system and is broken down to urea which is excreted by the
kidneys. But when blood is shunted past the liver due to collateral circulation, or the liver is unable to convert
ammonia to urea, large quantities of ammonia remain in the blood. Ammonia crosses the blood-brain barrier
neuro toxicity….lethargy, irritability, memory loss, confusion, drowsiness, insomnia, slow slurred speech, slow
deep respirations, hyperactive reflexes, disorientation, liver flap (asterixis… when arms extended outward, the
patient cannot hold this position and there will be a rapid flexion and extension of hand movements). Treated
with lactulose (Decreases the ph of the colon decreased diffusion of ammonia from the colon into the
blood decreased blood ammonia levels.)
7.
How would Zach’s diagnosis of liver disease be made?
Liver function tests: elevated liver enzymes (AST, ALT, alk phos) r/t release of enzymes from damaged liver.
Serum albumin: decreased
Total protein: decreased
PT: Prolonged
Serum bilirubin: increased
Liver biopsy
8. What nursing interventions would be appropriate for Zach?
Nursing interventions are aimed at promoting rest to decrease the demands on the liver and increase the blood
supply to the liver.
Diet: high protein diet supplemented with vitamins (B complex, A, C, K). Small frequent meals if ascites is
present. But protein is restricted if encephalopathy develops that cannot be successfully managed with
lactulose. Sodium restriction to prevent ascites and edema.
Skin care r/t edema, immobility if hospitalized, jaundice, pruitis.
Risk of bleeding: Use only electric razor. Soft-bristled toothbrush only. Apply extra pressure to venipuncture
sites.
I and O
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