Nursing Care Plan – Cirrhosis of the Liver

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Cirrhosis (pronounced /sɪˈroʊsɪs/) is a consequence of chronic liver disease characterized by replacement of liver tissue by fibrosis, scar tissue and regenerative nodules (lumps that occur as a result of a process in which damaged tissue is regenerated), leading to loss of liver function. Cirrhosis is most commonly caused by alcoholism, hepatitis B and C, and fatty liver disease, but has many other possible causes. Some cases are idiopathic, i.e., of unknown cause.

Ascites (fluid retention in the abdominal cavity) is the most common complication of cirrhosis, and is associated with a poor quality of life, increased risk of infection, and a poor long-term outcome. Other potentially life-threatening complications are hepatic encephalopathy (confusion and coma) and bleeding from esophageal varices. Cirrhosis is generally irreversible, and treatment usually focuses on preventing progression and complications. In advanced stages of cirrhosis the only option is a liver transplant.

The word "cirrhosis" derives from Greek κιρρός [kirrós] meaning yellowish, tawny (the orange-yellow colour of the diseased liver) + Eng. med. suff. -osis. While the clinical entity was known before, it was René Laennec who gave it the name "cirrhosis" in his 1819 work in which he also describes the stethoscope.

Pathophysiology of Liver Cirrhosis

 Cirrhosis of the liver is a chronic disease that causes cell destruction and fibrosis (scarring) of hepatic tissues. Fibrosis alters normal liver structure and vasculature, impairing blood and lymph flow and resulting in hepatic insufficiency and hypertension in the portal vein. Complications include hyponatremia, water retention, bleeding esophageal varices, coagulopathy, spontaneous bacterial peritonitis, and hepatic encephalopathy.
Cirrhosis is known in three major forms. In Laennec’s (alcohol-induced) cirrhosis, fibrosis occurs mainly around central veins and portal areas. This is the most common form of cirrhosis and results from chronic alcoholism and malnutrition. Postnecrotic (micronodular) cirrhosis consist of broad bands of scar tissue and results from previous acute viral hepatitis or drug-induced massive hepatic necrosis. Biliary cirrhosis consists of scarring of bile ducts and lobes of the liver and results from chronic biliary obstruction and infection (cholangitis), and is much rarer than the preceding forms.



May be hospitalized on a medical unit during initial or recurrent acute episodes with potentially life-threatening complications. Otherwise, this condition is handled at the community level.

  1. Alcohol: acute withdrawal
  2. Substance dependence/abuse rehabilitation
  3. Fluid and electrolyte imbalances
  4. Psychosocial aspects of care
  5. Renal dialysis
  6. Renal failure: acute
  7. Total nutritional support: parenteral/enteral feeding
  8. Upper gastrointestinal/esophageal bleeding
  9. Patient Assessment Database
  10. Data depend on underlying cause of the condition.

  • May report: Weakness, fatigue, exhaustion
  • May exhibit: Lethargy
  • Decreased muscle mass/tone

  1. May report: History of/recent onset of HF, pericarditis, rheumatic heart disease, or cancer (causing liver impairment leading to failure)
  2. Easy bruising, nosebleeds, bleeding gums
  3. May exhibit: Hypertension or hypotension (fluid shifts)
  4. Dysrhythmias, extra heart sounds (S3, S4)
  5. JVD; distended abdominal veins
  6. Jaundiced skin, sclera

  • May report: Flatulence
  • Diarrhea or constipation; gradual abdominal enlargement
  • May exhibit: Abdominal distention (hepatomegaly, splenomegaly, ascites)
  • Decreased/absent bowel sounds
  • Clay-colored stools, melena
  • Dark, concentrated urine; oliguria (renal failure)

  1. May report: Anorexia, food intolerance/ingestion
  2. Nausea/vomiting
  3. May exhibit: Weight loss or gain (fluid)
  4. Tissue wasting
  5. Edema generalized in tissues
  6. Dry skin, poor turgor
  7. Halitosis/fetor hepaticus, bleeding gums

  • May report: SO(s) may report personality changes, depressed mentation
  • May exhibit: Changes in mentation, confusion, hallucinations, coma
  • Slowed/slurred speech
  • Asterixis (involuntary jerking movements of hands/tongue/feet associated with hepatic encephalopathy)

  • May report: Abdominal tenderness/RUQ pain
  • Itching
  • Pins/needles sensation, burning pain in extremities
  • May exhibit: Guarding/distraction behaviors
  • Self-focus

  1. May report: Dyspnea
  2. May exhibit: Tachypnea, shallow respiration, adventitious breath sounds
  3. Limited thoracic expansion (ascites)
  4. Hypoxia

  • May report: Severe itching of the skin/dryness
  • May exhibit: Fever (more common in alcoholic cirrhosis)
  • Jaundice, ecchymosis, petechiae
  • Spider angiomas/telangiectasis, palmar erythema

  • May report: Menstrual disorders (women), impotence (men)
  • May exhibit: Testicular atrophy, gynecomastia, loss of hair (chest, underarm, pubic)

  1. May report: History of long-term alcohol use/abuse, alcoholic liver disease
  2. History of biliary disease, hepatitis, exposure to toxins; liver trauma; upper GI bleeding; episodes of bleeding esophageal varices; use of drugs affecting liver function
  3. Discharge plan
  4. DRG projected mean length of inpatient stay: 6.4 days
  5. May need assistance with homemaker/management tasks
  6. Refer to section at end of plan for postdischarge considerations.


  1. Liver scans/biopsy: Detects fatty infiltrates, fibrosis, destruction of hepatic tissues, tumors (primary or metastatic), associated ascites.
  2. Percutaneous transhepatic cholangiography (PTHC): May be done to rule out/differentiate causes of jaundice or to perform liver biopsy.
  3. Esophagogastroduodenoscopy (EGD): May demonstrate presence of esophageal varices, stomach irritation or ulceration, duodenal ulceration or bleeding.
  4. Percutaneous transhepatic portal angiography (PTPA): Visualizes portal venous system circulation.
  5. Serum bilirubin: Elevated because of cellular disruption, inability of liver to conjugate, or biliary obstruction.
  6. Liver enzymes:
  7. AST/ALT, LDH, and isoenzymes (LDH5): Increased because of cellular damage and release of enzymes.
  8. Alkaline phosphatase (ALP) and isoenzyme (LAP1): Elevated because of reduced excretion.
  9. Gamma glutamyl transpeptidase (GTT): Elevated.
  10. Serum albumin: Decreased because of depressed synthesis.
  11. Globulins (IgA and IgG): Increased synthesis.
  12. CBC: Hb/Hct and RBCs may be decreased because of bleeding. RBC destruction and anemia is seen with hypersplenism and iron deficiency. Leukopenia may be present as a result of hypersplenism.
  13. PT/activated partial thromboplastin time (aPTT): Prolonged (decreased synthesis of prothrombin)
  14. Fibrinogen: Decreased.
  15. BUN: Elevation indicates breakdown of blood/protein.
  16. Serum ammonia: Elevated because of inability to convert ammonia to urea.
  17. Serum glucose: Hypoglycemia suggests impaired glycogenesis.
  18. Electrolytes: Hypokalemia may reflect increased aldosterone, although various imbalances may occur. Hypocalcemia may occur because of impaired absorption of vitamin D.
  19. Nutrient studies: Deficiency of vitamins A, B12, C, K; folic acid, and iron may be noted.
  20. Urine urobilinogen: May/may not be present. Serves as guide for differentiating liver disease, hemolytic disease, and biliary obstruction.
  21. Fecal urobilinogen: Decreased.

  1. Maintain adequate nutrition.
  2. Prevent complications.
  3. Enhance self-concept, acceptance of situation.
  4. Provide information about disease process/prognosis, potential complications, and treatment needs.

  1. Nutritional intake adequate for individual needs.
  2. Complications prevented/minimized.
  3. Dealing effectively with current reality.
  4. Disease process, prognosis, potential complications, and therapeutic regimen understood.
  5. Plan in place to meet needs after discharge.

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