NCP Cirrhosis of the Liver

Cirrhosis is a chronic disease of the liver characterized by alteration in structure, degenerative changes and widespread destruction of hepatic cells, impairing cellular function and impeding blood flow through the liver. Causes include malnutrition, inflammation (bacterial or viral), and poisons (e.g., alcohol, carbon tetrachloride, acetaminophen).

Cirrhosis is the fourth leading cause of death in the United States among people ages 35 to 55 and represents a serious threat to long-term health.


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.


Alcohol: acute withdrawal

Substance dependence/abuse rehabilitation

Fluid and electrolyte imbalances

Psychosocial aspects of care

Renal dialysis

Renal failure: acute

Total nutritional support: parenteral/enteral feeding

Upper gastrointestinal/esophageal bleeding

Patient Assessment Database

Data depend on underlying cause of the condition.


May report: Weakness, fatigue, exhaustion

May exhibit: Lethargy

Decreased muscle mass/tone


May report: History of/recent onset of HF, pericarditis, rheumatic heart disease, or cancer (causing liver impairment leading to failure)

Easy bruising, nosebleeds, bleeding gums

May exhibit: Hypertension or hypotension (fluid shifts)

Dysrhythmias, extra heart sounds (S3, S4)

JVD; distended abdominal veins

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)


May report: Anorexia, food intolerance/ingestion


May exhibit: Weight loss or gain (fluid)

Tissue wasting

Edema generalized in tissues

Dry skin, poor turgor

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


Pins/needles sensation, burning pain in extremities

May exhibit: Guarding/distraction behaviors



May report: Dyspnea

May exhibit: Tachypnea, shallow respiration, adventitious breath sounds

Limited thoracic expansion (ascites)



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)


May report: History of long-term alcohol use/abuse, alcoholic liver disease

History of biliary disease, hepatitis, exposure to toxins; liver trauma; upper GI bleeding; episodes of bleeding esophageal varices; use of drugs affecting liver function

Discharge plan
DRG projected mean length of inpatient stay: 6.4 days

May need assistance with homemaker/management tasks

Refer to section at end of plan for postdischarge considerations.


Liver scans/biopsy: Detects fatty infiltrates, fibrosis, destruction of hepatic tissues, tumors (primary or metastatic), associated ascites.

Percutaneous transhepatic cholangiography (PTHC): May be done to rule out/differentiate causes of jaundice or to perform liver biopsy.

Esophagogastroduodenoscopy (EGD): May demonstrate presence of esophageal varices, stomach irritation or ulceration, duodenal ulceration or bleeding.

Percutaneous transhepatic portal angiography (PTPA): Visualizes portal venous system circulation.

Serum bilirubin: Elevated because of cellular disruption, inability of liver to conjugate, or biliary obstruction.

Liver enzymes:

AST/ALT, LDH, and isoenzymes (LDH5): Increased because of cellular damage and release of enzymes.

Alkaline phosphatase (ALP) and isoenzyme (LAP1): Elevated because of reduced excretion.

Gamma glutamyl transpeptidase (GTT): Elevated.

Serum albumin: Decreased because of depressed synthesis.

Globulins (IgA and IgG): Increased synthesis.

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.

PT/activated partial thromboplastin time (aPTT): Prolonged (decreased synthesis of prothrombin)

Fibrinogen: Decreased.

BUN: Elevation indicates breakdown of blood/protein.

Serum ammonia: Elevated because of inability to convert ammonia to urea.

Serum glucose: Hypoglycemia suggests impaired glycogenesis.

Electrolytes: Hypokalemia may reflect increased aldosterone, although various imbalances may occur. Hypocalcemia may occur because of impaired absorption of vitamin D.

Nutrient studies: Deficiency of vitamins A, B12, C, K; folic acid, and iron may be noted.

Urine urobilinogen: May/may not be present. Serves as guide for differentiating liver disease, hemolytic disease, and biliary obstruction.

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.