Liver Cirrhosis Nursing Care Plan & Management

 Description

• Is a chronic disease that causes cell destruction and fibrosis (scarring) of hepatic tissue.
• 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.

    Three major forms:

1. 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.
2. Postnecrotic (micronodular) Cirrhosis
   • Consist of broad bands of scar tissue and results from previous acute viral hepatitis or drug-induced massive hepatic necrosis.
3. Biliary Cirrhosis
   • Consist 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.

Causes/ Risk Factors

• 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.

Pathophysiology

Assessment

1. Early complaints including fatigue, anorexia, edema of the ankles in the evening, epistaxis, bleeding gums, and weight loss.
2. In later disease:
   • Chronic dyspepsia, constipation and diarrhea.
   • Esophageal varices; dilated cutaneous veins around umbilicus (caput medusa); internal hemorrhoids, ascites, splenomegaly.
   • Fatigue, weakness, and wasting caused by anemia and poor nutrition.
   • Deterioration of mental function.
   • Estrogen-androgen imbalance causing spider angioma and palmar erythema; menstrual irregularities in women; testicular and prostatic atrophy, gynecomastia, loss of libido, and impotence in men.
   • Bleeding tendencies and hemorrhage.
3. Enlarged, nodular liver.

Diagnostic Evaluation

1. Elevated serum liver enzyme levels, reduced serum albumin.
2. Liver biopsy detects cell destruction and fibrosis of hepatic disease.
3. Liver scan shows abnormal thickening and a liver mass.
4. CT scan determines the size of the liver and its irregular nodular surface.
5. Esophagoscopy determines the presence of esophageal varices.
6. Percutaneous transhepatic cholangiography differentiates extrahepatic from intrahepatic obstructive jaundice.
7. Paracentesis examines ascitic fluid for cell, protein, and bacteria counts.

Primary Nursing Diagnosis

• Fluid volume excess related to retention

Therapeutic Intervention / Medical Management

Medical management is based on presenting symptoms.

• Treatment includes antacids, vitamins, balanced diet, and nutritional supplements; potassium-sparing diuretics (for ascites); avoidance of alcohol.
• Colchicine may increase the length of survval in patients with mild to moderate cirrhosis.

Surgical Intervention

1. Transjugular intrahepatic portosystemic shunt may be performed in patients whose ascites prove resistant. This percutaneous procedure creates a shunt from the portal to systemic cisculation to reduce portal pressure and relieve ascites.

   
   

Pharmacologic Intervention

• Provide asymptomatic relief measures such as pain medications and antiemetics.
• Diuretic therapy, frequently with spironolactone, a potassium-sparing diuretic that inhibits the action of aldosteroe on the kidneys.
• I.V albumin to maintain osmotic pressure and reduce ascites.
• Administration of lactulose or neomycin through a nasogastric tube or retention enema to reduce ammonia levels during periods of hepatic encephalopathy.

Nursing Intervention

• Observe stools and emesis for color, consistency, and amount, and test each one for occult blood.
• Monitor fluid intake and output and serum electrolyte levels to prevent dehydration and hypokalemia, which may precipitate hepatic encephalopathy.
• Maintain some periods of rest with legs elevated to mobilize edema and ascites. Alternate rest periods with ambulation.
• Encourage and assist with gradually increasing periods of exercise.
• Encourage the patient to eat high-calorie, moderate protein meals and supplementary feedings. Suggest small, frequent feedings.
• Encourage oral hygiene before meals.
• Administer or teach self-administration of medications for nausea, vomiting, diarrhea or constipation.
• Encourage frequent skin care, bathing with soap, and massage with emollient lotions.
• Keep the patient’s finger nails short to prevent scratching from pruritus.
• Keep the patient quiet and limit activity if signs of bleeding are evident.
• Encourage the patient to eat foods high vitamin C content.
• Use small gauge needles for injections and maintain pressure over injection site until bleeding stops.
• Protect from sepsis through good handwashing and prompt recognition and management of infection.
• Pad side rails and provide careful nursing surveillance to ensure the patient’s safety.
• Stress the importance of giving up alcohol completely.
• Involve the person closest to the patient, because recovery usually is not easy and relapses are common.