Hepatic Cirrhosis Nursing Care Management and Study Guide

Cirrhosis is end-stage liver disease, and the cirrhotic patient stays alive on the details: protect against bleeding, manage ascites and fluid, watch mental status for encephalopathy, and remember that a damaged liver cannot detoxify the drugs you give. It is a chronic disease marked by diffuse destruction and fibrotic regeneration of liver cells.

What Is Hepatic Cirrhosis?

As necrotic liver tissue gives way to fibrosis, the disease alters liver structure and normal vasculature, impairs blood and lymph flow, and ultimately causes hepatic insufficiency. The prognosis is better in noncirrhotic hepatic fibrosis, which causes minimal dysfunction and does not destroy liver cells.

Classification

The clinical types reflect the diverse etiology:

• Laennec's cirrhosis: the most common type, in 30% to 50% of cirrhotic patients, up to 90% of whom have a history of alcoholism.
• Biliary cirrhosis: from injury or prolonged obstruction.
• Postnecrotic cirrhosis: from various types of hepatitis.
• Pigment cirrhosis: from disorders such as hemochromatosis.
• Cardiac cirrhosis: from right-sided heart failure.
• Idiopathic cirrhosis: no known cause.

Pathophysiology

Alcohol consumption is the major causative factor. Cirrhosis runs through episodes of necrosis of the liver cells, which are gradually replaced with scar tissue. This diffuse destruction and fibrotic regeneration alters liver structure and vasculature, impairs blood and lymph flow, and causes hepatic insufficiency.

Statistics and Incidences

By type: Laennec's cirrhosis occurs in 30% to 50% of cirrhotic patients, biliary in 15% to 20%, postnecrotic in 10% to 30%, pigment in 5% to 10%, and idiopathic in about 10%.

Causes

Excessive alcohol consumption is the most common cause. Injury or prolonged obstruction causes biliary cirrhosis. The various types of hepatitis cause postnecrotic cirrhosis. Diseases such as hemochromatosis cause pigment cirrhosis. Right-sided heart failure causes cardiac cirrhosis, a rare form.

Clinical Manifestations

The manifestations are similar across types regardless of cause. Early signs are usually GI: anorexia, indigestion, nausea, vomiting, constipation, or diarrhea. Respiratory symptoms come late from hepatic insufficiency and portal hypertension, such as pleural effusion and limited thoracic expansion from ascites, interfering with gas exchange and causing hypoxia. CNS signs of hepatic encephalopathy also appear late: lethargy, mental changes, slurred speech, asterixis (flapping tremor), peripheral neuritis, paranoia, hallucinations, extreme obtundation, and ultimately coma. Hematologically, the patient has bleeding tendencies and anemia. Endocrine changes include testicular atrophy in men and menstrual irregularities, gynecomastia, and loss of chest and axillary hair in women. Skin shows severe pruritus, extreme dryness, poor turgor, abnormal pigmentation, spider angiomas, palmar erythema, and possibly jaundice. Hepatic effects include jaundice, ascites, hepatomegaly, leg edema, hepatic encephalopathy, and hepatorenal syndrome.

Complications

Portal hypertension is elevated pressure in the portal vein when blood flow meets increased resistance. Esophageal varices are dilated, tortuous veins in the submucosa of the lower esophagus. Hepatic encephalopathy presents as deteriorating mental status and dementia or as abnormal involuntary and voluntary movements. Fluid volume excess occurs from increased cardiac output and decreased peripheral vascular resistance.

Assessment and Diagnostic Findings

A liver scan shows abnormal thickening and a liver mass. Liver biopsy is the definitive test, detecting destruction and fibrosis of hepatic tissue. CT, ultrasound, and MRI confirm the diagnosis by visualizing masses, abnormal growths, metastases, and venous malformations. Cholecystography and cholangiography visualize the gallbladder and biliary duct system. Splenoportal venography visualizes the portal venous system. Percutaneous transhepatic cholangiography differentiates intrahepatic from extrahepatic obstructive jaundice and discloses hepatic pathology and gallstones. CBC shows decreased white blood cell count, hemoglobin, hematocrit, albumin, or platelets.

Medical Management

Treatment removes or alleviates the underlying cause. The patient may benefit from a high-calorie, medium-to-high protein diet, though developing hepatic encephalopathy mandates restricted protein intake. Sodium is usually restricted to 2 g/day and fluids to 1 to 1.5 liters/day. Rest and moderate exercise are essential. Paracentesis can relieve ascites. The Sengstaken-Blakemore or Minnesota tube can control hemorrhage by applying pressure on the bleeding site.

Pharmacologic therapy requires caution because the cirrhotic liver cannot detoxify harmful agents effectively. Octreotide may be prescribed for esophageal varices. Diuretics may be given for edema but need careful monitoring, since fluid and electrolyte imbalance can precipitate hepatic encephalopathy. Encephalopathy is treated with lactulose, and antibiotics are used to decrease intestinal bacteria and reduce ammonia production, one of its causes.

Surgical Management

The transjugular intrahepatic portosystemic shunt (TIPS) procedure treats varices by upper endoscopy with banding to relieve portal hypertension.

Nursing Management

Care focuses on promoting rest, improving nutrition, providing skin care, reducing injury risk, and monitoring and managing complications.

Assessment

Check the skin, gums, stools, and vomitus for bleeding. Weigh the patient and measure abdominal girth at least once daily to assess fluid retention. Assess level of consciousness often and watch closely for changes in behavior or personality.

Diagnosis

• Activity intolerance related to fatigue, lethargy, and malaise
• Imbalanced nutrition, less than body requirements, related to abdominal distention, discomfort, and anorexia
• Impaired skin integrity related to pruritus from jaundice and edema
• High risk for injury related to altered clotting mechanisms and altered level of consciousness
• Disturbed body image related to changes in appearance, sexual dysfunction, and role function
• Chronic pain and discomfort related to enlarged liver and ascites
• Fluid volume excess related to ascites and edema formation
• Disturbed thought processes related to abnormal liver function and increased serum ammonia
• Ineffective breathing pattern related to ascites and restricted thoracic excursion

Planning and Goals

• Decrease fatigue and increase participation in activities
• Maintain a positive nitrogen balance, no further muscle loss, and meet nutritional requirements
• Reduce the potential for pressure ulcers and skin breakdown
• Reduce the risk of injury
• Verbalize improved body image and self-esteem
• Increase comfort
• Restore normal fluid volume
• Improve mental status, maintain safety, and cope with cognitive and behavioral changes
• Improve respiratory status

Interventions

Promoting rest: position the bed for maximal respiratory efficiency and provide oxygen if needed; prevent respiratory, circulatory, and vascular disturbances; encourage gradual increases in activity, planning rest with activity and mild exercise.

Improving nutrition: provide a nutritious, high-protein diet supplemented with B-complex vitamins and vitamins A, C, and K. Offer small, frequent meals, honor patient preferences, and give protein supplements if indicated. Provide nutrients by feeding tube or total parenteral nutrition if needed. For patients with steatorrhea, give water-soluble forms of the fat-soluble vitamins A, D, and E, plus folic acid and iron to prevent anemia. Switch to a temporary low-protein diet if signs of impending or advancing coma appear, and restrict sodium if needed.

Skin care: reposition frequently, avoid irritating soaps and adhesive tape, apply lotion to soothe irritated skin, and prevent scratching.

Reducing injury risk: use padded side rails if the patient becomes agitated or restless; orient to time, place, and procedures; instruct the patient to ask for help getting out of bed; evaluate any injury carefully for internal bleeding; use an electric razor and soft toothbrush; and apply pressure to venipuncture sites to minimize bleeding.

Monitoring complications: monitor for bleeding and hemorrhage; watch mental status closely and report changes so encephalopathy treatment starts promptly; monitor serum electrolytes and correct abnormalities; give oxygen if desaturation occurs and watch for fever or abdominal pain that may signal bacterial peritonitis or other infection; assess cardiovascular and respiratory status, give diuretics, implement fluid restrictions, and optimize positioning as needed; monitor intake and output, daily weight, abdominal girth, and edema; and watch for nocturia and later oliguria, which indicate worsening liver dysfunction.

Home management: provide dietary instruction including exclusion of alcohol; refer to Alcoholics Anonymous, psychiatric care, counseling, or a spiritual advisor if indicated; continue sodium restriction and stress avoidance of raw shellfish; give written instructions and reinforcement to patient and family; encourage rest and a lifestyle change (adequate, well-balanced diet and elimination of alcohol); teach the family the symptoms of impending encephalopathy and the risk of bleeding and infection; offer support and positive feedback; and refer to a home care nurse to ease the transition home.

Evaluation

Care is effective when the patient meets the planned goals: reduced fatigue with more activity, a positive nitrogen balance with no further muscle loss, lower risk of skin breakdown and injury, improved body image and self-esteem, increased comfort, restored fluid volume, improved mental status with maintained safety, and improved respiratory status.

Discharge and Home Care

Dietary instruction is the focus. Most important is excluding alcohol, which may require referral to Alcoholics Anonymous, psychiatric care, or counseling. Sodium restriction continues for a considerable time, if not permanently. Teach the patient and family the symptoms of impending encephalopathy, possible bleeding tendencies, and susceptibility to infection.

Documentation

Document level of activity, causative or precipitating factors, vital signs before, during, and after activity, the plan of care, responses to interventions and teaching, the teaching plan, changes to the plan, attainment of or progress toward outcomes, caloric intake, individual cultural or religious restrictions and personal preferences, availability and use of resources, duration of the problem, perception of pain and its effects on lifestyle and expectations of therapy, and results of laboratory tests, diagnostic studies, and mental status and cognitive evaluation.