In 2005, cirrhosis and other liver disorders were listed as the 12th leading cause of death in the United States. Liver transplantation is currently the only life-saving procedure for end-stage disease.
In 2005, cirrhosis and other liver disorders were listed as the 12th leading cause of death in the United States. Liver transplantation is currently the only life-saving procedure for end-stage disease.
In 2005, cirrhosis and other liver disorders were listed as the 12th leading cause of death in the United States. Liver transplantation is currently the only life-saving procedure for end-stage disease.
a. Alteration in structure and degenerative changes resulting from buildup of diffuse bands of fibrotic connective tissue causing widespread destruction of hepatic cells, impairing liver function, and impeding blood flow through the liver b. Compensated cirrhosis: Liver function may continue for some time, even with significant scarring, but metabolic abnormalities can occur, such as coagulation defects and malnutrition. c. Decompensated cirrhosis: progression of failure with significant complications, such as portal hypertension with bleeding varices, ascites, peritonitis, hepatorenal syndrome, and encephalopathy II. Etiology a. Rate of progression of fibrosis to cirrhosis varies for unknown reasons. b. Multiple causation (Wolf, 2007) i. Hepatitis C (26%), B, and D (15%) ii. Alcoholic liver disease (21%) iii. Cholestatic diseases: biliary atresia, primary biliary cirrhosis, cystic fibrosis, primary sclerosing cholangitis iv. Miscellaneous liver disorders, including autoimmune, Wilsons disease, alpha 1 -antitrypsin deficiency, hemochromatosis v. Injury from trauma, drugs, or other environmental toxins III. Treatment a. Goals are to slow the progression of the disease and alleviate the symptoms. b. Liver transplantation is currently the only life-saving procedure for end-stage disease. IV. Statistics a. Morbidity: In 2005, 112,000 hospitalizations for chronic liver disease or cirrhosis; approximately 17,000 individuals awaiting liver transplant (Scientific Registry of Transplant Recipients [SRTR], 2007). b. Mortality: Approximately 35,000 deaths annually due to chronic liver disease and cirrhosis (Wolf, 2007); in 2005, cirrhosis and other liver disorders were listed as the 12th leading cause of death in the United States (Hsiang-Ching, 2008). GLOSSARY Ascites: Buildup of fluid in the abdomen, due to a number of conditions including severe liver disease. Asterixis: Involuntary jerking movements of hands and feet associated with hepatic encephalopathy. Ecchymosis: Skin discoloration consisting of a large, irregularly formed hemorrhagic area with colors changing from blue-black to greenish-brown or yellow; commonly referred to as a bruise. Fetor hepaticus: Particularly foul-smelling breath, which frequently precedes hepatic coma. Hematemesis: Bloody vomitus. Hepatic encephalopathy: Brain dysfunction directly due to liver dysfunction seen in advanced cirrhosis, resulting in disturbances of consciousness and progressing to coma. Hepatomegaly: Enlarged liver. Hepatorenal syndrome: Represents a continuum of kidney dysfunction observed in individuals with cirrhosis caused by the vasoconstriction of large and small renal arteries. Jaundice: Yellow staining of the skin and sclerae (and sometimes other tissues and body fluids) because of abnormally high blood levels of bilirubin. Melena: Bloody stools. Oliguria: Urinary output less than 400 mL/day. Palmar erythema: Redness of the palms of the hands caused by dilation and congestion of capillaries. Peritoneovenous shunt: Surgically implanted device for continuous draining of ascitic fluid into the venous system. Fluid is removed via a pressure-sensitive one-way valve. It is connected to a tube under the subcutaneous tissue of the chest wall to the neck, where it enters the internal jugular vein and terminates in the superior vena cava. Petechiae: Tiny red dots on the skin caused by minute hemor-rhage, indicating low platelet count or other blood disorder. Spider angiomas: Abnormal collection of blood vessels near the surface of the skin; can occur anywhere, but are most common on the face and trunk. Splenomegaly: Enlarged spleen. Telangiectasis: Visibly dilated blood vessel on the skin or mucosal surface. Care Setting Client may be hospitalized on a medical unit during initial or recurrent acute episodes with potentially life-threatening complications. Otherwise, this condition is managed at the community, outpatient level. Related Concerns 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 Client Assessment Database Data depend on underlying cause of the condition. DIAGNOSTIC DIVISION MAY REPORT MAY EXHIBIT ACTIVITY/REST Weakness Fatigue, exhaustion Lethargy Decreased muscle mass and tone CIRCULATION History of or recent onset of heart failure (HF), pericarditis, rheumatic heart disease, or cancer, causing liver impairment leading to failure Easy bruising, nosebleeds, bleeding gums Hypertension or hypotension (fluid shifts) Dysrhythmias, extra heart soundsS 3 , S 4
Jugular vein distention (JVD), distended abdominal veins, spider angiomas, collateral circulation Ecchymosis, petechiae Anemia, leukopenia, thromboctyopenia, coagulation disorders, splenomegaly ELIMINATION Flatulence Diarrhea or constipation Gradual abdominal enlargement Abdominal distention (hepatomegaly, splenomegaly, ascites) Decreased or absent bowel sounds Clay-colored stools, melena Hemorrhoidal varices Dark, concentrated urine; oliguria (hepatorenal syndrome, failure) FOOD/FLUID Anorexia Food intolerance, ingestion Nausea, vomiting Hematemesis Weight loss or gain (fluid) Tissue wasting, delayed wound healing Edema generalized in tissues Dry skin, poor turgor Halitosis or fetor hepaticus, bleeding gums Hypoalbuminemia NEUROSENSORY Significant other (SO)/family may report personality changes, depressed mentation Changes in mentation, confusion, hallucinations, coma Slowed, slurred speech Asterixis PAIN/DISCOMFORT Abdominal tenderness and right upper quandrant (RUQ) pain Severe itching Pins-and-needles sensation, burning pain in extremities (peripheral neuropathy) Guarding or distraction behaviors Self-focus RESPIRATION Dyspnea Tachypnea, shallow respiration, adventitious breath sounds Limited thoracic expansion because of ascites Hypoxia SAFETY Itching, dryness of the skin (pruritus) Fevermore common in alcoholic cirrhosis Jaundiced skin and sclera Spider angiomas, telangiectasis Palmar erythema Confusion progressing to delirium and coma (hepatic encephalopathy) Unsteady or shaky, jerking movements SEXUALITY Menstrual disorders (women) Impotence (men) Testicular atrophy, gynecomastia, loss of hair chest, underarm, pubic TEACHING/LEARNING History of long-term alcohol or injection drug use or abuse, alcoholic liver disease, use of drugs affecting liver function History of biliary system disease, hepatitis, exposure to toxins, liver trauma
DISCHARGE PLAN CONSIDERATIONS May need assistance with self-care and other activities of daily living (ADLs), homemaking and maintenance tasks Refer to section at end of plan for postdischarge considerations.
Diagnostic Studies TEST WHY IT IS DONE WHAT IT TELLS ME BLOOD TESTS Serum bilirubin (total and indirect unconjugated): Bilirubin results from the breakdown of hemoglobin. Elevated because of cellular disruption, or biliary obstruction, causing jaudice. Liver enzymes:
Aspartate aminotransferase/alanine aminotransferase (AST/ALT), lactate dehydrogenase (LDH), and isoenzymes (LDH 5 ): Detects liver damage. Increased because of cellular damage and release of enzymes. Most specific indicator of hepatitis as cause (Murphy, 2006). Alkaline phosphatase (ALP) and isoenzyme (APL 1 ): Enzyme found in high concentration in the liver cells Elevated in biliary obstruction. forming the bile ducts as well as in other tissues. APL 1 is more specific to the liver and helpful in determining type and extent of cirrhosis. Gamma glutamyl transpeptidase (GGTP): Screens for liver disease and alcohol abuse. Level is elevated. Serum albumin: Protein of the highest concentration in plasma. Transports substances, such as bilirubin, calcium, progesterone, and drugs, and regulates osmotic pressure of blood, keeping fluid from leaking out into the tissues. Because albumin is made by the liver, decreased serum albumin may result from liver disease. Decreased albumin may also be explained by malnutrition or a low-protein diet. Immunoglobulin (Ig) A, G, and M: Proteins found in blood or other bodily fluids used by the immune system to identify and neutralize foreign objects, such as bacteria and viruses. Levels are increased. Complete blood count (CBC): Battery of screening tests, which typically includes hemoglobin (Hgb); hematocrit (Hct); red blood cell (RBC) count, morphology, indices, and distribution width index; platelet count and size; white blood cell (WBC) count and differential. Hb, Hct, and RBCs may be decreased because of bleeding and RBC destruction. Anemia is seen with hypersplenism and iron deficiency. Leukopenia may be present as a result of hypersplenism. Bleeding/clotting: Prothrombin time (PT): Measures length of time required for blood sample to clot. Prolonged because of decreased production of clotting proteins and fat-soluble vitamin K deficiency, leading to easy bleeding. Fibrinogen and other clotting factors: Used to monitor the progression of liver disease over time. Decreased; chronically low levels seen in end-stage liver disease. Blood urea nitrogen (BUN): Urea is the end product of protein metabolism formed in the liver from amino acids and from ammonia compounds. Elevation indicates breakdown of blood proteins and possible kidney dysfunction because of diuretic use in treatment of ascites. Serum ammonia: Product of breakdown of protein, which is normally converted to urea and excreted. Elevated because of inability to convert ammonia to urea. Serum glucose: One of the simple sugars in the blood, which serves as primary energy source for cells. Low blood glucose (hypoglycemia) suggests impaired synthesis of glycogen from glucose (glycogenesis). Electrolytes: Substances that dissociate into ions in solution and acquire the capacity to conduct electricity. Common electrolytes include sodium, potassium, chloride, calcium, and phosphate. Low potassium (hypokalemia) may reflect increased aldosterone, although various imbalances may occur. Low calcium (hypocalcemia) may occur because of impaired absorption of vitamin D. Nutrient studies: Evaluate nutritional status. Deficiency of vitamins A, B 12 , C, and K; folic acid; and iron may be noted. Viral tests: Determine if cirrhosis is caused by viral Hepatitis B, C, or D may be present. hepatitis. OTHER DIAGNOSTIC STUDIES
Abdominal ultrasonography with Doppler: Diagnostic technique that uses sound waves to produce an image of internal body structures. May be first assessment performed in individual with suspected liver disease to detect ascites and enlarged liver and spleen. It can also identify biliary duct obstruction or bile stones. Nodularity, irregularity, and atrophy are ultrasonographic hallmarks of cirrhosis. In advanced disease, the gross liver appears small and multinodular, ascites may be detected, and Doppler flow can be significantly decreased in the portal circulation. Liver biopsy: Biopsy can be performed via percutaneous, transjugular, laparoscopic, open operative, or computed tomography (CT)-guided fine-needle approaches. Samples are obtained for microscopic evaluation. Detects fatty infiltrates, fibrosis, destruction of hepatic tissues, tumors (primary or metastatic), and associated ascites. Percutaneous transhepatic cholangiography (PTHC): X-ray procedure where dye is injected directly into the drainage system of the liver. If necessary, a catheter may be inserted to allow the bile to drain into a collection bag outside the body or into the small intestine. Shows whether there is a blockage in the liver or the bile ducts that drain it. May be done to differentiate causes of jaundice or to perform biliary drainage. Hepatobiliary iminodiacetic acid (HIDA) scan: The client is given a radioactive tracer intravenously (IV) that is excreted by the liver into bile ducts. Identifies blockages in the biliary system. Urine and stool urobilinogen: Serves as guide for differentiating liver disease, hemolytic disease, and biliary obstruction. May or may not be present. Nursing Priorities 1. Maintain adequate nutrition. 2. Prevent complications. 3. Enhance self-concept and acceptance of situation. 4. Provide information about disease process, prognosis, potential complications, and treatment needs. Discharge Goals 1. Nutritional intake adequate for individual needs. 2. Complications prevented or minimized. 3. Deals effectively with current reality. 4. Disease process, prognosis, potential complications, and therapeutic regimen understood. 5. Plan in place to meet needs after discharge. NURSING DIAGNOSIS: imbalanced Nutrition: Less than Body Requirements May be related to Inadequate diet; inability to process, digest nutrients Anorexia, nausea, vomiting, indigestion, early satiety (ascites) Abnormal bowel function Possibly evidenced by Weight loss Changes in bowel sounds and function Poor muscle tone, muscle wasting; fatigue Imbalances in nutritional studies Desired Outcomes/Evaluation CriteriaClient Will Nutritional Status NOC Demonstrate progressive weight gain toward goal with client-appropriate normalization of laboratory values. Experience no further signs of malnutrition.
ACTIONS/INTERVENTIONS RATIONALE Nutrition Therapy NIC Independent Evaluate clients risk for malnutrition. Eighty-five percent to 90% of the blood that leaves the stomach and intestines carries nutrients to the liver where they are converted into substances the body can use. The client with liver dysfunction often has malnutrition because of inadequate dietary intake due to poor food choices or preference for alcohol rather than food and may currently have malabsorption syndrome due to inability to process or digest nutrients, anorexia, nausea or vomiting, indigestion, or early satiety associated with ascites. Because of the decreased secretion of bile into the gut, client may have difficulty absorbing fat and fat-soluble vitamins A, D, E, and K. These deficiencies can lead to such complications as decreased vision in the dark, due to vitamin A deficiency; bone disease, due to vitamin D deficiency; neurological impairment, due to vitamin E deficiency; and decreased production of clotting proteins in the liver, due to vitamin K deficiency (Brettler, 2003). Determine interest in eating and ability to chew, swallow, and taste. Discuss eating habits, including food preferences, intolerances, or aversions. Note availability and use of support systems. Factors that affect ingestion and digestion of nutrients. Determine dietary intake and perform calorie count if client is eating. Provides information about intake, needs, and deficiencies. Client with cirrhosis requires a balanced protein diet providing 2,000 to 3,000 calories per day to permit liver cell regeneration. Weigh, as indicated. Compare changes in fluid status and recent weight history. It may be difficult to use weight as a direct indicator of nutritional status in view of edema and ascites. Note: Undigested fat that passes into the large intestine can cause diarrhea and lead to weight loss (Brettler, 2003). Assist or encourage client to eat; explain reasons for the types of diet. Feed client if tiring easily, or have SO assist client. Consider preferences in food choices. Improved nutrition is vital to recovery. Client may eat better if family is involved and preferred foods are included as much as possible. Client and family must understand protein intake limitations and how best to meet needs and desires within limitations. Encourage client to eat all meals and supplementary feedings. Client may demonstrate loss of interest in food because of nausea, generalized weakness, and fatiguewhich is often first reported symptom and seen in approximately 70% of clients with cirrhosis (Taylor, 2008). Recommend or provide small, frequent meals. Poor tolerance to larger meals may be due to increased intra-abdominal pressure or ascites. Limit such high-salt foods as canned soups and vegetables, processed meats, and condiments. Provide salt substitutes if allowed, avoiding those containing ammonia. Salt limitations can help manage fluid complications in cirrhosis, including ascites or tissue edema. Salt substitutes enhance the flavor of food and aid in increasing appetite; ammonia potentiates risk of encephalopathy. Restrict intake of caffeine and gas-producing or spicy and excessively hot or cold foods. Aids in reducing gastric irritation, diarrhea, and abdominal discomfort that may impair oral intake and digestion. Encourage or provide frequent mouth care, especially before meals. Client is prone to sore and bleeding gums and bad taste in mouth, which contributes to anorexia. Provide assistance with activities as needed. Promote undisturbed rest periods, especially before meals. Conserving energy reduces metabolic demands on the liver and promotes cellular regeneration. Recommend cessation of smoking. Reduces excessive gastric stimulation and risk of irritation and bleeding. Collaborative Monitor nutritional laboratory studies: serum glucose, prealbumin or albumin, total protein, and ammonia. Glucose may be decreased because of impaired glycogenesis, depleted glycogen stores, or inadequate intake. Protein may be low because of impaired metabolism, decreased hepatic synthesis, or loss into peritoneal cavity (ascites). Protein-calorie malnutrition contributes to further development of fatty liver and deterioration of function. Elevation of ammonia level may require restriction of protein intake to prevent serious complications. Maintain nothing by mouth (NPO) status, when indicated. Gastrointestinal (GI) rest may be required in acutely ill clients to reduce demands on the liver and production of ammonia and urea in the GI tract. When this is the case, nutrition must be supplied by another methodenteral or parenteral feedings. Determine nutritional and caloric needs using appropriate methods, such as total energy expenditure (TEE), body mass index (BMI), Harris- Benedict equation, or indirect calorimetry test, as indicated. Identifies energy requirements and deficits. Skinfold measurements and indirect calorimetry are useful in assessing changes in muscle mass, energy expenditure, and subcutaneous fat reserves. Consult with dietitian or nutritionist to provide diet that is high in calories and simple carbohydrates, low in fat, and low to moderate in protein. Limit sodium, as necessary. Provide liquid supplements, as indicated. Because clients intake is usually limited, high-calorie foods are desired. Carbohydrates supply readily available energy. Fats are poorly absorbed because of liver dysfunction and may contribute to abdominal discomfort. Proteins are needed to improve serum protein levels, reducing edema and promoting liver cell regeneration. However, protein can also elevate ammonia levels and must be restricted if ammonia level is elevated or if client has clinical signs of hepatic encephalopathy. In addition, these individuals may tolerate vegetable protein better than meat protein. Provide enteral tube feedings or total parenteral nutrition (TPN), if indicated. May be required to supplement diet or to provide nutrients when client is too nauseated or anorexic to eat or when esophageal varices interfere with oral intake. (Refer to CP: Total Nutritional Support: Parenteral/Enteral Feedings.) Administer medications, as indicated, for example: Vitamin supplements (especially fat-soluble vitamins Replacement required because of the inability of the A, D, E, K) and B vitamins (thiamine, iron, folic acid) liver to process or store vitamins. Zinc sulfate Improves sense of taste and may enhance appetite. Digestive enzymes, such as pancrelipase (Niokase) and lactulose May be tried to promote digestion of fats and reduce incidence of steatorrhea and diarrhea. Antiemetics, such as trimethobenzamide (Tigan) Used with caution to reduce nausea and vomiting and enhance oral intake.
NURSING DIAGNOSIS: excess Fluid Volume May be related to Compromised regulatory mechanismsyndrome of inappropriate antidiuretic hormone (SIADH), decreased plasma proteins, malnutrition Excess sodium and fluid intake Possibly evidenced by Edema, anasarca, weight gain Intake greater than output, oliguria, changes in urine specific gravity Dyspnea, adventitious breath sounds, pleural effusion Blood pressure (BP) changes, altered central venous pressure (CVP) JVD, positive hepatojugular reflex Altered electrolyte levels Change in mental status Desired Outcomes/Evaluation CriteriaClient Will Fluid Balance NOC Demonstrate stabilized fluid volume, with balanced intake and output (I&O), stable weight, vital signs within clients normal range, and absence of edema.
ACTIONS/INTERVENTIONS RATIONALE Fluid/Electrolyte Management NIC Independent Measure I&O, noting positive balanceintake in excess of output. Weigh daily, and note gain more than 0.5 kg/day. Reflects circulating volume status, developing or resolving fluid shifts, and response to therapy. Positive fluid balance and weight gain often reflects continuing fluid retention. Note: Decreased circulating volume and fluid shifts can directly affect renal function and urine output, resulting in hepatorenal syndrome. Monitor BP and CVP, if available. Note JVD and abdominal vein distention. BP elevations are usually associated with fluid volume excess but may not occur because of fluid shifts out of the vascular space. JVD and presence of distended abdominal veins are associated with vascular congestion. Assess respiratory status, noting increased respiratory rate and dyspnea. Indicative of pulmonary congestion or edema. Auscultate lungs, noting diminished or absent breath sounds and developing adventitious sounds crackles. Increasing pulmonary congestion may result in consolidation, impaired gas exchange, and complications, such as pulmonary edema. Monitor for cardiac dysrhythmias. Auscultate heart sounds, noting development of S3/S4 gallop rhythm. May be caused by HF, decreased coronary arterial perfusion, or electrolyte imbalance. Assess degree of peripheral and dependent edema. Fluids shift into tissues as a result of sodium and water retention, decreased albumin, and increased antidiuretic hormone (ADH). Measure abdominal girth. Reflects accumulation of fluid or ascites resulting from loss of plasma proteins and fluid into peritoneal space. Note: Excessive fluid accumulation can reduce circulating volume, resulting in hypotension and dehydration. Encourage bedrest when ascites is present. May promote recumbency-induced diuresis. Provide frequent mouth care and occasional ice chips, particularly if NPO; schedule fluid intake around the clock. Decreases sensation of thirst, especially when fluid intake is restricted. Collaborative Monitor serum albumin and electrolytes, particularly potassium and sodium. Decreased serum albumin affects plasma colloid osmotic pressure, resulting in edema formation. Reduced renal blood flow, accompanied by elevated ADH and aldosterone levels and the use of diuretics to reduce total body water, may cause various electrolyte shifts and imbalances. Monitor serial chest x-rays. Vascular congestion, pulmonary edema, and pleural effusions frequently occur. Restrict sodium and fluids, as indicated. Sodium may be restricted to minimize fluid retention in extravascular spaces. Fluid restriction may be necessary to correct dilutional hyponatremia. Administer salt-free albumin and plasma expanders, as indicated. Albumin may be given to increase the colloid osmotic pressure in the vascular compartment, thereby increasing effective circulating volume and decreasing formation of ascites. Administer medications, as indicated, for example: Diuretics, such as spironolactone (Aldactone) and furosemide (Lasix) Used with caution to control edema and ascites, block effect of aldosterone, and increase water excretion while sparing potassium when conservative therapy with bedrest and sodium restriction do not alleviate problem. Diuretic given in coordination with albumin administration may enhance fluid removal. Potassium Serum and cellular potassium are usually depleted because of liver disease and urinary losses. Positive inotropic drugs and arterial vasodilators Given to increase cardiac output and improve renal blood flow and function, thereby reducing excess fluid.
NURSING DIAGNOSIS: risk for impaired Skin Integrity Risk factors may include Altered circulation and metabolic state Accumulation of bile salts in skin Poor skin turgor, skeletal prominence, presence of edema, ascites Possibly evidenced by (Not applicable; presence of signs and symptoms establishes an actual diagnosis) Desired Outcomes/Evaluation CriteriaClient Will Risk Control NOC Maintain skin integrity. Identify individual risk factors and demonstrate behaviors or techniques to prevent skin breakdown.
ACTIONS/INTERVENTIONS RATIONALE Skin Surveillance NIC Independent Discuss itching with client, addressing areas involved and time of day when client is most uncomfortable. Pruritus affects about two-thirds of clients with primary biliary cirrhosis; the cause is unknown. The itching often worsens during the evening and improves during the day. It typically begins in the palms and soles, and then spreads to the rest of the body. Prolonged, repeated scratching can result in excoriations and thickening and darkening of the skin (Heathcote, 2000). Inspect skin surfaces and pressure points routinely. Gently massage bony prominences or areas of continued stress. Use emollient lotions and limit use of soap for bathing. Edematous tissues are more prone to breakdown and to the formation of decubitus ulcers. Ascites may stretch the skin to the point of tearing in severe cirrhosis. Encourage and assist with repositioning on a regular schedule, while in bed or chair, and active or passive range-of-motion (ROM) exercises, as Repositioning reduces pressure on edematous tissues to improve circulation. Exercises enhance circulation and improve or maintain joint mobility. appropriate. Recommend elevating lower extremities. Enhances venous return and reduces edema formation in extremities. Keep linens dry and free of wrinkles. Moisture aggravates pruritus and increases risk of skin breakdown. Suggest clipping fingernails short and provide mittens or gloves, if indicated. Prevents client from inadvertently injuring the skin, especially while sleeping. Encourage, or provide, perineal care following urination and bowel movement. Prevents skin excoriation breakdown from bile salts. Collaborative
Use alternating pressure mattress, egg-crate or foam mattress, waterbed, or sheepskins, as indicated. Reduces dermal pressure, increases circulation, and diminishes risk of tissue ischemia and breakdown. Apply calamine lotion and provide baking soda baths. May be soothing and provide relief of itching. Administer medications, such as cholestyramine (Questran), colestipol (Colestid), hydroxyzine (Atarax), and dronabinol (Marinol), if indicated. Although the cause of pruritus is unknown, it may be associated with jaundice or bile salts in skin and may respond to these treatments.
NURSING DIAGNOSIS: risk for ineffective Breathing Pattern Risk factors may include Intra-abdominal fluid collection (ascites) Decreased lung expansion, accumulated secretions Decreased energy, fatigue Possibly evidenced by (Not applicable; presence of signs and symptoms establishes an actual diagnosis) Desired Outcomes/Evaluation CriteriaClient Will Respiratory Status: Ventilation NOC Maintain effective respiratory pattern and be free of dyspnea and cyanosis, with arterial blood gases (ABGs) and vital capacity within acceptable range.
ACTIONS/INTERVENTIONS RATIONALE Ventilation Assistance NIC Independent
Monitor respiratory rate, depth, and effort. Rapid, shallow respirations or dyspnea may be present because of hypoxia or fluid accumulation in abdomen. Auscultate breath sounds, noting crackles, wheezes, and rhonchi. Indicates developing complicationspresence of adventitious sounds reflects accumulation of fluid while diminished sounds suggest atelectasis increasing risk of pulmonary infection. Investigate changes in level of consciousness (LOC). Changes in mentation may reflect hypoxemia and respiratory failure, which often accompany hepatic coma. Keep head of bed elevated. Position client on side. Facilitates breathing by reducing pressure on the diaphragm and minimizes risk of aspiration of secretions. Encourage frequent repositioning, deep-breathing exercises, and coughing, as appropriate. Aids in lung expansion and mobilizing secretions. Monitor temperature. Note presence of chills, increased coughing, and changes in color or character of sputum. Indicative of onset of infection, such as pneumonia. Collaborative
Monitor serial ABGs, pulse oximetry, vital capacity measurements, and chest x-rays. Reveals changes in respiratory status and developing pulmonary complications. Provide supplemental oxygen (O2) as indicated. May be necessary to treat or prevent hypoxia. If respirations or oxygenation are inadequate, mechanical ventilation may be required. Demonstrate and assist with respiratory adjuncts, such as incentive spirometer. Reduces incidence of atelectasis and enhances mobilization of secretions. Prepare for and assist with acute care procedures, such as:
Paracentesis Occasionally done to remove ascites fluid to relieve abdominal pressure when respiratory embarrassment is not corrected by other measures. Peritoneovenous shunt Surgical implant of a catheter to return accumulated fluid in the abdominal cavity to systemic circulation via the vena cava; provides long-term relief of ascites and improvement in respiratory function.
NURSING DIAGNOSIS: risk for Bleeding Risk factors may include Abnormal blood profile; altered clotting factorsdecreased production of prothrombin, fibrinogen, and factors VIII, IX, and X; impaired vitamin K absorption; and release of thromboplastin Portal hypertension, development of esophageal varices Possibly evidenced by (Not applicable; presence of signs and symptoms establishes an actual diagnosis) Desired Outcomes/Evaluation CriteriaClient Will Coagulation Status NOC Maintain homeostasis with absence of bleeding. Risk Control NOC Demonstrate behaviors to reduce risk of bleeding.
ACTIONS/INTERVENTIONS RATIONALE Bleeding Precautions NIC
Independent
Assess for signs and symptoms of GI bleeding; for instance, check all secretions for frank or occult blood. Observe color and consistency of stools, nasogastric (NG) drainage, or vomitus. The GI tractesophagus and rectumis the most usual source of bleeding because of its mucosal fragility and alterations in homeostasis associated with cirrhosis. Observe for presence of petechiae, ecchymosis, and bleeding from one or more sites. Subacute disseminated intravascular coagulation (DIC) may develop secondary to altered clotting factors. Monitor pulse, BP, and CVP, if available. An increased pulse with decreased BP and CVP may indicate loss of circulating blood volume, requiring further evaluation. Note changes in mentation and LOC. Changes may indicate decreased cerebral perfusion secondary to hypovolemia or hypoxemia. Avoid rectal temperature; be gentle with GI tube insertions. Rectal and esophageal vessels are most vulnerable to rupture. Encourage use of soft toothbrush and electric razor, avoiding straining for stool, forceful nose blowing, and so forth. In the presence of clotting factor disturbances, minimal trauma can cause mucosal bleeding. Use small needles for injections. Apply pressure to small bleeding or venipuncture sites for longer than usual. Minimizes damage to tissues, reducing risk of bleeding and hematoma. Recommend avoidance of aspirin-containing products. Prolongs coagulation, potentiating risk of hemorrhage. Collaborative
Monitor Hgb and Hct, platelets, and clotting factors. Indicators of anemia, active bleeding, or impending complications, such as DIC. Administer medications, as indicated, for example: Supplemental vitamins, such as vitamins K, D, and C Promotes prothrombin synthesis and coagulation, if liver is functional. Vitamin C deficiencies increase susceptibility of GI system to irritation and bleeding. Stool softeners Prevents straining for stool with resultant increase in intra-abdominal pressure and risk of bleeding hemorrhoidal varices, especially when client has portal hypertension. Provide gastric lavage with cool saline solution or water, as indicated. In presence of acute bleeding, evacuation of blood from GI tract may reduce ammonia production and risk of hepatic encephalopathy. (Refer to CP: Upper Gastrointestinal/Esophageal Bleeding.) Assist with insertion and maintenance of intestinal or esophageal tube, such as Sengstaken-Blakemore tube. Temporarily controls bleeding of esophageal varices by balloon tamponade when control by other means, such as lavage, and hemodynamic stability cannot be achieved. Prepare for procedures, such as direct ligation or banding of varices, esophagogastric resection, transjugular intrahepatic portosystemic shunt (TIPS), and splenorenal-portacaval anastomosis. May be needed to control active hemorrhage or to decrease portal and collateral blood vessel pressure to minimize risk of recurrence of bleeding. TIPS is a nonsurgical procedure to relieve portal hypertension and decompress varices by creating a shunt between the systemic and portal venous systems to redirect portal blood flow.
NURSING DIAGNOSIS: risk for acute Confusion Risk factors may include Alcohol abuse Inability of liver to detoxify certain enzymes and drugs Possibly evidenced by (Not applicable; presence of signs and symptoms establishes an actual diagnosis) Desired Outcomes/Evaluation CriteriaClient Will Cognition NOC Maintain usual level of mentation and reality orientation. Initiate behaviors or lifestyle changes to prevent or minimize recurrence of problem.
ACTIONS/INTERVENTIONS RATIONALE Reality Orientation NIC
Independent
Observe for changes in behavior and mentation: lethargy, confusion, drowsiness, slowing or slurring of speech, and irritability. Arouse client at intervals, as indicated. Ongoing assessment of behavior and mental status is important because of fluctuating nature of hepatic encephalopathy or impending hepatic coma. Review current medication regimen. Adverse drug reactions or interactions may potentiate or exacerbate confusion. Evaluate sleep and rest schedule. Difficulty falling asleep or staying asleep leads to sleep deprivation, exacerbating cognition problems and fatigue. Note development or presence of asterixis, fetor hepaticus, and seizure activity. Suggests elevating serum ammonia levels and increased risk of progression to encephalopathy. Consult with SO about clients usual behavior and Provides baseline for comparison of current status. mentation. Have client write name periodically and keep this record for comparison. Report deterioration of ability. Have client do simple arithmetic computations. Easy test of neurological status and muscle coordination. Reorient to time, place, person, and situation, as needed. Assists in maintaining reality orientation, reducing confusion and anxiety. Maintain a pleasant, quiet environment and approach in a slow, calm manner. Encourage uninterrupted rest periods. Reduces excessive stimulation and sensory overload, promotes relaxation, and may enhance coping. Provide continuity of care. If possible, assign same nurse over a period of time. Familiarity provides reassurance, aids in reducing anxiety, and provides a more accurate documentation of subtle changes. Reduce provocative stimuli and confrontation. Refrain from forcing activities. Assess potential for violent behavior. Avoids triggering agitated, violent responses; promotes client safety. Discuss current situation and future expectations. Client and SO may be reassured that intellectual as well as emotional function may improve as liver involvement resolves. Maintain bedrest and assist with self-care activities. Reduces metabolic demands on liver, prevents fatigue, and promotes healing, lowering risk of ammonia buildup. Identify and provide for safety needs, such as supervision during smoking, bed in low position, side rails up, and pad, if necessary. Provide close supervision. Reduces risk of injury when confusion, seizures, or violent behavior occurs. Investigate temperature elevations. Monitor for signs of infection. Infection may precipitate hepatic encephalopathy caused by tissue catabolism and release of nitrogen. Recommend avoidance of narcotics or sedatives, anti-anxiety agents, and limiting or restricting use of medications metabolized by the liver. Certain drugs are toxic to the liver, whereas other drugs may not be metabolized because of cirrhosis, causing cumulative effects that affect mentation, mask signs of developing encephalopathy, or precipitate coma. Collaborative
Monitor laboratory studies, such as ammonia, electrolytes, pH, blood urea nitrogen (BUN), glucose, and CBC with differential. Elevated ammonia levels, hypokalemia, metabolic alkalosis, hypoglycemia, anemia, and infection can precipitate or potentiate development of hepatic coma. Eliminate or restrict protein in diet. Provide glucose supplements and adequate hydration. Ammonia is responsible for mental changes in hepatic encephalopathy. Dietary changes may result in constipation, which also increases bacterial action and formation of ammonia. Glucose provides a source of energy, reducing need for protein catabolism. Administer medications, as indicated, for example:
Ursodeoxycholic acid (urosodiol, UDCA, Actigall) Major medication used to slow the progression of the disease; may delay need for transplantation. Immunosuppressive agents, such as corticosteroids (Prednisolone, DeltaCortef), methotrexate (Rheumatrex/Folex), and cyclosporine (Sandimmune/Neoral); anti-inflammatory agents, such as colchicines These agents may inhibit immune reactions that mediate inflammatory processes and progression of the disease. Electrolytes Corrects imbalances and may improve cerebral function and metabolism of ammonia. Stool softeners, colonic purges such as magnesium sulfate, enemas, and lactulose Removes protein and blood from intestines. Acidifying the intestine produces diarrhea and decreases production of nitrogenous substances, reducing risk or severity of encephalopathy. Note: Long-term use of lactulose may be required for clients with hepatic encephalopathy to reduce ammonia on a daily or regular basis. Bactericidal agents, such as neomycin (Mycifradin) and kanamycin (Kantrex) Destroys intestinal bacteria, reducing production of ammonia, to prevent encephalopathy. Administer supplemental O2. Mentation is affected by O2 concentration and utilization in the brain. Assist with procedures as indicated, such as dialysis, plasmapheresis, or extracorporeal liver perfusion. May be used to reduce serum ammonia levels if encephalopathy develops or other measures are not successful.
NURSING DIAGNOSIS: Self-Esteem [specify]/disturbed Body Image May be related to Biophysical changes, altered physical appearance Uncertainty of prognosis, changes in role function Personal vulnerability Self-destructive behavioralcohol-induced disease Possibly evidenced by Verbalization of change or restriction in lifestyle Fear of rejection or reaction by others Negative feelings about body and abilities Feelings of helplessness, hopelessness, or powerlessness Desired Outcomes/Evaluation CriteriaClient Will Self-Esteem NOC Verbalize understanding of changes and acceptance of self in the present situation. Identify feelings and methods for coping with negative perception of self.
ACTIONS/INTERVENTIONS RATIONALE Self-Esteem Enhancement NIC
Independent
Discuss situation and encourage verbalization of fears and concerns. Explain relationship between nature of disease and symptoms. Client is very sensitive to body changes and may also experience feelings of guilt when cause is related to alcohol or other drug use. Support and encourage client; provide care with a positive, friendly attitude. Caregivers sometimes allow judgmental feelings to affect the care of client and need to make every effort to help client feel valued as a person. Encourage family/SO to verbalize feelings, visit freely, and participate in care. Family/SO may feel guilty about clients condition and may be fearful of impending death. They need nonjudgmental emotional support and free access to client. Participation in care helps them feel useful and promotes trust between staff, client, and family/SO. Assist client/SO to cope with change in appearance; suggest clothing that does not emphasize altered appearance, such as use of red, blue, or black clothing. Client may present unattractive appearance as a result of jaundice, ascites, and ecchymotic areas. Providing support can enhance self-esteem and promote clients sense of control. Collaborative
Refer to support services, such as counselors, psychiatric resources, social service, clergy, and alcohol treatment program. Increased vulnerability and concerns associated with this illness may require services of additional professional resources.
NURSING DIAGNOSIS: deficient Knowledge [Learning Need] regarding condition, prognosis, treatment, self-care, and discharge needs May be related to Lack of exposure or recall; information misinterpretation Unfamiliarity with information resources Possibly evidenced by Questions, request for information, statement of misconception Inaccurate follow-through of instructions, development of preventable complications Desired Outcomes/Evaluation CriteriaClient Will Knowledge: Illness Care NOC Verbalize understanding of disease process, prognosis, and potential complications. Correlate symptoms with causative factors. Knowledge: Health Behaviors NOC Identify and initiate necessary lifestyle changes. Actively participate in care.
ACTIONS/INTERVENTIONS RATIONALE Teaching: Disease Process NIC
Independent
Review disease process and future expectations. Provides knowledge base from which client can make informed choices. Emphasize importance of avoiding alcohol. Give information about medical and community services available to aid in alcohol rehabilitation, if indicated. Alcohol is one of the leading causes for the development of cirrhosis. Inform client of altered effects of medications with cirrhosis and the importance of using only drugs prescribed or cleared by a healthcare provider who is familiar with clients history. Some drugs are hepatotoxic, especially opioids, sedatives, and hypnotics. In addition, the damaged liver has a reduced ability to metabolize all drugs, potentiating cumulative effect and aggravation of bleeding tendencies. Review procedure for maintaining function of peritoneovenous shunt when present. Several types of shunts are available, so it is important that client and SO understand care needed for clients shunt. For example, Denver shunt requires client to periodically pump the chamber to maintain patency of the device, and client with a LeVeen shunt may wear an abdominal binder or engage in a Valsalvas maneuver to maintain shunt function. Assist client with identifying support person(s). Because of length of recovery, potential for relapses, and slow convalescence, support systems are extremely important in maintaining behavior modifications. Emphasize the importance of good nutrition. Recommend avoidance of high-protein and salty foods, onions, and strong cheeses. Provide written dietary instructions. Proper dietary maintenance and avoidance of foods high in sodium and protein aid in remission of symptoms and help prevent ammonia buildup and further liver damage. Written instructions are helpful for client to refer to at home. Stress necessity of follow-up care and adherence to therapeutic regimen. Chronic nature of disease has potential for life- threatening complications. Provides opportunity for evaluation of effectiveness of regimen, including patency of shunt if used. Discuss sodium and salt substitute restrictions and necessity of reading labels on food, OTC drugs, Minimizes ascites and edema formation. Overuse of substitutes may result in other electrolyte and herbal agents. imbalances. Food, OTC medications, and personal care products, including antacids and some mouthwashes, may contain sodium or alcohol and may be toxic to the liver or be primarily metabolized by the liver. Encourage scheduling activities with adequate rest periods. Adequate rest decreases metabolic demands on the body and increases energy available for tissue regeneration. Promote diversional activities that are enjoyable to client. Prevents boredom, facilitates rest, and minimizes anxiety and depression. Recommend avoidance of persons with infections, especially upper respiratory infections. Decreased resistance, altered nutritional status, and impaired immune responses potentiate risk of infection. Instruct client and SO of signs and symptoms that warrant notification of healthcare provider, such as increased abdominal girth, rapid weight loss or gain, increased peripheral edema, increased dyspnea, fever, blood in stool or urine, excess bleeding of any kind, and jaundice. Prompt reporting of symptoms provides opportunity to treat complications before they become life- threatening. Note: Client may be evaluated for additional medical or surgical interventions, including liver transplantation. Instruct SO to notify healthcare providers of any confusion, untidiness, night wandering, tremors, or personality change. Changes reflecting deterioration in mental status may be apparent to SO, although insidious changes may be noted by others with less frequent contact with client. POTENTIAL CONSIDERATIONS following acute hospitalization (dependent on clients age, physical condition and presence of complications, personal resources, and life responsibilities) Fatiguedecreased metabolic energy production, states of discomfort, altered body chemistry, such as changes in liver function, effect on target organs, alcohol withdrawal imbalanced Nutrition: Less than Body Requirementsinadequate diet, inability to process and digest nutrients, anorexia, nausea and vomiting, indigestion, early satiety (ascites), abnormal bowel function risk for ineffective self Health Managementperceived benefit, social support deficit, economic difficulties. dysfunctional Family Processesabuse of alcohol, resistance to treatment, inadequate coping and lack of problem-solving skills, addictive personality and codependency risk for Caregiver Role Strainaddiction or codependency; family dysfunction before caregiving situation; presence of situational stressors, such as economic vulnerability, hospitalization, changes in employment