Cirrhosis

CIRRHOSIS OF THE LIVER I. Pathophysiology (Murphy, 2006)

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, Wilson’s disease, alpha1-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 sounds—S3, S4

• 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) • Fever—more 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 (LDH5):

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 (APL1):

Enzyme found in high concentration in the liver cells

Elevated in biliary obstruction.

forming the bile ducts as well as in other tissues.

APL1 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, B12, 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 Criteria—Client 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 client’s 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

fatigue—which 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 method—enteral 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 client’s 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 mechanism—syndrome 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 Criteria—Client Will

Fluid Balance NOC

Demonstrate stabilized fluid volume, with balanced intake and output (I&O), stable weight, vital signs

within client’s normal range, and absence of edema.

ACTIONS/INTERVENTIONS RATIONALE

Fluid/Electrolyte Management NIC

Independent

Measure I&O, noting positive balance—intake 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 Criteria—Client 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 Criteria—Client 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 complications—presence 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 factors—decreased 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 Criteria—Client 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 tract—esophagus and rectum—is 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 Criteria—Client 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 client’s 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 behavior—alcohol-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 Criteria—Client 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 client’s 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 client’s 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 Criteria—Client 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 client’s 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 client’s 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 Valsalva’s

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 client’s age,

physical condition and presence of complications, personal resources, and life responsibilities)

• Fatigue—decreased 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 Requirements—inadequate diet, inability to process and

digest nutrients, anorexia, nausea and vomiting, indigestion, early satiety (ascites), abnormal

bowel function

• risk for ineffective self Health Management—perceived benefit, social support deficit, economic

difficulties.

• dysfunctional Family Processes—abuse of alcohol, resistance to treatment, inadequate coping

and lack of problem-solving skills, addictive personality and codependency

• risk for Caregiver Role Strain—addiction or codependency; family dysfunction before caregiving

situation; presence of situational stressors, such as economic vulnerability, hospitalization,

changes in employment