Care Plan I

Care Plan I

 

Learning Objectives

After studying this chapter, you should be able to:

1. Describe the pathophysiology and complications associated with cirrhosis of the liver.

2. Interpret laboratory test findings commonly seen in clients with cirrhosis.

3. Analyze assessment data from clients with cirrhosis to determine priority nursing diagnoses and collaborative problems.

4. Formulate a collaborative plan of care for the client with severe late-stage cirrhosis.

5. Identify emergency interventions for the client with bleeding esophageal varices.

6. Evaluate care for clients with cirrhosis.

7. Develop a community-based teaching plan for the client with cirrhosis of the liver.

8. Compare and contrast the transmission of hepatitis A, B, and C viral infections.

9. Explain ways in which each type of hepatitis can be prevented.

10. Discuss the primary concerns about the increasing incidence of hepatitis C in the United States.

11. Identify treatment options for clients with cancer of the liver.

12. Describe the typical complications that result from liver transplantation.

 

The liver is the largest and one of the most vital internal organs, performing more than 400 functions and affecting every system in the body. When the liver cannot perform its complex activities, hepatic failure results. Liver diseases range in severity from mild hepatic inflammation to chronic end-stage cirrhosis.

CIRRHOSIS

 OVERVIEW

Cirrhosis is a chronic, progressive liver condition. It usually develops insidiously and has a prolonged, destructive course. As an end-stage process, it is essentially an irreversible reac­tion to hepatic inflammation and necrosis.

 Pathophysiology

Cirrhosis is characterized by diffuse fibrotic bands of connec­tive tissue that distort the liver’s normal architecture. Extensive degeneration and destruction of hepatocytes (hepatic [liver] cells) occur. In attempts to regenerate with new nodule forma­tion, a disorganized lobular pattern develops. Flow alterations in the vascular system and lymphatic bile duct channels result from compression caused by the proliferation of fibrous tissue.

TYPES OF CIRRHOSIS

There are four major types of cirrhosis (Table 59-1):

1.  Laennec’s, or alcoholic cirrhosis

2.  Postnecrotic cirrhosis

3.  Biliary cirrhosis

4.  Cardiac cirrhosis

LAENNEC’S CIRRHOSIS. Laennec’s cirrhosis, or alcoholic cirrhosis, is also called nutritional, or portal, cir­rhosis. Alcohol has a direct toxic effect on the liver cells (he­patocytes) and causes liver inflammation (alcoholic hepati­tis), which usually precedes the onset of alcoholic cirrhosis. Metabolic changes in the liver that are induced by alcohol lead to fatty infiltration of the hepatocytes and scarring be­tween the lobules. The liver becomes enlarged, with cellular degeneration and infiltration by fat, leukocytes, and lym­phocytes (white blood cells). As the inflammatory process decreases, the destructive phase increases. Early scar forma­tion is caused by fibroblast infiltration and collagen forma­tion. Damage to the hepatic parenchyma progresses as a result of malnutrition and repeated exposure to the hepato-toxin (alcohol). If alcohol is withheld, the fatty infiltration is reversible. If alcohol abuse continues, widespread scar tis­sue formation and fibrosis infiltrate the liver as a result of cellular necrosis.

 

      MAJOR TYPES OF CIRRHOSIS OF THE LIVER

LAENNEC’S CIRRHOSIS

•  Most common type

•  Caused by long-term use of alcohol

•  Liver becomes enlarged, firm, and hard in early disease,and smaller and nodular in end-stage disease

POSTNECROTIC CIRRHOSIS

•      Caused by massive hepatic cell necrosis, usually fromacute viral hepatitis or exposure to certain hepatotoxins,such as industrial chemicals

BILIARY CIRRHOSIS

•  Caused by chronic biliary obstruction, bile stasis, and in­flammation

•  Liver becomes fibrotic; hepatic cells are destroyed

CAR0IAC CIRRHOSIS

•  Caused by severe or chronic heart failure (also called vas­cular cirrhosis).

•  Liver becomes enlarged and congested with venousblood, resulting in cell necrosis from anoxia

In early cirrhosis, the liver capsule is enlarged, firm, and hard. The regenerated nodules give the capsule a hobnailed, or bumpy, appearance. As the pathologic process of cirrhosis progresses, the liver shrinks in size. The capsule is covered with fine nodules surrounded by gray connective tissue.

POSTNECROTIC CIRRHOSIS. Postnecrotic cirrho­sis occurs after massive liver cell necrosis. Broad bands of scar tissue cause the destruction of liver lobules and entire lobes. The liver enlarges and then becomes shrunken with large nodules, representing macronodular structural changes throughout the organ. Postnecrotic cirrhosis occurs most often as a complication of acute viral hepatitis or after exposure to industrial or chemical hepatotoxins (e.g., carbon tetrachlo-ride). This type of cirrhosis is suspected in clients who exhibit signs of chronic liver disease and do not have a history of ex­cessive alcohol intake.

BILIARY CIRRHOSIS. Biliary cirrhosis develops as a result of chronic biliary obstruction, bile stasis, inflammation, or diffuse hepatic fibrosis. Primary biliary cirrhosis results from intrahepatic bile stasis. Secondary biliary cirrhosis is caused by obstruction of the hepatic or common bile ducts, which produces bile stasis in the liver. The accumulation of excessive hepatic bile leads to progressive fibrosis, hepatocel-lular destruction, and regenerated nodules. Severe obstructive jaundice is a key clinical manifestation in both types of biliary cirrhosis.

CARDIAC CIRRHOSIS. Cardiac cirrhosis, or vascular cirrhosis, is associated with severe right-sided heart failure. It develops in clients with long-standing heart failure after cor pulmonale, constrictive pericarditis, and valvular insuffi­ciency (see Chapter 35). The liver becomes enlarged, is con­gested with venous blood, and appears edematous and dark in color. The liver serves as a reservoir for large amounts of ve­nous blood that the failing heart cannot pump back into the systemic circulation. The increase in hepatic volume and pressure causes severe venous congestion. The liver becomes anoxic, which results in hepatic cell necrosis and fibrosis.

 

 COMPLICATIONS OF CIRRHOSIS

Common problems and complications associated with hepatic cirrhosis depend on the amount of damage sustained by the liver. The loss of hepatic function contributes to the develop­ment of metabolic abnormalities. Hepatic cell degeneration may lead to the following:

•  Portal hypertension

•  Ascites (accumulation of abdominal fluid)

•  Bleeding esophageal varices

•  Coagulation defects

•  Jaundice

•  Portal-systemic encephalopathy (PSE) with hepatic coma

•  Hepatorenal syndrome

PORTAL  HYPERTENSION. Portal hypertension, apersistent increase in pressure within the portal vein, is a ma­jor complication of cirrhosis. It results from increased resist­ance to or obstruction of the flow of blood through the portal vein and its tributaries. The blood meets resistance to flow and seeks collateral venous channels around the high-pressure area. Blood flow backs into the spleen, causing splenomegaly. Veins in the esophagus, stomach, intestines, abdomen, and rectum become dilated. Portal hypertension can result in as­cites, esophageal varices, prominent abdominal veins (caput medusae), and hemorrhoids.

ASCITES. Ascites is the accumulation of free fluid con­taining almost pure plasma within the peritoneal cavity. In­creased hydrostatic pressure from portal hypertension causes plasma to leak into the peritoneal cavity. The accumulation of plasma protein, primarily albumin, in the peritoneal fluid re­duces the amount of circulating plasma protein in the blood. When this decrease is combined with the inability of the liver to synthesize albumin because of impaired hepatocyte func­tioning, the effective serum colloid osmotic pressure is de­creased in the circulatory system.

Increased hepatic lymph formation also contributes to as­cites formation. The lymphatic system is unable to channel the increased amounts of lymph, and weeping of liver plasma (“liver sweat”) occurs as a result. The decrease of effective in-travascular circulation from massive ascites may cause renal vasoconstriction, triggering the renin-angiotensin system. This results in sodium and water retention, which increases hydrostatic pressure and lymph formation, and the vicious circle of ascites formation continues.

BLEEDING ESOPHAGEAL VARICES. As the blood backs up away from the liver, it enters the esophageal and gas­tric vessels that carry it into the systemic circulation. Bleed­ing esophageal varices occur when these fragile, thin-walled esophageal veins become distended or irritated and rupture. Variceal bleeding may be caused by the following:

•  Any chemical irritant, such as alcohol, medications, and refluxed gastric acid

•  Mechanical trauma from abrasions by poorly chewed food, vomiting, or nasogastric (NG) tube insertion

•  Increased pressure in the esophagus caused by vigorous physical exercise, coughing, or retching and vomiting

Varices occur most often in the distal end of the esopha­gus but are also noted in the proximal esophagus and stom­ach. Gastric ulceration or erosion also puts the client at risk for hemorrhage from the stomach. Endoscopy, if possible, can differentiate between gastrointestinal and esophageal bleeding.

The client with bleeding esophageal varices loses large volumes of blood from hematemesis and may go into shock from hypovolemia. This condition is a medical emergency and needs immediate medical intervention (see Potential for Hemorrhage, p. 1308).

COAGULATION DEFECTS. With cirrhosis, there is a decrease in the synthesis of bile fats in the liver; this prevents the absorption of fat-soluble vitamins (e.g., vitamin K). With­out vitamin K, clotting factors II, VII, IX, and X are not pro­duced in sufficient quantities, and the client is susceptible to bleeding and easy bruising. Therefore when a client has bleeding esophageal varices, the blood does not clot and hem­orrhage occurs.

CRITICAL THINKING CHALLENGE

You are the nurse for a client with Laennec’s cirrhosis. You go into the client’s room and find the client in the bath­room vomiting what appears to be hematemesis (blood in the vomitus).

• What actions will you take?

• In what order of priority should you implement these inter­ventions?

• How can you differentiate if this is a gastrointestinal bleed or an esophageal bleed?

JAUNDICE. Jaundice in clients with hepatic cirrhosis is caused by one of two mechanisms (Table 59-2): hepatocellu­lar disease or intrahepatic obstruction. Hepatocellular jaun­dice develops because the liver cannot metabolize bilirubin. The liver’s normal uptake of bilirubin from the blood is thus impaired. This decreased excretion results in excessive circu­lating bilirubin levels. Intrahepatic obstructive jaundice re­sults from edema, fibrosis, or scarring of the hepatic bile channels and bile ducts, which interferes with normal bile and bilirubin excretion.

PORTAL-SYSTEMIC ENCEPHALOPATHY. Portalsystemic encephalopathy (PSE) is also known as hepatic en-cephalopathy and hepatic coma in the later stages. It is a clin­ical disorder seen in end-stage hepatic failure and cirrhosis. PSE is manifested by neurologic symptoms and is character­ized by an altered level of consciousness, impaired thinking processes, and neuromuscular disturbances.

PSE may develop insidiously in clients with chronic liver disease and go undetected until the late stages. Symptoms de­velop rapidly in acute liver dysfunction. Four stages of devel­opment have been identified: prodromal, impending, stu-porous, and comatose (Table 59-3). The client’s symptoms may gradually progress to coma or fluctuate among the four stages.

The exact mechanisms of PSE have not been identified. The most probable cause is impaired ammonia metabolism. Most of the ammonia in the body is found in the gastroin­testinal (GI) tract. Protein provided by the diet is transported to the liver by the portal vein. The liver breaks down protein by a series of enzymatic reactions. Protein is initially broken down into glutamine (a nontoxic substance) and ammonia. Ammonia is further broken down into urea. Urea diffuses into the body fluids and is eventually excreted in the urine by the kidneys.

Some ammonia is normally formed in the GI tract by the action of intestinal bacteria on protein products. Gastric juices are also a source of ammonia, and peripheral tissue metabo­lism produces some ammonia. The kidney may be a source of endogenous ammonia if hypokalemia is present.

 

If the liver is incapable of adequate protein degradation and cannot convert ammonia to urea, an excessive amount of circulating ammonia develops. Elevated ammonia levels are toxic to central nervous system tissue (glial and nerve cells), interfering with normal cerebral metabolism and function.

Factors that may precipitate PSE include the following:

•  High-protein diet

•  Infections

•  Hypovolemia (deficient fluid volume)

•  Hypokalemia (deficient serum potassium)

•  Constipation

•  GI bleeding (causes a large protein load in the intestines)

•  Drugs (e.g., hypnotics, opioids, sedatives, analgesics, diuretics)

PSE may also occur after paracentesis or shunting proce­dures. The prognosis for a client with PSE depends on the severity of the underlying cause, the precipitating factors, and the degree of liver dysfunction.

HEPATORENAL SYNDROME. The development of hepatorenal syndrome indicates a poor prognosis for the client with hepatic failure. It is one of the primary causes of death in end-stage cirrhosis. Progressive oliguric renal failure associated with hepatic failure results in functional impair­ment of kidneys with normal anatomic and morphologic fea­tures. This syndrome is manifested by the following:

·        A sudden decrease in urinary flow

·        Elevated blood urea nitrogen and creatinine levels, withabnormally decreased urine sodium excretion

·        Increased urine osmolarity

Hepatorenal syndrome often occurs after clinical deteriora­tion from GI bleeding or the onset of PSE. Drugs such as in-domethacin (Indocin) and possibly acetaminophen (Tylenol, Exdol^) and aspirin (acetylsalicylic acid [ASA]) may precipi­tate renal failure when administered to the client with cirrhosis. Hepatorenal syndrome is generally accompanied by elevated serum ammonia levels with an increase in jaundice and serum bilirubin levels. The kidneys cannot excrete these products in the urine. Hepatorenal syndrome may also complicate other liver diseases, including acute hepatitis and hepatic malignancy.

Etiology

The exact factors contributing to cirrhosis have not been clearly defined. There is a genetic component, with a familial tendency to develop cirrhosis and a familial hypersensitivity to alcohol in some people. Many alcoholics do not experience cirrhosis, whereas others have cirrhosis even when adequate nutrition is maintained.

The cause of cirrhosis varies with the type. Chronic infec­tion with the hepatitis B virus is the number-one cause of cir­rhosis in the world (Rollier et al., 1999). Laennec’s (alco­holic) cirrhosis results from the hepatotoxic effect of alcohol. Poor nutritional intake compounds the problem of a malnour­ished liver in most adults. Postnecrotic cirrhosis usually oc­curs after acute viral hepatitis, which may result from blood transfusions. It is seen after exposure to industrial or chemi­cal hepatotoxins (e.g., carbon tetrachloride, arsenic, and phos­phorus). Biliary cirrhosis results from chronic biliary obstruc­tion and inflammation. Cardiac cirrhosis is associated with prolonged hepatic venous congestion. Cirrhosis often devel­ops as an idiopathic process.

Incidence/Prevalence

Cirrhosis may develop at any age. Cirrhosis and chronic liver disease was the tenth leading cause of death in 1997, ac­counting for 25,175 deaths (Centers for Disease Control and Prevention [CDC], 1999). Of all cases of cirrhosis, 10% to 30% are postnecrotic and 5% to 10% are primary biliary. Laennec’s cirrhosis is the most common type of cirrhosis in industrialized countries. Most cases of cirrhosis could be pre­vented by eliminating alcohol intake. The death rate for cir­rhosis in men is two times the rate for females, regardless race or ethnicity (National Institutes of Health [NIH], 1999).

CULTURAL CONSIDERATIONS

 In the United States, mortality from cirrhosis is higher in African Americans and Hispanics (CDC, 1999). The cause is unknown.

 COLLABORATIVE MANAGEMENT

Assessment

  HISTORY

The nurse obtains historical data from clients with suspected cirrhosis, including age, sex, race, history of or present sub­stance use, and employment history, especially exposure to harmful chemical toxins. The nurse determines whether there is a history of alcoholism in the family. The client is asked to describe his or her alcohol intake, including the amount con­sumed during a given period of time. The nurse also asks the client about previous medical conditions, such as acute viral hepatitis, biliary tract disorders, viral infections, blood trans­fusions, and a history of heart failure or respiratory disorders.

 PHYSICAL ASSESSMENT/CLINICAL MANIFESTATIONS

Because cirrhosis has an insidious onset, many of the early signs and symptoms are vague and nonspecific. The client may report the following:

·        Generalized weakness

·        Weight loss

·        GI symptoms (loss of appetite, early morning nausea andvomiting, dyspepsia, flatulence, and changes in bowelhabits, with constipation and bouts of diarrhea)

·        Abdominal pain and liver tenderness (both of which are often ignored by the client)

Hepatic function abnormalities are often detected when a physical examination or laboratory tests are completed for an unrelated illness or problem. The development of late signs of advanced cirrhosis may cause the client to seek medical treat­ment. GI bleeding, jaundice, ascites, and spontaneous bruis­ing indicate deteriorating hepatic function and represent com­plications of cirrhosis.

The nurse thoroughly assesses the client with liver dys­function or hepatic failure, because it affects every body sys­tem (Figure 59-1). The clinical picture and course vary from client to client depending on the severity of hepatic failure. An inspection may reveal the following:

·        Obvious yellowing of the skin (jaundice) and the sclerae (icterus)

·        Dry skin

·        Rashes

·        Purpuric lesions, such as petechiae (round, pinpoint, redpurple lesions) or ecchymosis (large purple, blue, or yel­low bruises)

·        Warm and bright red palms of the hands (palmar erythema)

·        Vascular   lesions   with   a  red   center   and   radiating branches, known as “spider angiomas” (telangiectasias,spider nevi, or vascular spiders), on the nose, cheeks, up­per thorax, and shoulders

·        Peripheral dependent edema of the extremities and sacrum

 

ABDOMINAL ASSESSMENT. The nurse may read­ily detect massive ascites as a distended abdomen with bulging flanks. The umbilicus may protrude, and dilated ab­dominal veins (caput medusae) may radiate from the umbili­cus. Ascites can cause physical problems; for example, or-thopnea and dyspnea from increased abdominal distention can interfere with lung expansion. The client may have diffi­culty maintaining an erect body posture, and problems with balance may affect walking. The nurse inspects and palpates for the presence of inguinal or umbilical hernias, which are likely to develop in clients with ascites because of increased intra-abdominal pressure.

Minimal ascites is often more difficult to detect. Advanced assessment techniques, such as the percussion test for shifting dullness and the presence of a fluid wave, may be performed by the health care provider.

When performing an assessment of the abdomen, the nurse keeps in mind that hepatomegaly occurs in 60% of all cases of early cirrhosis. The advanced practice nurse or other health care provider palpates the right upper quadrant for he­patomegaly (enlarged liver) below the costal (rib cage) bor­der. The presence of hepatomegaly may be determined by percussing for dullness over the enlarged liver.

The nurse measures the client’s abdominal girth to evalu­ate the progression of ascites (Figure 59-2). To measure ab­dominal girth, the client lies flat while the nurse pulls a tape measure around the largest diameter of the abdomen. The girth is measured at the end of exhalation. The abdominal skin and flanks should be marked to ensure the same tape measure placement on subsequent readings.

OTHER PHYSICAL ASSESSMENT. The nurse as­sesses nasogastric (NG) tube drainage (if present), vomitus, and stool for the presence of blood. This may be indicated by frank blood in the excrement or by a positive result of an o-toluidine test for occult blood content (Hema-Check, Hematest). Gastri­tis, stomach ulceration, or oozing esophageal varices may be responsible for the presence of blood (melena).

The nurse may note fetor hepaticus, which is the distinc­tive breath odor of chronic liver disease and portal-systemic encephalopathy (PSE). It is characterized by a fruity or musty odor. Fetor hepaticus results from the inability of the damaged liver to metabolize and detoxify mercaptan, which is pro­duced by bacterial degradation of methionine, a sulfurous amino acid.

Amenorrhea may occur in women, and men may exhibit testicular atrophy, gynecomastia (enlarged breasts), and im­potence as a result of inactive hormones. Clients with prob­lems of the hematologic system caused by hepatic failure may have bruising, petechiae (small, purplish hemorrhagic spots on the skin), and an enlarged spleen.

The nurse continually assesses the client’s neurologic functioning. Subtle changes in mentation and personality of­ten progress to coma, a late complication of PSE. The nurse also assesses for asterixis (liver flap or flapping tremor), a coarse tremor characterized by rapid, nonrhythmic extensions and flexions in the wrists and fingers. Asterixis also appears in the ankles, corners of the mouth, eyelids, and tongue. Fig­ure 59-3 illustrates the technique used to elicit asterixis dur­ing physical assessment.

PSYCHOSOCIAL ASSESSMENT

The client with hepatic cirrhosis may undergo subtle or obvi­ous personality, cognitive, and behavior changes, such as agitation and belligerence. He or she may experience sleep pat­tern disturbances or may exhibit signs of emotional lability, euphoria, or depression. The nurse performs a psychosocial assessment to identify needs and help guide client care. For reasons unknown, individuals living in poorer, inner city com­munities experience a disproportionate percentage of liver disease (Frieden et al., 1999)

Repeated hospitalizations are common for clients with alcohol-induced cirrhosis who do not adhere to treatment plans. The nurse assesses the impact of the hospitalizations on the client’s lifestyle and self-esteem. Social workers assess the client’s financial capabilities to help determine whether assistance is needed.

LABORATORY ASSESSMENT

Characteristic abnormalities are common in laboratory stud­ies of clients with liver disease (Table 59-4). Serum levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and lactate dehydrogenase (LDH) are elevated be­cause these enzymes are released into the blood with the de­struction of hepatic cells. Alkaline phosphatase levels are sen­sitive to mild extrahepatic or intrahepatic biliary obstruction and therefore increase in clients with cirrhosis.

Total serum bilirubin levels also rise. Indirect bilirubin lev­els rise in clients with cirrhosis because of the inability of the failing liver to conjugate bilirubin. Therefore bilirubin is pres­ent in the urine (urobilinogen) in increased amounts. Fecal urobilinogen concentration is decreased in clients with biliary tract obstruction, which occurs in biliary cirrhosis. These clients exhibit light- or clay-colored stools.

Total serum protein and albumin levels are decreased in clients with severe or chronic liver disease as a result of de­creased synthesis by the liver. Serum levels of globulins (al­pha, beta, and gamma) are elevated because of their increased synthesis by the reticuloendothelial system of the liver, which indicates an immune response to hepatic disease.

Prothrombin time (PT) is prolonged because the liver de­creases the synthesis of prothrombin, reflecting hepatocellular or obstructive biliary tract disease. Anemia may be reflected by an altered complete blood count (CBC), with decreased he­moglobin and hematocrit values. The white blood cell (WBC) count may also be decreased. Increased toxins in the blood lead to premature cell death. Ammonia levels are elevated in the presence of advanced liver disease and PSE because the conversion of ammonia to urea for excretion is decreased.

 RADIOGRAPHIC ASSESSMENT

Abdominal x-ray studies may reveal an enlarged liver, gas or cysts within the liver and biliary tract, calcification of the liver, and massive ascites.

The upper gastrointestinal (GI) radiographic series is an examination of the esophagus, stomach, and small bowel. It may show the presence of esophageal varices or gastric or duodenal ulceration, all of which complicate the care of a client with cirrhosis.

The physician may order angiographic studies to identify actual arterial bleeding sites within the stomach. A computed tomography (CT) scan is helpful in detecting minimal ascites and provides information about the volume and character of fluid collections.

 OTHER DIAGNOSTIC ASSESSMENT

The physician may perform an esophagogastroduodenoscopy (EGD) to directly visualize the upper GI tract and to detect the presence of bleeding or oozing esophageal varices, stom­ach irritation and ulceration, or duodenal ulceration and bleeding. Injection sclerotherapy may be performed as a pal­liative measure during the endoscopic procedure to halt variceal bleeding (see Potential for Hemorrhage, p. 1308).

Radioisotope liver scans show abnormal hepatic thicken­ing and identify liver masses. The physician may use liver biopsy as the definitive test for cirrhosis. A hepatic tissue biopsy reveals destruction and fibrosis of the hepatic cells, which is indicative of the disease.

Analysis

m COMMON NURSING DIAGNOSES AND COLLABORATIVE PROBLEMS

The most commoursing diagnosis for clients with cirrhosis is Excess Fluid Volume related to portal hypertension (causing ascites) and decreased serum colloid osmotic pressure.

The following are the primary collaborative problems for clients with cirrhosis:

1.  Potential for Hemorrhage

2.  Potential for Portal-Systemic Encephalopathy (PSE)

ADDITIONAL NURSING DIAGNOSES AND COLLABORATIVE PROBLEMS

In addition to the commoursing diagnoses and collabora­tive problems, clients with cirrhosis may have one or more of the following:

Imbalanced Nutrition: Less than Body Requirements re­lated to anorexia, nausea, and faulty absorption, metabo­lism, and storage of nutrients and vitamins

·        Ineffective Breathing Pattern related to ascites and de­creased diaphragmatic excursion and pressure on the di­aphragm from ascites

·        Impaired Comfort related to abdominal pressure

·        Risk for Infection related to a decreased number of white blood cells

·        Risk for Impaired Skin Integrity related to pruritus secondary to jaundice, edema, and ascites

·        Ineffective Coping related to a chronic and potentially fatal disease process

·        Sexual Dysfunction related to altered hormonal function and decreased libido

 

·        Disturbed Body Image related to distended abdomen and skin lesions

·        Additional collaborative problems include the following:

·        Potential for Drug Toxicity

·        Potential for Hypokalemia

 Planning and Implementation

 EXCESS FLUID VOLUME

PLANNING: EXPECTED OUTCOMES. The client with cirrhosis is expected to experience a decrease in extravas-cular and intra-abdominal fluid as indicated by (1) a decrease or absence of ascites, (2) serum electrolytes within normal lim­its (WNL), and (3) blood pressure in expected range (IER).

INTERVENTIONS. Fluid accumulations are minimal during the early stages of ascites, and therefore interventions are aimed at preventing the accumulation of additional fluid and mobilizing the existing fluid collection. Nonsurgical treatment measures usually control ascites. If respiratory or abdominal functioning is compromised, surgical measures may be necessary. (See the Concept Map for chronic liver failure on p. 1306.)

NONSURGICAL MANAGEMENT. Supportive measures to control abdominal ascites include diet therapy, drugs, para-centesis, and comfort measures. The nurse also carefully monitors fluid and electrolyte status.

DIET THERAPY. The health care provider usually places the client with abdominal ascites on a low sodium diet as an initial means of controlling fluid accumulation in the abdom­inal cavity. The amount of daily sodium intake restriction typ­ically varies from 500 mg to 2 g. In collaboration with the di­etitian, the nurse explains the purpose of the diet and advises the client to eliminate table salt and salty foods. (See Chapter 13 for a list of high-sodium foods.) The absence of salt in low-sodium diets is distasteful to most people, so the dietitian sug­gests alternative flavoring additives such as lemon, vinegar, parsley, oregano, and pepper.

The health care provider may limit the client’s fluid intake if serum sodium levels fall. The kidneys retain sodium, and dilutional hyponatremia results, primarily from excessive fluid volume. Intravenous (IV) and oral fluids are restricted to 1000 to 1500 mL/day in an effort to reverse the fluid overload and raise the serum sodium level. The nurse calculates the permitted amount of oral fluids on the basis of the ordered IV intake.

In general, clients with cirrhosis are malnourished and have multiple dietary deficiencies. Vitamin supplements, such as thiamine, folate, and multivitamin preparations, are typi­cally added to the IV fluids because of the inability of the liver to store vitamins. Oral vitamins are given when IV fluid administration is discontinued.

DRUG THERAPY. The health care provider usually orders a diuretic to reduce fluid accumulation and to prevent cardiac and respiratory impairment.

The nurse monitors the effect of diuretic therapy by as­sessing intake and output, weighing the client daily, measur­ing abdominal girth, and monitoring electrolyte levels. Seri­ous electrolyte imbalances, such as hypokalemia (decreased potassium) and hyponatremia (decreased sodium), may ac­company diuretic therapy. (See Chapter 13 for discussion of electrolyte imbalances.) Depending on the diuretic selected, the provider may order an oral or IV potassium supplement. Clients with cirrhosis often require antacid therapy for GI symptoms. Because most antacids are high in sodium, the physician prescribes a low-sodium antacid such as magaldrate (Riopan).

PARACENTESIS. Abdominal paracentesis may be indi­cated if dietary restrictions and drug administration fail to control ascites (Chart 59-1). The procedure is performed at the bedside. The physician inserts a trocar catheter into the abdomen to remove and drain ascitic fluid from the peritoneal cavity.

Once a primary treatment modality for ascites, paracentesis is more commonly used as a diagnostic tool to examine ascitic fluid. It is also used as a palliative measure to relieve abdomi­nal pressure, because ascites may cause severe respiratory and abdominal distress. To relieve acute symptoms, the physician slowly drains the ascitic fluid (usually 1 to 3 L). Hypovolemia with a fluid volume deficit may occur with rapid fluid removal, because these clients have adjusted to the excessive fluid vol­ume in the abdomen. Rapid, drastic removal of ascitic fluid leads to decreased abdominal pressure, which may contribute to vasodilation and shock. The nurse observes for impending signs of shock from fluid shifts during and immediately after the procedure.

Repeated paracentesis procedures are contraindicated be­cause of the increased incidence of protein depletion, hypovo­lemia, and electrolyte imbalances (hypokalemic alkalosis), which can contribute to the development of portal-systemic encephalopathy in the client with cirrhosis.

COMFORT MEASURES. Excessive ascitic fluid volume in the abdomen may cause the client to experience respiratory difficulty. Dyspnea may develop as a result of increased intra-abdominal pressure, which limits thoracic expansion and di­aphragmatic excursion. The nurse or assistive nursing person­nel elevates the head of the bed to at least 30 degrees or as high as the client wishes in an effort to minimize shortness of breath. The client is encouraged to sit in a chair. This upright position, with his or her feet elevated to discourage dependent ankle edema, often relieves dyspnea.

To weigh the client, the nurse or assistive nursing person­nel uses a standard upright bedside scale (if the client can stand). Weighing on a bed scale necessitates that the client lie flat; this supine position can cause the client to feel increas­ingly short of breath and can increase anxiety.

 FLUID/ELECTROLYTE MANAGEMENT. The nurse mon­itors the client for fluid and electrolyte imbalances as a result of the disease or treatment. Laboratory tests, such as blood urea nitrogen (BUN), serum protein, hematocrit, and elec­trolytes help to determine fluid and electrolyte status. Nursing activities are listed in Chart 59-2.

SURGICAL MANAGEMENT. When medical manage­ment fails to control ascites, the physician may choose surgi­cal intervention to divert ascites into the venous system by creating a shunt. However, the shunt has limited use as an ef­fective treatment for ascites. Clients with ascites are poor surgical risks because of their susceptibility to infection, as evi­denced by the following:

·        A decreased WBC count

·        Disseminated intravascular coagulation (DIC)

·        Bleeding esophageal varices

·        Anesthesia reactions

Mortality in these clients having shunt procedures can be as great as 11% perioperatively; complication rates are ap­proximately 30% (Ziser et al., 1999).

PREOPERATIVE CARE. Because the client with cirrhosis has many underlying medical problems, an optimal physical state is desired before surgery is performed. Electrolyte im­balances are corrected, and abnormal coagulation is treated with the administration of fresh frozen plasma and vitamin K. Packed red blood cells are made available for transfusion, be­cause these clients have bleeding tendencies.

OPERATIVE PROCEDURES. One of several types of shunts may be created, such as the peritoneovenous and Den­ver shunts.

Peritoneovenous Shunt. A peritoneovenous shunt, also known as a peritoneojugular or LeVeen shunt (Figure 59-4), drains ascites through a one-way valve into a silicone rubber tube that terminates in the superior vena cava. A pressure gra­dient develops between the peritoneal cavity and the vena cava, facilitating the flow of ascitic fluid through the valve into the venous system. During inspiration, the diaphragm de­scends, which increases peritoneal fluid (ascites) pressure; pressure in the superior vena cava also increases, which cre­ates the needed gradient. A pressure difference of greater than 3 cm H₂O is necessary to open the valve. The valve closes when the pressure is decreased.

After the shunt has been inserted, the client is expected to lose weight, show a decrease in abdominal girth, have in­creased urinary output, and exhibit an increased renal excre­tion of sodium. These clinical improvements result from re­stored adequate peripheral circulation.

Denver Shunt. The Denver shunt has a subcutaneous pump that can be manually compressed. It is often preferred for clients whose ascites contains large particles (common in neoplastic ascites). These particles can cause the flow to become sluggish and result in a clotted shunt. Compressing the pump of the Denver shunt helps to irrigate the tubing to main­tain patency.

POSTOPERATIVE CARE. The nurse provides the usual postoperative care for a client undergoing abdominal surgery (see Chapter 19). The nurse remains aware that the ascitic fluid is routed into the venous system, resulting in vascular volume expansion and hemodilution. The vital signs are mon­itored carefully; an increase in blood pressure reflects an in­crease in vascular volume. If the client has a central venous or pulmonary artery catheter in place, the nurse determines whether pressure is elevated. Breath sounds are auscultated for the presence of crackles, which indicates excessive lung fluid. A diuretic, such as furosemide (Lasix), is usually or­dered to rid the body of excessive fluid.

The nurse notes any abnormal results of coagulation stud­ies (prothrombin time [PT] and partial thromboplastin time [PTT]). Reabsorption of clotting factors in ascitic fluid may further inhibit an already altered clotting mechanism and lead to DIC and bleeding abnormalities.

The nurse or assistive nursing personnel measures the client’s weight, abdominal girth, and urinary output each shift to determine the effectiveness of the shunting procedure.

 

 

 POTENTIAL FOR HEMORRHAGE

PLANNING: EXPECTED OUTCOMES. If the client experiences hemorrhage, it is expected to be controlled through medical and nursing interventions.

INTERVENTIONS. During the acute phase of bleeding, early interventions are based on identifying the source of bleeding and initiating treatment to halt it. Because massive esophageal bleeding can cause rapid blood loss, emergency interventions are initiated. If the client is a known alcoholic with a history of variceal bleeding, measures to treat the esophageal varices are initiated and therefore valuable time is not wasted looking for another source of bleeding.

NONSURGICAL MANAGEMENT. The health care team intervenes quickly to control bleeding by providing gastric in­tubation, balloon tamponade, drug therapy, replacement of blood products, injection sclerotherapy, or transjugular intra-hepatic portal-systemic shunt (TIPS). The client is managed in the critical care unit. After the acute bleeding episode has been controlled, the client may require surgical intervention to decrease portal hypertension, thereby decreasing the risk of further variceal bleeding.

GASTRIC INTUBATION. Early in the hospitalization, the client’s reports of hematemesis should be investigated. The physician usually inserts an 18-gauge Salem sump tube and lavages the stomach until the fluid returned is clear. The in­troduction of saline or water lavage may be used to achieve vasoconstriction of the bleeding gastric ulceration or varices. The physician may add norepinephrine (Levophed) to the so­lution to produce further constriction. If endoscopy identifies the bleeding site as a gastric ulcer, the physician initiates medical treatment with drug therapy (antacids and histamine receptor antagonists) and blood prod­uct replacement. If bleeding continues from the ulcer, surgi­cal intervention is necessary.

ESOPHAGOGASTRIC BALLOON TAMPONADE. If the physician suspects that hematemesis has occurred because of bleeding esophageal varices, he or she inserts an esopha-gogastric tamponade tube. Bleeding varices are a medical emergency and necessitate immediate intervention. The pri­mary nursing intervention is maintaining a patent airway. Vomiting and the accumulation of blood in the oropharynx may result in aspiration, occlusion of the airway, and respira­tory compromise. The nurse attempts to keep the client’s oropharynx clear by suctioning secretions, turning the client’s head, and keeping the head of the bed elevated during vomit­ing episodes to prevent aspiration.

 

Types of Esophagogastric Tubes. The classic method of treating bleeding esophageal varices is by compressing the bleeding vessels with an esophagogastric tube, such as the Sengstaken-Blakemore tube (Blakemore tube), which has two balloons. This type of tube is also referred to as a tamponade tube. When inflated, the large esophageal balloon compresses the esophagus. The smaller gastric balloon helps anchor the tube and exerts pressure against bleeding varices in the distal esophagus and the cardia of the stomach. A third lumen ter­minates in the stomach and is connected to suction, allowing the aspiration of gastric contents and blood. A Salem sump tube is used in conjunction with the Sengstaken-Blakemore tube and is placed in the proximal esophagus to enable clear­ing of collected esophageal secretions, saliva, and blood.

Insertion of an Esophagogastric Tube. Before the physician inserts the tube, the nurse inspects it and inflates and deflates the balloons to check for integrity and leaks. Each lumen is identified and labeled to prevent errors in adding or removing pressure and air volume.

The physician usually anesthetizes the client’s nose and oropharynx, introduces the tube through the nares, and gently inserts it into the stomach. After tube placement is verified, the stomach is aspirated and irrigated. The gastric balloon is inflated with up to 300 mL of air. The nurse assists the physi­cian in securing the tube and applying traction, which pro­vides additional tamponading pressure. This is accomplished by taping the tube to the face guard of a football helmet or by securing it to an overbed traction apparatus and applying a 1-pound (0.45-kg) traction weight.

Care of the Client with an Esophagogastric Tube. Inflation of the esophageal balloon is measured with a sphyg-momanometer. Pressure should be maintained between 20 and 25 mm Hg. The nurse periodically checks the balloon pressures and volumes to prevent loss of pressure (with fur­ther bleeding or erosion) or rupture of the esophagus caused by overinflation (Chart 59-3). The esophagogastric balloon is usually removed after 48 hours. The nurse attaches the esophageal and gastric drainage lumina to low intermittent suction and monitors the amount and type of drainage.

Placement of the tamponade tube should halt variceal bleed­ing. After bleeding is controlled, the traction is released, and esophageal pressure is gradually decreased. The gastric balloon is deflated, and the tube is removed. Another tube should be kept at the bedside for potential reinsertion if bleeding recurs.

The nurse and assistive nursing personnel should be alert for sudden respiratory compromise with acute distress caused by airway obstruction from upward displacement of the esophageal balloon. A pair of scissors is always kept at the bedside. If the tube becomes dislodged, the nurse cuts both balloon ports to rapidly deflate the balloon and quickly removes the tube.

BLOOD TRANSFUSIONS. Massive hemorrhage necessi­tates replacement by blood products. Blood is drawn to iden­tify the client’s blood type. Until the blood is available, the nurse administers large crystalloid (IV fluids) or colloid (plasma) volumes, as ordered, into large-bore IV access routes to maintain blood pressure.

The nurse administers packed red blood cells and fresh frozen plasma (per physician order and agency policy) to re­place blood volume and clotting factors. The physician and the nurse monitor trends in hemoglobin and hematocrit levels, and additional blood products are transfused as indicated.

DRUG THERAPY. To prevent the incidence of esophageal hemorrhage, the client may be placed on propranolol (Inderal, Apo-Propranolol^) therapy. By decreasing heart rate and sys­temic blood pressure, the chance of bleeding may be reduced.

In a client who is actively bleeding, the physician may use a vasoconstrictor (e.g., vasopressin [Pitressin]), to temporar­ily control hemorrhage by lowering pressure within the portal blood flow system. This drug causes contraction of smooth muscle in the vascular bed. By constricting preportal splanch­nic arterioles, blood flow is decreased to the abdominal or­gans, which reduces portal pressure and portal blood flow.

Vasopressin is administered by infusion pump intra­venously or through a catheter placed in the superior mesenteric artery.

The IV route is indicated initially because it al­lows easy, rapid access. The insertion of a superior mesenteric artery catheter is an invasive procedure performed by the physician or radiologist through fluoroscopy. Both infusion methods have demonstrated effective short-term control of variceal bleeding, but recurrent hemorrhage is common. An initial bolus dose of 20 to 40 units of vasopressin in 100 to 200 mL of 5% dextrose in water (D₅W) is typically given, fol­lowed by a continuous infusion of 200 units in 500 mL of D₅W at 0.2 to 0.4 units/min.

The nurse closely monitors the pulse, blood pressure, and intake and output ratio of the client receiving vasopressin. The occurrence of abdominal cramping, chest pain, and cardiac dysrhythmias is noted and reported immediately to the health care provider. Vasopressin may precipitate acute angina or myocardial infarction in clients with coronary artery disease. The nurse immediately reports any abnormal assessment find­ings to the physician. Concurrent IV administration of nitro-glycerin, a vasodilator, may help prevent vasoconstriction of the coronary arteries during vasopressin therapy.

INJECTION SCLEROTHERAPY. The use of endoscopic injection sclerotherapy in clients with bleeding esophageal varices is a treatment reserved for clients who have repeated hemorrhagic episodes despite conservative medical manage­ment. Before the endoscopy, the nurse obtains baseline vital signs values. The physician usually administers the first dose of sedative, usually diazepam (Valium) or midazolam hy-drochloride (Versed). The physician sprays the client’s throat with a topical anesthetic, such as benzocaine (Cetacaine).

Injection sclerotherapy is performed in conjunction with esophagogastroduodenoscopy. During the endoscopic examination, the physician introduces a sclerosing agent, or scle-rosant, through a flexible injector (Figure 59-5).

Bleeding from the varices should stop within 2 to 5 min­utes. If it continues, the physician makes a second injection attempt below the bleeding site. Prophylactic injection scle-rotherapy may be performed on other distended, nonbleeding varices. Because the procedure is usually done during an acute bleeding episode, the nurse or assistive nursing person­nel closely monitors the client’s vital signs during this hour-long procedure, which is done at the bedside or in an en-doscopy clinic.

The client may report noncardiac chest discomfort for 24 to 72 hours after the injection; this discomfort is relieved by analgesia. The nurse assesses the complaint of chest pain and administers pain medication. Esophageal perforation and ul-ceration are other complications of injection sclerotherapy and cause severe chest pain. The nurse immediately reports acute changes to the physician.

Because aspiration may occur and cause pneumonia and pleural effusion, the nurse assesses lung sounds for decreased aeration and adventitious sounds. After injection sclerother­apy, caution is necessary wheasogastric (NG) tubes are used and inserted. Some physicians prefer not to reinsert NG tubes to decrease the risk of injury to the sclerosed esophagus.

ENDOSCOPIC LIGATION. Endoscopic variceal ligation uses bands to ligate the bleeding varices and can be used to prevent esophageal varices from bleeding. This procedure is similar to sclerotherapy except that the varices are ligated with bands instead of injected. This procedure is thought to be safer and more cost-effective than propranolol therapy in pre­venting esophageal varices from bleeding (Sarin et al., 1999).

TRANSJUGULARINTRAHEPATIC PORTAL-SYSTEMIC SHUNT. Insertion of a transjugular intrahepatic portal-systemic shunt (TIPS) is a nonsurgical procedure performed in the radiology department in a special procedures room or an interventional radiology suite. This procedure is usually re­served for clients who have not responded to any other non-surgical management. With the client under IV conscious se­dation, the physician passes a shunt through a catheter and implants it between the portal vein and the hepatic vein. This technique reduces portal venous pressures and therefore con­trols bleeding.

Before the procedure, the physician obtains informed con­sent from the client. The client should know that the proce­dure is painful even though droperidol (Inapsine), meperidine hydrochloride (Demerol), or midazolam hydrochloride (Versed) is given in high doses for IV conscious sedation. Complications may include stenosis and thrombosis. After TIPS, the client can usually go home within 2 to 4 days.

SURGICAL MANAGEMENT. Portal-systemic shunts are considered a last-resort intervention for clients with portal hy­pertension and esophageal varices. The high mortality rate as­sociated with shunting procedures occurs because clients with end-stage liver disease have coagulation abnormalities, are susceptible to infection, tolerate anesthesia poorly, and have ascites. In recent years, liver transplantation has also been commonly performed for end-stage cirrhosis (see Liver Transplantation, p. 1324).

Surgical bypass shunting procedures decrease portal hy­pertension by diverting a portion of the portal vein blood flow from the liver. The goal is to decrease the incidence of variceal bleeding while maintaining sufficient blood flow to the liver, thereby preserving hepatocellular function.

PREOPERATIVE CARE. The client with hepatic cirrho­sis has multiple underlying problems. The client with esophageal bleeding must be transfused before surgery with packed red blood cells and fresh frozen plasma to correct clotting deficiencies.

OPERATIVE PROCEDURES. The shunting procedures most commonly used are the portacaval and splenorenal shunts (Figure 59-6).

The portacaval shunt diverts the portal venous blood flow into the inferior vena cava to decrease portal pressure. The portal vein is anastomosed to the inferior vena cava. Splenore­nal shunting involves splenectomy with anastomosis of the splenic vein and left renal vein. There are several variations of these procedures. With the mesocaval shunt, the superior mesenteric vein is anastomosed to the inferior vena cava.

Portal-systemic decompression shunting procedures are not as common as they once were because of complications such as bleeding, portal-systemic encephalopathy (PSE), shunt thrombosis, and infection, as well as the increase iumber of liver transplants. A shunt may decrease the occurrence of variceal bleeding, but survival time is usually not prolonged.

POSTOPERATIVE CARE. The client is usually admitted to the critical care unit immediately after surgery. The extent of care needed depends on the client’s preoperative health sta­tus, extent of hepatic disease, and magnitude of the procedure.

The nurse provides constant observation and careful mon­itoring, including a frequent assessment of vital signs, central venous pressure, and pulmonary artery pressure (if indicated), as well as an hourly intake and urinary output measurements. In collaboration with the physician and the respiratory thera­pist, the nurse monitors respiratory status if the client is intu-bated, protects the client’s artificial airway (endotracheal tube), and checks the ventilator for correct settings. The usual postoperative care measures to prevent atelectasis and pneu­monia are instituted.

Although the intubated client has an increased need for seda­tives, the nurse exercises discretion in providing opioid analgesics for pain relief and sedation during the postoperative pe­riod. These drugs are contraindicated in clients with chronic he­patic failure, because most drugs are metabolized in the liver.

After these shunting procedures, clients are susceptible to oliguria. They are often hypovolemic as a result of the following:

·        Uncompensated blood loss

·        Excessive fluid loss from prolonged exposure of the peritoneal space during surgery, resulting in fluid evaporation

·        The recurrence of ascites

·        Preoperative fluid restriction

·        Diuretic therapy

The nurse administers the ordered fluid volume and as­sesses the effects of the volume by monitoring for increased blood pressure, decreased heart rate, and increased urinary output. Excessive increases in the central venous pressure or pulmonary artery pressure after fluid challenge are reported. Volume replacement may be given as fresh frozen plasma (to correct postoperative coagulopathy), IV solution boluses, and packed red blood cells.

Recurrent esophageal variceal bleeding after a portal-systemic shunt is not uncommon and may indicate the return of elevated portal pressures caused by a thrombosed (clotted) shunt. A rapid reaccumulation of abdominal fluid may also suggest a failed shunt or excessive sodium administration. The physician may need to reinstitute diuretic therapy. The nurse continues to measure the client’s abdominal girth and reports sudden girth increases to the physician.

The nurse should be alert for the development of postshunt encephalopathy, because it is common in these clients (see care measures for portal-systemic encephalopathy [PSE] in the next section).

Clients requiring portal-systemic shunts have increased nutritional requirements and are often given total parenteral nutrition (TPN) to provide the needed calories, vitamins, and minerals. The nurse also administers albumin intravenously several times per day to replace the albumin lost in ascites. (See Chapter 61 for care associated with TPN administration.) <JIE» Bleeding Precautions. The nurse monitors the client closely for hemorrhage. Coagulation studies, including pro-thrombin time (PT), partial thromboplastin time (PTT), platelet count, and International Normalized Ratio (INR), are also monitored carefully. Chart 59-2 lists additional interven­tions for clients at risk for bleeding.

 POTENTIAL FOR PORTAL-SYSTEMIC ENCEPHALOPATHY

PLANNING: EXPECTED OUTCOMES. It is ex­pected that the nurse report and document findings for clients who exhibit signs of portal-systemic encephalopathy (PSE).

INTERVENTIONS. During the early stages of PSE in clients with hepatic cirrhosis, interventions are focused on de­creasing ammonia formation in an effort to decrease progres­sive cerebral dysfunction. The diseased liver cannot convert ammonia to a less toxic form, and ammonia is carried by the circulatory system to the brain, where high levels of ammonia are toxic to normal cerebral function. The aim of PSE man­agement is to halt this process.

Because ammonia is formed in the gastrointestinal (GI) tract by the action of bacteria on protein, nonsurgical treat­ment measures to decrease ammonia production include di­etary limitations and drug therapy to reduce bacterial break­down. The nurse collaborates with the dietitian and physician to plan and implement these treatment measures.

DIET THERAPY. The client with cirrhosis has increased nutritional requirements. The client needs high-carbohy­drate, moderate-fat, and high-protein foods. The diet is often modified for clients who have elevated serum ammonia lev­els and exhibit the signs of PSE. The client’s intake of di­etary protein is typically limited in an effort to reduce the excessive breakdown of protein into ammonia by intestinal bacteria.

The diet for a client with PSE or elevated ammonia levels usually includes low-protein foods and simple carbohydrates, such as fruit juice. As the client’s mental status deteriorates, proteins may be totally eliminated from the diet. When PSE fluctuates among the four stages, the nurse avoids giving foods high in protein content, such as meat, fish, poultry, eggs, and dairy products.

Clients with cirrhosis often experience GI bleeding, which results in the formation of increased amounts of ammonia as in­testinal bacteria attempt to metabolize the blood cells. GI bleed­ing may precipitate hepatic coma (stage IV of PSE). These clients are maintained oothing by mouth (NPO) status with a nasogastric (NG) tube or an esophageal tamponade tube, de­pending on the source of the bleeding. Nutritional maintenance with IV total parenteral nutrition is ofteecessary.

DRUG THERAPY. Several types of drugs can eliminate or reduce ammonia levels in the body.

LACTULOSE. The health care provider orders the admin­istration of lactulose (Cephulac) to promote the excretion of ammonia in the stool. Lactulose, a disaccharide with high mo­lecular weight, is a viscous, sticky, sweet-tasting liquid that the nurse administers either orally or by NG tube. When giv­ing the drug orally, the nurse dilutes the lactulose with fruit juice to help the client tolerate the sweet taste. Lactulose re­tention enemas are ofteecessary when the client cannot tol­erate oral administration or when liquids are contraindicated in the upper GI tract.

Lactulose creates an acidic environment in the bowel by keeping ammonia in its ionized state; this decreases the colon’s pH from 7 to 5. This causes ammonia to leave the cir­culatory system and move into the colon, which reverses the normal passage of ammonia from the colon to the blood­stream. The acidic environment also discourages the growth of bacteria. Lactulose draws water into the bowel because of its high osmotic gradient, producing a laxative effect and fa­cilitating the evacuation of ammonia from the bowel.

The desired effect of lactulose is two to three soft stools per day with an acidic fecal pH. During the acute phase of PSE, 20 to 30 g of lactulose is administered at 4-hour inter­vals until stools are achieved; the dosage is then decreased to three or four times per day. As a retention enema, 200 g of lac­tulose diluted in 1000 mL of water is administered at 4- to 6-hour intervals.

The nurse or assistive nursing personnel observes closely for watery diarrheal stools, which may signify excessive lac­tulose administration. The client may complain of intestinal bloating and cramping. The nurse also monitors daily for de­creasing ammonia levels, which would reflect a positive ef­fect of drug therapy, and for hypokalemia and dehydration, which can result from numerous stools.

NEOMYCIN SULFATE. Neomycin sulfate (Mycifradin Sulfate), a broad-spectrum antibiotic, is given to act as an in­testinal antiseptic. It destroys the normal flora in the bowel, diminishing protein breakdown and decreasing the rate of am­monia production. Maintenance doses of neomycin are given orally but may also be administered as a retention enema.

Because constipation may lead to increased bacterial ac­tion on retained stool, with a resulting increase in ammonia levels, stool softeners should be included in the long-term treatment plan. The administration of medications that are po­tentially toxic to the liver, such as opioid analgesics, seda­tives, and barbiturates, must be restricted.

OTHER DRUGS. Because the client with PSE exhibits progressive neurologic changes and is often confused, com­bative, uncooperative, or belligerent, the nurse may need to give sedatives to prevent him or her from self-harm or harm of others. In such cases, the judicious use of drugs such as ox-azepam (Serax) is warranted.

Levodopa (Dopar, Larodopa) has been used with some success in the treatment of chronic PSE. The use of levodopa (a precursor of dopamine and norepinephrine) is based on the theory that encephalopathy involves defective neurotransmit-ters. Deficient dopamine and norepinephrine are replaced by false transmitters—amine products from the breakdown of di­etary protein. Synthetic levodopa provides the pathway for normal transmission.

 NEUROLOGIC MONITORING. The nurse or assistive nursing personnel continually assesses for changes in level of consciousness and orientation (see Chart 59-2). An indi­vidualized neurologic assessment is developed for each client and includes the assessment of simple tasks such as name writing, bilateral handgrasping, and serial subtractions and additions.

The nurse also continually assesses for the presence of as-terixis (liver flap) and fetor hepaticus (liver breath). These signs suggest worsening encephalopathy.

CRITICAL THINKING CHALLENGE

You are caring for a client in the prodromal stage of PSE.

•  In planning care, which common medications are hepatotoxic and should be avoided?

•  What type of dietary restrictions might be ordered?

•  How will you maintain the client’s safety?

•  For what signs and symptoms indicating worsening PSE will you be observing?

 Community-Based Care

If the client with hepatic cirrhosis survives life-threatening complications, he or she is usually discharged to the home or to a long-term care facility after treatment measures have combated the acute medical problems. A home care referral may be needed if the client is discharged to the home. These chronically ill clients are often readmitted, and community-based care is aimed at preventing rehospitalization. The client may benefit from hospice care. A case manager is often needed to coordinate interdisciplinary care.

 HEALTH TEACHING

The client is discharged to the home setting with an individu­alized teaching plan (Chart 59-4) that covers diet therapy, drug therapy, and alcohol abstinence.

DIET THERAPY. In collaboration with the dietitian, the nurse provides strict dietary instructions. Most clients need a diet high in calories, protein, and vitamins. Depending on the resence or absence of ascites, the client may require a diet low in sodium. The dietitian plans meals and menus with the client’s favorite foods and provides lists of foods high in calo­ries, protein, and vitamins.

 

CLIENT EDUCATION GUIDE

Cirrhosis

Diet Therapy

·        Consume a diet high in calories, protein, and vitamins unless your health care provider has told you to avoid high-protein foods.

·        If you have excessive fluid in the abdomen, follow the low-sodium diet prescribed for you.

·        Eat small, frequent meals that are nutritionally well balanced.

·        Include in your diet daily supplemental liquids (e.g., Ensure or Ensure Plus) and a multivitamin. Low-protein supplements are available if needed.

Drug Therapy

·        Take the diuretics prescribed for you. If you experience weakness or cardiac irregularities, report these symp­toms to your health care provider. Take the H₂-receptor antagonist prescribed for you to prevent gastrointestinal bleeding.

·        Do not take any other medication unless specifically or­dered by your health care provider.

Alcohol Abstinence

·        Do not consume any alcohol.

·        • Seek support services for help.

The client with portal-systemic encephalopathy (PSE) must avoid high-protein foods at home in an effort to decrease the incidence of progressive neurologic dysfunction. If the client’s nutritional intake is decreased after discharge, multi-vitamin supplements and supplemental liquid feedings (e.g., Ensure) are usually needed.

DRUG THERAPY. The client is often discharged while receiving diuretics. The nurse provides written instructions and the health care provider’s prescription for the diuretic. Written information about the signs and symptoms of poten­tial electrolyte imbalances that may result from diuretic ther­apy (e.g., hypokalemia) is also essential. The client may need to take a potassium supplement.

If the client has had problems with bleeding from gastric ulcers, the provider prescribes antacids or an H₂-receptor an­tagonist agent, such as ranitidine hydrochloride (Zantac). The nurse provides written guidelines and administration sched­ules for all medications to be taken at home.

The nurse advises the client to avoid all over-the-counter medications and to consult the physician for follow-up med­ical care. The client is instructed to notify the physician im­mediately if any gastrointestinal (GI) bleeding is noted so that re-evaluation can be initiated quickly.

ALCOHOL ABSTINENCE. One of the most important aspects of ongoing care for the nurse to stress is the need for alcohol abstinence (see Chapter 8). Avoiding alcohol can do the following:

·        Prevent further fibrosis of the liver from scarring

·        Allow the liver to regenerate

·        Prevent gastric and esophageal irritation

·        Reduce the incidence of bleeding

·        Prevent other life-threatening complications

HOME CARE MANAGEMENT

The nurse, case manager, client, and family or significant other should identify any physical adaptations needed to pre­pare the client’s home for convalescence. The client’s rest area should be close to a bathroom, because diuretic therapy increases the frequency of urination. If the client has difficulty reaching the toilet, additional equipment (e.g., urinals, bed­pans, and bedside commodes) is necessary. Special, adult-sized incontinence pads or briefs may be helpful if the client has an altered mental status and has urinary incontinence.

Initial home activity may be limited for the client who has undergone surgical intervention. If the client experiences shortness of breath from massive ascites, elevating the head of the bed and maintaining the client in a semi-Fowler’s to high Fowler’s position may help alleviate respiratory distress. Al­ternatively, a reclining chair with a foot elevator may be used.

HEALTH CARE RESOURCES

The client with chronic cirrhosis may require a home care nurse to assess the client’s tolerance of dietary restrictions. The home care nurse can also monitor the effectiveness of drug therapy or the surgical shunt in controlling ascites. Indi­vidual and group therapy sessions may be arranged to assist the client in dealing with alcohol abstinence. The nurse may refer the client and family to self-help groups, such as Alco­holics Anonymous and Al-Anon. The client may also desire spiritual support. Other possible resources include hospice and long-term care in a nursing home.

 Evaluation: Outcomes

The nurse evaluates the care of the client with cirrhosis on the basis of the identified nursing diagnoses and collaborative problems. The expected outcomes include that the client will:

·        Experience a decrease in or no ascites

·        Have electrolytes withiormal limits (WNL)

·        Have blood pressure WNL

·        Not experience hemorrhage, or be managed immediately f bleeding occurs

·        Not experience PSE, or be managed immediately if PSE ccurs

·        Have the optimal quality of life possible

HEPATITIS

OVERVIEW

Hepatitis is the widespread inflammation of liver cells. Viral hepatitis is the most prevalent type and can be either acute or chronic. Viral hepatitis results from an infection caused by one of five major categories of viruses:

·        Hepatitis A virus (HAV)

·        Hepatitis B virus (HBV)

·        Hepatitis C virus (HCV)

·        Hepatitis D virus (HDV)

·        Hepatitis E virus (HEV)

Hepatitis F and G have also been identified but are uncommon. Liver injury with inflammation can also develop after ex­posure to a number of pharmacologic and chemical agents by inhalation, ingestion, or parenteral (IV) administration. Toxic and drug-induced hepatitis can result from exposure to hepa-totoxins (e.g., industrial toxins, alcohol, and medications). epatitis may also occur as a secondary infection during the course of infections with other viruses, such as Epstein-Barr, herpes simplex, varicella-zoster, and cytomegalovirus.

Clients usually recover from hepatitis but may have resid­ual liver damage. Mortality from hepatitis is relatively low, but severe hepatitis may be fatal. With increasing numbers of people developing chronic hepatitis, the mortality is rising.

Pathophysiology

After the liver has been exposed to causative agents (e.g., a virus), it becomes enlarged and congested with inflammatory cells, lymphocytes, and fluid, resulting in right upper quad­rant pain and discomfort. As the disease process continues and progresses, the liver’s normal lobular pattern becomes distorted as a result of widespread inflammation, necrosis, and hepatocellular regeneration. This distortion increases pressure within the portal circulation, interfering with the blood flow into the hepatic lobules. Edema of the liver’s bile channels results in intrahepatic obstructive jaundice.

Specific data on the pathogenesis of hepatitis A, C, D, and E are limited. Clinical manifestations of acute HBV inflam­mation are determined by an immunologic response of the host (client). Immune complex-mediated tissue damage may contribute to the extrahepatic manifestations of acute hepati­tis B. Clinical responses include an urticarial rash (hives) and arthritic joint pain.

There are three phases of hepatitis. The preicteric or pro­dromal phase begins with the infection and the start of signs and symptoms and generally lasts a week. The icteric phase starts with the onset of jaundice and lasts approximately 4 to 6 weeks. The posticteric or recovery phase of hepatitis is marked by active phagocytosis and enzyme activity; damaged hepatic cells are removed, allowing for regeneration of the cells. This phase may last up to 4 months. Unless serious complications develop, most clients recover normal hepatic function after a viral hepatic insult.

CLASSIFICATION OF HEPATITIS AND ETIOLOGIES

VIRAL HEPATITIS. The five types of acute viral hepati­tis vary by mode of transmission, manner of onset, and incuba­tion periods (Table 59-5). These viruses are classified as enteral or parenteral in reference to the mechanism of transmission.

Enteral forms (hepatitis A and E) are transmitted by the fecal-oral route. Parenteral forms (hepatitis B, C, and D) are primarily transmitted via venous blood transfer or through in­timate sexual contact. Vaccines to prevent hepatitis A and B are currently available.

HEPATITIS A. The causative agent of hepatitis A, hepati­tis A virus (HAV), is a ribonucleic acid (RNA) virus of the en-terovirus family. HAV is characterized by a mild course sim­ilar to that of a typical viral syndrome and often goes unrecognized. It is spread via the fecal-oral route by the oral ingestion of fecal contaminants. Sources of infection include contaminated water, shellfish caught in contaminated water, and food contaminated by food handlers infected with HAV. The virus may also be spread by oral-anal sexual activity. The incubation period of hepatitis A is usually 15 to 50 days. The disease is usually not life threatening. Individuals exposed to he virus should be given immune globulin immediately and not later than 2 weeks after the exposure.

HEPATITIS B. Hepatitis B is caused by a double-shelled particle containing deoxyribonucleic acid (DNA) composed of a core antigen (HBcAg), a surface antigen (HBsAg), and an independent protein (HBeAg) that circulates in the blood.

The primary mode of transmission of hepatitis B virus (HBV) is via the skin and mucous membrane route by con­tamination with blood and serous fluid. Lower concentrations of HBV are also found in semen, vaginal fluid, and saliva. Al­though transmission can occur through bites, there are no doc­umented cases of transmission through kissing. Hepatitis B may be spread through the following modes of transmission:

•  Sexual contact with multiple partners (heterosexual and omosexual)

•  Sharing needles

•  Accidental needle sticks or injuries from sharp instru­ments in health care workers

•  Blood transfusion

•  Hemodialysis

•  Acupuncture, tattooing, ear or body piercing

•  Maternal-fetal route

The clinical course of hepatitis B may be varied. It may have an insidious onset with mild signs and symptoms, or it may result in serious complications such as fulminant hepati­tis, chronic hepatitis, cirrhosis, and hepatocellular carcinoma, a rare but increasing problem in the United States. The incu­bation period is generally 45 to 180 days, but hepatitis B com­monly develops 60 to 90 days after exposure. Chronic HBV infection develops in about 1% to 10% of adult clients with acute HBV infection (CDC, 1999).

HEPATITIS C. The causative virus of hepatitis C (HCV) is an enveloped, single-stranded RNA virus. It is transmitted by exposure of the skin and mucous membrane to blood and plasma; it is rarely transmitted sexually or from mother to fetus.

HCV is spread by contaminated items such as the following:

•  Illicit IV drug needles (highest incidence)

•  Tattoo, ear, or body piercing needles

•  Razors, nail clippers, and scissors

•  Toothbrushes and Water Piks

•  Tampons or sanitary napkins

•  Blood, blood products, or organ transplants received be­fore 1992

Health care workers, such as nurses and phlebotomists, are also at risk for HCV infection following a needle stick injury with HCV-contaminated blood. HCV infection is also com­mon in hemodialysis centers.

The incubation period for HCV is 21 to 140 days, with an average incubation period of 7 weeks. Approximately 85% of infected individuals develop chronic hepatitis (Hoofnagle, 1999). Approximately 2.7 million Americans are chronically infected with HCV, with 65% between 30 and 49 years of age (Alter, 1999). This suggests that the health care system may be burdened as infected individuals age and develop worsen­ing liver damage (see the Cost of Care box on p. 1316).

Hepatitis C is a leading cause of cirrhosis and hepatocellu­lar carcinoma worldwide. Approximately half of the liver transplants performed in the United States are for end-stage hepatitis C (Hepatitis Foundation International, 1999). Unfortunately, the newly transplanted liver often becomes reinfected with the virus (see the Legal/Ethical Issues box below, left).

 

 

 

COST OF CARE

HEPATITIS C

Cost of Care

• An estimated 3.9 million Americans, nearly 2% of the pop­ulation, are chronically infected with hepatitis C.

• The cost of hepatitis C infections and related diseases ismore than $600 million dollars per year.

• More than half of the liver transplants performed in theUnited States are for hepatitis C. The average first-year costfor a liver transplant exceeds $200,000.

• From the year 2010 through 2019, the projected cost in di­rect medical expenses is $10.7 billion, with 165,900 deathsdue to chronic liver disease and 27,200 deaths due to he-patocellular carcinoma.

Implications for Nursing

Nurses are at high risk for getting hepatitis C and becoming part of these statistics. As these costs rise, health care will be impacted further from this disease. Nurses must strive to dis­seminate information about this disease to prevent others from obtaining it and to help reduce costs.

 

HEPATITIS D. Hepatitis D (delta hepatitis, or HDV) is caused by a defective RNA virus that needs the helper function of HBV. HDV co-infects with HBV and needs its presence for viral replication. Hepatitis D can co-infect a client with HBV or can occur as a superinfection in a client with chronic HBV. Su-perinfection usually develops into chronic HDV. The incuba­tion period is approximately 14 to 56 days. As with HBV, the disease is transmitted primarily by parenteral routes.

CULTURAL CONSIDERATIONS

‘ In the United States, Canada, and northern Europe, hep­atitis D (delta infection) is most prevalent in people exposed to blood and blood products (e.g., drug addicts and hemophiliacs). The prevalence of hepatitis D usually corresponds to the prevalence of hepatitis B. Southern Italy, Africa, South Amer­ica, and parts of Russia and Romania have a high prevalence, whereas northern Italy, Spain, Turkey, and Egypt have a mod­erate prevalence (CDC [Hepatitis Branch], 1997).

 

 

HEPATITIS E. The hepatitis E virus (HEV) was originally identified by its association with waterborne epidemics of hepatitis in the Indian subcontinent. Since then, it has oc­curred in epidemics in Asia, Africa, the Middle East, Mexico, and Central and South America. Many large outbreaks have occurred after heavy rains and flooding.

In the United States, hepatitis E has been found only in travelers returning from these endemic areas. The nonen-veloped, single-stranded RNA virus is transmitted via the fecal-oral route, and the clinical course resembles that of hep­atitis A. HEV has an incubation period of 15 to 64 days. There is no evidence at this time of a chronic form of HEV.

 OXIC AND DRUG-INDUCED (CHEMICAL) HEP­ATITIS. Two major types of toxic hepatitis have been recog­nized—direct toxic hepatitis and idiosyncratic toxic hepatitis.

 

DIRECT TOXIC HEPATITIS. Direct toxic hepatitis (DTH) results iecrosis and fatty infiltration of the liver. Agents caus­ing toxic hepatitis are generally systemic poisons or are con­verted in the liver to toxic metabolites. People with repeated, regular exposure to an offending agent (e.g., alcohol [alcoholic hepatitis]) or with a dose-related toxicity range can have direct toxic hepatitis. For example, acetaminophen (Tylenol), a com­monly used over-the-counter (OTC) analgesic, can cause se­vere hepatic necrosis when taken in large amounts, such as in suicide attempts or accidental ingestion by children. ndustrial toxins such as carbon tetrachloride, trichloroeth-ylene, and yellow phosphorus also have a direct toxic effect on the liver.

IDIOSYNCRATIC TOXIC HEPATITIS. Idiosyncratic toxic hepatitis (ITH) results in morphologic changes to the liver that are similar to those found in viral hepatitis. In idiosyncratic drug reactions, the occurrence of hepatitis is unpredictable and un­common. It may occur at any time during or shortly after expo­sure to the drug. Examples of agents that result in idiosyncratic toxic hepatitis are isoniazid (INH, Isotamine+O, an antitubercu-losis drug, and phenytoin (Dilantin), an anticonvulsant.

Treatment of toxic and drug-induced hepatitis is support­ive. Transplantation may be considered if fulminating liver failure is present. Withdrawal of the suspected agent is indi­cated at the first sign of a reaction. Chemical exposure of the liver to drugs and toxins has resulted in the development of chronic active hepatitis and cirrhosis.

COMPLICATIONS OF HEPATITIS

Failure of the liver cells to regenerate, with progression of the necrotic process, results in a severe and often fatal form of hepatitis known as fulminant hepatitis. This form of massive hepatic necrosis is rare.

Hepatitis is considered to be chronic when liver inflamma­tion lasts longer than several months (usually defined as 6 months). Chronic hepatitis usually occurs as a result of hep­atitis B or hepatitis C. Superimposed infection with hepatitis D (HDV) in clients with chronic HBV may also result in chronic hepatitis.

With chronic active hepatitis (CAH), liver damage is pro­gressive and is characterized by hepatic necrosis, acute inflam­mation, and progressive fibrosis. The client may be asympto­matic for long periods of the hepatic disease process, or the continued fibrosis may lead to liver failure, cirrhosis, and death. Chronic active hepatitis may be manifested by the following:

Persistent clinical symptoms and hepatomegaly • The continual presence of HBsAg (hepatitis B surface antigen) or anti-HCV (HCV antibodies) Elevated, fluctuating serum levels of aspartate amino-transferase (AST), bilirubin, and alkaline phosphatase for 6 months or longer after the acute hepatitis episode Liver biopsy is necessary to establish the diagnosis of chronic hepatitis. In people with chronic persistent hepatitis and chronic lo-bar hepatitis, liver damage does not progress after the initial insult. These types of hepatitis result from infections with hepatitis B and C viruses. Most clients with chronic persistent hepatitis are asymptomatic, and physical findings are normal. Laboratory data may reveal a mild elevation of serum AST and alkaline phosphatase levels that may persist for up to 1 year. Routine screening of blood donors and the elimination of commercial blood sources have virtually eliminated the in­cidence of hepatitis B or C caused by blood transfusion. Case reporting to local health departments for all types of viral hep­atitis is mandatory. Measures to prevent viral hepatitis for health care workers and others in contact with infected clients are listed in Charts 59-5 and 59-6.

 

BEST PRACTICE j«r

Prevention of Viral Hepatitis in Health Care Workers

·        Use standard precautions to prevent the transmission of isease between clients or between clients and health are staff (see Chapter 26).

·        Eliminate needles and other sharps by substituting eedleless systems. (Needle sticks are the major source of hepatitis B transmission in health care workers.)

·        Take the hepatitis B vaccine (Hepatovax-B, Recombivax HB), which is given in a series of three injections. This vaccine also prevents hepatitis D. (See Chapter 26 for more information on this requirement of the United States Occupational Safety and Health Administration OSHA].)

·        For postexposure prevention of hepatitis A or B, seek medical attention immediately for immunoglobulin (IG) administration.

·        Report all cases of hepatitis to the local health department.

CLIENT EDUCATION GUIDE

Prewention of Vira! Hepatitis

·        Maintain adequate sanitation and personal hygiene. Wash your hands before eating and after using the toilet.

·        Drink water treated by a water purification system.

·        If traveling in underdeveloped or nonindustrialized coun­tries, drink only bottled water. Avoid food washed or prepared with tapwater, such as raw vegetables, fruits, and soups.

·        Use adequate sanitation practices to prevent the spread of the disease between family members.

·        Do not share bed linens, towels, eating utensils, or drink­ing glasses.

·        Do not share needles for injection, body piercing, or tat­tooing.

·        Do not share razors, nail clippers, toothbrushes, or Water Piks.

·        Use a condom during sexual intercourse.

 

 Etiology

In addition to the hepatitis A, B, C, D, and E viruses, other causes of hepatitis include the following:

·        Drugs, chemicals, and toxins

·        Blood transfusion reactions from exposure to the hepati­tis virus

·        Hyperthyroidism

·        Ingestion of ethyl alcohol (ETOH), resulting in alcoholic hepatitis

·        Wilson’s disease (increased serum copper)

·        Other viruses, such as Epstein-Barr, cytomegalovirus, and yellow fever

Incidence/Prevalence

There are an estimated 125,000 to 200,000 infections of hep­atitis A every year. Approximately one third of Americans have evidence of past infection, but many are not aware that they were infected (CDC, 1999). Hepatitis B occurs primarily in young adults between 20 and 39 years of age. The incidence of hepatitis B is between 140,000 to 320,000 infections each year. There has been a de­crease during the first half of the 1990s, most likely as a re­sult of the hepatitis B vaccine. Approximately 10% of clients with hepatitis B develop chronic hepatitis.

The prevalence of hepatitis C is highest in individuals with high-risk drug behaviors, such as sharing needles. The incidence is approximately 36,000 new infections per year. It is estimated that 4 million of the U.S. population has been infected. The chronic form develops in approximately 85% of those infected.

 COLLABORATIVE MANAGEMENT

Assessment

 HISTORY

If viral hepatitis is suspected, the nurse asks the client whether he or she has had known exposure to a person with hepatitis. The nurse determines whether the client has had recent blood transfusions or undergoes hemodialysis for renal failure. The client should be asked about the following:

•  Sexual activities

•  Social activities

•  Injectable drug use

•  Recent ear or body piercing and/or tattooing

•  Close living accommodations, such as military barracks, correctional institutions, overcrowded apartments, longterm care facilities

•  Receiving blood, blood products, or a transplant before 1992

The client’s employment history is obtained. The nurse specifically asks about employment as a health care worker. The client is asked about recent travel to a foreign country or to an area with inadequate environmental sanitation. The client is also questioned about the ingestion of water from a possibly contaminated source or the recent ingestion of shellfish.

PHYSICAL ASSESSMENT/CLINICAL MANIFESTATIONS

VIRAL HEPATITIS. The courses and clinical manifesta­tions of all five types of viral hepatitis are somewhat similar (see Table 59-5). The nurse assesses the client’s general sub­jective complaints, determining whether symptoms occurred acutely (hepatitis A and E) or insidiously (hepatitis B and C).

The client may verbalize feelings of fatigue and loss of ap­petite. The nurse explores further to assess whether the client is experiencing the following: Abdominal pain

·        Arthralgia (joint pain)

·        Myalgia (muscle pain)

·        Diarrhea/constipation

·        Fever

·        Irritability

·        Lethargy

·        Malaise

·        Nausea/vomiting

The nurse lightly palpates the right upper abdominal quad­rant to assess for liver tenderness. The client may report right upper quadrant pain with jarring movements. The skin, sclerae, and mucous membranes are inspected for the presence of jaundice. The client may present for medical treatment only after jaundice appears, believing that other vague symptoms are related to an influenza-like syndrome.

Jaundice in hepatitis results from intrahepatic obstruction and is caused by edema of the liver’s bile channels. Dark urine and clay-colored stools are often reported by the client. The nurse obtains a urine and stool specimen for visual inspection and laboratory analysis. The skin is inspected for the presence of rashes in clients with suspected hepatitis B and hepatitis C. Irregular patches of redness or urticaria (hives) may occur. The client often reports pruritus (itching) and may have skin abrasions from scratching.

The client with hepatitis A usually has a fever, and the tem­perature may range from 100° to 104° F (38° to 40° C). Fever may be low-grade or absent with hepatitis B and hepatitis C.

TOXIC    AND    DRUG-INDUCED    HEPATITIS. The clinical picture in toxic and drug-induced hepatitis depends on the causative agent. Idiosyncratic reactions may result in clini­cal manifestations that are indistinguishable from those of viral hepatitis or may simulate extrahepatic bile duct obstruction symptoms such as severe jaundice, rash, arthralgia, and fever.

PSYCHOSOCIAL ASSESSMENT

Viral hepatitis usually occurs as an acute illness. Its symp­toms may be mild and abate rapidly or go undetected. Emo­tional problems for affected clients often center on their anger about being sick and being fatigued. General malaise, inactivity, and vague complaints contribute to depression and despondency. These clients worry about the long-term effects and complications.

Clients with viral hepatitis often feel guilty about having ex­posed others to the virus. Infectious diseases such as hepatitis continue to have a social stigma. The client may feel embar­rassed by the isolation and hygiene precautions that are imposed in the hospital and continue to be necessary at home. This em­barrassment may cause the client to limit social interactions. Self-imposed visitor restrictions may be instituted by the client out of fear of spreading the virus to family and friends.

Family members are sometimes afraid of contracting the disease and may distance themselves from the client. The nurse allows the client and family to verbalize these feelings and explores the reasons for these fears. Precautionary isola­tion measures evoke anxiety for the client and the family.

Clients are unable to return to work until the results of blood tests for serologic markers are negative. The loss of wages and the cost of hospitalization for a client without in­surance coverage may produce great anxiety and financial burden for the client and the family.

 CRITICAL THINKING CHALLENGE

 You are the nurse caring for a 52-year old man recently diagnosed with chronic hepatitis C. He denies any high-risk behavior but admits to getting a tattoo in Vietnam. How will you reply to his following questions?

• Could I have gotten this by a tattoo?

• Could my wife and children have hepatitis?

• How could I not have known I had hepatitis?What is the cure?

 

 

 

LABORATORY ASSESSMENT

The presence of hepatitis A, B, and C is usually indicated by acute elevations in levels of liver enzymes, indicating liver cellular damage, and by specific serologic markers.

SERUM LIVER ENZYMES. Levels of alanine amino-transferase (ALT) may be elevated to more than 1000 mU/mL and may rise to as high as 4000 mU/mL in severe cases of vi­ral hepatitis. Aspartate aminotransferase (AST) levels may rise to 1000 to 2000 mU/mL. Alkaline phosphatase levels may be normal (30 to 90 IU/L) or mildly elevated. Serum to­tal bilirubin levels are elevated to greater than 2.5 mg/dL and are consistent with the clinical appearance of jaundice. Ele­vated levels of bilirubin are also present in the urine.

SEROLOGIC MARKERS/ENZYME ASSAYS. The presence of hepatitis A is established when hepatitis A virus (HAV) antibodies (anti-HAV) are identified in the blood. On­going inflammation of the liver by HAV is evidenced by the presence of immunoglobulin M (IgM) antibodies, which per­sist in the blood for 4 to 6 weeks. Previous infection is indi­cated by the presence of immunoglobulin G (IgG) antibodies. These antibodies persist in the serum and provide permanent immunity to HAV.

The presence of the hepatitis B virus (HBV) is established if serologic testing confirms the presence of hepatitis B anti­gen-antibody systems in the blood. HBV is a double-shelled DNA virus consisting of an inner core and an outer shell. Antigens located on the surface (shell) of the virus (HBsAg) and IgM antibodies to hepatitis B core antigen (anti-HBc IgM) are the most significant serologic markers. The presence of these markers establishes the diagnosis of hepatitis B. The client is considered infectious as long as HBsAg is present in the blood. Persistence of this serologic marker after 6 months or longer indicates a carrier state or chronic hepatitis. HBsAg levels normally decline and disappear after the acute hepatitis B episode. The presence of antibodies to HBsAg (anti-HBs) in the blood indicates recovery and immunity to hepatitis B.

Enzyme-linked immunosorbent assay (ELISA) is the ini­tial screening test for clients suspected of being infected with hepatitis C virus (HCV), and it is the most commonly used enzyme test for HCV antibodies (anti-HCV). False-positive results can occur in clients with normal ALT levels and no risk factors. In these cases, a more specific assay called the re-combinant immunoblot assay (RIBA) is used. Because HCV can often be detected within 2 to 3 weeks of exposure, the virus may be measured directly using the reverse transcription polymerase chain reaction (RT-PCR) test.

The presence of hepatitis D virus (HDV) can be confirmed by the identification of intrahepatic delta antigen or, more often, by a rise in the hepatitis D virus antibodies (anti-HDV) titer.

Hepatitis E virus (HEV) testing is usually reserved for travelers in whom hepatitis is present, but the viruses cannot be detected. The presence of the hepatitis E antibodies (anti-HEV) is found in individuals infected with the virus.

OTHER DIAGNOSTIC ASSESSMENT

Chronic hepatitis is diagnosed by percutaneous liver biopsy. The biopsy distinguishes between chronic active and chronic persistent hepatitis. It is also the gold standard test for assess­ing the extent of injury and prognosis of HCV disease. The finding of fatty infiltrates in liver biopsy specimens and inflammation with neutrophils is consistent with Laennec’s (alcohol-induced) hepatitis.

 Interventions

The client with viral hepatitis can be mildly or acutely ill de­pending on the severity of the inflammation. Most clients are not hospitalized. The plan of care for all clients with viral hepatitis is based on measures to rest the liver, promote cellu­lar regeneration, and prevent complications (see the Client Care Plan on pp. 1320 and 1321).

NONSURGICAL MANAGEMENT. During the acute stage of viral hepatitis, interventions are aimed at resting the in­flamed liver to promote hepatic cell regeneration. Rest is an es­sential intervention to reduce the liver’s metabolic demands and increase its blood supply. Treatment is generally supportive.

PHYSICAL REST. The nurse and assistive nursing per­sonnel assess the client’s response to activity and rest periods. Strict bedrest may be indicated during the early icteric phase of hepatitis. The client is usually tired and expresses feelings of general malaise. Complete bedrest is usually not required, but rest periods alternating with periods of activity are indi­cated and are often sufficient to promote hepatic healing.

The nurse individualizes the client’s plan of care and changes it as needed to reflect the severity of symptoms, fa­tigue, and the results of liver function tests and enzyme deter­minations. The client and nursing staff should adhere to sched­uled rest periods. Activities such as self-care and ambulating are gradually added to the activity schedule as tolerated.

PSYCHOLOGIC REST. Emotional and psychologic rest is essential for the client. Because bedrest and inactivity can pro­duce anxiety, the nurse includes diversional activities in the plan of care. The nurse asks the hospitalized client’s family to bring in small craft projects, reading materials (e.g., maga­zines, books, newspapers), or a portable radio. Staff and fam­ily members are encouraged to spend time in the client’s room.

DIET THERAPY. A special diet is usually not required. The diet should be high in carbohydrates and calories with moderate amounts of fat and protein. Small, frequent meals are often preferable to three standard meals. The nurse asks the client about food preferences, because favorite foods are tolerated better than randomly selected foods. The nurse or assistive nursing personnel encourages the client to select foods that are appealing. High-calorie snacks may be needed.

The health care provider typically orders supplemental vi­tamins. If caloric intake is low, the nurse may need to provide supplemental commercial feedings, such as Ensure.

DRUG THERAPY. An antiemetic to relieve nausea, such as trimethobenzamide hydrochloride (Tigan) and dimenhydri-nate (Dramamine), may be prescribed. Prochlorperazine maleate (Compazine), a phenothiazine, is avoided because of its potential hepatotoxic effects.

There are no drugs specific for hepatitis A management. Interferon, a biologic response modifier given by injection over several months, has been approved for the treatment of hepatitis B. However, interferon has a number of side effects that often are so severe the client cannot continue the therapy. Side effects include flu-like symptoms of headaches, fever, fatigue, loss of appetite, nausea, and vomiting. Other side ef­fects include hair loss, depression, and bone marrow suppres­sion that decreases white blood cell and platelet production.

Two antiviral drugs have recently been used to treat acute HBV: ribavirin (Virazole, Rebetol) and lamivudine (Epivir). Lamivudine is also used after liver and heart transplantation. Both of these drugs can cause sudden, severe anemia and car­diac arrest.

Hepatitis C can be treated with interferon (usually alfa), ribavirin (Virazole, Rebetol), or the more effective combina­tion of Rebetol and interferon alfa-2b, a recombinant called Rebetron. Long-term results are better with the combination drug, which is now considered the first-line drug for HCV (Dougherty & Dreher, 2001).

COMFORT MEASURES. Some foods and smells may stimulate nausea. If possible, the nurse or assistive nursing personnel removes the stimulus causing the nausea. In an ef­fort to stimulate appetite, the nurse or assistive nursing per­sonnel provides mouth care or instructs the client to perform mouth care before meals. The meal may be more palatable when the client is sitting up in a chair. The nurse empties bed­pans, urinals, and bedside commodes promptly and provides an air freshener for the room if the client can tolerate it.

SURGICAL MANAGEMENT. Liver transplantation may be performed for clients with chronic hepatitis, especially for hepatitis C, but many become reinfected (see the later discus­sion of liver transplantation, p. 1324).

 

 

 Community-Based Care

HEALTH TEACHING

The nurse teaches the client and the family to observe meas­ures to prevent infection transmission (see Chart 59-6). In ad­dition, the nurse instructs the client with viral hepatitis to avoid alcohol and any nonprescription, over-the-counter med­ications, particularly acetaminophen (Tylenol, Exdol^O and sedatives, for 3 to 12 months because of the hepatotoxic ef­fects (Chart 59-7). Clients who develop chronic hepatitis should always avoid these products.

The client must determine patterns for rest on the basis of physical tolerance of increased activity. The nurse encourages the client to increase activity gradually to prevent fatigue. The client should eat small, frequent meals of high-carbohydrate and low-fat foods. In collaboration with the dietitian, the nurse provides diet teaching and menu planning. The nurse teaches the client to follow precautionary measures and avoid sexual activity until the results of hepatitis B surface antigen (HBsAg) tests are negative.

■ HOME CARE MANAGEMENT

Home care management varies according to the type of hep­atitis. A primary focus is preventing the spread of the infection. For hepatitis transmitted by the fecal-oral route, careful handwashing and sanitary disposal of feces are important. Standard precautions are used for hepatitis transmitted per-cutaneously and permucosally. Education is therefore very important.

 

 

 

CLIENT EDUCATION GUIDE Vira! Hepatitis

• Avoid all medications, including over-the-counter drugs, such as acetaminophen (Tylenol, Exdol*), unless pre­scribed by your physician.

• Avoid all alcohol.

• Rest frequently throughout the day, and get adequate sleep at night.

• Eat small, frequent meals with a high-carbohydrate, lowfat content.

• Avoid sexual intercourse until antibody testing results are negative.

• Follow the guidelines for preventing transmission of the disease (see Chart 59-6).

HEALTH CARE RESOURCES

Clients with viral hepatitis and their families may contact the local health department for further information on infection control and prevention. Clients discharged home with limited activity tolerance or minimal family support may need the as­sistance of a home care aide in performing activities of daily living, particularly meal preparation.\

 

FATTY LIVER

A fatty liver is caused by the accumulation of triglycerides and other fats in the hepatic cells. In severe cases, fat may constitute as much as 40% of the liver’s weight and cause changes in liver function. Minimal, temporary fatty changes are usually reversible by eliminating the cause. The most common cause of fatty liver is chronic alcoholism. Other causes include the following:

·        Malnutrition

·        Diabetes mellitus

·        Obesity

·        Pregnancy

·        Prolonged total parenteral nutrition (TPN)

·        •Exposure to large doses of drugs toxic to the liver

Fatty infiltration of the liver may result from faulty fat metabolism in the liver and the mobilization of fatty acids from adipose tissue.

Many clients with a fatty liver are asymptomatic. The most common and typical finding is hepatomegaly. Other symp­toms include the following:

·        Right upper abdominal pain

·        Ascites

·        Edema

·        Jaundice

·        Fever

·        Signs of late cirrhosis, depending on the severity of the fat infiltration and the longevity of the occurrence

A liver biopsy confirms excessive fat in the liver. Interven­tions are aimed at removing the underlying cause of the infil­tration and providing dietary restrictions.

 

HEPATIC ABSCESS

OVERVIEW

Although hepatic abscesses are uncommon, they carry a high mortality rate. Liver abscesses occur when the liver is invaded by bacteria or protozoa. These organisms destroy the liver tis­sue, producing a necrotic cavity filled with infective agents, liquefied liver cells and tissue, and leukocytes. The infectious necrotic tissue walls off the abscess from the healthy liver.

A pyogenic liver abscess occurs when bacteria invade the liver. Infecting organisms include Escherichia coli and Kleb-siella, Enterobacter, Salmonella, Staphylococcus, and Entero-coccus species. A pyogenic abscess is generally solitary and confined to the right lobe, but occasionally they are multiple in nature. The usual cause is acute cholangitis, which occurs as a complication of cholelithiasis. Pyogenic liver abscesses may also result from liver trauma, abdominal peritonitis, and sepsis, or an abscess can extend to the liver after pneumonia or bacterial endocarditis.

The protozoan Entamoeba histolytica causes an amebic hepatic abscess, which may occur after amebic dysentery. These abscesses usually occur in the form of a single abscess in the right hepatic lobe.

COLLABORATIVE MANAGEMENT

Clients with hepatic abscesses are generally ill. On occasion, an abscess is not diagnosed until autopsy. In clients with a pyogenic liver abscess, the onset of symptoms is usually sud­den. Amebic abscesses cause a more insidious onset of symp­toms. Common complaints include the following:

•  Right upper abdominal pain with a palpable, tender liver

•  Anorexia

•  Weight loss

•  Nausea and vomiting

•  Fever and chills

•  Shoulder pain

•  Dyspnea

•  Pleural pain if the diaphragm is involved

A hepatic abscess is usually diagnosed by liver scan. He­patic arteriography differentiates an abscess from a malig­nancy. Blood cultures assist in identifying the causative or­ganism in pyogenic abscesses, and stool cultures may identify E. histolytica. With ultrasonographic guidance, a liver abscess may be aspirated percutaneously. Surgical drainage is indi­cated only for a single pyogenic abscess or for an amebic ab­scess that fails to respond to long-term antibiotic treatment.

LIVER TRAUMA

OVERVIEW

The liver is the most common organ to be injured in clients with penetrating trauma of the abdomen (e.g., gunshot wounds, stab wounds, and rib fractures) and is the second most commonly injured organ in clients who have blunt ab­dominal trauma. Liver damage or injury should be suspected whenever any upper abdominal or lower chest trauma is sus­tained. The liver is often injured by steering wheels in vehic­ular accidents. Common injuries to the liver include simple lacerations, multiple lacerations, avulsions (tears), and crush injuries. The liver is a highly vascular organ and receives approxi­mately 29% of the body’s cardiac output. When hepatic trauma occurs, blood loss can be massive. The client may ex­hibit signs of hemorrhagic shock, such as the following:

·        Hypotension

·        Tachycardia

·        Tachypnea

·        Pallor

·        Diaphoresis

·        Cool, clammy skin

·        Confusion

A decreased hematocrit may confirm suspected blood loss. Clinical manifestations include right upper quadrant pain with abdominal tenderness, distention, guarding, and rigidity. Ab­dominal pain exaggerated by deep breathing and referred to the right shoulder (Kehr’s sign) may indicate diaphragmatic irritation (Chart 59-8).

COLLABORATIVE MANAGEMENT

When hepatic and other abdominal organ trauma is suspected, the physician performs an emergency peritoneal lavage to confirm injury. If trauma is present, the lavage reveals gross blood or a high red blood cell count.

The physician then performs an exploratory laparotomy to identify and control the source and type of bleeding. Minor surgical interventions, such as suture placement, wound pack­ing, decompression, or a combination of these procedures, are often performed to halt bleeding. Liver lobe resection is re­quired in some extensive liver injuries.

Clients with hepatic trauma require the administration of multiple blood products, packed red blood cells, and fresh frozen plasma, as well as massive volume infusion to main­tain adequate hydration. Postoperatively, the client with he­patic trauma is admitted to a critical care unit. The nurse mon­itors the client for persistent bleeding. Complete blood count and coagulation studies must be closely monitored for trends in changes.

CANCER OF THE LIVER

OVERVIEW

Primary hepatic cancer, or hepatocellular carcinoma (cancer originating in the liver), is one of the leading causes of death in the world. The incidence is higher in African-American males and is increasing in people age 40 to 60 years of age (El-Serag & Mason, 1999). Possible reasons for this trend in­clude the increase in people with hepatitis B and hepatitis C infections, which often lead to cancer of the liver.

CULTURAL CONSIDERATIONS

  Hepatocellular carcinoma (HCC) is rare in the United States but is one of the most common malignancies in other parts of the world (e.g., Africa). The geographic variation prob­ably reflects the prevalence of chronic hepatitis B and chronic hepatitis C infection in other countries. Hepatitis B or C virus is thought to be the primary carcinogen in as many as 80% of clients with HCC worldwide. Men are affected three times more than women, and blacks worldwide are affected twice as often as Caucasians (El-Serag & Mason, 1999).

Carcinoma of the liver most often develops as a metastatic process. Because of the increased vascularity of the liver, the organ is a common site for metastasis from (1) primary can­cers of the esophagus, stomach, colon, rectum, breasts, and lungs; or (2) a malignant melanoma.

Between 30% and 70% of clients with primary hepatic cancer also have cirrhosis, and the risk is 40 times greater in clients with cirrhosis. Men with cirrhosis are more likely than women to develop HCC. Increased testosterone and de­creased estrogens may promote the development of HCC in men with cirrhosis (Tanaka et al., 2000).

Primary hepatic cancer has also been associated with trauma, nutritional deficiencies, and exposure to carcinogens and hepatotoxins, such as aflatoxin, thorium dioxide, Senecio alkaloids, and the fungus Aspergillus.

COLLABORATIVE MANAGEMENT

Clients with liver metastasis initially complain of epigastric or right upper quadrant abdominal pain, fatigue, anorexia, and weight loss. Later they typically experience the same mani­festations of HCC, such as jaundice, ascites, bleeding, and en-cephalopathy. A nuclear radioisotope liver scan detects metas­tasis in many cases, but ultrasonography with needle biopsy may be required to confirm the metastasis.

Liver cancer is usually fatal within 6 months of diagnosis. Surgical management may be indicated for clients with a sin­gle metastatic lesion confined to one liver lobe. Liver lobe re­section for surgical excision of metastasis has been successful in achieving survival rates of up to 5 years.

Unfortunately, 75% of clients are not candidates for surgi­cal excision because their tumors are unresectable. A newer procedure, cryosurgical ablation of the liver, has produced re­missions that offer hope for long-term survival (Leininger, 1997). In this procedure, the surgeon makes a subcostal or midline abdominal incision and selects which tumors are ap­propriate for either resection or cryoablation. The cryotherapy probes circulate liquid nitrogen and freeze the tumors. Post­operatively, the client is admitted to the critical care unit for monitoring of complications, including hypothermia, renal failure, and bleeding.

Other standard treatments for liver cancer include high-dose chemotherapy, usually with fluorouracil (5-FU) and he­patic artery ligation to deprive the metastatic lesion of oxy­gen. Both treatments can be accomplished without systemic effect because of the unique portal vein circulation in the liver. Hepatic chemotherapy is administered by a surgically implanted infusion pump, which enables controlled infusion for up to 14 days at a time. (See Chapter 25 for a discussion of intra-arterial chemotherapy.) Transplantation may also be used to treat liver cancer.

LIVER TRANSPLANTATION

OVERVIEW

The first liver transplantation was performed in 1963, and in 1983 it was decided that liver transplantatioo longer be considered experimental. In 1998, 4487 liver transplants were performed, and 1-year survival rates are now approx­imately 84% (United Network for Organ Sharing (UNOS), 1998).The client with end-stage liver disease who has not responded to conventional medical or surgical intervention is a potential candidate for liver transplantation. In the adult, diseases treated by liver transplantation include the following:

·        Primary or secondary biliary cirrhosis

·        Chronic active hepatitis with cirrhosis

·        Hepatic metabolic diseases, such as protoporphyria and Wilson’s disease

·        Budd-Chiari syndrome (hepatic vein thrombosis)

·        Primary sclerosing cholangitis

·        Lanneac’s cirrhosis, if the person has abstained from al­cohol

Liver transplantation is not commonly performed for clients with malignant neoplasms. Because the tumor is likely to recur in immunosuppressed clients, the procedure remains controversial.

The client for potential transplantation undergoes exten­sive physiologic and psychologic assessment and evaluation by physicians and transplant coordinators to identify con­traindications to the procedure.

Clients who are not considered candidates for transplanta­tion are those with severe end-stage liver disease with life-threatening complications, such as the following:

·        Repeated episodes of esophageal variceal bleeding

·        Sepsis

·        Severe cardiovascular instability with advanced cardiac disease

·        Acquired immunodeficiency syndrome (AIDS)

·        Diabetes mellitus

·        Severe respiratory disease

Additional identified risk factors include the existence of the following:

·        Portal vein thrombosis

·        Advanced catabolic state

·        Active alcoholism

·        Age older than 60 years

·        Primary and metastatic malignant disease

A lack of knowledge and understanding of the procedure and necessary postoperative care measures

·        A poor psychosocial support system

·        Psychologic instability

Liver transplantation has become the most effective treat­ment for clients with an increasing number of acute and chronic liver diseases, although they are more common in children than in adults. Indications and contraindications con­tinue to vary among transplantation centers and are continu­ally revised as treatment options change and surgical tech­niques improve.

Donor livers are obtained primarily from head trauma vic­tims and in the United States. They are distributed through a nationwide program, the United Network of Organ Sharing (UNOS). This system distributes donor livers on the basis of regional considerations and recipient acuity. A new program for living donors has also been established. Recipients with the highest level of acuity receive highest priority.

Acute Graft Rejection

The success of all transplantations has greatly improved since the introduction in 1980 of cyclosporine (cyclosporin A), an immunosuppressant drug. Cyclosporine has been the primary agent to prevent rejection of the donor organ graft, but aza-thioprine (Imuran) and prednisone (Deltasone) are also used. Most recipients receive a combination of cyclosporine, steroids, and azathioprine.

A newer immunosuppressant agent discovered in 1984, tacrolimus (FK 506), is more potent than cyclosporine. FK 506 has been shown to be effective as a form of rescue ther­apy for clients who continue to reject a liver graft. Mycophe-nolate mofetil (CellCept) is the one of the newest approved immunosuppressants for the treatment of rejection in liver transplants and for those who are unable to tolerate cy­closporin or FK 506.

A majority of clients still experience a rejection response after liver transplantation beginning 1 to 2 weeks after sur­gery. Clinical manifestations of acute rejection include tachy­cardia, fever, right upper quadrant or flank pain, decreased bile pigment and volume, and increasing jaundice. Laboratory findings include elevated serum bilirubin, alkaline phos-phatase levels, and increased prothrombin time and amino-transferase levels.

Transplant rejection is treated with IV doses of methyl-prednisolone (Solu-Medrol). If this drug is not effective, anti­bodies to lymphocytes such as muromonab-CD3 (OKT3) may also be used. OKT3 is T-cell specific and is more potent, but it increases the client’s risk of infection. Mycophenolate mofetil may also be used against rejection. As with all rejec­tion treatments, the client is at a greater risk for infection. If none of these drugs is effective, a rapid deterioration of liver function occurs. Multisystem organ failure, including respira­tory and renal involvement, develops along with diffuse coag-ulopathies and portal-systemic encephalopathy. The only al­ternative for treatment is emergency transplantation.

Infection

Infection is another potential threat to the transplanted graft and the client’s survival. Immunosuppressant therapy, which must be used to prevent and treat organ rejection, significantly increases the client’s susceptibility to and risk for infection. Other risk factors include the presence of multiple tubes and intravascular lines, immobility, and prolonged anesthesia.

The average liver transplant client acquires at least one bacterial infection and has a 40% to 50% chance of develop­ing a viral or fungal infection. In the early post-transplantation period, common infections include pneumonia, wound infections, and urinary tract infections. Opportunistic infec­tions usually develop after the first postoperative month and include cytomegalovirus, mycobacterial infections, and para­sitic infections. Latent infections such as tuberculosis and herpes simplex are often reactivated.

Transplant complications cause clients to be very anxious. The nurse and other members of the health care team assure the client that these problems are common and usually suc­cessfully treated (see the Evidence-Based Practice for Nurs­ing on box at right).

The physician prescribes broad-spectrum antibiotics for prophylaxis during and after surgery. The nurse obtains cul­ture specimens from all lines and tubes and collects speci­mens for culture at predetermined time intervals as dictated by the agency’s policy. If an infection is detected, the physi­cian prescribes organism-specific anti-infective agents.

Other Complications

The biliary anastomosis is susceptible to breakdown, obstruc­tion, and infection. If leakage occurs or if the site becomes necrotic or obstructed, an abscess can form or peritonitis, bac-teremia, and cirrhosis may develop. Other potential complica­tions include the following:

·        Hemorrhage

·        Hepatic artery thrombosis

·        Fluid and electrolyte imbalances

·        Pulmonary atelectasis

·        Acute renal failure

·        Chronic graft rejection

·        Psychologic maladjustment

 

How much anxiety is experienced by clients undergoing a liver transplant?

The purpose of this study was to describe the anxiety of adult liver transplant recipients during their hospitalization. Speilberg’s model of state and trait anxiety was the frame­work for the study. Speilberg’s State Trait Anxiety Inventory (STAI) and a visual analog scale (VAS) were completed at the following stages: admission for transplantation, transfer to the nursing floor, first liver biopsy, first signs of infection, first signs of a rejection episode, immediately after the first teach­ing session with the transplant coordinator, and discharge from the hospital. The highest mean anxiety scores occurred at the first liver biopsy, the first episode of rejection, and the first infection.

Critique. Although the sample size for this study was small, the researchers aimed to explore the psychosocial as­pects of this major surgery and life-changing event. Data from this study can help nurses better care for their clients by ad­dressing both their psychosocial needs and their physical needs.

Implications for Nursing. Nurses should anticipate that clients will be extremely anxious during the first liver biopsy and during episodes of rejection or infection. Nurses caring for clients during these procedures and times should exercise ad­ditional support. Other people on the health care team, as well as the clients’ families, should also be made aware that clients will experience anxiety at these times; they should be taught to be as supportive and understanding as possible.

 

 

 COLLABORATIVE MANAGEMENT

Care of the client undergoing liver transplantation requires an interdisciplinary team approach. Case managers are an im­portant part of the team. After the client is identified as a can­didate and a donor organ is procured, the actual liver trans­plantation surgical procedure usually takes 8 hours. The length of the procedure can vary greatly. The procedure in­volves five anastomoses between recipient and donor organs, including the following vascular anastomosis sites:

·        Suprahepatic inferior vena cava

·        Infrahepatic vena cava

·        Portal vein

·        Hepatic artery

·        Biliary tract

The biliary anastomosis site varies depending on the client’s extrahepatic biliary tract. Two common sites are end-to-end anastomosis between the donor and the recipient com­mon bile duct and anastomosis between the donor common bile duct and the recipient jejunum.

In the immediate postoperative period, the client who has undergone liver transplantation is managed in the critical care unit and requires aggressive monitoring and care. The nurse assesses for signs and symptoms of complications of surgery and immediately reports their occurrence to the physician (Table 59-6).

The nurse monitors the client’s temperature and reports temperatures greater than 100° F (38° C) and increased ab­dominal pain, distention, and rigidity, which are indicators of peritonitis. Nursing assessment also includes monitoring for a change ieurologic status that could indicate encephalopa-thy from a nonfunctioning liver. Signs of coagulopathy (e.g., continuous bloody oozing from a catheter, a drain, and inci­sion sites; petechiae; or ecchymosis) are reported to the physi­cian immediately because they can indicate impaired function of the transplanted liver.

 

 

 

Interventions for Clients with Malnutrition and Obesity

 

Objectives

After studying this chapter, you should be able to:

 

1.   Identify three anthropometric measurements that the nurse can use to evaluate a client’s nutritional status.

2.   Explain the potential consequences and complications associated with malnutrition.

3.   Describe the risk factors for malnutrition, especially for older adults.

4.   Discuss the role of laboratory testing in the diagnosis of malnutrition.

5.   Analyze assessment data to determine common nursing diagnoses for the client with malnutrition.

6.   Identify expected outcomes for clients who are malnourished.

7.   Describe the nursing care of clients receiving total enteral nutrition (TEN).

8.   Prioritize nursing care for clients receiving total parenteral nutrition (TPN).

9.   Identify complications associated with TPN.

10.Explain the potential consequences and complications associated with obesity.

11.Discuss the role of culture and gender as factors in the prevalence of obesity.

12.Identify the role of drug therapy in the management of obesity.

13.Develop a postoperative teaching plan for clients having a gastroplasty or intestinal bypass.

 

 

Nutrition plays a major role in promoting and maintain­ing health. Nutritional health not only contributes to positive care outcomes but also saves health care dollars. As part of a comprehensive health assessment, the nurse should include nutritional screening to identify clients who have nutritional deficits or are at risk for developing nutritional deficits. Nurses may also conduct a complete nutritional assessment (Grindel & Costello, 1996).

NUTRITION STANDARDS

 Dietary Planning

Several national standards are available for planning and eval­uating nutrition. The standard most widely accepted in the United States is the Recommended Dietary Allowance (RDA), established in 1943 by the Food and Nutrition Board (FNB) of the National Research Council/National Academy of Sciences. The most current revision in 1989 establishes recommendations for energy intake, protein, vitamins, and minerals for a healthy population. Healthy adults require ap­proximately 1800 calories/day and 0.8 g of protein/kg of body weight to meet basal energy needs.

The RDA can be used to estimate the adequacy of nutrient in­take over time. If a client does not meet 100% of the RDA, it is incorrect to assume that he or she is nutritionally deficient. The risk of inadequate intake for any nutrient is not presumed to be increased until less than 70% of the RDA is consumed. It is also incorrect to assume that all clients in a specific population who meet 100% of the RDA are not at risk for malnutrition.

The FNB, with the involvement of Health Canada, has rec­ommended Dietary Reference Intakes (DRI) replace the RDA. The first DRI released recommended the intake of nutrients re­lated to bone health (Food and Nutrition Board, 1997). The es­tablished standard of Canada, the Recommended Nutrient In­take (RNI), is similar to that of the United States.

Disease Prevention and Health Promotion

The role of diet and nutrition in disease has been a subject of interest for many years. The current focus is on health promo­tion and the prevention of disease. In 1995, the Dietary Guide­lines for Americans were revised by the U.S. Department of Agriculture (USDA) and the U.S. Department of Health and Human Services (DHHS). These seven guidelines emphasize the importance of selecting foods to maintain a healthful diet with balance, moderation, and variety (Figure 61-1). One of the most noticeable changes from previous editions occurs in the weight guideline. For the first time, diet and physical ac­tivity are emphasized in the second guideline with the goal of maintaining or improving body weight (Kennedy, Meyers, & Layden, 1996). The Nutrition Recommendations for Canadians (Table 61-1) are similar to the Dietary Guidelines for Americans. In addition, they recommend limiting the caffeine content of the diet to no more than the equivalent of four cups of cof­fee per day, as well as adding fluoride to community water supplies to a level of 1 mg/L.

 

The USDA developed the Food Guide Pyramid in 1992 to translate food recommendations into a practical graphic for­mat (Figure 61-2). A pyramid format was chosen to commu­nicate three key dietary principles: variety, moderation, and proportionality. The pyramid design emphasizes building the diet on a base of grains, fruits, and vegetables. Moderate quantities of lean meats, protein sources, and dairy products are added, and the intake of fats and sweets is limited. This guide to daily food choices has replaced the basic four foodgroups as the standard for evaluating the nutritional adequacy of dietary intake. Table 61-2 suggests the daily servings of each food group and clarifies the size of a serving. Adhering to this pattern results in a nutritionally adequate intake if a va­riety of foods is chosen.

A variety of vegetarian diet patterns are being adopted by increasing numbers of people for health, environmental, and moral reasons. The lacto-vegetarian eats milk, cheese, and dairy foods but avoids meat, fish, poultry, and eggs. The lacto-ovo-vegetarian also includes eggs. The vegan eats only foods of plant origin. Vegans can develop megaloblastic ane­mia as a result of vitamin B₁₂ deficiency. Vegans should in­clude a daily source of vitamin B₁₂ in their diets, such as a for­tified breakfast cereal, fortified soy beverage, or meat analog (Messina & Burke, 1997). All vegetarians should ensure that they get adequate amounts of calcium, iron, zinc, and vita­mins D and B₁₂. Well-planned vegetarian diets can provide adequate nutrition. The Vegetarian Food Pyramid, endorsed by the Vegetarian Resource Group, can assist vegetarians with daily food choices (Figure 61-3).

NUTRITIONAL ASSESSMENT

Malnutrition and obesity are commoutrition problems that occur as progressive changes within the client. Wheutri­tional deficiencies or excesses develop, the body adapts through the use of homeostatic mechanisms. As the intake moves farther away from the accepted range, however, the body accommodates by reducing functional levels or chang­ing the status or size of the affected body compartments. The nutritional status of a client can be determined by the pres­ence or absence of these adaptations.

Nutritional status reflects the balance between nutrient re­quirements and nutrient intake. Factors affecting nutrient re­quirements include disease, infection, and psychologic stress. Nutrient intake is influenced by disease, eating behavior, eco­nomic factors, emotional stability, medication, and cultural factors.

 

 

 

 

 

 CULTURAL CONSIDERATIONS

 Lactose intolerance (inability to tolerate milk and milk products) is a relatively common condition that occurs in a number of ethnic groups. It is found in more than 66% of Mexican Americans and 79% of African Americans, as well as in some Native American tribes, Asian Americans, and Ashkenazic Jews (Giger & Davidhizar, 1999). A small percent­age of Caucasians are also lactose intolerant. The cause of lactose intolerance is an insufficient amount of the lactase en­zyme, which converts lactose into absorbable glucose.

Optimal nutritional care is a major interdisciplinary out­come for clients with malnutrition and obesity. Evaluation of nutritional status is an important part of total client assess­ment. A thorough assessment of nutritional status includes the following:

·        Review of the diet history

·        Food and fluid intake record

·        Laboratory data

·        Food-medication interactions

·        Physical examination and health history

·        Anthropometric measurements

·        Psychosocial assessment

Monitoring the nutritional care of a client is as important as the initial assessment. The health care provider, nurse, and dieti­tian collaborate to identify clients at risk for nutritional problems.

 

Initial Nutritional Screening

Not every client needs a complete nutritional assessment, but it is important to identify clients at risk for nutritional prob­lems through screening. An initial nutritional screening pro­vides the nurse with an inexpensive, quick way of determin­ing which clients need more extensive nutritional assessment by the health care provider and dietitian.

The initial nutritional screening includes visual inspection, measured height and weight, weight history, usual eating habits, ability to chew and swallow, and any recent changes in appetite or food intake. Questions that may alert the nurse to clients at risk for nutritional problems can be incorporated into the history and physical assessment (Chart 61-1).

 CONSIDERATIONS FOR OLDER ADULTS

BIO Nutritional screening can take place in the home, ambu­latory care setting, hospital, or nursing home. The Nutrition Screening Manual for Professionals Caring for Older Ameri­cans (1991) is a multidisciplinary project of the American Di­etetic Association, the American Academy of Family Physi­cians, and the National Council on the Aging. The goal of this 5-year initiative was to use a collaboration of health care professionals to promote routine nutrition screening to older Americans in all community health and medical care settings. Risk factors for malnutrition in older adults include inappropri­ate intake, poverty, social isolation, dependency or disability, acute or chronic diseases or conditions, and chronic medica­tion use. The Nutrition Screening initiative developed a three-tiered approach to nutrition screening:

1.The DETERMINE Your Nutritional Health Checklist to alert older adults about the warning signs for poor nutritional health (Figure 61-4)

2.The Level I screen developed for use by professionals in health or social service settings, such as adult day-care centers, congregate meal programs, and assisted-living facilities

3.The Level II screen developed for use in medical settings such as acute care hospitals, physicians’ offices, and long-term care facilities.

Another nutritional assessment tool, the Mini Nutritional Assessment (MNA), has recently been designed and tested worldwide to provide a single, rapid assessment of older adults in ambulatory care, hospitals, and nursing homes (Vellas et al, 1999). The MNA can be completed in about 10 minutes; a low score indicates malnutrition or a risk for malnutrition.

Anthropometric Measurements

Anthropometric measurements are noninvasive methods of evaluating nutritional status. These measurements include height and weight and assessment of body fat.

 

 

BEST PRACTICE/or

Initial Nutrition Screening Assessment

The presence of one or more of the following conditions should alert the nurse that the client is at risk for malnutrition or has had a condition in the past requiring special nutritional care.

 

General

• Does the client have any conditions that cause nutrient loss, such as malabsorption syndromes, draining abscesses, wounds, fistulas, or protracted diarrhea?

• Does the client have any conditions that increase the need for nutrients, such as fever, burn, injury, sepsis, or antineoplastic therapies?

• Has the client been on NPO status for 3 days or more?

• Is the client receiving a modified diet or a diet restricted in one or more nutrients?

• Is the client being enterally or parenterally fed?

• Does the client describe food allergies, lactose intolerance, or limited food preferences?

• Has the client experienced a recent, unexplained weight loss?

• Is the client taking medications, either prescription, over-the-counter, or herbal/natural products?

Gastrointestinal

• Does the client complain of nausea, indigestion, vomiting, diarrhea, or constipation?

• Does the client exhibit glossitis, stomatitis, or esophagitis?

• Does the client have difficulty chewing or swallowing?

• Does the client have a partial or total gastrointestinal obstruction?

• What is the client’s state of dentition?

Cardiovascular

•  Does the client have ascites or edema?

•  Is the client able to perform activities of daily living?

•  Does the client have congestive heart failure?

Genitourinary

•  Does fluid input approximately equal fluid output?

•  Does the client have an ostomy?

•  Is the client hemodialyzed or peritoneally dialyzed?

Bespiratory

•  Is the client receiving mechanical ventilatory support?

•  Is the client receiving oxygen via nasal prongs?

•  Does the client have chronic obstructive pulmonary disease (COPD) or asthma?

Integumentary

•  Does the client have nail or hair changes?

•  Does the client have rashes or dermatitis?

•  Does the client have dry or pale mucous membranes or de­creased skin turgor?

•  Does the client have pressure areas on the sacrum, hips, orankles?

Extremities

•  Does the client have pedal edema?

•  Does the client exhibit cachexia?

 

MEASUREMENT OF HEIGHT AND WEIGHT

Height and weight provide a baseline determination of nutri­tional status. The nurse or assistive nursing personnel obtains accurate measurements, because clients who report their own measurements tend to overestimate height and underestimate weight. Subsequent measurements may indicate an early change iutritional status.

Height

Clients should be measured and weighed while wearing min­imal clothing and no shoes. The nurse or assistive nursing per­sonnel determines the client’s height in inches or centimeters with the measuring stick of a weight scale. The client should stand erect and look straight ahead, with the heels together and the arms at the sides.

CONSIDERATIONS FOR OLDER ADULTS

BBS Some older adults may have difficulty standing erect, and their actual height may be less than their height on recall. If height cannot be measured directly, it should be estimated by arm span or with use of a knee-height caliper, which provides a more precise height estimate.

 Weight

The nurse or assistive nursing personnel weighs ambulatory clients with an upright balance beam scale. Nonambulatory clients can be weighed with a movable wheelchair balance beam scale or a bed scale. The manufacturer should calibrate weight scales twice yearly to ensure accurate readings. For daily or sequential weights, the nurse or assistive nursing per­sonnel notes the time and obtains the weight at the same time each day, if possible. Conditions such as heart failure and re­nal disease affect fluid balance and, therefore, weight.

Normal weights for adult men and women are shown in the Metropolitan Life tables (Table 61-3). The latest U.S. Depart­ment of Agriculture (USDA) and U.S. Department of Health and Human Services (DHHS) Dietary Guidelines contain weight guidelines that emphasize both weight maintenance and weight loss. The same healthy weight guideline applies to all adults. Older adults are no longer permitted a higher weight standard. The weight range appears in the guidelines as a chart with three categories: healthy weight, moderate overweight, and severe overweight (Figure 61-5). Either the Metropolitan Life tables or the New Weight Guidelines from the USDA and the DHHS may be used for comparison with a client’s height and weight. Some health care professionals prefer the Metropolitan Life tables be­cause they consider body build differences by gender.

Changes in body weight can be expressed by three differ­ent formulas:

 

 

 

 

 

 

 

 

An involuntary weight loss of 10% at any time signifi­cantly affects nutritional status. Weights may need to be taken daily, several times a week, or weekly for monitoring status and the effectiveness of nutritional support.

ASSESSMENT OF BODY FAT I Body Mass Index

The body mass index (BMI), or Quetelet index, is a measure of nutritional status that does not depend on frame size. The BMI indirectly estimates total fat stores within the body by the relationship of weight to height:

BMI can also be determined using a nomogram. The least risk of death from malnutrition is associated with scores be­tween 20 and 25 (Mahan & Escot-Stump, 1996). BMIs above and below these values are associated with increased health risks. Older, healthy adults should have a BMI between 24 and 27.

Skin Fold Measurements

Skin fold measurements estimate body fat. The nurse or di­etitian may measure the client. The triceps and subscapular skin folds are most commonly measured. Both are com­pared with standard measurements and are recorded as per-centiles.

The nurse or dietitian can measure the triceps skin fold thick­ness by using a tape measure to locate and mark the midpoint on the client’s upper arm. To obtain the midpoint, the left arm is bent 90 degrees at the elbow, and the forearm is placed palm down across the middle of the body. The midpoint is half the dis­tance between the tip of the shoulder (acromion process) and the tip of the elbow (olecranon process). The skin should be marked at this point before any measurements are made. The triceps skin fold is measured on the back of the left arm over the triceps mus­cle at the marked midpoint. The nurse holds a double fold of skin and subcutaneous adipose tissue between the fingers and thumb. The skin fold is held until the jaws of the skin fold caliper are placed perpendicular to the length of the skin fold at the marked midpoint. The nurse records this measurement.

Subscapular skin fold thickness indirectly estimates body fat. The body position is the same as for triceps skin fold thickness, and the same caliper is used. The nurse holds a double fold of skin and subcutaneous adipose tissue in a line from the inferior angle of the left scapula to the left elbow, ap­plies the calipers, and records the measurement.

Arm Circumference

The midarm circumference (MAC) can be obtained to mea­sure muscle mass and subcutaneous fat. To measure MAC, the nurse or dietitian places a flexible tape around the arm at the same marked midpoint used to measure skin fold thickness, taking care to hold the tape firmly but gently to avoid com­pressing the tissue. This measurement is recorded in centime-

ters. The midarm muscle mass (MAMM) measures the amount of muscle in the body and is a more sensitive indica­tor of protein reserves. It can be computed from the MAC and the triceps skin fold measure.

MALNUTRITION 

 

OVERVIEW

Carbohydrates, protein, and fat supply the body with energy. Under healthy conditions, the majority of this energy under­goes digestion and is absorbed from the gastrointestinal tract. Food energy is used to maintain body temperature, respira­tion, cardiac output, muscle function, protein synthesis, and the storage and metabolism of food sources.

Energy balance refers to the relationship between energy ex­pended and energy stored. When energy expended exceeds en­ergy intake, energy stores are used to supply the deficit; this re­sults in weight loss. Body proteins are used for energy when calorie intake is insufficient. The body attempts to meet its calo­rie requirements even if it is at the expense of proteieeds.

Many severely ill or traumatized hospitalized clients are at risk for protein-calorie malnutrition (PCM), also known as protein-energy malnutrition (РЕМ). PCM may present in three forms: marasmus, kwashiorkor, and maras-mic-kwashiorkor. Marasmus is generally a calorie malnu­trition in which body fat and protein are wasted. Serum proteins are often preserved. Kwashiorkor is a lack of pro­tein quantity and quality in the presence of adequate calo­ries. Body weight is more normal, and serum proteins are low. Marasmic-kwashiorkor is a combined protein and energy malnutrition. This problem often presents clinically when metabolic stress is imposed on a chronically starved client. The outcome of unrecognized or untreated PCM is often dysfunction or disability and increased morbidity and mortality.

Pathophysiology

Malnutrition is a multinutrient problem because foods that are good sources of calories and protein are also good sources of other nutrients. In the malnourished client, protein catabolism exceeds protein intake and synthesis, resulting iegative nitrogen balance, weight loss, decreased muscle mass, and weakness.

 CONSIDERATIONS FOR OLDER ADULTS

BfiaOlder adults are at a high risk for poor nutrition due to cog­nitive impairments, complicated physical conditions, or chronic disease. Malnutrition in older adults has been associated with increased complications from infections and slower recovery from physiologic stresses such as surgical wounds, bone frac­tures, pressure ulcers, and loss of functional capacity (Ander­son, 2000). PCM has been shown to be a strong independent risk factor for 1 -year posthospital discharge mortality.

The functional ability of the liver, heart, lungs, gastroin­testinal tract, and immune system diminishes in the client with malnutrition. A decrease in serum proteins (hypopro-teinemia) occurs as protein synthesis in the liver decreases. Vital capacity is also reduced as a result of respiratory muscle atrophy; cardiac output diminishes. Malabsorption occurs be­cause of atrophy of gastrointestinal mucosa and the loss of in­testinal villi.

Other complications of severe malnutrition in adults in­clude the following:

·        Leanness and cachexia (muscle wasting)

·        Decreased effort tolerance

·        Lethargy

·        Intolerance to cold

·        Edema

·        Dry, flaking skin and various types of dermatitis Poor wound healing and a higher than usual number of infections, particularly postoperative infection

 Etiology

Malnutrition results from inadequate nutrient intake, in­creased nutrient losses, and increased nutrient requirements. Inadequate nutrient intake can be linked to poverty, lack of education, substance abuse, decreased appetite, and a decline in functional ability to eat independently. Infectious diseases, such as tuberculosis and human immunodeficiency virus (HIV) infection, are also precipitating factors in PCM. Dis­eases that produce diarrhea and respiratory and other infec­tions leading to anorexia result iegative calorie and protein balance; anorexia then leads to poor food intake. Vomiting leads to decreased absorption with increased nutrient losses. Medical treatments such as chemotherapy can also cause mal­nutrition. In addition, catabolic processes increase nutrient re­quirements and metabolic losses.

Inadequate nutrient intake can also result when a person is admitted to the hospital or nursing home (Dudek, 2000). De­creased staffing may not allow time for clients who need to be fed, especially older adults who may eat slowly (Anderson, 2000). Many diagnostic tests and surgery require a period of having nothing by mouth (NPO).

Unrecognized dysphagia is a common problem in nursing homes and can cause malnutrition, dehydration, and aspiration pneumonia. A study by Kayser-Jones and Pengilly (1999) found that 45 of 82 residents in one nursing home had some degree of dysphagia (difficulty swallowing) ranging from mild to profound. Only 10 of the 45 residents had been referred for dysphagia evaluation by a speech-language pathologist.

Eating disorders, such as anorexia nervosa and bulimia ner-vosa, also lead to malnutrition. Anorexia nervosa is a self-induced starvation resulting from a fear of fatness, even though the client is underweight. Bulimia nervosa is characterized by episodes of binge eating in which the client ingests a large amount of food in a short time. The binge eating is followed by some form of purging behavior, such as self-induced vom­iting and/or an excessive use of laxatives and diuretics. If not treated, death can result from starvation, infection, or suicide. Information about eating disorders can be found in textbooks on mental health nursing.

Incidence/Prevalence

Malnutrition is present in many hospitalized clients (Dudek, 2000). In a review of eight studies with more than 1347 hospi­talized adults, 40% to 55% were determined to be malnour­ished or at risk for malnutrition, and up to 12% were severely malnourished. Malnourished clients heal more slowly, suffer more complications, and have a higher mortality rate. Surgical clients with a likelihood of malnutrition were two to three times more likely to experience minor and major complica­tions and excess mortality. Length of hospitalization in mal-

nourished medical-surgical clients can be extended by as much as 90%, which clearly increases health care costs (Gallagher-Allred et al., 1996).

The prevalence of PCM in long-term care facilities has been reported to range from 10% to 85% (Anderson, 2000). In one study, the prevalence of malnutrition in 100 clients ad­mitted consecutively to a skilled nursing facility was 39%. The highest prevalence of malnutrition was found in clients admitted from acute care hospitals (Nelson et al., 1993).

Acute PCM may develop in clients who were adequately nourished before hospitalization if they experience starvation while in a catabolic state from infection, stress, or injury. Chronic PCM can occur in clients who have cancer, end-stage renal or hepatic disease, or chronic neurologic disease.

 WOMEN’S HEALTH CONSIDERATIONS As many as 25% of the general older adult population may be malnourished, most of them women (Wellman, 1997). Older women are particularly at risk for PCM (Chart 61 -2) be­cause of the following:

•  Acute and chronic disease

•  Processes that lead to a reduction of food intake

•  Malabsorption and maldigestion

•  Decreased efficiency of nutrient use

•  Multiple medication therapy

•  Poverty

•  Social isolation

•  Dependency/disability

Women, especially adolescents and young adults, are more likely than men to have eating disorders. Caucasian women are at the highest risk for these health problems.

CULTURAL CONSIDERATIONS

 In Western countries, cultural factors do not seem to have a major influence on the development of malnutrition. However, newly arriving immigrants from developing countries may be at risk for malnutrition because of limited food sup­plies, poverty, and eating habits.

In the Native American population of the United States, poor nutrition has also been directly related to several leading causes of death, including heart disease and cirrhosis of the liver. The diets of many Native American tribes continue to be inadequate in protein, calcium, and vitamins A and С These deficiencies may result from an unavailability of or a lack of money to purchase foods that are high in these nutrients (Giger & Davidhizar, 1999).

 COLLABORATIVE MANAGEMENT

 

Assessment

history

The nurse reviews the medical history to determine the diag­nosis, possibility of increased metabolic needs or nutritional losses, chronic disease, recent surgery of the gastrointestinal tract, drug and alcohol abuse, and recent, significant weight loss. Each of these conditions can contribute to malnutrition. For older adults, the nurse also explores mental status deteri­oration, poor eyesight or hearing, diseases affecting major or­gans, constipation or incontinence, slowed reactions, a review of prescription and over-the-counter medications (including herbal and natural supplements), and physical disabilities.

For clients who live independently, the nurse or occupa­tional therapist assesses the performance of instrumental ac­tivities of daily living (IADLs). Functional status can best be evaluated for institutionalized clients by assessing their per­formance of activities of daily living (ADLs). An inability to perform any of the eight IADLs or any of the six ADLs indi­cates a high level of dependence and the potential for disease and poor nutritional status (Nutrition Screening Manual, 1991). When functional status is evaluated with nutritional status, there appears to be a strong predictability of infections and complications among institutionalized adults. Chapter 10 describes functional assessment in detail.

The nurse interviews the client to obtain information about his or her usual daily food intake, eating behaviors, change in appetite, and recent weight changes. The client is asked to de­scribe the usual foods eaten daily and the times of meals and snacks. This information is then compared with the Food Guide Pyramid for gross deficiencies. The dietitian can more thoroughly analyze the diet, if necessary.

The nurse explores with the client any changes in eating habits as a result of illness. Any change in appetite, taste, and weight loss is recorded. A weight loss of 5% or more in 30 days, a weight loss of 10% in 6 months, or a weight that is be­low ideal body weight is significant for malnutrition.

Difficulty or pain in chewing or swallowing is also as­sessed. The nurse asks the client whether any foods are avoided and why. The occurrence of nausea, vomiting, heart­burn, or any other symptoms of discomfort with eating is also recorded. Finally, the client is asked about dental health prob­lems, including the presence of dentures. Dentures or partial plates that do not fit well interfere with food intake.

 

 

 

PHYSICAL ASSESSMENT/CLINICAL MANIFESTATIONS

The nurse assesses for signs and symptoms of various nutri­ent deficiencies (Table 61-4). The nurse inspects the client’s hair, eyes, oral cavity, nails, and musculoskeletal and neuro­logic systems. The condition of the skin, including any red dened or open areas, is observed. The anthropometric mea­surements previously described may also be obtained. The nurse or assistive nursing personnel monitors all food and fluid intake, observes the client at mealtime, and notes any mouth pain or difficulty in chewing or swallowing.

 

 

 

PSYCHOSOCIAL ASSESSMENT

The psychosocial history provides information about the client’s economic status, occupation, educational level, living and cooking arrangements, and mental status. The nurse de­termines whether financial resources are adequate for pro­viding the necessary food. If resources are inadequate, the social worker may refer the client to available community services.

 

 LABORATORY ASSESSMENT

Routine laboratory tests provide additional information about nutritional status. These tests supply objective data that can support subjective data and identify preclinical deficien­cies. Laboratory tests must be carefully interpreted with re­gard to the total client; an isolated value may yield an inac­curate conclusion.

HEMATOLOGY. Hemoglobin is measured to detect iron deficiency anemia. A low hemoglobin level may indicate ane­mia, recent hemorrhage, or hemodilution caused by fluid re­tention. Hemoglobin may be low secondary to conditions such as low serum albumin, infection, catabolism, or cancer. High hemoglobin levels may indicate hemoconcentration or dehydration, or they may be secondary to liver disease.

Hematocrit, a measure of cell volume, indicates iron sta­tus. Low hematocrit levels may reflect anemia, hemorrhage, excessive fluid, renal disease, or cirrhosis. High hematocrit levels may indicate dehydration or hemoconcentration.

PROTEIN STUDIES. Serum albumin, transferrin, and thyroxine-binding prealbumin can be measured in the labora­tory. Serum albumin indicates the body’s protein status but is not sensitive enough to detect early changes iutritional sta­tus. The normal serum albumin level for men and women is greater than 3.5 g/dL. Table 61-5 indicates the level of protein depletion based on the serum albumin level.

Serum transferrin, an iron-transport protein, can be mea­sured directly or calculated as an indirect measurement of to­tal iron-binding capacity (TIBC) as follows:

Calculated transferrin = (0.68 x TIBC) + 21

Serum transferrin has a shorter half-life of 8 to 10 days and therefore is a more sensitive indicator of protein status than is albumin. Table 61-6 indicates the level of protein depletion based on serum transferrin level.

Thyroxine-binding prealbumin (PAB) provides a more sensitive indicator of protein deficiency because of its short half-life of 2 days. Depending on the laboratory test used, the normal PAB range is 17 to 40 mg/dL. PAB can also assess improvement iutritional status with refeeding; levels can increase by 1 mg/dL/day with adequate nutritional support. However, this test is expensive, and its cost may be prohibi­tive except at large facilities.

SERUM CHOLESTEROL. Cholesterol levels normally range between 160 and 200 mg/dL in adult men and women. Values are typically low with malabsorption, liver disease, per­nicious anemia, terminal stages of cancer, sepsis, or stress. A cholesterol level below 160 mg/dL has been identified as a possible indicator of malnutrition.

 

OTHER LABORATORY TESTS. Total lymphocyte count (TLC) can be used to assess immune function. Malnu­trition suppresses the immune system and leaves the client more vulnerable to infection. When a client is malnourished, the TLC is usually decreased below 1500 mm³ (Bender et al., 2000).

 Analysis

COMMON NURSING DIAGNOSES AND COLLABORATIVE PROBLEMS

The most common diagnosis for the client with malnutrition is unbalanced Nutrition: Less Than Body Requirements related to inadequate food intake or increased nutrient requirements.

К   ADDITIONAL NURSING DIAGNOSES AND COLLABORATIVE PROBLEMS

In addition to the commoursing diagnosis, clients with malnutrition may have one or more of the following:

•        Risk for Impaired Skin Integrity related to depleted pro­tein stores

Risk for Infection related to suppressed immune system

•        Risk for Disturbed Body Image related to physical changes from weight loss

 

Some clients with malnutrition are at risk for collaborative problems such as the following:

•  Anemia

•  Immunocompromised state

• 

 

 Planning and Implementation

 

■   UNBALANCED NUTRITION: LESS THAN BODY REQUIREMENTS

PLANNING: EXPECTED OUTCOMES. The client with malnutrition is expected to (1) demonstrate an adequate nutrient intake, (2) maintain body mass and weight withiormal limits (WNL), and (3) maintain laboratory values WNL (e.g., albumin).

INTERVENTIONS. The preferred route for feeding is through the gastrointestinal tract because it enhances the im­mune system and is safer, easier, less expensive, and more physiologically sound (Chart 61-3).

 NUTRITION MANAGEMENT. In collaboration with the health care provider and dietitian, the nurse provides high-calorie, high-protein foods (e.g., milkshakes, cheese and crackers). A feeding schedule of six small meals benefits many clients. If the client has difficulty chewing or is edentu­lous (toothless), a pureed or dental soft diet may facilitate food intake.

Malnourished ill clients ofteeed to be encouraged to eat. The nurse provides a quiet environment, which is conducive to eating. Some clients, especially older adults, may take a long time to eat even small quantities of food.

Restorative feeding programs help nursing home residents who need special assistance. These residents eat in a separate dining area so that time and attention can be given to them. Chart 61-4 offers additional interventions to increase nutri­tional intake for older adults in any setting.

DRUG THERAPY. Medications may be given to some clients to stimulate appetite. For example, cyproheptadine (Periactin), an antihistamine, may be ordered for clients who are underweight, especially those with eating disorders. Megestrol acetate (Megace), an antineoplastic drug, may be used to increase appetite in clients who have cachexia, ac­quired immunodeficiency syndrome (AIDS), or unexplained weight loss. The mechanism for how these drugs work to in­crease appetite is unknown.

PARTIAL ENTERAL NUTRITION. The dietitian calcu­lates the nutrients required daily and translates these require­ments into meals for the client. If the client cannot ingest suf­ficient nutrients as food, partial enteral nutrition with fortified medical nutritional supplements (MNSs) (e.g., En­sure or Carnation Instant Breakfast) may be given, especially for older adults. Many commercial enteral products are avail­able. For clients with medical diagnoses such as liver and re­nal disease, special products that meet their needs are also available. The client must enjoy the taste of the product for acceptability and optimal intake.

CONSIDERATIONS FOR OLDER ADULTS

Supplements used in acute care, long-term care, and home care are costly. In addition, older adults may refuse them, and the supplements are then wasted. Bender at al. (2000) found that a more successful alternative to having the MNS distributed by food service or nursing assistant staff in the nursing home was to have the supplements delivered by nurses during their usual medication passes. In this study, the nurses gave 60 mL or more of the MNS at least four times a day with the clients’ medications. The subjects increased weight and had fewer pressure ulcers, thus making the pro­gram very cost-effective.

Nutritional supplements are supplied as liquid formulas, powders, bars, and puddings in a variety of flavors. They come in different degrees of sweetness and are also available as modular supplements that provide single nutrients. Examples of modular supplements are Polycose for carbohydrates and ProPac for protein. Carbohydrate modulars are useful only if additional calories are needed. Protein modulars are indicated when metabolic stress causes a need for higher protein intake.

The nurse bases adequate daily fluid intake on 30 mL of fluid per kilogram of body weight. This recommendation is not for clients with severe cardiac problems or fluid restric­tions. The health care provider may also prescribe vitamin and mineral supplements.

 

The nurse or assistive nursing personnel maintains a daily calorie count and fluid intake to assess whether the client can meet the goals of nutritional therapy. The dietitian usually asks the nursing staff to keep the food intake record for at least 3 consecutive days. Accurate daily or weekly weights are also essential depending on the amount of depletion.

TOTAL ENTERAL NUTRITION. Clients often cannot meet the goals of nutritional therapy through their usual oral intake because of increased metabolic demands or a decreased ability to eat. In such cases, enteral tube feeding may be necessary to supplement oral intake or to provide total nutritional support.

CANDIDATES   FOR   TOTAL   ENTERAL   NUTRITION.

Clients likely to receive total enteral nutrition (TEN) can be divided into three groups:

Clients who can eat but cannot maintain adequate nutri­tion by oral intake of food alone Clients who have permanent neuromuscular impairment and cannot swallow

Clients who do not have permanent neuromuscular im­pairment but are critically ill and cannot eat because of their condition

Clients in the first group are often older adults or clients re­ceiving cancer treatment who cannot meet their calorie and proteieeds (see the Legal/Ethical Issues in Health Care box below). Clients in the second group usually have permanent swallowing problems and require some type of feeding tube for delivery of the enteral product on a long-term basis. Ex­amples of conditions that can cause permanent swallowing problems are strokes, severe head trauma, and advanced mul­tiple sclerosis. Clients in the third group receive enteral nutri­tion for as long as their illness lasts. The feeding is discontin­ued when the client improves and can eat again. Total enteral nutrition is contraindicated for clients with diffuse peritonitis, severe pancreatitis, intestinal obstruction, intractable vomit­ing or diarrhea, and paralytic ileus (Bowers, 1996).

TYPES OF ENTERAL PRODUCTS. Many commercially prepared enteral products are available. An appropriate com­bination of carbohydrates, fat, vitamins, minerals, and trace elements is available in liquid form. Differences among prod­ucts allow the dietitian to select the right formula for each client. An order from the health care provider is required for enteral nutrition, but the dietitian usually makes the recom­mendation and computes the amount and type of product needed for each client.

METHODS OF ADMINISTRATION OF TOTAL EN­TERAL NUTRITION. TEN is administered as “tube feedings” through one of the available gastrointestinal tubes, either via a nasoenteric tube (NET) or an enterostomal tube.

Types of Tubes. A nasoenteric tube is any feeding tube inserted nasally and then advanced into the gastrointestinal tract. Commonly used NETs include the nasogastric (NG) tube and the nasoduodenal tube (NDT). A nasojejunal tube (NJT) is also available but is used less often than the other NETs. NDTs and NJTs are usually indicated for critically ill clients at risk for aspiration or delayed stomach emptying.

NETs are used for delivering short-term enteral feedings be­cause they are easy to use and are safer for the client at risk for aspiration if the tip of the tube is placed below the pyloric sphinc­ter of the stomach. Small-bore polyurethane or silicone tubes from 8 to 12 French external diameter are preferred over large-bore plastic or latex tubes. The smaller tubes are more comfort­able and are less likely to cause complications such as nasal irri­tation, sinusitis, tissue erosion, and pulmonary compromise.

Enterostomal feeding tubes are used for clients who need long-term enteral feeding. The most common types are gas-trostomies and jejunostomies. The physician directly accesses the gastrointestinal tract using various surgical, endoscopic, and laparoscopic techniques.

A gastrostomy is a stoma created from the abdominal wall into the stomach through which a short feeding tube is inserted by the physician. The gastrostomy may require a small abdom­inal incision or may be placed endoscopically; these tubes are called percutaneous endoscopic gastrostomy (PEG) or dual access gastrostomy-jejunostomy (PEG/J) tubes. The PEG does not require general anesthesia and is more secure and more durable than traditional gastrostomies. An alternative to either device is the low-profile gastrostomy device (LPGD). The LPGD is available with a firm or balloon-style internal bumper or retention disk. An antireflux valve keeps gastrointestinal contents from leaking onto the skin. This device is less irritat­ing to the skin, longer lasting, and more cosmetically pleasing, and it allows greater client independence. However, skin-level devices do not allow easy access for checking residuals.

Jejunostomies are used less often than gastrostomies. A je-junostomy is used for long-term feedings when it is desirable to bypass the stomach, such as with gastric disease, upper gastrointestinal obstruction, and abnormal gastric or duodenal emptying.

 

 

Types of Feedings. Tube feedings are administered by bolus feeding, continuous feeding, and cyclic feeding. Bolus feeding is an intermittent feeding of a specified amount of en-teral product at specified times during a 24-hour period— typically every 4 hours. This method can be accomplished manually or by infusion through a mechanical pump or con­troller device. A more popular method of tube feeding is con­tinuous enteral feeding. Continuous feeding is similar to IV herapy in that small amounts are continuously infused (by gravity drip or by a pump or controller device) over a speci­fied time. Cyclic feeding is the same as continuous feeding except that the infusion is stopped for a specified time in each 24-hour period, usually 6 to 10 or more hours (“down time”). Down time typically occurs in the morning to allow bathing, bed making, and other treatments.

Infusion rates for continuous and cyclic feedings (and to some extent for intermittent bolus feeding) vary with the total amount of solution to be infused, the specific composition of the product, and the response of the client to the procedure.

The health care provider and dietitian usually decide the type, rate, and method of tube feeding, as well as the amount of additional water needed. If the client can swallow small amounts of food, he or she may also eat orally while the tube is in place.

The nurse is responsible for the care and maintenance of the feeding tube and the enteral feeding. Chart 61-5 lists the major nursing interventions for the client receiving an enteral feeding.

COMPLICATIONS OF TOTAL ENTERAL NUTRITION.

The nurse is responsible for the prevention, assessment, and management of complications associated with tube feeding. Some complications of therapy result from the type of tube used to administer the feeding, and other complications result from the enteral product itself. The most common problem as­sociated with feeding tubes is the development of a clogged tube. Chart 61-6 lists nursing interventions for maintaining a patent tube.

A less common but more serious complication is dislodge-ment of the tube. Several techniques should be used to con­firm proper placement. An x-ray study is the most accurate confirmation method and should always be done on initial tube insertion. After the initial placement is confirmed, the nurse checks the placement before each intermittent feeding or at least every 8 hours during continuous or cyclic feeding.

The traditional auscultatory method is not reliable, espe­cially for clients with small-bore tubes (see the Evidence-Based Practice for Nursing box on p. 1371). In this method, the nurse instills 20 to 30 mL of air into the tube while listen­ing over the stomach with a stethoscope. The whooshing sound that results does not guarantee correct tube placement. The nurse should instead aspirate a sample of the gastroin­testinal content, observe its color, and test its pH. When aspi­rating fluid, the nurse waits at least 1 hour following medica­tion administration, then flushes the tube with 20 mL of air to clear it. The aspirate is collected and tested with pH paper. The pH of gastric fluid ranges from 0 to 4.0. If the tube has migrated down into the intestines, the pH will be between 7.0 and 8.0. If the tube is in the lungs, the pH will be greater than 6.0 (Metheney at al., 1998). The pH may also be as high as 6 if the client takes certain medications, such as H₂ blockers (e.g., ranitidine [Zantac] and famotidine [Pepcid]).

 

 

 

Fluid Imbalances. Clients receiving enteral nutrition therapy are at an increased risk for fluid imbalances. Clients who receive this therapy are often older or debilitated and may also have cardiac or renal problems. Fluid imbalances as­sociated with enteral nutrition are usually related to the body’s response to increased serum osmolarity.

Increased Osmolarity. Osmolarity is the amount or con­centration of particles dissolved in solution. This concentra­tion exerts a specific osmotic pressure within the solution. Normal osmolarity of extracellular fluid (ECF) ranges be­tween 270 and 300 mOsm. Enteral feeding products range in osmolarity from isotonic (about 300 mOsm) to extremely hy-pertonic (600 mOsm). Electrolytes (including sodium) con­tribute to this hypertonicity, but more of the osmolarity is de­termined by the concentration of proteins and sugar molecules in the enteral product. Even when the product is isotonic, the ECF can become hyperosmolar unless some hy-potonic fluids are also administered to the client. This situa­tion is most likely to develop in clients who are unconscious, unable to respond to the thirst reflex, on fluid restrictions, or receiving hyperosmotic enteral preparations.

An increase in the osmolarity of the plasma increases the osmotic pressure of the plasma. Because this increased osmo­larity is largely a result of extra glucose and proteins (which tend to remain in the plasma rather than move to interstitial spaces), the plasma osmotic pressure (water-pulling pressure) is increased. In this situation, intracellular and interstitial wa­ter move into and expand the plasma volume. This volume ex­pansion results in an increased renal excretion of water (among clients with normal renal function) and leads to os­motic dehydration. If clients do not have normal renal and cardiac function, the expansion of the plasma volume can lead to circulatory overload and the formation of pulmonary edema, especially in older adults. The nurse assesses for signsand symptoms of circulatory overload and collaborates with the dietitian and physician in planning the correct amount of fluid to be provided to the client.

Dehydration. Excessive diarrhea may develop when hy­perosmolar enteral preparations are delivered quickly. This situation can also lead to dehydration through excessive water loss. The nurse consults with the health care provider and di­etitian for recommendations to prevent diarrhea.

First, the dietitian usually changes the feeding to a more iso-osmolar formula. Most of these formulas can be started full-strength but slowly at 15 to 20 mL/hr. The rate is gradu­ally increased as the client tolerates and as the expected nu­tritional outcome is achieved. If diarrhea continues, the client should be evaluated for Clostridium difficile and its toxins.

In some cases, diarrhea may be the result of liquid med­ications, such as elixirs and suspensions that have a very high osmolality. Examples include acetaminophen, digoxin, furos-emide, phenytoin, and potassium chloride. Clients receiving multiple liquid medications need to be evaluated to determine if their drug regimen can be changed to prevent diarrhea. Di­luting these liquids may also be an option.

Another cause of diarrhea-related fluid imbalance among clients receiving enteral feeding preparations is lactose intol­erance. Clients receiving milk-based enteral feeding prepara­tions may become lactose intolerant. Most commercial en­teral products, such as Ensure, are lactose free.

Vines et al. (1992) conducted a comprehensive review of research on diarrhea related to tube feeding. They concluded that diarrhea often results from bacterial contamination, and they implemented interventions for decreasing this risk.

Electrolyte Imbalances. Depending on the client’s state of health, certain electrolyte imbalances can be avoided. This is achieved by the use of enteral preparations containing lower concentrations of the electrolytes that the client cannot handle well.

In addition to the client’s specific electrolyte imbalances, the two most common electrolyte imbalances associated with enteral nutrition therapy are hyperkalemia and hypernatremia. Both of these conditions may be related to hyperglycemia-in-duced hyperosmolarity of the plasma and the resultant os­motic diuresis. Electrolyte imbalances are discussed in detail in Chapter 13.

 CRiTICAL THINKING CHALLENGE

W An older adult in your nursing home has been eating less than 50% of her meals since admission the previous week. She has lost 3 pounds in 5 days. The nursing assistant reports to you today that the resident has a reddened area on her sacrum that does not blanch. When you speak to this client, she tells you that she is upset about being “put in a home.”

•  What other assessments should you perform at this time?

•  What are her priority nursing diagnoses?

•  What interventions are appropriate for her now?

PARENTERAL NUTRITION. When a client cannot effec­tively use the gastrointestinal tract for nutrition, parenteral nu­trition therapy may maintain or improve his or her nutritional status. This form of IV therapy differs from standard IV ther­apy in that all nutrients (carbohydrates, proteins, fats, vita­mins, minerals, and trace elements) are delivered to the client.

 

One liter of fluid containing 5% dextrose, which is often used as standard IV therapy, provides only 170 kcal. A hospitalized client typically receives 3 or 4 L a day for a total number of calories ranging between 500 and 700 a day. This calorie in­take is not sufficient when the client requires IV therapy for a prolonged period and cannot eat an adequate diet or has in­creased calorie needs for tissue repair and building.

Parenteral nutrition (hyperalimentation, or “hyperal”) is subdivided into two categories:

•        Partial parenteral nutrition, or peripheral parenteral nu­trition

•        Total parenteral nutrition, or central parenteral nutritionAs suggested by the names, these categories differ by the site of administration and the content of the solutions.

PARTIAL PARENTERAL NUTRITION. Partial parenteral nutrition (PPN) provides nutritional support to clients who are unable or unwilling to take a feeding via the gastrointestinal tract. PPN is typically used when a client has a prolonged post­operative ileus or when placement of a central IV line is not ad­vised. It is used wheutritional support is needed less than 14 days. The client should be able to tolerate large fluid volumes and have readily accessible peripheral veins.

PPN is usually delivered through a cannula or catheter in a large distal vein of the arm. Two types of solutions are com­monly used in various combinations for PPN: lipid (fat) emul­sions and amino acid dextrose solutions.

Most lipid emulsions (20%) are isotonic, but the tonicity of commercially prepared amino acid dextrose solutions ranges from 300 mOsm to nearly 1200 mOsm. Amino acid dextrose solutions are considered more stable than the lipid emulsions, and therefore additives (e.g., vitamins, minerals, electrolytes, and trace elements) tend to be mixed with the amino acid dex­trose solutions. The amino acid dextrose solution must be de­livered through an in-line filter. Lipids and amino acid dex­trose solutions are administered by a pump or controller device for accuracy and constancy in delivery rate.

A newer product for PPN is a mixture of lipids (10% or 20% fat emulsion) and an amino acid dextrose (usually 10%) solution. This mixture of three types of nutrients is referred to as a 3:1, total nutrient admixture (TNA), or triple-mix solu­tion; it is available in 3-L bags.

TOTAL PARENTERAL NUTRITION. When the client re­quires intensive nutritional support for an extended time, the health care provider prescribes centrally administered total parenteral nutrition (TPN). TPN is delivered through access to central veins, usually the subclavian or internal jugular veins. Central venous catheters and associated nursing care are described in detail in Chapter 14.

TPN solutions contain higher concentrations of dextrose and proteins, usually in the form of synthetic amino acids or protein hydrolysates (3% to 5%). These solutions are hyper-osmotic (three to six times the osmolarity of normal blood). The base solutions are available as commercially prepared so­lutions. The hospital or community pharmacist adds compo­nents (specific electrolytes, minerals, trace elements, and in­sulin) according to the client’s nutritional needs. This therapy provides needed calories and spares body proteins from ca-tabolism for energy requirements.

TPN solutions are administered with a pump or an infusion controller device. The osmolarity of the fluid and the concentrations of the specific components make controlled delivery essential.

COMPLICATIONS    OF    PARENTERAL    NUTRITION.

Clients receiving PPN or TPN are at risk for a wide variety of serious and potentially life-threatening complications. Com­plications may result from the PPN and TPN solutions or from the central venous catheter. The following discussion is limited to the complications of PPN and TPN that involve fluid or electrolyte balance. Complications of IV cannulas and central venous catheters are discussed in Chapter 14.

Fluid Imbalances. Clients receiving PPN or TPN are at increased risk for fluid imbalance. Not only is fluid delivered directly into the venous system, but the extreme hyperosmo-larity of the solutions stimulates fluid shifts between body fluid compartments.

The hyperosmolarity of parenteral nutrition solutions is caused by their amino acid and dextrose concentrations. In­creased dextrose causes hyperglycemia. As a result, some of the dextrose moves into the interstitial and intracellular spaces, where it is metabolized. However, dextrose remains in the plasma volume when the solutions are administered too rapidly, without enough insulin coverage, or in the presence of hyponatremia and hypokalemia. The result is a shift of wa­ter from the interstitial and intracellular spaces into the plasma. Expansion of the plasma volume together with hy­perglycemia can cause osmotic diuresis and lead to serious dehydration and hypovolemic shock. If the client has an ac­companying cardiac or renal dysfunction, the situation can lead to overhydration, congestive heart failure, and pul­monary edema.

The nurse monitors for these complications by taking daily weights and by recording accurate intake and output while the client is receiving parenteral nutrition. Serum glucose and electrolyte values are also monitored (Chart 61-7). Any major changes or abnormalities are reported to the health care provider.

 

 

Electrolyte Imbalances. Clients receiving either PPN or TPN are at an increased risk for many different electrolyte im­balances, depending on the electrolyte composition of the so­lution and whether a fluid imbalance occurs. The health care provider usually orders daily determinations of serum elec­trolyte levels to detect these imbalances. The risk of metabolic and electrolyte complications is reduced when the rate of ad­ministration is carefully controlled and clients are closely monitored for response to treatment. Potassium and sodium imbalances are common among clients receiving PPN and TPN, especially when insulin is also administered as part of the therapy. Calcium imbalances, especially hypercalcemia, are associated with PPN and TPN, although immobility may play more of a role than the actual parenteral therapy in the development of this imbalance.

EFFECTS OF MEDICATION. There is no specific drug therapy for malnutrition, although multivitamins and an iron preparation may be prescribed to treat or prevent anemia. The nurse carefully reviews the client’s medications because of food-medication interactions. Medications can affect nutri­tional status, and the foods ingested can affect the efficacy of medications.

 Community-Based Care

Malnourished clients can be cared for in a variety of settings, including the acute care hospital, subacute unit, nursing home, or their own home. Malnutrition is often diagnosed when the client is admitted to the acute care hospital or as a consequence of events that occur after hospitalization, such as poor wound healing or sepsis. If the client is severely com­promised, he or she may require admission to a subacute unit or traditional nursing home for either transitional or long-term care and be followed by a case manager. If adequate home support is available, the client may be discharged to home in the care of a family member, significant other, or other care-giver. Home care nurses may be needed to monitor and direct the care.

 HEALTH TEACHING

The dietitian instructs the malnourished client and the family about high-calorie, high-protein diet and nutritional supple­ments. The pharmacist reviews any parenteral solutions with the client and family or significant others.

The nurse reinforces the importance of adhering to the diet and reviews any medications the client may be taking. If the client takes an iron preparation, the nurse teaches the impor­tance of taking the medication immediately before or during meals. The nurse also cautions the client that iron tends to cause constipation. For the older adult already susceptible to constipation, the nurse stresses measures for prevention, in­cluding adequate fiber intake, adequate fluids, and exercise.

HEALTH CARE RESOURCES

The malnourished client may need help from community re­sources. Once nutrition therapy has progressed, the client may be discharged to the home setting or to a long-term care facil­ity. The nurse collaborates with the case manager or discharge planner to find the best placement for each client. If the client is discharged to home, a home care nurse may visit until the client is stable.

Whether the client is discharged to home or to another fa­cility, the dietitian provides written instructions about the diet and nutritional supplements. Communication with the new care provider is essential for continuity of care.

 Evaluation: Outcomes

noo The nurse evaluates the care of the malnourished client on the basis of the identified nursing diagnoses and collaborative problems. Expected outcomes include that the client:

•  Has an adequate intake of all required nutrients on a daily basis

•  Experiences no further weight loss or has a weight in­ crease

•  Has laboratory values withiormal limits (WNL)

 

 

OBESITY

 OVERVIEW

The terms obesity and overweight are often used inter­changeably, but they refer to different conditions. Overweight is an increase in body weight for height compared with a ref­erence standard, such as the Metropolitan Life height and weight tables (see Table 61-3) or 10% greater than ideal body weight. However, this weight may not reflect excess body fat. It is possible for well-developed athletes to appear overweight because of increased muscle mass; in such cases the propor­tion of muscle to fat is greater than average.

An obese person weighs at least 20% above the upper limit of the normal range for ideal body weight. Morbid obesity refers to a weight that has a negative effect on health—usually more than 100% above ideal body weight.

 

 

 

■  HOME CARE MANAGEMENT

The malnourished client needs a variety of resources at home to continue aggressive nutrition support. If the client can con­sume food by the oral route, the case manager or other dis­cbarge planner determines whether his or her financial re­sources are adequate for providing the necessary food and nutrition supplements. If the hospital provides ambulatory nu­trition counseling services, the client is scheduled for follow-up after discharge for assessment of weight gain. The nurse assesses the ability of the client and family to understand and comply with instructions.

The malnourished client discharged to home on enteral or parenteral nutrition support needs the specialized services of a home nutrition therapy team. This team generally consists of the physician, nurse, dietitian, pharmacist, and social worker. Several commercial companies supply these services to clients in addition to the feeding supplies and formulas.

Pathophysiology

Obesity refers to an excess amount of body fat. It is possible to be obese at a weight that is withiormal range according to a reference standard. The normal amount of body fat in men is between 15% and 20% of body weight. Obese young men have body fat greater than 22%, and older obese men have body fat greater than 25%. For women, the normal amount of body fat is 18% to 32%. Obese young women have body fat greater than 35% (Bray, 1994). Body fat can be measured in several ways. Height and weight are the easiest and most practical measurements for determining the degree of overweight.

OBESITY INDICES

To establish the percentage of ideal body weight (IBW), the height and weight of the client are compared with the mid­point of the desirable weight for a medium frame of the client’s height and sex in the Metropolitan Life height and weight tables (see Table 61-3). The body mass index (BMI), as described previously on p. 1363, is a measure of heaviness and is only an indirect indicator of body fat. It reflects the combined effects of body build, proportions, lean body mass, and body fat. However, BMI has exhibited substantial corre­lations with fat mass for adult men and women and has been validated as a risk factor for cardiovascular disease. As a gen­eral rule, a BMI of 27 indicates obesity and an increased risk for health problems. Arm circumference and skin fold meas­urements more completely define body composition and adiposity.

The distribution of excess body fat rather than the degree of obesity has been used to predict increased health risks. The waist-to-hip ratio (WHR) or abdominal/gluteal ratio (AGR) differentiates a predominantly peripheral (gynecoid) lower body obesity from a central (android) upper body obe­sity. A WHR of 0.95 or greater in men (0.8 or greater in women) indicates android obesity with excess fat at the waist and abdomen; this pattern carries the greatest health risk. Two risk groups have been identified by location of ab­dominal fat: one with subcutaneous fat and one with intra-abdominal fat. The group with subcutaneous fat had fewer complications than did the group with excess intra-abdomi-nal fat. Cross-sectional studies have shown that increased abdominal fat has been related to stroke, insulin resistance, hyperinsulinemia, and frank diabetes mellitus. Excessive ab­dominal fat may also enhance the risk for gallbladder dis­ease (Pi-Sunyer, 1993).

COMPLICATIONS OF OBESITY

Obesity is a major public health problem and is associated with many complications, including death. As a result of this increasing problem, the Healthy People 2010 agenda ad­dresses the need to reduce the proportion of children, adoles­cents, and adults who are obese. Nurses can help meet this goal through education and role modeling (see the Meeting Healthy People 2010 Objectives box above).

Complications of obesity that improve with weight loss in­clude the following:

·        Diabetes mellitus

·        Hypertension

·        Hyperlipidemia (increased serum lipids)

·        Cardiac disease

·        Sleep apnea

·        Cholelithiasis

·        Chronic back pain

·        Early degenerative arthritis

·        Certain types of cancer

Obese people are also more susceptible to infectious dis­eases than are thinner people.

CLASSIFICATION

Bray (1994) has developed a classification of obesity based on BMI and the corresponding risk for disease (Table 61-7). This classification system eliminates describing obesity in un­flattering and prejudicial terms such as morbid or gross.

Etiology

The cause of obesity involves complex interrelationships of many factors, including the following: ¹ Genetic

Environmental

·        Psychologic

·        Social

·        Cultural

·        Pathologic

·        Physiologic

Five major causes of both human and animal obesity have been identified (Bray, 1994). The first, neuroendocrine causes, include injury to the hypothalamus, Cushing’s dis­ease, polycystic ovary failure, hypogonadism, and growth hormone deficiency and insulinoma.

 

A second cause is dietary obesity associated with high-fat diets. Data suggest that obesity associated with a high-fat diet is more pronounced when the diet contains a significant amount of saturated fat.

Genetic factors are being studied as a third cause. They are found in clinically uncommon states, such as Prader-Willi syn­drome. Genetic composition may predispose some people but not others to obesity. Researchers have recently identified the ob gene in mice, which helps to regulate energy balance. Lep­tin, the hormone encoded by the ob gene, appears to send a message to the brain that the body has stored enough fat; this serves as a signal to stop eating. For obese humans, a variant in this gene may mean that the body does not receive the sig­nal to stop eating. More recent evidence suggests that energy balance and adiposity are regulated not only by the hormonal action of leptin and its receptors but also by the interaction of leptin and insulin with the hypothalamic neuropeptide Y sys­tem (Schwartz & Seeley, 1997).

The fourth cause of obesity is drug treatment. Drugs that promote obesity include the following:

·        Corticosteroids

·        Estrogens

·        Nonsteroidal anti-inflammatory drugs

·        Antihypertensives

·        Antidepressants

·        Antiepileptics

·        Phenothiazines

Physical inactivity has been identified as the fifth cause. The major identified barriers to increasing physical activity include a lack of time and a lack of safe environments in which to be active. Regular exercise is associated with lower death rates for adults of any age. It also increases lean mus­cle, decreases body fat, aids in weight control, and enhances psychologic well-being. Regular exercise can also decrease the risk of falling in older adults.

Incidence/Prevalence

The number of overweight children, adolescents, and adults has continued to rise over the past four decades. In the United States, the total cost (medical cost and lost productivity) of obesity is more than $100 billion each year. Phase 1 of the third National Health and Nutrition Examination Survey (NHANES III) was conducted between 1988 and 1991 and concluded that 58 million adults in the United States were overweight. This figure represents 33.4% of Americans. “Overweight” in this study was a BMI equal to or greater than 27.8 for men (approximately 124% of IBW) and a BMI equal to or greater than 27.3 for women (approximately 120% of IBW) (Kuczmarski et al., 1994). In 2000, an esti­mated 107 million adults in the United States were over­weight or obese.

Familial and genetic factors play an important role in obe­sity. When both parents are overweight, approximately 80% of their children will be overweight. If neither parent is over­weight, fewer than 10% of the children will be overweight. In studies of identical twins, nonidentical twins, and parent-sibling relationships, about 50% of the difference in body fat­ness is transmitted to children, and approximately 50% of this amount is genetically controlled. A combination of improper diet and lack of physical activity produces obesity in geneti­cally predisposed people.

CULTURAL CONSIDERATIONS

Culture seems to be a factor in the prevalence of obe­sity. The prevalence of obesity among ethnic minorities, in­cluding African Americans, Hispanic Americans, Asian Ameri­cans and Pacific Islanders, Native Americans, Native Alaskans, and Native Hawaiians, is substantially higher than in Caucasians, especially among women (Kumanyika, 1993). A study by Harrell and Gore (1998) found that African-American women of low and middle socioeconomic status (SES) were much more likely to be obese and inactive than were African-American women of high SES. Among Caucasian women, those with low SES had the greatest prevalence of obesity and inactivity. After controlling for income and education, African-American women were twice as likely as Caucasian women to be obese and inactive.

Further research by Gore (1999) found that African Ameri­cans’ frame of reference for “normal” body weight is much larger that the standard indicator for weight. Another factor contributing to larger body size in African-American women is that Caucasian women engage in weight loss methods for sig­nificantly longer periods of time than do African-American women (Tyler, Allan, & Alcozer, 1997).

A descriptive study of Hispanic women and their daughters demonstrated that daughters ate more fat than did their moth­ers (Garcia-Maas, 1999). The greater the fat intake, the more negatively women seemed to perceive their health status.

 

 COLLABORATIVE MANAGEMENT

 

Assessment

 HISTORY

The   nurse or dietitian collects the following informationabout the client:

·        Economic status

·        Usual food intake

·        Eating behavior

·        Cultural background

·        Attitude toward food

·        Appetite

·        Chronic diseases

·        Medications

·        Physical activity

A diet history usually incorporates a 24-hour recall of food intake and the frequency with which foods are consumed. The nurse or dietitian is objective but understands the personal na­ture of these questions. The adequacy of the diet can be rap­idly evaluated by comparing the amount and types of foods consumed daily with the Dietary Guidelines for Americans (see Figure 61-1). Gross inadequacies for specific nutrients can be identified with this approach. The dietitian can provide a more detailed analysis of dietary intake.

WOMEN’S HEALTH CONSIDERATIONS

 Women have a unique risk for nutrition-related diseases and conditions and weight-related problems due to biologic, social, and political factors. The American Dietetic Association (ADA) and the Canadian Dietetic Association (CDA) issued a joint position paper on women’s health and nutrition (ADA, 1995). Five of the leading causes of morbidity and mortality in North American women are cardiovascular disease, cancer, osteoporosis, diabetes, and overweight. Women are vulnerable to several weight-related health risks associated with being overweight. Recent estimates of North American women who are overweight range from 25% to 33%, with certaiative and ethnic populations reporting even higher percentages.

Being overweight adds many risks for women, especially if the fat stores are located in the abdominal or truncal areas of the body. A waist/hip ratio of 0.85 puts women at higher risk for coronary heart disease, hypertension, dyslipidemia, diabetes, gallstone formation, and cancer of the reproductive organs. In addition to these medical risks, women are vulnerable to the social, economic, and emotional pressures associated with be­ing overweight. Overweight women may find it difficult to feel good about themselves when challenged by society’s discrimi­nation against the overweight. The constant struggle for many women to lose weight often ends in failure and leads to patterns of weight cycling or disordered eating. Prevention and early in­tervention programs for overweight women and their families remain a critical need. The ADA and CDA will continue their ef­forts to include nutrition in clinical and preventive services for women because it is such a critical component of both risk re­duction and treatment for weight-associated conditions.

PHYSICAL ASSESSMENT/CLINICAL MANIFESTATIONS

In collaboration with the dietitian, the nurse accurately ob­tains the client’s height and weight and calculates the per­centage of ideal body weight (% IBW) and the body mass in­dex (BMI). The dietitian may:

•  Calculate the waist/hip ratio

•   Make the necessary skin fold measurements and record them in the chart

The nurse also examines the skin of the obese client for reddened or open areas; these may not be easily visible be­cause of excess fat.

 PSYCHOSOCIAL ASSESSMENT

The nurse obtains a psychosocial history to determine the client’s circumstances and emotional factors that might pre­vent success of therapy or be worsened by it. The nurse or so­cial worker interviews the client to determine his or her per­ception of current weight. The client may or may not view weight as a problem, which will affect treatment and outcome. The nurse explores the client’s past history to assess the following:

·        Cause and duration of weight gain

·        Family history of obesity

·        Past attempts at weight reduction and outcomes

·        The nurse asks about the following:

·        Current reasons for wanting to lose weight

 

·        Stressors (e.g., home, employment, personal, financial, or community) that might prevent success

·        Exercise patterns

·        Current medications

·        Perceptions of self-worth

The diet history provides a detailed analysis of the client’s eating habits. As a member of the health care team, the nurse can evaluate the data to coordinate an interdisciplinary ap­proach that incorporates diet, exercise, behavior modification, and psychologic support. The client may be referred to a com­munity support group if one is available.

 LABORATORY ASSESSMENT

There are no significant laboratory tests for obesity. However, the nurse should review all laboratory test results to assess the nutritional status of the client.

 Analysis

В   COMMON NURSING DIAGNOSES AND COLLABORATIVE PROBLEMS

The following are the most commoursing diagnoses for clients with obesity or overweight:

1. Imbalanced Nutrition: More Than Body Requirements related to a dysfunctional eating pattern or neuroendocrine disorder

2. Activity Intolerance related to a sedentary lifestyle

 ADDITIONAL NURSING DIAGNOSES AND COLLABORATIVE PROBLEMS

In addition to the commoursing diagnoses, clients may have one or more secondary problems associated with obesity and overweight, which include the following:

•   Situational Low Self-Esteem or Chronic Low Self-Esteem related to guilt associated with eating style

•   Disturbed Body Image related to physical appearance

•   Disturbed Thought Processes related to depression

•   Ineffective Sexuality Patterns related to body image per­ception, rejection by partner, or difficulty assuming sex­ual positions

•   Impaired Social Interaction related to poor self-esteem and rejection by others

•   Impaired Physical Mobility related to decreased strength and endurance

•  

 

Some clients with obesity are at risk for collaborative problems, which include the following:

•   Diabetes mellitus

•   Cardiovascular disease

•   Hypertension

Planning and Implementation

  IMBALANCED NUTRITION: MORE THAN BODY REQUIREMENTS

PLANNING: EXPECTED OUTCOMES. The client with obesity or overweight is expected to (1) participate in a structured weight loss program, (2) approach ideal body weight, and (3) establish a lasting, healthful dietary pattern that will result in permanent, sustained weight loss.

INTERVENTIONS. Weight is lost only when energy ex­pended is greater than intake. Weight loss may be accom­plished by dietary restriction with or without the aid of drugs. Clients who are candidates for surgical treatment:

•   Repeatedly fail at nonsurgical techniques

•   Have a body mass index (BMI) equal to or greater than 40 (class IV)

•   Weigh more than 100% above ideal body weight (IBW)

•   Have medically significant obesity

NONSURGICAL MANAGEMENT. The first clinical prac­tice Guidelines for Treatment of Adult Obesity outlines treat­ment decisions based on risk assessment. Recommendations for appropriate weight reduction strategies or weight maintenance to prevent further weight gain are also included (Shape Up America and American Obesity Association, 1996). Vari­ous diet programs and medications have attempted to help obese clients achieve permanent weight loss.

DIET PROGRAMS. Modalities for helping people lose weight include fasting, very-low-calorie diets, balanced and unbalanced low-energy diets, and novelty diets.

Fasting. Short-term fasting programs have not been suc­cessful in treating morbidly obese clients, and prolonged fast­ing does not produce permanent benefits. Most clients regain the weight that was lost by this method. In addition, the risks associated with fasting (e.g., severe ketosis) require close medical supervision.

Very-Low-Calorie Diets. Very-low-calorie diets gener­ally provide 200 to 800 calories/day. Two types of very-low-calorie diets are the protein-sparing modified fast and the liq­uid formula diet.

The protein-sparing modified fast provides protein of high biologic value (1.5 g/kg of desirable body weight/day) within a limited number of calories. The diet produces rapid weight loss while preserving lean body mass. The liquid formula diet provides between 33 and 70 g of protein daily.

Both diets require an initial cardiac evaluation, supervision by an interdisciplinary health team with monitoring by a physi­cian, nutrition counseling by a registered dietitian, and supple­mentation with vitamins and minerals. These diets are only one part of a weight reduction program. Clients who are following these diets should receive nutrition education, psychologic counseling, exercise, and behavior therapy. Comparable weight losses have been achieved with both diets, but most clients do not sustain the weight loss and regain the weight.

Balanced and Unbalanced Low-Energy Diets. Nutri­tionally balanced diets generally provide 1200 calories/day with a conventional distribution of carbohydrate, protein, and fat. Vitamin and mineral supplements may be necessary if en­ergy intakes fall below 1200 calories for women and 1800 calories for men. This diet provides conventional foods that are economical and easy to obtain; thus the goal of weight loss is facilitated, and that loss is maintained.

Unbalanced low-energy diets, such as the low-carbohydrate diet (e.g., Atkins diet), restrict one or more nutrients. No evi­dence supports the claim that the restricted nutrient increases or decreases weight loss beyond the calorie deficit it produces.

Novelty Diets. Novelty diets, such as the grapefruit diet, are ofteutritionally inadequate. This type of diet implies that a certain food increases metabolic rate or accelerates the oxidation of body fat. Weight loss is achieved because energy is restricted by food choice, but clients do not sustain weight loss after terminating the diet.

DIET THERAPY. Diet recommendations for each client should be developed through close interaction between the client, physician, and dietitian. The diet should meet the client’s needs and habits and should be realistic.

The dietitian develops a diet plan and instructs the client. At a minimum, the diet should:

·        Have a scientific rationale

·        Be nutritionally adequate for all nutrients except energy

·        Have a low risk/benefit ratio

·        Be practical and conducive to long-term success

 

 

  Calorie estimates are easily calculated. Resting metabolicrate is determined using a gender-specific formula that incor­porates the appropriate activity factor. This figure reflects the total calories needed daily for maintaining current weight. To encourage a weight loss of 1 pound (2.2 kg) a week, the die­titian subtracts 500 calories/day. To encourage a weight loss of 2 pounds (4.4 kg) a week, the dietitian subtracts 1000 calo­ries/day. The amount of weight lost varies with the client’s food intake, level of physical activity, and water losses. Car­bohydrate, protein, and fat can be calculated as in Table 61-8. A reasonable goal of 5% to 10% loss of body weight has been shown to improve glycemic control and reduce cholesterol and blood pressure, and these benefits continue if the weight loss is sustained (Wing & Jeffery, 1995).

DRUG THERAPY. A BMI of 30, or a BMI of 27 with co-morbidities, is one indicator for the use of drug therapy (Shape Up America and American Obesity Association, 1996). Anorec-tic drugs suppress appetite, which reduces food intake and over time may result in weight loss. These drugs play a valuable role in a comprehensive weight reduction program but should be used only as part of such a program. Currently available drugs to treat obesity act on either the noradrenergic or serotonergic systems in the central nervous system. The most commonly used anorectic drug for the treatment of obesity is sibutramine (Meridia). Sibutramine is an anorectic drag that inhibits the re-uptake of serotonin (which enhances satiety [feeling full when eating]) and norepinephrine (which raises metabolic rate). Ad­verse effects include dry mouth, constipation, and insomnia.

Orlistat (Xenical) is a different type of drag that inhibits li-pase and leads to partial hydrolysis of triglycerides. Because fats are only partially digested and absorbed, calorie intake is decreased. Most clients taking orlistat experience gastroin­testinal symptoms that include loose stools, abdominal cramps, and nausea.

 

 

 

BEHAVIORAL TREATMENT. Behavioral treatment of obe­sity consists of various strategies to change daily eating habits to achieve weight loss. This ongoing process should produce a change in behavior. Self-monitoring techniques include keeping a record of foods eaten (food diary), exercise patterns, and emo­tional and situational factors. Stimulus control involves control­ling the external cues that promote overeating. Reinforcement techniques are used to self-reward the behavior change. Cogni­tive restructuring involves modifying negative beliefs by learn­ing positive coping self-statements.

Fairbum and Cooper (1996) have developed a cognitive behavioral approach to the acquisition of weight maintenance behavior skills. Clients are encouraged to accept modest weight loss goals and are further discouraged from losing more weight. The treatment focuses on the acquisition of weight maintenance skills and on cognitive factors and any tendency to evaluate self-worth in terms of body size. The client’s focus is shifted from physical appearance to a concern for health.

 CRITICAL THINKING CHALLENGE

 You are caring for a 42-year-old female hospitalized client who is preparing to have bilateral knee replacements. She tells you that she has been obese her entire life and now has severe arthritis in both knees. She has tried every novelty diet available but regains the weight shortly after completing the diet. Her husband left her last year because he was em­barrassed to be with her.

• What are the priority nursing diagnoses related to her obesity?

• What other options does she have for managing her nutri­tional problem?

• What is the psychologic impact of being obese?

SURGICAL MANAGEMENT. Clients who do not respond to traditional dietary intervention may be considered for a sur­gical procedure aimed at producing permanent weight loss. All clients with a body mass index (BMI) >40, or a BMI >35 with additional risk factors, should be considered for surgery (Shape Up America and American Obesity Association, 1996). Most surgical procedures fall into three categories:

1. Mechanical or physical (adipose tissue removal or in­ take restriction)

2. Malabsorptive (bypass of the gastrointestinal tract)

3. Regulatory (directly affecting hunger or thirst)

PREOPERATIVE CARE. The nurse reinforces health teaching before the client has surgery. Preoperative care is similar to that for any client undergoing abdominal surgery (see Chapter 17).

OPERATIVE PROCEDURES. Surgical procedures that physically restrict the intake of food include the following:

·        Maxillomandibular fixation (jaw wiring) Esophageal banding

·        Gastroplasty (banding or stapling the stomach)

·        Intestinal bypass, in which the stomach and jejunum are connected

One of the most common procedures is gastroplasty, which decreases the size of the stomach. Stapling horizontally across the top of the stomach leaves only a small opening (0.8 to 1 cm) into the distal stomach. However, the fundic pouch created is of often stretched too much, which inhibits weight loss. The vertical banded gastroplasty evolved from earlier forms of gastroplasty. It is designed with a less distensible vertical pouch that reduces the capacity for a meal by 100-fold. The small pouch outlet delays emptying and provides an internal cue for satiety. Gastric restrictive operations sometimes produce maladaptive eating behaviors, such as the following:

·        Soft calorie syndrome” (consumption of excessive amounts of soft or liquid, calorically dense foods)

·        Vomiting from inadequate chewing

·        Inappropriate consumption of liquids after solids

An intestinal bypass reduces the size of the stomach with stainless steel staples but connects a small opening in the upper portion of the stomach to the small intestine by means of an intestinal loop (Figure 61-6). Complications of the intestinal bypass include bloating of the pouch. The incidence of nausea and vomiting is similar to that with gastroplasty. Intestinal bypass usually leads to greater weight loss that does gastroplasty, in part because of dumping syndrome as the use of the lower part of the stomach is omitted. Intestinal bypass operations have been modified to avoid blind loop bacterial overgrowth  yndromes and are now performed as a biliointestinal bypass, jejunoileal bypass with ileogastrostomy, or duodenoileal bypass. Surgical treatment of clinically severe obesity by either vertical banded gastroplasty or Roux-en-Y gastric bypass is a viable option for selected clients (NIH Consensus Development Conference Panel, 1991). Maximum weight loss from these procedures generally occurs 18 to 24 months after surgery. Two years after surgery, Roux-en-Y clients lost 60% to 70% of their weight, whereas gastroplasty clients lost 40% to 60%.

 

POSTOPERATIVE CARE.

 The client has a nasogastric (NG) tube put in place immediately after gastroplasty or intestinal bypass. In gastroplasty, the NG tube drains both the proximal pouch and the distal stomach. The nurse closely

monitors the tube for patency. The tube is never repositionedbecause its movement can disrupt the suture line. The NG tube is removed on the third day if the client has bowel sounds and is passing flatus. The nurse gives the client 1 ounce (30 mL) of water in a 1-ounce medicine cup and instructs the client to sip it slowly over 1 hour. Clear liquids are given if the client can tolerate water, and 1-ounce cups are used for each serving. Pureed foods, juice, and soups thinned with broth, water, or milk are added to the diet 24 to 48 hours after clear liquids are tolerated. Typically, the client can increase the volume to 1 ounce over 5 minutes or until satisfied, but the diet is limited to liquids or pureed foods for 6 weeks. The client then progresses to three meals a day, with an emphasis outrient-dense foods. Nausea, vomiting, or discomfort occurs if too much liquid is ingested. Before discharge from the hospital, the nurse instructs the client to take liquid or chewable multivitamins daily and to consume adequate protein to promote wound healing. To avoid blockage of the pouch opening, clients are encouraged to eat slowly, chew foods well, and avoid swallowing chunks of food that cannot be liquefied completely.

 

ACTIVITY INTOLERANCE

PLANNING: EXPECTED OUTCOMES. The client with obesity or overweight is expected to (1) tolerate usual activity as evidenced by endurance, energy conservation, and selfcare; and (2) incorporate daily exercise into his or her lifestyle.

 

INTERVENTIONS. Management of the overweight or obese client is an interdisciplinary effort. The nurse collaborates with the physician, dietitian, and physical therapist or exercise physiologist to meet the goal of improving the client’s physical activity tolerance. The major intervention is to increase the type and amount of daily exercise to create a calorie deficit along with modification of eating habits. Adding exercise to a diet interven­tion produces more weight loss than just dieting alone. More of the weight lost is fat, which preserves lean body mass. An in­crease in exercise produces a reduction in the waist/hip ratio.

Increasing and maintaining physical activity levels is impor­tant in maintaining weight loss. Many overweight or obese clients are so unfit that it may take several months of condition­ing before they can exercise sufficiently to achieve weight loss.

The nurse or physical therapist or exercise physiologist first obtains a clinical exercise history. It is important to de­termine the client’s current exercise pattern and exercise habits over a lifetime. The client should understand the im­portance of an exercise component in a weight loss program. The nurse also ascertains the client’s desire to participate in an exercise program and his or her preferred types of exercise.

The health care provider evaluates the client by an exercise stress test. Not all clients need a stress test, but those with chronic disease may need a stress test and more specific exer­cise recommendations. The nurse counsels clients about un­usual signs and symptoms during exercise (e.g., chest pain) and

what to do if they occur. The physical therapist or exercise physiologist first emphasizes the importance of exercising con­sistently and then stresses duration, intensity, and frequency.

A minimal-level workout should be developed for the client so that consistency can be achieved. The goal for the client is to maintain a lifetime of increased physical activity. The client is apt to be less fatigued and discouraged with a low-intensity, short-duration program. Sedentary clients are encouraged to increase their activity by walking 30 to 40 min­utes daily (15 to 20 minutes/mile) or the equivalent. The ac­tivity may be performed all at once or divided over the course of the day. The nurse teaches the client to exercise only under the supervision of the physician. All members of the interdis­ciplinary team should provide encouragement and support for any increase in physical activity.

 Community-Based Care

Obese clients can be cared for in a variety of settings, includ­ing the acute care hospital and subacute unit (particularly fol­lowing surgical treatment for obesity) or in their own home. Obesity is a chronic, lifelong problem. Diets, drug therapy, exercise, and behavior modification can produce short-term weight losses with reasonable safety. However, most clients who do lose weight often regain the weight. Treatment of obe­sity should focus on the long-term reduction of health risks and medical problems associated with obesity, improving quality of life, and promoting a health-oriented lifestyle. In­terdisciplinary team members need to provide a nonjudgmen-tal, supportive atmosphere that encourages the client to in­crease physical activity, decrease fat intake and reliance on medication use, establish a normal eating pattern in response to physiologic hunger, and address psychologic problems. Frequent, long-term ambulatory care follow-up coordinated by a case manager is essential for successful treatment.

HEALTH TEACHING

The most important features of client education focus on health-related behavior patterns. The dietitian counsels the client on a healthful eating pattern. The nurse provides sup­port and reinforces the importance of maintaining a healthful eating pattern. The physical therapist or exercise physiologist recommends an appropriate exercise program. A psychologist recommends cognitive restructuring approaches that help al­ter dysfunctional eating patterns.

HOME CARE MANAGEMENT

The overweight or obese client needs proper weighing de­vices and measuring utensils to follow the diet prescribed by the physician. No other home care preparation is needed.

 HEALTH CARE RESOURCES

The chances for success in a weight control program are en­hanced if additional support is available. The nurse provides the client with a list of available community resources, such as Weight Watchers, Overeaters Anonymous, Take Off Pounds Sensibly (TOPS), comprehensive interdisciplinary treatment programs, and a list of professionals that includes a registered dietitian, psychologist, and exercise physiologist who may provide frequent follow-up in an ambulatory care setting.

Evaluation: Outcomes

 The nurse evaluates the care of the client with obesity or overweight on the basis of the identified nursing diagnoses and collaborative problems. Expected outcomes include that the client:

·        Establishes a lasting, healthful dietary pattern that re­sults in permanent, sustained weight loss

·        Slowly increases the amount of physical exercise to aid in promoting weight loss

·        Incorporates daily exercise into lifestyle

·        Participates in usual daily activities