Practice nursing care for Clients with Liver Problems I
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.
Fig (A) Patient with alcoholic cirrhosis who shows ascites, an umbilical hernia, and wasting of muscle.
(B) After 2 years of abstinence and appropriate nutrition, the patient gained back muscle mass and his ascites improved.
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 from acute 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 venous blood, 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, with abnormally 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
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
COMMON NURSING DIAGNOSES AND COLLABORATIVE PROBLEMS
The most common nursing 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 withiormal 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
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
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
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
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.
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
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
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
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.
Assist the physician with tube placement. Before the gastric balloon is inflated, make sure that a chest x-ray film is obtained and is available immediately on tube insertion. Elevate the head of the bed when the tube is in place. Clearly label all lumina of the tamponade tube. Keep a pair of scissors at the bedside. Cut the tube and remove it immediately if signs of respiratory distress or airway obstruction occur.
Apply gentle tension to the tube by securing it to the face guard of a football helmet or by applying an overhead traction setup with a 1 -pound (0.45-kg) traction weight. Apply a cut gauze sponge around the tube under the client’s nose.
Insert a drainage tube into the esophagus, above the inflated balloon, if the tamponade tube does not have an esophageal drainage port. If an esophageal drainage port is available, maintain drain patency. Provide the client with frequent mouth care. Restrain the client’s hands loosely if necessary to prevent dislodgement of the tube.
Maintain the specified balloon pressures and volumes. (Esophageal balloon pressure is measured in millimeters of mercury; gastric balloon volume is measured in milliliters or cubic centimeters.) Release the pressure at specified intervals. (The client may experience substernal pressure when the esophageal balloon is inflated. This is an expected feeling.) Assess the client’s sudden report of back and upper abdominal pain. Monitor vital signs for a drop in blood pressure and an increase in the heart rate. Report these signs immediately.
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
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
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 is more than $600 million dollars per year.
• More than half of the liver transplants performed in the United States are for hepatitis C. The average first-year cost for 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 deaths due to chronic liver disease and 27,200 deaths due to hepatocellular carcinoma.
Implications for Nursing
Nurses are at high risk for getting hepatitis C an D
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
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?
Ø Could I have gotten this by a tattoo?
Ø Could my wife and children have hepatitis?
Ø 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.
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. 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
Ø Avoid all medications, including over-the-counter drugs, such as acetaminophen (Tylenol, Exdol*), unless prescribed by your physician.
Ø Avoid all alcohol.
Ø Rest frequently throughout the day, and get adequate sleep at night.
Ø Eat small, frequent meals with a high-carbohydrate, lowfat content.
Ø Avoid sexual intercourse until antibody testing results are negative.
Ø 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:
Ø Malnutrition
Ø Diabetes mellitus
Ø Obesity
Ø Pregnancy
Ø Prolonged total parenteral nutrition (TPN)
Ø 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:
Ø Right upper abdominal pain
Ø Ascites
Ø Edema
Ø Jaundice
Ø Fever
Ø 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 iature. 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.