Care of the Patient With a Gallbladder, Liver, Biliary Tract, or Exocrine Pancreatic Disorder

Rationale

The liver is a storehouse of many enzymes. Injury or diseases affecting the liver cause release of these intracellular enzymes into the bloodstream, and their levels become elevated. Some of these enzymes are also produced in other organs, and injury or disease affecting these organs will raise the serum level. Therefore, although elevation of these serum enzymes is found in pathologic liver conditions, the test is not specific for liver diseases alone.

Nursing Interventions

Provide information to the patient regarding blood draws and what test is being performed. Monitor the venipuncture site for bleeding.

Rationale

One way to assess the liver's functional status is to measure the products it synthesizes. One of these products is protein, especially albumin. When a dis­order or disease affects liver cells (i.e., hepatocytes), they lose their ability to synthesize albumin and the serum albumin level falls markedly. A low serum albumin level may also result from excessive loss of albumin into urine (as in nephrotic syndrome) or into third-space volumes (as in ascites), as well as in liver disease, increased capillary permeability, or protein-calorie malnutrition.

Nursing Interventions

Provide information to the patient regarding blood draws and what tests are being performed. Monitor the venipuncture site for bleeding.

Nursing Interventions

To prevent an allergic reaction, the nurse determines whether the patient is allergic to iodine because the dye typically used for this test is iodine-based. If the patient is not allergic to iodine, administer six tablets orally (e.g., iopanoic acid [Telepaque], iodalphionic acid [Priodax], or ipodate [Oragrafin]), one every 5 minutes, beginning after the evening meal. The patient is put on NPO status from midnight. The patient may be given a high-fat meal or beverage to stimulate emptying of the gallbladder after the test has begun. No other food or fluids are allowed until after the examination.

Nursing Interventions

During the preoperative phase ensure that the patient is not allergic to iodine. Preparation of the patient also includes maintaining NPO status after midnight and until the examination is completed. Administer a cleansing enema on the morning of the examination, if ordered.

Postoperatively, the patient is protected from sepsis by connecting the T-tube (if left in place) to a sterile closed-drainage system. If the T-tube is removed, cover the T-tube tract site with a sterile dressing to prevent bacteria from entering the ductal system.

Nursing Interventions

The patient is on NPO status from midnight prior to the test. If the patient has had recent barium contrast studies, request an order for laxatives because ultrasound cannot penetrate barium, and the study will not be adequate.

Nursing Interventions

Reassure the patient that exposure to radioactivity is minimal, because only a trace dose of the radioisotope is used. The patient is on NPO status from midnight until the examination is complete.

Nursing Interventions

After the health care provider has explained the procedure to the patient the nurse verifies that the patient has signed the consent form. Ensure that measurements of platelets, clotting or bleeding time, prothrombin time, and International Normalized Ratio (INR) have been ordered; report any abnormal values to the health care provider. After the procedure observe the patient for symptoms of bleeding. Monitor the patient's vital signs every 15 minutes (two times), then every 30 minutes (four times), and then every hour (four times). The nurse keeps the patient lying on the right side for at least 2 hours to splint the puncture site. In this position, the liver capsule (a connective tissue layer covering the liver) is compressed against the chest wall, decreasing the risk of hemorrhage or bile leak.

Some pain is common. When leakage involves a large quantity of blood or bile, the peritoneal reaction is great and the resulting pain severe. Assess the patient for pneumothorax (collapsed lung) caused by improper placement of the biopsy needle into the adjacent chest cavity or for bile peritonitis. Immediately report to the health care provider signs and symptoms of pneumothorax such as shortness of breath, change in respiratory and cardiac rate, or decreased breath sounds on the affected side.

Nursing Interventions

The patient is on NPO status from midnight before the test. Assure patients that they will not be exposed to a large amount of radioactivity, since only trace doses of isotopes are used.

Rationale

Ammonia is a by-product of protein metabolism. Most of the ammonia is made by bacteria acting on proteins in the intestine. By way of the portal vein, ammonia goes to the liver, where it is normally converted into urea and then excreted by the kidneys. When the patient has severe liver dysfunction or altered blood flow to the liver, ammonia cannot be catabolized, the serum ammonia level rises, and the blood urea nitrogen level decreases. The serum ammonia level is primarily used as an aid in diagnosing hepatic encephalopathy and hepatic coma. Elevated serum ammonia levels suggest liver dysfunction as the cause of these signs and symptoms.

Nursing Interventions

Notify the laboratory of any antibiotics the patient is currently taking. Certain broad-spectrum antibiotics such as neomycin can cause a decreased ammonia level, thus giving inaccurate test results.

Rationale

Hepatitis is an inflammation of the liver caused by viruses, bacteria, and noninfectious causes such as alcohol ingestion and drugs. Five viruses, designated A through E, can cause this disease. Hepatitis A, B, and C viruses are the most common hepatitis viruses. Hepatitis D virus is carried by the hepatitis B virus (HBV). Both hepatitis D and E viruses are seen less frequently in the United States than are the hepatitis A, B, or C viruses. The various types of hepatitis virus can be detected by their various antigen and antibody levels, and their different incubation periods must be considered.

Nursing Interventions

Use standard precautions and handle the serum specimen as if it were capable of transmitting viral hepatitis. Don gloves when handling any blood or body fluids, and wash hands carefully after handling equipment.

Rationale

The serum amylase test can aid in quickly diagnosing pancreatitis in its early stages. Damage to pancreatic cells (as in pancreatitis) or obstruction to the pancreatic ductal flow (as in pancreatic carcinoma) causes an outpouring of this enzyme into the intrapancreatic lymph system and the free peritoneum. Blood vessels draining the free peritoneum and absorbing the lymph pick up this excess amylase. An abnormal rise in the serum level of amylase occurs within 2 hours of the onset of pancreatic disease. Because amylase is rapidly cleared by the kidney, serum levels may return to normal within 36 hours. Persistent pancreatitis, duct obstruction, or pancreatic duct leak (e.g., pseudocysts) cause persistent elevated serum amylase levels.

Nursing Interventions

Note on the laboratory order whether the patient is receiving intravenous dextrose or any medications, since these can cause a false-negative result.

Rationale

Levels of amylase in the urine remain elevated for 7 to 10 days after the onset of pancreatitis. Urine amylase is particularly useful in detecting pancreatitis late in the disease course. This fact is important for diagnosing pancreatitis in patients who have had symptoms for 3 days or longer.

Nursing Interventions

Record the exact time at the beginning and end of the collection period. A 2-hour spot urine or 6-hour, 12-hour, or 24-hour collection can be performed, depending on the health care provider's order. The collection begins after the patient empties the bladder and discards that specimen. All subsequent urine is collected, including the voiding at the end of the collection period. Keep the specimen on ice or refrigerated until it is sent to the laboratory.

Rationale

Like serum amylase, serum lipase is elevated in acute pancreatitis and is a helpful complementary test because other disorders (e.g., mumps, cerebral trauma, and renal transplantation) may also cause an increase in serum amylase. Lipase appears in the bloodstream after damage to the pancreas. The lipase levels rise a little later than amylase levels (4 to 48 hours after the onset of pancreatitis), peak around 24 hours, and remain elevated for at least 14 days. Because lipase peaks later and remains elevated longer than amylase, it is more useful in the diagnosis of acute pancreatitis later in the course of the disease.

Nursing Interventions

Instruct the patient to remain on NPO status from midnight, except for water.

Nursing Interventions

Fluids and food are withheld for 8 hours before the examination. If an endoscopic ultrasound is being performed, the same interventions should be implemented as for an EGD (see Chapter 5). If the patient's abdomen is distended with gas or if the patient has had a recent barium examination, the study should be postponed, since gas and barium interfere with sound wave transmission.

Nursing Interventions

Fluids and food are withheld from midnight until the examination is complete; however, this test can be performed on an emergency basis on patients who have recently eaten. If possible, show the patient a picture of the machine and encourage the patient to verbalize fears because some patients suffer claustrophobia when enclosed in the machine.

Nursing Interventions

Withhold food and fluids for 8 hours before the examination, and obtain the patient's signature on a consent form. Assess prothrombin time and INR before the procedure. Tell patients that the test takes approximately 1 to 2 hours, during which time they must lie completely motionless on a hard x-ray table, which may be uncomfortable. After the procedure, keep the patient on NPO status until the gag reflex returns; assess for abdominal pain, tenderness, and guarding, which could be signs of perforation. Assess for signs and symptoms of pancreatitis (the most common ERCP complication), including increasingly intense abdominal pain, nausea, fever, chills, vomiting, and diminished or absent bowel sounds. Assess for signs of hypovolemic shock, including decreased blood pressure, increased pulse and respirations, shortness of breath, cool and clammy skin, and decreased urine output.

Clinical Manifestations

Clinical manifestations of cirrhosis of the liver differ, depending on the stage of the disease. In the early stages the liver is firm and therefore easier to palpate, and abdominal pain may be present because rapid enlargement produces tension on the organ's fibrous covering. Later stages of the disease are characterized by dyspepsia, changes in bowel habits, gradual weight loss, ascites, enlarged spleen, malaise, nausea, jaundice, ecchymoses, and spider telangiectases (small, dilated blood vessels with a bright red center point and spiderlike branches). Spider telangiectases occur on the nose, cheeks, upper trunk, neck, and shoulders. These later manifestations are the result of scarring of liver tissue that produces chronic failure of liver function and also fibrotic changes that cause obstruction of the portal circulation.

When enough cells of the liver become involved to interfere with its function and obstruct its circulation, the GI organs and the spleen become congested and cannot function properly. Anemia occurs because of the body's decreased ability to produce red blood cells (RBCs). The cirrhotic liver cannot absorb vitamin K or produce the clotting factors VII, IX, and X. These factors cause the patient with cirrhosis to develop bleeding tendencies.

Assessment

Subjective data in the early stages include the patient's description of flulike symptoms (loss of appetite, nausea and vomiting, general weakness, and fatigue), indigestion, abnormal bowel function (either constipation or diarrhea), flatulence, and abdominal discomfort. The anatomical area most commonly affected is in the epigastric region or the right upper quadrant of the abdomen.

Subjective data in the later stages typically include the same early-stage symptoms, but now more intense in the later stages. The patient may complain of dyspnea, pruritus, and severe fatigue that interfere with the ability to carry out routine activities. Pruritus results from an accumulation of bile salts under the skin, the result of jaundice.

Collection of objective data in the early stages includes observing low hemoglobin, fever, weight loss, and jaundice (yellow discoloration of the skin, mucous membranes, and sclerae of the eyes [scleral icterus], caused by greater than normal amounts of bilirubin in the serum). Collection of objective data in the later stages includes noting epistaxis, purpura, hematuria, spider angiomas (telangiectases), and bleeding gums. Late symptoms include ascites, hematologic disorders, splenic enlargement, and hemorrhage from esophageal varices or other distended GI veins. The patient may also appear mentally disoriented and display abnormal behaviors and speech patterns due to increased ammonia levels in the brain. Any prolonged interference with gas exchange leads to hypoxia, coma, and ultimately death.

Diagnostic Tests

Many diagnostic tests aid in the diagnosis of cirrhosis. Poor liver function may be manifested as abnormal electrolyte values; elevated serum bilirubin, AST, ALT, LDH, and GTT; decreased total protein and serum albumin; elevated ammonia; low blood glucose (hypoglycemia) from impaired gluconeogenesis; prolonged prothrombin time; increased INR; and decreased cholesterol levels. Visualization through ERCP (to detect common bile duct obstruction), esophagoscopy with barium esophagography to visualize esophageal varices, scans and biopsy of the liver, and ultrasonography are used to diagnose cirrhosis. Paracentesis (a procedure in which fluid is withdrawn from the abdominal cavity) relieves ascites and also provides fluid for laboratory examination.

Medical Management

When possible causes have been identified, the initial treatment is to eliminate those causes, decrease the buildup of fluids in the body, prevent further damage to the liver, and provide individual supportive care. Eliminating alcohol, hepatotoxins (e.g., acetaminophen [Tylenol]), or environmental exposure to harmful chemicals is essential to prevent further damage to the liver. Diet therapy is aimed at correcting malnutrition, promoting the regeneration of functional liver tissue, and compensating for the liver's inability to store vitamins, while avoiding fluid retention and hepatic encephalopathy. A diet that is well balanced, high in calories (2500 to 3000 calories/day), moderately high in protein (75 g of high-quality protein per day), low in fat, low in sodium (1000 to 2000 mg/day), and with additional vitamins and folic acid will usually meet the needs of the patient with cirrhosis and improve deficiencies. A protein-restricted diet may be prescribed for a patient recovering from an acute episode of hepatic encephalopathy.

Antiemetics may be prescribed to control nausea or vomiting. Monitor the patient closely for toxicity, which develops quickly when the poorly functioning liver cannot clear these drugs from the system. Diphenhydramine (Benadryl) or dimenhydrinate (Dramamine) may be given, whereas prochlorperazine maleate (Compazine), hydroxyzine pamoate (Vistaril), or hydroxyzine hydrochloride (Atarax) are contraindicated in severe liver dysfunction.

Later manifestations may be severe and result from liver failure and portal hypertension. Jaundice, peripheral edema, esophageal varices, hepatic encephalopathy, and ascites develop gradually (Figure 45-2).

Complications and treatment.

The severity of fluid retention from ascites and edema determines the treatment. Initially the patient is placed on bed rest with accurate monitoring of intake and output (I&O). Restrictions are placed on the amount of fluid (500 to 1000 mL/day) and sodium (1000 to 2000 mg/day). Diuretic therapy may be added if the diet does not control the ascites and edema. Spironolactone (Aldactone) at 300 to 1000 mg/day may be used to obtain the desired diuresis. Other diuretics may be added, including furosemide (Lasix) or hydrochlorothiazide (HydroDIURIL). Vitamin supplements include vitamin K, vitamin C, and folic acid. Salt-poor albumin may be administered in an attempt to restore plasma volume if the intravascular volume is decreased significantly. Complications of diuretic therapy include plasma volume deficit, decreased renal function, and electrolyte imbalance.

Another method of treatment for ascites and edema is the LeVeen continuous peritoneal jugular shunt (Figure 45-3). This procedure allows the continuous shunting of ascitic fluid from the abdominal cavity through a one-way, pressure-sensitive valve into a silicone tube that empties into the superior vena cava. Patients with this shunt are monitored for complications, which include congestive heart failure, leakage of ascitic fluid, infection at the insertion sites, peritonitis, septicemia, and shunt thrombosis.

Paracentesis (see Chapter 15), in which fluid is removed from the abdominal cavity by either gravity or vacuum, provides temporary relief from ascites. It is imperative that patients urinate immediately before the procedure to prevent puncture of the bladder. The patient should sit on the side of the bed or be placed in a high Fowler's position. An incision is made in the skin, and a hollow trocar, cannula, or catheter is passed through the incision and into the cavity. The fluid is removed over a period of 30 to 90 minutes to prevent sudden changes in blood pressure, which could lead to syncope. Monitor the patient closely for signs of hypovolemia and electrolyte imbalances. Apply a dressing over the insertion site, and observe for bleeding and drainage.

Esophageal varices (a complex of longitudinal, tortuous veins at the lower end of the esophagus) enlarge and become edematous as the result of portal hypertension. They are susceptible to ulceration and hemorrhage; avoiding this is a main goal of treatment. For patients who have not bled from esophageal varices, prophylactic treatment with nonselective beta blockers (e.g., propranolol [Inderal]) has been shown to reduce the risk of bleeding and bleeding-related deaths. Varices can rupture as a result of anything that increases abdominal venous pressure, such as coughing, sneezing, vomiting, or the Valsalva maneuver. Rupture may occur slowly over several days or suddenly and without pain. An endoscopy may be performed to identify varices or to rule out bleeding from other sources. Endoscopic therapies include sclerotherapy (the injection of chemicals used to cause inflammation, followed by fibrosis and destruction of the vessels causing the bleeding) and ligation of varices.

Therapeutic management of a ruptured esophageal varix is a medical emergency. The patient's airway must be maintained, the bleeding varix controlled, and IV lines established for fluids and blood replacement as needed. The hormone vasopressin (VP), administered intravenously or directly into the superior vena cava, is used to decrease or stop the hemorrhaging. VP produces vasoconstriction of the vessels, decreases portal blood flow, and decreases portal hypertension. Current drug therapy in some institutions is a combination of VP and nitroglycerin (NTG). NTG reduces the detrimental effects of VP, which include decreased coronary blood flow and increased blood pressure. VP should be avoided or used cautiously in the older adult because of the risk of cardiac ischemia (i.e., a restriction in blood supply to the heart). If the VP drip does not stop or control bleeding, a Sengstaken-Blakemore tube with openings at the tip may be inserted. This triple-lumen tube has a lumen for inflating the esophageal balloon, one for inflating the gastric balloon, and one for gastric lavage (Figure 45-4). The tube is passed through the nose, and the balloon in the stomach, the one in the esophagus, or both are inflated to press against the bleeding vessels and control the hemorrhage. The gastric aspiration is attached to low, intermittent suction. When either balloon is inflated, a Levin tube is passed into the esophagus through the mouth and attached to low suction to drain the saliva that cannot drain into the stomach. The balloon must be deflated periodically to prevent necrosis. Give the patient nothing by mouth and elevate the head of the bed 30 to 45 degrees to help prevent aspiration of stomach contents and help the patient breathe.

Gastric lavage is performed to remove any swallowed blood from the stomach. Some facilities use iced isotonic saline solutions for the lavage to facilitate vasoconstriction. Endoscopic sclerotherapy may also be used to control the bleeding.

Other methods used to treat bleeding esophageal varices include band ligation. In this procedure an endoscope is passed into the esophagus and elastic bands are placed to tie off bleeding vessels. This procedure is also performed to prevent esophageal varices from bleeding. Band ligation has a small risk of causing scarring of the esophagus. The medication octreotide (Sandostatin) is sometimes used in combination with band ligation when treating bleeding varices. Octreotide (Sandostatin) slows the flow of blood from internal organs to the portal vein. This helps to reduce pressure in the portal vein and is administered for 5 days following an esophageal hemorrhage (Mayo Clinic, 2013).

Patients suffering from portal hypertension and esophageal varices may benefit from surgical shunting procedures that divert blood from the portal system to the venous system. The portacaval shunt diverts blood from the portal vein to the inferior vena cava. The splenorenal shunt requires the removal of the spleen, and the splenic vein is anastomosed to the left renal vein. The mesocaval shunt involves anastomosis of the superior mesenteric vein to the inferior vena cava. These procedures are associated with a high mortality rate. They may be performed in an emergency to control acute esophageal varix bleeding or in a therapeutic situation when a patient has already bled. Complications of surgical shunting procedures are hepatic encephalopathy, GI bleeding, ascites, and liver failure.

Care of the patient who has hemorrhaged from an esophageal varix includes maintenance of oxygen content levels within the blood and administration of fresh frozen plasma and packed RBCs, vitamin K (AquaMEPHYTON), histamine (H₂) receptor blockers such as cimetidine (Tagamet), and electrolyte replacements as needed without fluid overload. Ammonia buildup is avoided with the use of cathartics (e.g., lactulose [Chronulac]) and neomycin. Preventing ammonia buildup keeps hepatic encephalopathy from occurring.

Hepatic encephalopathy is a type of brain damage caused by liver disease and consequent ammonia intoxication. It is thought to result from a damaged liver being unable to metabolize substances that can be toxic to the brain, such as ammonia. The patient's signs and symptoms progress from inappropriate behavior, disorientation, asterixis, and twitching of the extremities to stupor and coma. Asterixis is a hand-flapping tremor in which the patient stretches out an arm and hyperextends the wrist with the fingers separated, relaxed, and extended. A rapid, irregular flexion and extension (flapping) of the wrist occurs in the patient who is acutely ill. Treatment of the patient with hepatic encephalopathy consists of supportive care to prevent further damage to the liver.

In the past, a low-protein diet was often prescribed for patients with cirrhosis of the liver. Restricting protein intake was thought to decrease the amount of ammonia produced in the intestine, thus preventing hepatic encephalopathy. It is now believed that protein should not be restricted because these patients often have existing malnutrition. On occasion, protein is decreased in the diet of a patient with an exacerbation of hepatic encephalopathy. In addition, carbohydrates are necessary for the patient with cirrhosis. To provide extra calories, a protein-free supplement such as glucose polymer (Polycose) can be used during an exacerbation of hepatic encephalopathy. Other supplemental enteral formulas containing amino acid and calorie supplementation may be given to the patient who has protein-calorie malnutrition (Lewis et al., 2011).

Teach the patient to avoid potentially hepatotoxic over-the-counter drugs such as acetaminophen and to abstain from alcohol. Medications may be given to cleanse the bowel and help decrease the serum ammonia level. Lactulose decreases the bowel's pH from 7 to 5, thus decreasing the production of ammonia by bacteria within the bowel. Lactulose may be administered orally, as a retention enema, or via nasogastric (NG) tube. It also functions as a cathartic. The lactulose traps ammonia in the gut, and the drug's laxative effect expels the ammonia from the colon. Antibiotics such as neomycin, which are poorly absorbed from the GI tract, are given orally or rectally. They reduce the bacterial flora of the colon. Bacterial action on protein in feces results in ammonia production. Because neomycin may cause renal toxicity and hearing impairment, lactulose is frequently preferred.

Nursing Interventions and Patient Teaching

Check vital signs every 4 hours, or more often if evidence of hemorrhage is present. Observe the patient for GI hemorrhage as evidenced by hematemesis, melena, anxiety, and restlessness.

Most patients require a well-balanced, moderate, high-protein, high-carbohydrate diet with adequate vitamins. With impending liver failure, protein and fluids are restricted. Sodium restriction is frequently necessary, which can make providing a palatable diet more difficult. Provide frequent oral hygiene and a pleasant environment to help the patient increase food intake.

A major nursing focus for many patients is to help them deal with alcoholism. This requires establishing trust that the health team is interested in the patient's well-being. Patients must admit that they have a drinking problem before they can be helped. Provide information regarding community support programs, such as Alcoholics Anonymous, for help with alcohol abuse.

Because of pruritus, malnutrition, and edema, the patient with cirrhosis is prone to skin lesions and pressure sores. Initiate preventive nursing interventions to avoid impairment of skin integrity, such as an alternating pressure air mattress, frequent turning, and back rubs. Apply soothing lotion to relieve pruritus.

Observe the patient's mental status and report changes such as disorientation, headache, or lethargy. Assist in activities of daily living (ADLs) as needed to promote good hygiene while allowing the patient to conserve energy. Observe for edema by measuring ankles daily, and observe for ascites by measuring abdominal girth. Record accurate I&O and daily weight. Nursing intervention with concern and warmth regardless of physical changes is essential in helping the patient maintain self-esteem.

Refer to Nursing Care Plan 45-1 for a sample nursing care plan for the patient with cirrhosis of the liver. The patient with cirrhosis must understand the need for getting adequate rest and avoiding infections. Plan activity around complete bed rest until strength is regained. Turning the patient at least every 2 hours and providing range-of-motion exercises will help avoid infection and prevent thrombophlebitis. Instruct the patient to use a soft-bristled toothbrush, use an electric razor, blow the nose cautiously, and avoid straining at stools to prevent bleeding as a result of a lack of vitamin K and certain clotting factors. Avoid soap, perfumed lotion, and rubbing alcohol because they will further dry the skin. For pruritus and dry skin, administer diphenhydramine (Benadryl). Explain the relationship of the therapeutic diet to the diagnosis and the liver's ability to function.

Help the patient and family identify community resources for home health care and alcohol rehabilitation to assist them in dealing with problems that arise after discharge. Because of the seriousness of the disease, the patient and the family need understanding and support throughout the treatment (see Home Care Considerations box).

Clinical Manifestations and Diagnostic Tests

Diagnosing carcinoma of the liver is difficult. In its early stages many of the clinical manifestations (e.g., hepatomegaly, weight loss, peripheral edema, ascites, portal hypertension) are similar to those of cirrhosis of the liver. Other common manifestations include dull abdominal pain in the epigastric or right upper quadrant region, jaundice, anorexia, nausea and vomiting, and extreme weakness. Palpation may reveal an enlarged, nodular liver. Patients frequently have pulmonary emboli. Tests to assist in the diagnosis are a liver scan, ultrasound, CT scan, magnetic resonance imaging, hepatic arteriography, ERCP, and needle liver biopsy. The test for alpha-fetoprotein (AFP) may be positive in hepatocellular carcinoma. AFP helps distinguish primary cancer from metastatic cancer (ACS, 2013a).

Medical Management and Nursing Interventions

Treatment of cancer of the liver is largely palliative. Surgical excision (lobectomy) is sometimes performed if the tumor is localized to one portion of the liver. Only a small percentage of patients have surgically resectable disease; usually the cancer is too advanced for surgery when it is detected. Surgical excision or transplantation offers the only chance for cure. Medical management is similar to that for cirrhosis of the liver. Chemotherapy may be used, but the response is usually poor. Portal vein or hepatic artery perfusion with chemotherapy agents such as 5-fluorouracil (5-FU) may be attempted.

Nursing interventions for the patient with liver carcinoma focus on keeping the patient as comfortable as possible. Because the problems are the same as with advanced liver disease, the nursing interventions discussed for cirrhosis of the liver apply.

Prognosis

The 5-year survival rate for liver cancer depends on the extent of the cancer when it is diagnosed. For early-stage (i.e., small) tumors that can be resected surgically the 5-year survival rate is 50% if the patient has no other serious health problems. Unfortunately, since many liver cancers are not discovered until late in the disease process the 5-year survival rate for all stages combined is less than 15% (ACS, 2013a).

Clinical Manifestations

The clinical manifestations for viral hepatitis vary greatly; some patients are asymptomatic, whereas others develop hepatic failure or hepatic encepha­lopathy.

Assessment

Subjective data include patients' reports of general malaise, aching muscles, photophobia, lassitude, headaches, and chills. Abdominal pain, dyspepsia, nausea, diarrhea, and constipation are reported also. The patient may complain of pruritus from the buildup of bile salts in the skin. The patient complains of tenderness in the liver and remains fatigued for several weeks.

Collection of objective data includes observing hepatomegaly, enlarged lymph nodes, and weight loss. Jaundice appears because of the damaged liver's inability to metabolize bilirubin; the resultant signs are yellowish skin; discoloration of the sclera (scleral icterus) and mucous membranes; dark, tea-colored urine; and clay-colored stools. Relapses are common in the convalescent stage.

Diagnostic Tests

Changes in the liver caused by viral hepatitis result in elevated direct bilirubin, GGT, AST, ALT, LDH, and alkaline phosphatase levels; a prolonged prothrombin time and increased INR; and, in severe hepatitis, decreased serum albumin. Leukopenia (low white blood cell count) is common in these patients, followed by lymphocytosis (high white blood cell count). Hypoglycemia is present in approximately 50% of patients with hepatitis. Serum is examined for the presence of antigens associated with hepatitis A, B, C, D, or G. A CT scan of the abdomen reveals hepatomegaly.

Medical Management

Providing supportive therapy for existing signs and symptoms and preventing transmission of the disease are important aspects of treatment of the patient with viral hepatitis. Hospitalization is an option for patients whose bilirubin concentrations in the blood are more than 10 mg/dL and for those with a prolonged prothrombin time and increased INR, but usually patients are cared for at home. Bed rest for several weeks is commonly prescribed.

Drug therapy for chronic hepatitis B focuses on decreasing the viral load, decreasing the rate of disease progression, and monitoring for detection of drug-resistant HBV. At present, several drugs are useful in suppressing viral activity and decreasing viral load in patients with HBV. The percentage of patients seroconverting (developing antibodies against the virus) remains relatively low. Lamivudine (Epivir, 3TC), interferon-beta, and adefovir dipivoxil (Hepsera) are three drugs being used in the treatment of chronic hepatitis B. Telbivudine (Tyzeka) is a new drug used to treat chronic HBV infection. Telbivudine has been shown to decrease the viral load more effectively than lamivudine and adefovir (www.cdc.gov/hepatitis/HBV/HBVfaq.htm#treatment). Patients should be informed of the possibility of serious or life-threatening liver damage. Lactic acidosis (buildup of acid in the blood) can occur with the use of some of these newer drugs used to treat HBV (National Library of Medicine [NLM], 2010).

In chronic hepatitis C, drug therapy is also directed at reducing the viral load, decreasing progression of the disease, and promoting seroconversion. Treatment options for HCV are interferon alfa-2b (Intron A), ribavirin (Rebetol), and pegylated interferon alfa-2a (Pegasys). This combination therapy eradicates the virus more effectively than monotherapy. Another treatment option is liver transplantation. In fact, half of all liver recipients are HCV positive. Most transplanted livers eventually become infected with HCV, but recipients can increase both quantity and quality of life by avoiding risky behaviors (CDC, 2012).

The patient is not allowed alcohol for at least 1 year and may need supportive care from the community to comply. Most patients tolerate small, frequent meals of a low-fat, high-carbohydrate diet. If the patient is dehydrated, IV fluids are given with addition of vitamin C for healing, vitamin B complex to assist the damaged liver's inability to absorb fat-soluble vitamins, and vitamin K to combat prolonged coagulation time. Avoid all unnecessary medications, particularly sedatives.

Give gamma globulin or immune serum globulin as soon as possible to people who have been in direct contact with a person with hepatitis A during the infectious period (2 weeks before and 1 week after onset of symptoms). A dose of 0.02 mL/kg of body weight, given intramuscularly, is effective in preventing hepatitis A in 80% to 90% of cases. At present, three vaccines are used to prevent hepatitis A: Havrix, Vaqta, and Avaxim.

Primary immunization consists of a single dose administered intramuscularly in the deltoid muscle. A booster is recommended between 6 and 12 months after the primary dose to ensure adequate antibody titers and long-term protection. However, primary immunization provides immunity within 30 days after a single dose.

Until routine vaccination of children is feasible, people who are at risk for infection should be vaccinated for hepatitis A. This includes people traveling to countries where hepatitis A is endemic; sexually active homosexual and bisexual men; patients with chronic liver disease; injecting drug users; and people at risk for occupational infection, such as those who work with hepatitis A in research laboratory settings.

Individuals who have been exposed to HBV via a needle puncture or sexual contact should be protected with hepatitis B immune globulin. A dose is administered intramuscularly as quickly after exposure as possible. This dose is repeated 1 month later. People identified as being at high risk for developing hepatitis B should be vaccinated if they are not already immune. These people include the following:

The CDC Advisory Committee on Immunization Practices (2009) recommends making hepatitis B vaccine a part of routine vaccination schedules for all newborns and adolescents. The protection program consists of three vaccinations: an initial vaccination, a vaccination 1 month later, and a third vaccination 6 months after the first injection. The hepatitis B vaccine has been shown to provide protection for 3 to 5 years in approximately 90% of the people treated. It is hoped that universal vaccination will lead to eventual prevention and control of hepatitis B.

Hepatitis B, C, D, and G are spread through blood transfusions. The blood used should be screened for elevated ALT and anti–hepatitis B core, and for anti–hepatitis C, anti–hepatitis D, and anti–hepatitis G antigens.

Nursing Interventions and Patient Teaching

The patient who has a liver transplant requires competent and highly skilled nursing interventions, in either an ICU or another specialized unit. Postoperative nursing care includes assessing neurologic status; monitoring for signs of hemorrhage; preventing pulmonary complications; monitoring drainage, electrolyte levels, and urinary output; and monitoring for signs and symptoms of infection and rejection. Common respiratory problems include pneumonia, atelectasis (collapsed lung), and pleural effusions. Have the patient use measures such as coughing, deep breathing, incentive spirometry, and repositioning to prevent these complications. Measure and record drainage from the Jackson-Pratt drain, NG tube suctioning, and T-tube, and note the color and consistency of drainage. A critical aspect of nursing interventions after liver transplantation is monitoring for infection. The first 2 months after the surgery are critical. Infection can be viral, fungal, or bacterial. Fever may be the only sign of infection. Emotional support and teaching the patient and family are essential.

The care of the patient with viral hepatitis includes ensuring rest, maintaining adequate nutrition, providing adequate fluids, and caring for the skin. The care of the patient with hepatitis continues over time, and support and patient education are necessary throughout the entire illness.

Preventing transmission of the disease is of primary importance in caring for the patient with viral hepatitis. The patient, family, and health care providers must be knowledgeable about routes of transmission of the virus and take steps to avoid such transmission. Proper personal hygiene and good sanitation, as well as hepatitis A vaccination, will help prevent the spread of hepatitis A. Give patients a thorough explanation of the reasons for the precautions, and instruct them in the proper handling of their own secretions and body wastes and in thorough methods of hand hygiene. Wear gown and gloves when handling excreta, giving enemas, taking rectal temperatures, handling food waste, handling needles, disposing of urine, or carrying out any other procedure or hygiene measure that involves direct contact with the patient's body fluids.

Not all patients know they are infected with hepatitis, so following standard precautions with all patients prevents the spread of all blood-borne pathogenic diseases. Health care personnel should always take the utmost care in handling syringes, needles, and other instruments that are contaminated with the patient's serum. Maintaining standard precautions while exposed to blood and body fluids such as saliva, semen, and vaginal secretions is essential to prevent the transmission of hepatitis B. Appropriate transmission-based precautions should be followed as designated by facility policy. Use enteric precautions for 7 days after the onset of hepatitis A. Use standard precautions for all patients.

Nursing diagnoses and interventions for the patient with hepatitis include but are not limited to the following.

For the patient with viral hepatitis being cared for at home, teach the family necessary precautions. Patients should avoid sexual activity during the acute stage of hepatitis B, C, and D. Sexual precautions should be taken, and needles and razors should not be shared. Patients with hepatitis A must wash their hands thoroughly after toileting, must disinfect feces-soiled articles (boil for 1 minute), and must not prepare foods for others while symptomatic. If possible, the patient should use separate bathroom facilities. Personal care items and drinking glasses should not be shared. The patient's clothes should be laundered separately in hot water. Contaminated items should be disposed of properly. Sexual intercourse should be avoided while in the acute stage of hepatitis A.

Inform the patient and family about signs and symptoms associated with hepatitis, including light-colored stools, dark-colored urine, jaundice, fever, GI disturbances, unusual bleeding that might be indicative of a prolonged prothrombin time and increased INR, and tenderness or pain in the abdomen. The danger of alcohol use and its effect on the liver should be clearly understood.

Prognosis

The prognosis for the patient with hepatitis differs, depending on the causative agent. Recovery from hepatitis A is high, since the virus does not remain in the body after the infection has resolved. Within 3 months after diagnosis over 85% recover and nearly all recover within 6 months. The mortality rate for hepatitis A is 0.5% (CDC, n.d., National Institutes of Health, n.d.). The acute stage of the illness typically lasts up to 3 weeks, and it is usually 4 to 6 months before the liver returns to normal function. A small percentage of patients will develop chronic hepatitis and cirrhosis as a result of hepatitis B infection. Patients who do develop chronic hepatitis are at a higher risk for liver cancer. Approximately 1 in 100 people with hepatitis B die. Hepatitis C often progresses to chronic hepatitis. Approximately 75% to 85% of patients who acquire HCV go on to develop chronic infection. Cirrhosis develops in 5% to 20% of those infected. One to five percent of patients with hepatitis C will die from the disease (CDC, n.d., National Institutes of Health, n.d.). The prognosis for patients with chronic hepatitis C infection has greatly increased the demand for liver transplants. The acute phase of hepatitis D typically improves within 2 to 3 weeks and liver enzymes return to normal within 16 weeks. Chronic hepatitis develops in about 10% of patients with hepatitis D. Almost all patients with hepatitis E recover completely. Hepatitis E has a 10% to 30% mortality rate in pregnant women. The mortality rate in all others with the disease is about 1% (CDC, n.d., National Institutes of Health, n.d.). Hepatitis G infections frequently coexist with other hepatitis infections, such as hepatitis C. However, most hepatitis G infections are not associated with chronic hepatitis; thus the association of hepatitis G virus with liver disease is, at this time, uncertain.

Recovery from acute toxic hepatitis is rapid if the hepatotoxin is identified early and removed or if exposure to the agent has been limited. However, the prognosis is poor if the period between exposure and the onset of signs and symptoms is prolonged, since there are no effective antidotes.

Etiology and Pathophysiology

If the body is not successful in destroying bacteria, the bacterial toxins attack neighboring liver cells, and the necrotic tissue produced serves as a protective wall for the organism. Meanwhile, leukocytes migrate into the infected area. The result is an abscess: a cavity full of a liquid containing living and dead leukocytes and bacteria. Pyogenic (pus-producing) abscesses of this type may be single or multiple. Common sources of liver abscess include abdominal infections such as appendicitis, diverticulitis, and perforated colon. Other causes include any infection in the blood or bile ducts, and trauma to the liver.

Clinical Manifestations

Patients with liver abscess often present with vague signs and symptoms. Fever accompanied by chills, abdominal pain, and tenderness in the right upper quadrant of the abdomen are common complaints. Unintentional weight loss, jaundice, and weakness are additional symptoms that the patient experiences (University of Maryland Medical Center, 2013).

Assessment

Subjective data are related to the infection and to the inability of the liver to function normally. Symptoms include chills, complaints of dull abdominal pain, abdominal tenderness, and discomfort.

Objective data are also related to the infection and impaired function of the liver. Signs of liver abscess include fever, hepatomegaly, jaundice, and anemia. Clay-colored stools and dark urine are also commonly present because of the decreased amount of bile being excreted.

Diagnostic Tests

The diagnosis is established by demonstrating a space-occupying lesion in the liver radiographically (radiograph, ultrasound, CT, and liver scan). Liver biopsy may be performed to determine the presence of an abscess and a culture may be initiated to determine the infective agent. Common laboratory testing that aids in the diagnosis include bilirubin levels, liver enzymes, blood cultures for bacteria, and a complete blood count (CBC). Amebic liver abscess (caused by a microscopic, single-celled parasite) can also be confirmed by serologic examination (in which ameba-specific antibodies are detected in the patient's serum) (University of Maryland Medical Center, 2013).

Medical Management

Usually liver abscesses are managed by medical therapy. Treatment includes IV antibiotic therapy that is specific to the organism identified. Antibiotic therapy is often continued for 4 to 6 weeks.

Percutaneous (performed through the skin) drainage of a liver abscess is reserved for patients who do not respond to medical therapy or are at high risk for rupture. Open surgical drainage has been the standard in patients whose liver abscesses have ruptured into the peritoneal space, but some of these patients are now being managed with percutaneous drainage. All patients require a full course of antibiotic therapy.

Nursing Interventions and Patient Teaching

Continuous monitoring and supportive care are indicated because of the seriousness of the patient's condition. Monitoring objective and subjective symptoms is important. Notify the health care provider if signs and symptoms increase in severity.

The patient's response to drug therapy is determined by a decrease in fever, tenderness and rigidity of the abdomen, chills, and discomfort. If percutaneous or open surgical drainage is instituted, observe the drainage for amount, color, and consistency.

Nursing diagnoses and interventions for the patient with a liver abscess include but are not limited to the following:

In addition to the relationship of infection and nutrition, teach preoperative and postoperative procedures if the patient requires percutaneous or open surgical drainage. A thorough explanation and assessment for the patient's understanding are necessary. The seriously ill patient becomes less anxious as the knowledge base increases and the patient feels more in control of the situation.

Prognosis

The prognosis for patients with liver abscesses was very poor in the past, with an extremely high mortality rate. Sepsis was commonly the cause of death. The prognosis today is much improved because of advanced diagnostic tests, including CT and liver scans, and aggressive medical and nursing interventions.

Clinical Manifestations

The condition may be acute, with a sudden onset of indigestion; nausea and vomiting; and severe, colicky pain in the right upper quadrant of the abdomen. The pain may be referred to the right shoulder and scapula. Pain due to cholecystitis or cholelithiasis is sometimes mistaken for a cardiac problem because of the pain that is felt in the epigastric region and radiating to the back. If the condition is chronic, the patient usually has had several milder attacks of pain and a history of fat intolerance. When gallstones move through the biliary ducts the patient often complains of pain being intensified.

Assessment

Subjective data include complaints of indigestion after eating foods high in fat. The pain of acute cholecystitis is abrupt in onset, reaches peak intensity quickly, and remains at that level for 2 to 4 hours. It localizes in the right upper quadrant epigastric region. The pain radiates around the mid-torso to the right scapular area. Anorexia, nausea, vomiting, and flatulence (excess formation of gases in the stomach or intestine) are also noted. This pain is caused by the gallbladder contracting in an attempt to secrete bile for fat digestion. Patients may experience increased heart and respiratory rates and become diaphoretic (sweaty), leading them to think they are having a heart attack. These symptoms are decreased or absent in patients with chronic cholecystitis.

Objective data include a low-grade fever, increased pulse and respirations, nausea, vomiting, an elevated leukocyte count, mild jaundice, stools that contain fat (steatorrhea), and clay-colored stools caused by a lack of bile in the intestinal tract. The urine may be dark amber to tea colored and contain urobilinogen as the kidneys try to remove excess bilirubin from the bloodstream.

Diagnostic Tests

A number of diagnostic studies are performed to confirm a diagnosis of cholecystitis and cholelithiasis. Fecal studies, serum bilirubin tests, ultrasound of the gallbladder and biliary system, a HIDA scan, and an OCG may be done. Ultrasound of the gallbladder is highly accurate in diagnosing cholelithiasis. HIDA scanning is helpful in assessing the patency of the cystic and common bile ducts as well as the ability of the gallbladder to function efficiently. Operative cholangiography is a procedure in which the common bile duct is directly injected with radiopaque dye. This is frequently done at the time of gallbladder surgery.

Medical Management

If the attack of cholelithiasis is mild, the patient is treated conservatively. Bed rest is prescribed, an NG tube is inserted and connected to low suction, and the patient is placed on NPO status. This allows the GI tract, including the gallbladder, to rest. IV fluids are given to rehydrate the patient and to replace drainage from the NG tube.

Antispasmodic and analgesic drugs may be given to decrease pain. Meperidine (Demerol) and ketorolac (Toradol) are commonly used for pain management. An antispasmodic such as dicyclomine (Bentyl) may be used to decrease the incidence of spasms of the sphincter of Oddi (which controls the flow of pancreatic juices and bile into the duodenum). Morphine is generally not used for pain management since it often increases the tone of the sphincter of Oddi. Antibiotics may be given (1) prophylactically to prevent infection; (2) to treat an existing infection; and (3) after perforation, should it occur. A diet that is low in fat and cholesterol may be prescribed. Avoidance of spicy foods is also suggested (Steel, 2011) (see Complementary and Alternative Therapies box).

Surgical intervention.

The treatment of choice is cholecystectomy (removal of the gallbladder) with ligation of the cystic duct, vein, and artery. A laparoscopic cholecystectomy and open abdominal cholecystectomy are the two surgical procedures (see Figure 45-6 for stone retrieval). A Jackson-Pratt, Penrose, or Davol drain (which promotes drainage and prevents pressure and fluid accumulation under the diaphragm) may be inserted if an open cholecystectomy is performed. If the stones are in the common bile duct and edema is present, a biliary drainage tube, or T-tube, is inserted to keep the duct open and allow drainage of the bile until the edema resolves. The short end of the tube is placed in the common bile duct, and the longer end is brought to the surface through a stab wound (Figure 45-7). The long end is attached to a closed drainage system (bile bag) that is placed below the level of the common bile duct.

The T-tube also provides a route for postoperative cholangiography if desired (T-tube cholangiogram) to assess the patency of the common bile duct. The T-tube is removed 24 hours after the cholangiogram if the edema is resolved and the common bile duct appears normal. The T-tube is removed by cutting the anchoring stitches and pulling the tube out. The small opening is covered with an adhesive bandage or gauze dressing and heals on its own within a few days. The 24-hour period allows the dye to drain out of the common bile duct. If the edema does not resolve in this time, the patient may be discharged with the T-tube in place.

The most common treatment for cholecystitis and cholelithiasis is done by an endoscopic technique called laparoscopic cholecystectomy, in which a laser or cautery is used to remove the gallbladder. This procedure replaces the open surgical procedure 80% to 85% of the time. It involves removing the gallbladder through one of four small punctures in the abdomen (a comparatively minor procedure). During surgery, the abdominal cavity is inflated with 3 to 4 L of carbon dioxide to improve visibility. A laparoscope, which has a camera attached, is inserted into the abdomen. The surgeon removes the deflated gallbladder through the laparoscope. If the organ contains so much bile or gallstones that it cannot be collapsed, its contents will be aspirated first. Laparoscopic cholecystectomy offers several advantages over the common open abdominal cholecystectomy, including the following:

• It is less invasive (and thus there is less chance of wound infection or respiratory impairment) and has a shorter healing time and a shorter recuperative time.

• There is no unsightly scar.

• There is less pain and thus more rapid return to normal activities.

When a medical history, physical examination, and blood studies are complete, an ultrasound is done to locate gallstones and detect any dilation of the hepatic bile ducts. If choledocholithiasis (stones in the common bile duct) is confirmed, a sphincterotomy and stone extraction (see Figure 45-6) are performed before laparoscopic surgery.

It is important to obtain informed consent for endoscopic and open cholecystectomy in case converting from one procedure to the other is necessary. The conversion may be necessary if an extensive adhesion, gallstones within the common bile duct, unusual vascular or ductal anatomy, unsuspected pathologic condition of the abdomen, or excessive bleeding complicates the endoscopic procedure.

Nursing Interventions and Patient Teaching

Nursing interventions begin with careful assessment of the characteristics of pain (if it is present) and any signs of jaundice of the skin, sclera, and mucous membranes. Observe the patient's urine and stool for alterations in the presence of bilirubin.

When the patient is treated conservatively, nursing interventions center on keeping the patient comfortable by carefully administering the medications prescribed and monitoring the patient's response to the medications. The patient is kept on NPO status or on clear liquids. Administer antiemetics if nausea is present. Observe IV infusions for patency, correct rates, and entry sites that are free from erythema and edema. Measure I&O and describe carefully.

Preoperative care includes teaching the patient to turn, cough, and deep-breathe and to use an incentive spirometer to facilitate air movement in and out of the lungs to prevent pneumonia and atelectasis. To enable the patient to follow postoperative instructions more easily, teach him or her how to splint the abdomen with the hands, small pillow, or rolled bath blanket before attempting a cough; practice repositioning in the hospital bed; and assume a sitting position from a standing or lying position. If an open cholecystectomy is anticipated, explaining the IV tubing and urinary catheter and their functions will help relieve patient anxiety. The patient should be familiar with any medications that may be used to relieve pain and nausea and should understand that vitamin K and antibiotics may be given preoperatively to prevent hemorrhage and infection.

Postoperative care for open cholecystectomy includes monitoring vital signs and observing dressings frequently and carefully for exudate or hemorrhage. The dressings usually require reinforcement at the drain site. Place the patient in a semi-Fowler's position to facilitate drainage. Monitor the Jackson-Pratt, Penrose, or Davol drain for patency. Notify the surgeon if the drainage is excessive, contains bile, or is bright red.

The patient needs encouragement to perform deep breathing and coughing, and to use an incentive spirometer, because of the location of the incision. Provide analgesics frequently in the early postoperative period to facilitate movement and deep breathing. Help the patient to dangle (i.e., sit up with the legs hanging over the side of the bed) the night of surgery and ambulate the first postoperative day. Monitor the patient's neurologic status by checking ability to be aroused easily, orientation to the environment and family, and ability to move extremities equally on command.

Maintain fluid balance with IV therapy; potassium is usually added to compensate for loss from surgery. Check the health care provider's order before giving ice or clear liquids to the patient, and allow the patient to rinse the mouth frequently.

The nurse is responsible for the care of the T-tube if one is placed. The drainage bag for the T-tube is placed below the level of the common bile duct to prevent the reflux of bile. Position the bag so the tube is not kinked and bile can drain from the liver. Frequently check the position of the bag and tube and the color and amount of exudate during the first 24 hours and record the results. Place a gauze roll under the tube, anchoring it to the patient's abdomen and preventing tension and pull on the tube from the weight of the bag. The T-tube drains as much as 500 mL during the first 24 hours. The amount should decrease as the edema resolves and bile begins flowing through the common bile duct. Be careful not to dislodge the T-tube when changing the patient's dressings, as prescribed by the health care provider.

After oral intake is resumed, the health care provider may order the T-tube clamped for 1 to 2 hours before meals and unclamped 1 to 2 hours after the patient eats, to aid in the digestion of fat. While the T-tube is clamped, the patient may show signs of distress, including abdominal pain, nausea, vomiting, light brown urine, and clay-colored stools. If distress occurs, unclamp the tube immediately. Increase the time that the T-tube remains clamped as the patient tolerates the procedure. The tube may be left in place for as long as 10 days. The health care provider removes the tube when the common bile duct is patent for drainage of bile.

Check bowel sounds every 8 hours for the return of peristalsis by auscultating the abdomen. The nurse will also ask the patient if he or she is passing flatus. A clear liquid diet is usually ordered immediately or within the first 24 hours postoperatively and increased as tolerated. When solid food is started, it will usually be low in fat. Flatulence or nausea after eating certain foods may persist after surgery; instruct the patient to experiment with different foods.

The patient who undergoes a cholecystectomy must be observed for complications. These include jaundice (from an occluded common duct) and hemorrhage (indicated by decreased blood pressure, increased pulse, and increased exudate at the dressing site). An elevated temperature could indicate peritonitis or wound infection. Pancreatitis may occur after cholecystectomy.

Patients at high risk of not surviving a cholecystectomy may need a cholecystostomy (forming an opening into the gallbladder through the abdominal wall). This can be done using a local anesthetic. The opening provides a means of removing purulent exudate and possibly the stone. It also allows drainage of bile.

Nursing diagnoses and interventions for the patient with open cholecystectomy or cholecystostomy include but are not limited to the following:

Dietary teaching is necessary for the patient who is treated conservatively for cholecystitis, as well as for the patient who undergoes surgery. The patient who is treated conservatively must continue to avoid fatty foods, including fried foods, cream, whole milk, butter, margarine, peanut butter, nuts, chocolate, pastries, and gravies. For the postsurgical patient, provide instructions to try small amounts of foods that previously caused discomfort and gradually eliminate those that continue to do so. The patient can usually resume a normal diet without difficulty.

The patient should understand that stones may recur elsewhere in the biliary system. Teach the patient to identify the signs of complications that should be reported. These include jaundice caused by occlusion or stricture of a duct, hemorrhage or leakage of bile, elevated temperature, pain, and dietary intolerance associated with another attack. The patient should also be able to demonstrate care of the T-tube, if present on discharge; identify activity restrictions; and identify a date for a return visit to the health care provider.

Prognosis

To prevent complications from cholecystitis or cholelithiasis, assess the patient for signs and symptoms of gangrenous cholecystitis, subphrenic abscess, pancreatitis, cholangitis, biliary cirrhosis, fistulas, and rupture of the gallbladder with bile peritonitis. A stone occluding the common bile duct (choledocholithiasis) may cause obstructive jaundice (Lewis et al., 2010).

With prompt treatment of cholecystitis and cholelithiasis, the prognosis is excellent. Laparoscopic surgery has further decreased the number of complications. The prognosis is not as favorable in patients who develop pancreatitis (see Life Span Considerations box).

Clinical Manifestations

Manifestations include severe abdominal pain radiating to the back. The pain is usually located in the left upper quadrant. The pain is sometimes relieved by leaning forward, taking the stomach weight off the pancreas. Jaundice may be noted if the common bile duct is obstructed.

Assessment

Pain is the most common subjective data associated with pancreatitis. Pain may be gradual or have a sudden onset, and is often severe. The pain is caused by the enlargement of the pancreatic capsule, an obstruction, or chemical irritation from enzymes. The pain is usually decreased by flexing the trunk, leaning forward from a sitting position, or by assuming the fetal position. It is increased by eating or lying down. Other complaints include nausea, anorexia, malaise, and restlessness.

Collection of objective data includes noting the presence of low-grade fever, leukocytosis, hypotension, and vomiting. Jaundice is often seen if the common bile duct is obstructed. The abdomen usually appears swollen. Bowel sounds may be decreased or absent, leading to an ileus (paralysis of the bowel). The patient appears acutely ill (National Digestive Diseases Information Clearinghouse, 2012).

Diagnostic Tests

Both acute and chronic pancreatitis are diagnosed by radiologic studies (abdominal CT scan and ultrasound of the pancreas), endoscopy, and laboratory analysis of the pancreatic enzymes in the serum and urine. Laboratory tests reveal an increased level of serum amylase and lipase during the first few days and increased urine amylase thereafter. Amylase and lipase levels that are three times above normal are considered most definitive for pancreatitis. The amylase level is not a specific indicator for pancreatitis; abnormal levels also can be seen in cases of perforated peptic ulcer, perforated bowel, and diabetic ketoacidosis. Elevation of the pancreatic amylase level is a better indicator of pancreatitis. The level of lipase is more specific for diagnosing acute pancreatitis. The lipase level typically remains elevated for 12 days with pancreatitis. In chronic pancreatitis the serum lipase levels often remain elevated and the serum amylase remains normal. Leukocytosis, an elevated hematocrit level, hypocalcemia, hypoalbuminemia, and hyperglycemia may also be present. Pancreatic insulin production may be diminished if the islets of Langerhans become infected, and some patients develop diabetes mellitus.

Medical Management

Treatment is medical unless the precipitating cause is biliary tract disease; then surgery may be indicated. Food and fluids are withheld to avoid stimulating pancreatic activity, and IV fluids are administered. The patient is on NPO status, and an NG tube is inserted to decrease pancreatic stimulation, to treat or prevent nausea and vomiting, and to decrease abdominal distention. Analgesics prescribed by the health care provider should be administered as needed to control the pain associated with pancreatitis. Analgesics may be combined with an antispasmodic to achieve optimum pain control.

Parenteral anticholinergic medication, such as atropine or propantheline (Pro-Banthine), helps decrease pancreatic activity. This medication is contraindicated in paralytic ileus. Antacids or antihistamine H₂ receptor antagonists, such as cimetidine, may be given to prevent stress ulcers caused by decreased gastric pH. Some health care providers prescribe antibiotics to treat secondary infections.

Enteral feeding (i.e., tube feeding) is begun 24 to 48 hours after the onset of acute pancreatitis and is administered via the jejunum to prevent the release of pancreatic enzymes. Enteral feeding is preferred to the IV route because it is more nutritionally sound, is less costly, and has fewer complications. However, if enteral feeding is not tolerated in 5 to 7 days, the patient may need to be switched to total parenteral nutrition (TPN; intravenous feeding).

A clear liquid diet with gradual progression may be started once the patient's pain is under control for at least 24 hours. The diet should be low in fat and protein. The diet should also be free of caffeinated beverages since caffeine acts as a gastric stimulant. If the patient experiences increased pain from oral nutrition, hold all food and fluids and contact the health care provider. Oral hypoglycemic agents or insulin may be needed if there is destruction of the islets of Langerhans.

Nursing Interventions and Patient Teaching

Determine the presence and location of pain, as well as what aggravates or relieves the pain. Keep the patient as comfortable as possible through proper administration of analgesic and antispasmodic medications. The patient is usually on bed rest with bathroom privileges to decrease the flow of pancreatic enzymes. Nutritional needs are met by enteral feeding via the jejunum as long as necessary. If enteral feedings fail, the patient may need parenteral feedings. The patient who is addicted to alcohol may go through withdrawal while in the hospital. Be prepared to protect the patient from injury and provide supportive care to the patient and the family. Carefully monitor all replacement fluids and medications for proper administration.

Nursing diagnoses and interventions for the patient with pancreatitis include but are not limited to the following:

The patient remains on a low-fat, high-calorie, high-carbohydrate diet after discharge. Alcohol and beverages or foods containing caffeine are not allowed if full recovery is desired. Ensure that the patient understands the disease process and the severity of the disease and related complications.

Prognosis

The prognosis of pancreatitis depends on the course of the disease and complications, including pseudocysts and abscesses. In most patients, acute pancreatitis is mild, requiring less than 1 week of hospitalization. However, 5% to 25% of patients have a more com­plicated course. The severity of the disease varies according to the extent of pancreatic destruction. Some patients recover completely; others have recurring attacks. The overall mortality rate for acute pancreatitis is 10% to 15%. The mortality rate for patients with severe disease resulting in organ failure is approx­imately 30%. Complications can occur with mild, acute, chronic, or severe pancreatitis. Mortality rates for acute necrotizing pancreatitis are 20% and higher, depending on other organs that become involved (Gardner, 2013).

Etiology and Pathophysiology

The most common environmental risk factor for pancreatic cancer is cigarette smoking. Smoking is seen in 30% of patients diagnosed with the disease. Other risk factors include exposure to chemical carcinogens, diabetes mellitus, cirrhosis, and chronic pancreatitis. Diets high in red meat and pork (especially processed meat such as bacon), fat, and coffee are also linked to pancreatic cancer. Obesity, genetics, and being an African-American male increase the risk of developing pancreatic cancer.

The cancer may originate in the pancreas or be the result of metastasis from cancer of the lung, the stomach, the duodenum, or the common bile duct. Most often the head of the pancreas is involved and causes jaundice by compressing and obstructing the common bile duct. As the cancer spreads, it may invade the posterior wall of the stomach, the duodenal wall, the colon, and the common bile duct. Biliary obstruction and gallbladder dilation are subsequent complications. It is not uncommon for the tumor to grow rapidly and invade the vascular and lymphatic systems. Many patients live only 4 to 6 months after diagnosis, due to the diagnosis commonly being made late in the disease.

Clinical Manifestations

The insidious onset of the disease with initially vague symptoms generally accounts for delays in diagnosis. Complaints of anorexia, malaise, nausea, and fatigue are common. Abdominal pain in the mid-epigastric region or back occurs in many of the patients. About half the patients develop diabetes mellitus if islet cells are involved.

Assessment

A psychosocial history taken during patient assessment may reveal that the patient belongs to one of the at-risk populations such cigarette smokers, coal- and gas-plant employees, chemists, and workers exposed to beta-naphthol and benzidine. Subjective data include anorexia; fatigue; nausea; flatulence; a change in stools; and steady, dull, and aching pain in the epigastrium or referred to the back. The pain is usually worse at night.

Objective data include weight loss, often gradual and progressive, which is one of the earliest signs. Jaundice usually is progressive and may occur late. Pruritus accompanies the jaundice. Many patients have recent onset of diabetes mellitus.

Diagnostic Tests

Diagnosis of pancreatic cancer is based on the patient's history, signs and symptoms, and diagnostic studies. Diagnostic studies include transabdominal ultrasound and CT, endoscopic ultrasound (EUS) with fine needle biopsy to obtain specimens for cytologic examination, ERCP, and pancreatic scans. ERCP allows for visualization of the pancreatic duct and biliary system. With ERCP, pancreatic secretions and tissues can be collected for analysis of various tumor markers (see Figure 45-1).

The level of one tumor marker, cancer-associated antigen CA 19-9, is elevated in patients with pancreatic cancer. It is the most commonly used tumor marker to diagnose pancreatic adenocarcinoma and to monitor the patient's response to treatment. However, CA 19-9 can be elevated in other diseases such as cancer of the gallbladder and acute pancreatitis. Also, it is less sensitive in the early stages of the disease. CA 19-9 has proven to be more helpful for staging purposes and monitoring the patient posttreatment.

Medical Management

Often, malignant tumors of the pancreas are inoperable by the time they are diagnosed. Treatment of pancreatic cancer is primarily surgical and has been associated with a high mortality rate. Cancer of the head of the pancreas is usually treated by pancreatoduodenectomy; the Whipple procedure involves resection of the antrum of the stomach, the gallbladder, the duodenum, and varying amounts of the pancreas. Anastomoses are constructed between the stomach, the common bile duct and the pancreatic ducts, and the jejunum (Figure 45-8). In most cases, this procedure is performed by surgeons who are specially trained and experienced.

Another procedure is total pancreatectomy with resection of parts of the GI tract. Subtotal pancreatic resection has complications of postoperative pancreatic fistulas and is not recommended.

Combinations of drugs such as fluorouracil and gemcitabine (Gemzar) may produce a better response than a single chemotherapeutic agent. Gemcitabine is a main treatment for pancreatic cancer that has metastasized. The current role of chemotherapy in pancreatic cancer is limited. Adjuvant therapy—using surgical resection, radiation, and chemotherapy—is believed by some to be the most effective way to manage the almost always fatal cancer of the pancreas.

Nursing Interventions and Patient Teaching

Pancreatic surgery is radical and requires critical care nursing. Postoperative care focuses on maintaining fluid and electrolyte balance, preventing hemorrhage, preventing respiratory complications, and monitoring endocrine and exocrine functions of the pancreas.

Palliative care is crucial for the patient who is not a candidate or elects not to have treatment or surgery for pancreatic cancer. The patient may receive long-acting narcotic analgesics for chronic pain, supplemented by quick-acting opioids for breakthrough pain. Tricyclic antidepressants as well as antiemetics are often administered with the narcotic analgesic to potentiate (enhance) their effects. Nerve blocks or lysis of nerves of the celiac ganglia can be performed if pain control cannot be achieved with medications. Radiation therapy is also used to treat the pain associated with pancreatic cancer.

The health care provider caring for the patient with pancreatic cancer must offer compassionate physical and emotional assistance. Refer the patient and the family to social services and support groups. Hospice care is very beneficial to the family and patient.

Nursing diagnoses and interventions for patients with cancer of the pancreas include but are not limited to the following.

The patient is facing a life-threatening illness, and family members and close friends are important for the patient's well-being. If the patient has an inadequate support system, it is important to use the resources that are available. Health care personnel, support groups, and hospice care are essential resources for supportive care.

Prognosis

The prognosis for patients with cancer of the pancreas is very poor, due to the often late diagnosis. Median survival after diagnosis is only 5 to 12 months. The 1-year survival rate is approximately 24%, while the 5-year survival rate is approximately 5%. Resection of the tumor improves median survival to 17 to 20 months. Prognosis is related to the tumor's location and the stage at which the disease is diagnosed (Dragovich, 2013).