718-719, 726-736,749-753, 757-775,780-797, 800-805, 836-867 WH

bladder cancer

Cancer of the Bladder Cancer of the bladder is the most common kind of cancer of the urinary tract. It is most common in men, with the average age being 73. It is more common in Caucasians than in African Americans. The incidence of bladder cancer has been rising in the United States, and theAmerican Cancer Society (ACS) estimates that more than 72,570 new cases of bladder cancer occurred in 2013. Pathophysiology Cancer of the bladder often starts as a benign gro wth on the bladder wall that undergoes cancerous changes. Most bladder cancers begin in the inner lining of the bladder called the urothelium. They are called transition cell cancers. They come in a variety of forms and can behave in different ways. Some occur as small w artlike growths on the inside of the bladder. Others form large tumors that grow into the muscle wall of the bladder and require surgical removal. If the cancer affects only the inner lining of the bladder , it is known as a superficial cancer. If it has spread to the muscle w all, it is called an invasive cancer. Common sites for metastasis in- clude the liver, bones, and lungs. Etiology There is a strong correlation between cigarette smoking and bladder cancer. Those who smoke get bladder cancer twice asoftenaspeoplewhodonotsmoke.Specificchemicalsthat cause bladder cancer have been found in cigarette smoke. The more cigarettes smoked, the greater the risk. The lung absorbs the chemicals from tobacco. These chemicals are then passed via the bloodstream to the kidneys and collected in the urine. From there, they accumulate in the urine and damage the cells that line the bladder. Exposure to industrial pollution such as aniline dyes, benzidine and naphthylamine, leather finishings, metal machinery, and petroleum processing products also in- creases the incidence. It can take about 25 years after expo- sure to chemicals for bladder cancer to de velop. Bladder cancer is often diagnosed at a later stage in women. Signs and Symptoms Cancer of the bladder usually causes painless hematuria.The patient may notice that the urine is darker or more reddish in color than usual. Blood in the urine is one of theACS's seven warning signs of cancer. Initially the bleeding is intermittent, which often causes the patient to delay seeking treatment.As the disease progresses, the patient develops frank hematuria, bladder irritability, urine retention from clots obstructing the urethra, and fistula formation (an opening between the blad- der and an adjoining structure such as the v agina or bowel). Other common signs and symptoms of bladder cancer include pelvic pain, pain in the lower back, painful urination, changes in bladder habits, and inability to void. Diagnostic Tests Routine urinalysis can detect evidence of bladder cancer. A urine test for the enzyme telomerase has been found to be 90% accurate in detecting bladder cancer in early and late stages. Urine for cytology can be obtained to determine if cancer cells are present in the urine. Urine culture should also be done. Symptoms of bladder infection may be similar to those of bladder cancer. Diagnosis of bladder cancer may also be made with cystoscopy and transurethral biopsy. An IV Stent in place pyelogram or CT scan also may be done. Therapeutic Measures Treatment depends on the type and staging (se verity) of the bladder cancer. For small, confined tumors, chemotherapeutic agents are instilled into the bladder through a urinary catheter, allowed to dwell, and then removed along with the catheter. Systemic chemotherapy is also used and can be helpful to prolong life when other treatments are no longer indicated. The bacille Calmette-Guérin vaccine may be instilled into the bladder to prevent recurring tumors. Photodynamic therapy, in which drugs are given that make tumors sensitive to light, may be used. When light is applied to the tumor area, cancer cells are killed. Surgical treatment of bladder cancer includes a number of procedures. A cystoscopy and pyelogram with fulguration (de- struction of tissue with electrical current) may be done to burn off cancerous tissue. An alternate method is use of a laser to destroy tumor tissue. Partial cystectomy can be done for can- cer limited to one area. Advances in surgical techniques in- volve robotic and laparoscopic techniques. If the bladder requires removal, robotic laparoscopic radical c ystectomy with urinary diversion is an option. In this procedure, robotic surgical equipment, which imitates sur gical movements guided by the surgeon, allows more precision, steadiness, and maneuverability than manual surgery, as well as the use of small openings rather than larger incisions into the abdomen.Recovery time is reduced as a result. INCONTINENT URINARY DIVERSION. If the patient has a po- tentially curable disease with significant bladder involvement, complete removal of the bladder and creation of a urinary di- version may be done. A urinary diversion means that urine leaves the body in a different manner. A common surgery for urinary diversion is called an ileal conduit, an in volved sur- gery in which a 6- to 8-inch section of the ileum or colon is removed and used as a conduit for urine.The remaining por- tions of the bowel are stitched back together. The surgeon is careful to keep the blood and neurologic supply intact to the section of bowel that has been removed. The isolated section of bowel is closed off on one end, the ureters are stitched into it, and the other end is brought out as a stoma on the abdomen (urostomy) that almost continuously drains urine (Fig. 37.5). The urine from an ileal conduit contains mucus because it comes through the ileum, which normally secretes mucus. The patient must wear an ostomy appliance at all times over the stoma to collect urine. Box 37-2 e xplains how to apply an appliance to an ileal conduit stoma. CONTINENT URINARY DIVERSION. Continent urinary diver- sion surgeries are being done for patient convenience. One version is the Kock pouch (continent internal ileal reser - voir), which is created from a se gment of ileum that has been made into a reservoir for urine (see Fig. 37.5B). The ureters are implanted into the side of the reservoir. A special nipple valve is constructed and is the passage way through which the patient inserts a catheter at 4- to 6-hour intervals to drain urine. Another version of this surgery is the Indiana pouch (see Fig. 37.5C). A reservoir is created using a por- tion of the ascending colon and terminal ileum, making a larger pouch than the K ock pouch. Additional versions of this type of surgery use other parts of the bowel and include the Mainz pouch or Florida pouch. ORTHOTOPIC BLADDER SUBSTITUTION. This surgery involves formation of an orthotopic bladder using a section of the in- testine to make a neobladder (neo = new) and implanting both the ureters and the urethra into the neobladder. Various types of orthotopic bladder substitution surgery include the Studer pouch, hemi-Kock pouch, and ileal W-neobladder. After this surgery, the patient can void through the urethra, although in- continence may be a problem and intermittent catheterization may be needed. Nursing Care Nursing care of the postoperative patient is similar to care fol- lowing any major surgical procedure (see Chapter 12). It is important to ensure adequate urinary output and to detect and report any obstruction of urine drainage early to prevent com- plications. The skin around the stoma will require special care to prevent skin breakdown. The patient is taught how to care for the urinary diversion after surgery, either by frequent drain- ing with a catheter or by wearing an appliance. Be sensiti ve to the patient's anxiety about caring for the urinary diversion. Body image disturbance may occur because of the change in body function. A consultation with a nurse who specializes in wound, ostomy, and continence care (WOC nurse) or an ostomy support group may be helpful both before and after surgery. Cancer of the Kidney Pathophysiology and Etiology Cancer of the kidney is among the 10 most common cancers in both men and w omen. The ACS (2013) estimates about 65,150 new cases of kidney cancer will occur in 2013. The lifetime risk of kidney cancer is 1 in 63. Risk factors include genetics, smoking, obesity, hypertension, years of kidne y dialysis, and exposure to radiation, asbestos, and industrial pollution. Most patients with kidney cancer are over age 55. It is rare under the age of 45. Men ha ve twice the incidence of women. Often the cancer has metastasized before it is diagnosed because the kidney has such a large volume of cir- culating blood, which increases the risk of tumor spread. In addition, the disease has few early symptoms. Signs and Symptoms The three classic symptoms of kidney cancer are hematuria, dull pain in the flank area, and a mass in the area. Often, symptoms of kidney cancer do not occur until the tumor in- vades surrounding tissue. Less specif ic symptoms include fever, weight loss, night sweats, hypertension, anemia, poly- cythemia, swelling in the legs, fatigue, anorexia, and consti- pation. Symptoms of metastasis may be the first evidence of kidney cancer and include weight loss, cough, bone fractures, liver abnormalities, and increasing weakness. Diagnostic Tests A number of diagnostic tests will be done, including an IV pyelogram, cystoscopy and pyelogram, ultrasound examina- tion of the kidneys, CT scans of the abdomen, and magnetic resonance imaging (MRI). A definitive diagnosis is made with a renal biopsy. Therapeutic Measures Surgery is the commonly used treatment for cancer of the kid- ney. A radical nephrectomy removes the entire kidney along with the adrenal gland and other surrounding structures, in- cluding fascia, fat, and lymph nodes, in the area. Radiation therapy, immunotherapy, or chemotherapy may be used after the surgery. In nephron-sparing surgery, only the tumor is re- moved, and the healthy part of the kidney is saved. Nursing Care After nephrectomy, provide postoperative nursing care for any major surgery (see Chapter 12). Because the kidne y is highly vascular, it is essential that the nurse w atch for onset of bleeding and any signs of hypovolemic shock. Urine out- put is monitored. Changes in urine amount or color, bleeding, and signs of infection are reported. The patient should be as- sessed for shortness of breath or diminished breath sounds on the affected side. Surgically induced or spontaneous pneu- mothorax may occasionally occur after a nephrectomy. RENAL SYSTEM TRAUMA Renal trauma is the most common injury to the urinary sys- tem. The kidneys are highly vascular and have a lot of mo- bility, so they are vulnerable to vascular and tissue damage. The many causes of trauma to the kidney, ureters, and bladder include motor vehicle accidents, sports injuries, falls, gunshot wounds, and stabbing. Data collection includes a history of the injury and inspec- tion of the abdomen and flank for asymmetry and bruising or swelling of the flank area. Flank pain and hematuria may be present. Diagnostic tests include urinalysis, IV p yelogram, ultrasound, CT, and MRI. Treatment depends on the e xtent of the injury and ranges from bedrest to surgical intervention. Nursing care includes measuring intake and output, monitor- ing vital signs, and providing IV fluids and pain relief. Bladder trauma may occur with pelvic fractures and mul- tiple trauma from a blo w to the lo wer abdomen when the bladder is full. The weakest part of the bladder w all, which is the dome located at the top of the bladder , may rupture. Urine leaks out of the peritoneal cavity and around the bowel. The patient can ha ve symptoms of hematuria, abdominal pain, inability to void, shock, and pelvic hematoma noted on rectal examination. IV pyelogram and x-ray of the abdomen may be done. A urinary or suprapubic catheter is placed until the bladder heals.

Cancer of the pancreas

Cancer of the Pancreas Pancreatic cancer is the fourth leading cause of cancer deaths in the United States, killing more than 38,000 people each yea.r The incidence of pancreatic cancer has slowly been rising over the past 10 years. Nearly 45,000 ne w cases of cancer of the pancreas are diagnosed yearly (American Cancer Society , 2013); it most often affects people between ages 65 and 79. Pathophysiology Most primary tumors of the pancreas are ductal adenocarci- nomas and occur in the e xocrine (digestive secretion) parts of the pancreas. The tumors in the head and body of the pancreas tend to be lar ge. Cancer of the pancreas spreads rapidly by direct e xtension to the stomach, gallbladder , and duodenum. Cancer located in the body of the pancreas cancer, and gastric or duodenal obstruction. Postoperati ve usually spreads farther and more rapidly than do masses in the head. Cancer of the pancreas may spread by the lymphatic and vascular systems to distant organs and lymph nodes. Etiology The cause of pancreatic cancer is associated most commonly with smoking, then dietary factors (obesity, especially during early adulthood; red meat; processed meat), diabetes mellitus, chronic pancreatitis, and heredity. African American males have the highest rate of pancreatic cancer. Protection may be provided with high folate and lycopene fruits and vegetables. Signs and Symptoms The patient with pancreatic cancer e xperiences vague symptoms early in the disease. Epigastric or back pain, anorexia, nausea, fatigue, and malaise are early symptoms. Detection is often dif ficult because of the nonspecif ic symptoms identified by the patient. Weight loss is the classic sign of pancreatic cancer . The patient may report abdominal pain that is worse at night. The pain is described as gnawing or boring, and it radiates to the back. The pain may be lessened by a side-lying position with the knees drawn up to the chest or by bending o ver when walking. The pain becomes increasingly se vere and unrelenting as the cancer grows. Pruritus is annoying. Depression may be experienced. The patient may report a bloated feeling or fullness after eating. If the cancer obstructs the bile duct, the patient may ha ve jaundice, dark urine, pruritus, and light-colored stools. The patient's health history may include a recent diagnosis of diabetes mellitus. Complications Complications may occur before or after sur gical treatment. Preoperative complications include malnutrition, spread of the complications include infection, breakdo wn of the sur gical site, fistula formation, diabetes mellitus, and malabsorption syndrome. If the patient has had chemotherap y or radiation therapy, complications specific to those therapies can also occur. Thrombophlebitis is a common complication of cancer of the pancreas. As the tumor grows, by-products of the tumor growth appear to increase the levels of thromboplastic (clotting) factors in the blood, making clotting easier . The potential for thrombophlebitis increases if the patient is conf ined to bed or has surgery. Serum alkaline phosphatase, glucose, and bilirubin le vels may be elevated. Amylase and lipase are elevated if the can- cer has caused a secondary pancreatitis. Blood coagulation tests, such as clotting time, are done. Carcinoembryonic antigen is ordered to confirm the presence of cancer (normal: less than 5 ng/mL). Abdominal x-rays determine the size of the pancreas and the presence of masses. CT scan, magnetic resonance imaging (MRI), or ultrasonography are done to precisely locate masses in the pancreas. ERCP can be used to visualize the common ducts and to tak e tissue samples for microscopic analysis. Pancreatic biopsy is necessary for def initive diagnosis of pancreatic cancer. A tissue sample may be obtained by needle aspiration during ultrasonography. This procedure may cause seeding of the tumor along the needle pathway. Therapeutic Measures The prognosis for pancreatic cancer is poor. Survival time is often 4 to 6 months. If diagnosed early , treatment may be aimed at cure. If the patient' s cancer has progressed to distant involvement of other or gan structures and lymph nodes, treatment is directed at easing symptoms and making the patient more comfortable. Surgery is the primary treatment. A total pancreatectomy is one option. For tumors in the body and tail of the pancreas, a distal pancreatectomy is done. When the tumor is located at the head of the pancreas, the Whipple procedure is done to remove the head of the pancreas, the lower portion of the com- mon bile duct, most of the duodenum, and possibly parts of the stomach nearby (Fig. 35.6). Potential postoperati ve problems after the Whipple procedure include failure of the suture lines to hold, causing leakage of pancreatic enzymes and bile into the abdomen; pneumonia or atelectasis from shallow breathing because the incision line is directly under the diaphragm; paralyticileus;gastricretentionorulceration;woundinfection; fistula formation; unstable diabetes mellitus; and renal failure. Relief of biliary obstruction can sometimes be accomplished by implanting a stent or plastic tube in the common bile duct during an endoscopic procedure. P ain can be reduced by surgical removal of a portion of the greater splanchnic nerve. Chemotherapy and or radiation therap y can be used to shrink or destroy the tumor, treat or prevent metastasis, or provide relief of symptoms if the cancer has become too widespread for sur gery. (See Chapter 11 for care of the patient undergoing radiation or chemotherapy.) Nursing Process for the Patient With Pancreatic Cancer DATA COLLECTION. Observe the patient with cancer of the pancreas for evidence of malnutrition and fluid imbalance, including weight loss, inelastic skin tur gor, vomiting, fatty stools, and reports of anorexia or nausea. Review laboratory tests, especially blood glucose, li ver function studies, and clotting studies. Evaluate the patient every 2 to 4 hours for pain. Observe the skin for bruising, scaling, and yello wing, and question the patient about itching. Evaluate the patient's mental status for evidence of depression. NURSING DIAGNOSES, PLANNING, AND IMPLEMENTATION. The patient with cancer of the pancreas will ha ve numerous problems. Interventions for Imbalanced Nutrition: Less Than Body Requirements related to inability to digest food, anorexia, nausea, and vomiting, and Pain related to pancreatic tumor or surgical incision are the same as for patients with pancreatitis and are found in the "Nursing Care Plan for the P atient With Acute and Chronic P ancreatitis." Other care is listed ne xt. Additional interventions for patients with cancer , including psychosocial interventions, can be found in Chapter 11. Risk for Deficient Fluid Volume EXPECTED OUTCOME: The patient will have adequate fluid volume as evidenced by stable vital signs, elastic skin turgor, and moist mucous membranes. • Monitor the patient's intake and output carefully. Low intake increases risk of deficient fluid volume; low output is a sign of deficient fluid. • Monitor vital signs. Tachycardia, tachypnea, and low blood pressure may indicate excessive fluid loss. • Monitor laboratory values, especially serum sodium, potassium, calcium, and chloride levels. Report abnormal values. If electrolyte values are low, the physician may order IV replacement solutions. • Report low serum albumin level (normal is 3.4-4.8 g/dL) and assist with monitoring IV albumin therapy if ordered. Low albumin places the patient at risk for fluid imbalances. • Carefully observe the patient for signs of blood loss that may indicate abnormal bleeding: • Bruising, bleeding gums, or pink-tinged urine • Cullen's sign (bluish discolorations around the umbilicus) • Turner's sign (bluish discolorations on the flanks) • Bleeding at incision and drain sites and in drainage tubing • Teach the patient to use a soft-bristle toothbrush and electric razor rather than a straight razor to reduce risk of injury and bleeding. • Administer vitamin K as ordered to replace deficiency and to reduce risk for bleeding. Risk for Impaired Tissue Integrity related to itching and to leaking around drainage tubes EXPECTED OUTCOME: The patient's skin will remain intact. • Monitor the patient for reports of itching because scratch- ing can cause a break in the skin. • Help the patient keep fingernails short to reduce damage to skin with scratching. • Provide frequent skin care with products free of soap or alcohol to prevent further dryness and itching. • Protect skin around drains with skin-protective barrier products and ostomy bags to prevent skin damage. • Apply products such as calamine lotion as ordered to de- crease itching. • Exercise special care of any drains to prevent unnecessary tension that may cause sutures to give way. • Keep all drains patent, and keep drainage tubing and bags free from kinks to prevent fluid leakage onto the skin. • Place the patient in semi-Fowler's position to help with gravity drainage and reduce risk of fluid leakage. EVALUATION. The plan of care for the patient with pancreatic cancer is successful if the patient maintains body weight within 5% of normal body weight and e xperiences no nausea or vomiting; states that pain remains tolerable at 2 or less on a pain scale of 0 to 10; has urinary output greater than 30 mL/h,r elastic skin turgor, moist mucous membranes, pulse and blood pressure within 10% of patient's baseline, no sudden, excessive abdominal pain or rigidity, and incisions heal at the e xpected rate; demonstrates the appropriate self-care procedures for tubes, drains, dressings, and medication administration; and states the signs and symptoms of complications that are to be reported immediately. PATIENT EDUCATION. Teach the patient and f amily self- care measures such as blood glucose monitoring, insulin administration, signs and symptoms of hyper glycemia and hypoglycemia (see Chapter 40), and the re gimen for pancreatic enzyme replacement. Instruct the patient on how to manage dressing changes if he or she is to be discharged with tubes or drains. P atient and family should know the signs and symptoms of hemorrhage, gastric ulceration, infection, and fistula formation. A patient being cared for at home should have a referral for hospice care or home nursing care. For more information, visit the National P ancreas Foun- dation at www.pancreasfoundation.org.

Hepatitis

Hepatitis is an inflammation of the liver resulting from viral or bacterial infection, drugs, alcohol, or chemicals toxic to the liver, and metabolic or vascular disorders. Symptoms of hepatitis range from no symptoms to life-threatening symptoms due to death of liver tissue. Many people who are infected with hepatitis C, especially baby boomers (people born 1945-1965), are not a ware of it and can li ve for 20 years without symptoms. Those infected can de velop chronic infection, chronic li ver disease, cirrhosis, or li ver cancer. Risk factors for becoming infected with hepatitis C include sharing needles or other equipment to inject drugs. Also, health care providers (HCPs) who are exposed to the virus can become infected in the health care setting. Before 1992, when widespread screening of the blood supply began in the United States, hepatitis C was also commonly spread through blood transfusions and or gan transplants. It is recommended by the Centers for Disease Control and Prevention (CDC; www.cdc.gov) that all baby boomers be tested for hepatitis C. Viral hepatitis is quite common and discussed below. Pathophysiology and Etiology Viral hepatitis is usually caused by one of five viruses: • Hepatitis A virus (HAV) • Hepatitis B virus (HBV) • Hepatitis C virus (HCV) • Hepatitis D virus (HDV) • Hepatitis E virus (HEV) The viral agents vary by mode of transmission, incubation period, symptoms, diagnostic tests, and pre ventive vaccines (Table 35.1). The infecting organism causes inflammation of the liver, with resulting damage to liver cells and loss of liver function. If damage involves the bile canaliculi (thin tubes that collect secreted bile), obstructive jaundice will occur. If complications do not occur, cells regenerate and normal liver function eventually resumes. There are an estimated 72,000 ne w hepatitis A, B, and C infections in the United States each year (CDC, 2013). The incidence of all types of viral hepatitis is at a historic low. HAV is overall the most common cause of hepatitis and has a lo w mortality rate. However, HBV is more common among some groups, including health care w orkers and intravenous (IV) drug users. Prevention The hepatitis viruses are very resistant to a wide range of anti- infective measures, such as drying, heat, ultraviolet light ex- posure, freezing, and bleach and other disinfectants. At least 30 minutes in boiling water is required to destroy them. The best methods for preventing the transmission of the hepatitis viruses are careful attention to cleanliness and the use of vac- cines to HAV and HBV or the use of immunoglob ulin (Ig) after exposure. Ig can be given up to 2 weeks after exposure to HAV; upto1weekwithaseconddoseofIgin1month after HBV e xposure. Infection control precautions used should reflect the usual mode of transmission of the particular hepatitis virus. Ig provides temporary, passive, nonspecific immunity to hepatitis. A vaccine for HAV and HBV is available that provides permanent, active immunity. Health care workers are strongly encouraged (and often required by employers as a condition of employment) to be v accinated for HBV. Permanent, acti ve immunity is acquired from the body' s own antibodies in response to an actual viral infection. The active immunity is to the specific virus to which the body has developed antibodies. Public health measures such as health education programs, licensing and supervision of public f acilities, screening of blood donors, and screening of food handlers are general measures to prevent the transmission of hepatitis viruses.Signs and Symptoms Hepatitis usually sho ws a typical pattern of loss of li ver function, which generally occurs in three stages: 1. The prodromal (preicteric [prejaundice]) stage occurs about 2 weeks after exposure to the hepatitis virus and lasts about 1 week. The patient reports flulike symptoms of malaise, headache, anorexia, low-grade fever, possibly dull right upper quadrant (RUQ) pain, nausea, vomiting, and diarrhea or constipation. 2. With the appearance of jaundice (see Chapter 32), the icteric stage begins (Fig. 35.1). It occurs about 5 to 10 days after the prodromal stage and lasts 2 to 6 weeks. The patient continues to have prodromal symptoms. Dark urine can be present due to increased bilirubin. The liver is usually enlarged and tender on examination. 3. The convalescent stage (posticteric) begins when the patient starts feeling better. It can last from FIGURE 35.1 Jaundice of the conjunctivae and facial skin. From the Centers for Disease Control and Prevention/ Dr. Thomas F. Sellers; Emory University, 1963. 2 to 6 weeks. Recovery varies and depends on the type of hepatitis. Full recovery is measured by the return to normal of all liver function tests and may take as long as 1 year. The effects of hepatitis can be considered reversible if the patient adheres to a medical regimen of adequate rest, proper nutrition, and abstinence from alcohol and other liver-toxic agents for at least 1 year after liver function laboratory values return to normal. Complications Hepatitis may lead to fulminant (sudden, se vere), acute or chronic liver failure. Chronic infection can develop in those with HBV or HCV. Some people are asymptomatic carriers of HBV or HCV and never have an active illness. However, they can infect others and ha ve a greater risk of de veloping cancer of the liver. Diagnostic Tests Serum liver enzymes are ele vated (Table 35.2). Serum bilirubin may be elevated. In patients with severe hepatitis, prothrombin time may be prolonged. Serological tests can determine the specific virus causing the hepatitis via viral antigens and also identify the presence of antibodies to the virus (see Table 35.1). Abdominal x-ray examination may show an enlarged liver. Liver biopsy is done to assess liver damage and healing.herapeutic Measures Treatment goals are to identify the cause of hepatitis, monitor liver status, and provide symptom relief and supportive care. To promote healing with acute infection, limited activity with bathroom privileges and adequate nutrition and fluids are ordered. As the patient improves, activity may be increased as tolerated. Patients should avoid using alcohol or drugs that are known to be toxic to the liver (Box 35-1). To manage chronic hepatitis B infection, the anti virals adefovir (Hepsera) or lami vudine (Epivir) may be used. Interferon therapy (peginterferon alpha-2b [Pe g-Intron] or interferon alpha-2a [Pe gasys]) along with an anti viral medication (oral ribavirin [Rebetol]) is considered to pre- vent chronic hepatitis C infection. A new drug, sofosbuvir (Sovaldi; a nucleotide analog inhibitor) w as approved for treating adults with chronic hepatitis C infection. For more information, visit the websites of the Hepatitis Foundation International (www.hepfi.org), the CDC (www.cdc.gov), or the American Liver Foundation (Nursing Process for the Patient With Hepatitis DATA COLLECTION. Identify subjective data such as malaise, fatigue, pruritus (itching), nausea, anore xia, and R UQ abdominal pain. Objective data, such as baseline weight, vomiting, pale stools, dark-colored (tea-colored) urine, and jaundice, are recorded. The patient's vital signs are tak en, and a low-grade fever or any abnormal bruising or bleeding is reported immediately. Ask the patient about his or her knowledge of disease process and how to prevent spread of the disease. NURSING DIAGNOSES, PLANNING, AND IMPLEMENTATION. Pain related to inflammation and enlargement of the liver EXPECTED OUTCOME: The patient will state that pain level is acceptable. • Monitor pain level on 10-point scale, including WHAT'S UP? questions to determine treatment needs. • For continuous pain, provide analgesics around the clock and as needed (prn) analgesics for intermittent breakthrough pain to provide comprehensive pain relief. • Give analgesics as ordered, recognizing that lower doses might be needed with liver dysfunction, to control pain. • Avoid use of acetaminophen (Tylenol) and combination drugs containing acetaminophen due to risk of liver toxicity. • Encourage nondrug pain relief, such as distraction, imagery, and relaxation to supplement and possibly decrease need for analgesics. Imbalanced Nutrition, Less Than Body Requirements related to anorexia, nausea, or vomiting EXPECTED OUTCOME: The patient's weight will be stable and appropriate for height. • Obtain baseline nutritional status with a nutritional screen- ing tool to identify malnutrition and plan nutritional needs. • Monitor weight and nutritional intake recording percentage of food eaten to determine ongoing treatment needs. • Make dietary referral to develop nutritional plan. • Administer antiemetic drugs as ordered to reduce nausea and increase appetite. • Provide frequent, smaller meals because these may be better tolerated than larger meals. • Place the patient in an upright or sitting position for meals to decrease abdominal discomfort. • Serve meals in a quiet environment without unpleasant noise or odors to increase intake by making eating as pleasant as possible. • Teach patient to avoid alcohol and vitamin supplements unless specifically prescribed by the physician to prevent further damage to liver because alcohol and some vita- mins are metabolized by the liver. Risk for Impaired Liver Function related to viral infection • Monitor liver function tests to detect liver infections. • Monitor for signs of liver dysfunction: ascites, mental changes (check ammonia levels), bleeding (check coagulation studies) to report for implementation of supportive interventions. • Review medications for hepatotoxicity to protect liver function. • Calculate acetaminophen daily dosage so daily limit of 3000 mg or less is not exceeded if applicable to protect liver function. • Administer medication as ordered carefully in consideration of liver effects to preserve liver function. • Refer to alcohol cessation program if applicable to pre- serve liver function. Risk for Impaired Skin Integrity related to itching secondary to bilirubin pigment deposits in skin EXPECTED OUTCOME: The patient's skin will remain intact and free from secondary infection. • Administer antihistamines as ordered to decrease itching. • Encourage the patient not to scratch but to press firmly on the itchy area. Scratching can damage skin and increase risk for infection. • Encourage the patient to keep fingernails trimmed short so that vigorous scratching does not tear the skin. • Maintain room temperature at a comfortable level to decrease perspiration, which may increase itching. Risk for Ineffective Self Health Management related to lack of knowledge of hepatitis and its transmission and treatment EXPECTED OUTCOME: The patient will state how to self- manage the treatment regimen for viral hepatitis and how to prevent spread of the disease. • Determine patient's knowledge of hepatitis to plan teaching. • Teach patient how hepatitis affects the body and the importance of adequate rest and proper nutrition to promote recovery. • Teach the importance of avoiding alcohol and other liver-toxic drugs, to prevent further damage to liver. • Teach patient how to prevent spreading virus to others: hand washing after toileting, using soap and hot water to clean eating utensils, cookware, and food preparation surfaces, practicing safer sex (abstinence, condoms, monogamy), and not sharing needles because hepatitis is contagious. (See "Home Health Hints.") Managementofthepatientwithhepatitishas been successful if the patient reports pain is satisf actorily relieved; body weight is maintained within 2 pounds of pre- illness weight; skin has no breaks, cuts, or tears, or secondary infections; patient can def ine disease; and patient follo ws transmission precautions and treatment.

hydrnephrosis

Hydronephrosis Hydronephrosis is distention of the renal pelvis and calices. This condition results from untreated obstruction of urine flow in the urinary tract. The kidney enlarges as urine collects in the pelvis and kidne y tissue. Hydronephrosis is usually treatable once the condition is detected. Obstruction of urine flow can result from a stricture in a ureter or the urethra, kidney stones, a tumor, or an enlarged prostate. Because of the unrelieved obstruction, urine backs up and distends the ureters and then progresses to the kidney (Fig. 37.3). The capacity of the renal pelvis is normally 5 to 8 mL. Obstruction in the renal pelvis quickly distends it. Kid- ney pressure increases as the volume of urine increases. This enlargement of the kidney can be either unilateral or bilateral. Unrelieved pressure on the kidneys from urine causes the kid- neys to become sacs filled with urine instead of functioning kidneys. Sometimes, in a matter of hours, the blood v essels and renal tubules can be damaged extensively. If the onset of obstruction is gradual, the patient initially may be asymptomatic. Patients commonly develop UTIs be- cause of the obstruction of urine flo w and may have symp- toms of frequenc y, urgency, and dysuria. As the disease progresses, flank and back pain may occur . Eventually the patient develops symptoms of CKD (discussed later). Treatment of hydronephrosis always involves relieving the obstruction. Initial removal of the obstruction may be done by insertion of an indwelling urinary catheter. Long-term cor- rection depends on the cause and includes treatments and sur- geries to relieve obstruction from strictures, stones, tumor, or an enlarged prostate. At times, the obstruction cannot be re- lieved because a stone is too large or removal of tumor growth would result in the patient's death. In these situations, stents, which are tiny tubes, may be placed inside the ureters during a cystoscopy and pyelogram (C&P) to hold the ureters open, or a nephrostomy tube may be inserted directly into the kid- ney pelvis to drain urine. A nephrostomy tube exits through an incision in the flank area and allo ws urine to drain into a collecting bag so that function of the kidne y can be main- tained. Figure 37.4 shows a stent in place in a ureter and a nephrostomy tube. Complications associated with hydronephrosis include in- creased incidence of UTIs because of obstruction of urine flow and kidney failure from unrelieved pressure on the kidneys. Intake and output are carefully measured. Urine retention can worsen the condition and must be recognized and re- ported promptly. If the patient has a nephrostomy tube, ensure that it is draining adequately and prevent kinking or clamping of the tube. Kinking of the tube results in continuation of the hydronephrosis, and the resulting pressure will destro y kid- ney function. If both a nephrostomy tube and urinary catheter are present, output from each should be measured and docu- mented separately.

Colostomy

A colostomy is named according to where in the bowel it is formed: it may be an ascending, transv erse, descending, or sigmoid colostomy. The type of effluent is dependent on the location of the bowel used (Table 34.11). End Stoma An end stoma is formed when the proximal end of the bo wel is brought to the outside abdominal w all. If an abdominoper- ineal (AP) resection is done, the rectum is remo ved, and the proximal sigmoid or descending colon is brought out as a stoma. Another procedure that may be done involves removing FIGURE 34.8 Ileal J pouch-anal anastomosis. The two-loop ileal pouch is simple to construct, provides adequate storage capac- ity, and is evacuated spontaneously and fully. Cecostomy, ascending colostomy Left transverse colostomy Liquid to mushy, foul odor Semiformed, soft Descending or Soft to hard formed sigmoid colostomy the segment of diseased or injured bowel and using the proxi- mal portion to form the stoma. The remaining limb of bo wel is sutured closed and left in the peritoneal ca vity so that the rectum is intact. This is called a Hartmann's pouch, or mucous fistula, and may be permanent or temporary depending on the diagnosis. Because the rectum is intact, the patient may feel the urge to defecate. This is normal because the colon continues to produce mucus. As the rectal stump f ills with mucus, the sphincter is triggered and alerts the patient as if it were stool. Loop Stoma To create a loop stoma, a loop of bowel, usually the transverse colon, is pulled to the outside abdominal wall and a bridge is slipped under the loop to hold it in place.An incisional slit is made in the top of the e xposed colon to allow stool to exit. The entire loop of bowel is not cut through. Double-Barrel Stoma With a double-barrel stoma, the bo wel is completely dis- sected, and both ends of the colon are brought to the outside abdominal wall to form two separate stomas. The proximal stoma is the functioning stoma that e xpels stool. The distal stoma is called a mucous fistula because mucus produced by the bowel passes from it.A double-barrel stoma is often tem- porary, allowing the bowel to rest during healing after trauma or surgery. Preoperative Care A wound ostomy continence nurse (WOCN) should be con- sulted before surgery. The WOCN can help prepare the pa- tient both emotionally and physically for the sur gery. In addition, the WOCN has expertise in selecting the stoma site for the surgeon to ensure that it is easy to sit with it, care for it, and wear clothing over it. This involves observing the ab- domen as the patient assumes different positions and noting how clothing is worn, such as where the belt rides. The site for the stoma can then be chosen so it is visible to the patient for self-care, avoids skin or fat folds, and is where clothing will not interfere with the appliance. Properly planned stoma placement can prevent discomfort when sitting, inability to perform self-care, and uncomfortable, leaking, or poorly fit- ting appliances postoperatively. Routine preoperative instruction, including the importance of coughing and deep breathing, splinting, and early amb u- lation, is provided. Orders for cleansing of the bowel are per- formed to reduce the risk for infection follo wing surgery. Unless the patient has chronic diarrhea related to IBD, an oral agent to cleanse the bowel is given. Oral and IV antibiotics are given as ordered. For a patient with a new ostomy, in addition to routine post- operative assessment, a stoma should be inspected at least every 8 hours. The stoma should be pink to red, moist (sim- ilar to the inside of the mouth), and well attached to the surrounding skin (Fig. 34.9). A bluish stoma indicates in- adequate blood supply; a black stoma indicates necrosis. Either complication should be reported to the HCP imme- diately for treatment, which may require that the patient return to surgery. Note edema of stoma. The stoma size gradually decreases o ver the f irst few weeks follo wing surgery. For both new and established ostomies, skin is assessed for irritation around the pouch and under the pouch each time it is changed. Ostomy discharge (effluent) is monitored and documented. Unexpected changes, such as liquid stool from a descending ostomy, are reported. For the patient with a con- tinent ostomy pouch, assessing that regular emptying of the pouch is done is important to pre vent rupture and leakage. The characteristics of the stool are noted for any type of con- tinent ostomy so that problems can be reported. cient Knowledge related to ostomy EXPECTED OUTCOME: Patient will demonstrate how to care for ostomy. • Determine patient readiness and ability to learn and per- form self-care. The patient experiencing pain, nausea, or vomiting is not likely to be ready to look at the ostomy or learn about ostomy care. • Provide special instructions or a specific type of ostomy appliance for patients with special needs, such as blind- ness, deafness, language barrier, severe arthritis, or other physical conditions that limit ability to perform self-care, so they will be able to perform self-care. FIGURE 34.9 Types of stomas. Note moist, pink to red appear- ance of healthy stoma. Reproduced with permission of Hollister Inc., Libertyville, IL. • Include caregiver in teaching if the patient is not ready or able to learn. With short hospital stays, time for teaching is limited and must begin soon after surgery. • Ensure referral to home care nurse is made to continue teaching in the patient's home. • Consult a WOCN or ostomy equipment supplier if needed to identify appliances suited to individual patient's needs. Figure 34.10 shows types of appliances. • Explain how to change appliance (Fig. 34.11) to promote self-care. • Demonstrate how to apply appliance using moldable or traditional skin barrier to promote self-care. Moldable (able to change shape) skin barrier does not require measuring a pattern or cutting and does not leave a gap around the stoma. For the traditional skin barrier: • Measure stoma with a stoma-sizing guide initially with each appliance change because the stoma will shrink for up to 6 months. • Trace the stoma pattern on the cut to fit skin barrier and cut to fit, if using a nonmoldable barrier, to teach the patient proper size and shape because most stomas are not round. • Apply a moldable barrier ring or strips to the skin barrier as needed to fill in gaps or fit convex shapes to protect the skin and prevent leakage. • Fit the traditional skin barrier over the stoma on the skin with no gaps around the base of the stoma to prevent skin contact with stool. • Change appliance first thing in the morning every 3 days or every 10 to 14 days depending on the type of appliance to reduce skin shearing from frequent removal. • Change appliance immediately if leakage occurs to avoid peristomal skin irritation. • Use an open-ended or drainable pouch for all colostomies or ileostomies, especially during the first 8 weeks after surgery to facilitate emptying and comfort. • Explain to the patient who has a left-sided (descending or sigmoid) colostomy that the bowel can be regulated either by diet or regular irrigation of the stoma. After bowel regulation has been achieved, the patient may use a closed-end pouch or a stoma cap. • Explain daily care and hygiene: • Empty pouch when it is one-third to one-half full. The amount of effluent and the frequency of emptying de- pend on the location of the stoma in the bowel. If the pouch is allowed to get more than half full of stool, the weight of the effluent will pull on the pouch and weaken the seal of the skin barrier. Empty pouch and then clean inside of the tail of the pouch before the self-seal or clamp is replaced to help control odor. • Place deodorants in the pouch to control odor. • Bathe or shower with the appliance in place but check seal and retape or change it if it is loosening. Water will not harm stoma or leak into stoma. • Explain dietary considerations: • Identify foods that contribute to odor and gas. If foods that are known to cause odor or gas are eaten, the patient should know to empty the pouch of flatus more often and to be aware that more odor is probable.Identify foods that contribute to and control diarrhea and what to do for constipation. A list of foods that may con- tribute to ileostomy blockage must be given to the ileostomy patient (Box 34-2 and "Nutrition Notes"). Readiness for Enhanced Self Health Management related to difficulty carrying out self-care measures EXPECTED OUTCOME: Patient will demonstrate ability to perform self-care measures. • Identify financial ability to obtain supplies. The cost and availability of ostomy supplies is problematic for many patients. Most insurers, including Medicare, pay for ostomy supplies, although some limit the type of appliance and number allowed per month. Each state- funded Medicaid system is different. The type of appli- ance needed to eliminate leakage may not always be covered, requiring the patient either to pay the differ- ence or wear what the insurance company will provide. If the patient has no insurance, costs can be high. Some patients find they have to choose whether to purchase ostomy appliances or prescriptions with their limited funds. Fortunately, the pouches in most two-piece sys- tems can be washed out and reused to save money (see "Home Health Hints"). Home Health Hints • Patients with ostomies may be able to have some of their supplies covered by insurance. The home health nurse can work with the medical supply store to assist the patient in receiving the needed equip- ment. Most companies will deliver supplies to the patient's home. • Foods such as broccoli, cauliflower, Brussels sprouts, and cabbage can cause increased mal- odorous gas production. Encourage the patient with a colostomy to eat these in moderation. Offer alternative choices, such as green leafy vegetables, carrots, and cucumbers. • If the patient requires a stool for occult blood test, deliver a collection device (hat) before you visit to assist with obtaining the specimen. Plan to deliver the specimen to the laboratory the day it is collected. • Dietary instruction is important for home health patients with lower GI disorders. Give instructions both verbally and in writing. Written format allows the patient to have the information available for review and to assist with creating a shopping list. Sexual Dysfunction related to body image change or erectile dysfunction EXPECTED OUTCOME: Patient will discuss satisfying ac- ceptable sexual practices for self and partner. • Identify if male patient who had an AP resection is experi- encing erectile dysfunction. This impotence may be tran- sient, depending on the severity of nerve damage or edema associated with the surgery. • Ensure consultation with urologist is made to treat erectile dysfunction if present. • Encourage patients to discuss any concerns regarding sexuality with his or her sexual partner. This may help them work through any fears or embarrassment. • Explain that attractive pouch covers can be purchased and worn to help disguise the pouch and its contents. • Encourage personal hygiene and emptying ostomy pouch before sexual encounters to decrease odors and enhance experience • Refer to sex counselor who can suggest alternative sexual positions to increase satisfaction for partners. Risk for Injury related to skin and stomal complications EXPECTED OUTCOME: The patient will remain free from injury with intact skin, red, moist stoma, and functioning ostomy. • Identify allergies to prevent complications because allergic dermatitis from sensitivity to the adhesive may develop. • Consult WOCN for complications associated with care of the ostomy. A WOCN has had specialized instruction in caring for the stoma and peristomal skin and has a wealth of information to offer. • Use a protective skin paste to prevent skin breakdown from leakage. • Apply a stoma powder to absorb moisture from broken skin around the stoma to allow the skin to heal. • Remove tape and adhesive only when necessary to pre- vent skin shearing from frequent removal. • Leave pouches on for several days unless leakage occurs to prevent skin shearing from frequent removal. • Monitor for peristomal hernia to detect hernias that may develop around the stoma as a result of weakened abdom- inal muscles and cause leakage by the change in body contours associated with the hernia. • Use a more flexible ostomy appliance if peristomal hernia is present to fit body contours better. Monitor for and report stomal prolapse, especially in older adults. Weakened abdominal muscles contribute to the falling down (or out) of the intestinal mucosa, which can make pouching difficult. • Monitor stoma color and immediately report dusky or blue color, which occurs when there is circulatory com- promise. This may arise as a result of vascular collapse, blockage in the mesentery of the intestines, or edema in the intestine from obstruction proximal to the stoma. Usually, necrotic tissue occurs only at the very end of the stoma and will eventually slough off, revealing viable mucosa. Foods That Can Cause Ileostomy Blockage Vegetables: celery, Chinese vegetables, coleslaw, corn, green leafy (collards, lettuce, mustards, spinach), mushrooms, popcorn, potato skins Fruits: apple skins, coconut, dried fruits (apricots, dates, figs, raisins), grapes, orange membranes, pineapple, seedy fruits (raspberries, strawberries) Nuts and seeds (e.g., coconut, poppy seeds) Meats with casings: bologna, frankfurters, salami, other sausages Patients with ostomies may be able to have some of their supplies covered by insurance. The home health nurse can work with the medical supply store to assist the patient in receiving the needed equip- ment. Most companies will deliver supplies to the patient's home. • Foods such as broccoli, cauliflower, Brussels sprouts, and cabbage can cause increased mal- odorous gas production. Encourage the patient with a colostomy to eat these in moderation. Offer alternative choices, such as green leafy vegetables, carrots, and cucumbers. • If the patient requires a stool for occult blood test, deliver a collection device (hat) before you visit to assist with obtaining the specimen. Plan to deliver the specimen to the laboratory the day it is collected. • Dietary instruction is important for home health patients with lower GI disorders. Give instructions both verbally and in writing. Written format allows the patient to have the information available for review and to assist with creating a shopping list. Anticipating Dietary Management of Ostomies Ostomy patients receive a soft diet initially , progressing to a general diet as the surgeon prescribes. Stringy, high- fiber foods are initially avoided until a definite tolerance has been demonstrated and then are best tried in small amounts, one at a time. Stringy, high-fiber foods include the following: • Cabbage (including coleslaw, sauerkraut), corn, peas, spinach • Coconut, dried fruit, pineapple, membranes on citrus fruits • Popcorn, nuts, seeds, skins of fruits and vegetables. Some patients avoid beans, cruciferous vegetables (broccoli, Brussels sprouts), eggs, fish, beer, and carbon- ated beverages because they produce excessive odor. Di- etary restrictions are usually based on individual tolerance. Certain foods may be therapeutic because the y thicken the stool, including: • Applesauce, banana • Cheese • Creamy peanut butter • Pasta, white bread, white rice Patients with ostomies should be encouraged to do the following:Eat at regular intervals. • Chew food well to avoid blockage at the stoma site. • Drink adequate amounts of fluid. • Avoid foods that produce excessive gas, loose stools, offensive odors, and undesirable bulk. • Avoid excessive weight gain. • Explain colostomy irrigation if ordered for descend- ing or sigmoid colostomies (more formed stool): • Explain that colostomy irrigation is done to regu- late bowel movements at a regular time. • Show how to perform irrigation (similar to an enema), with special equipment used to instill fluid into the bowel via the stoma. Because a stoma does not have a sphincter, specially designed tubing with a cone at the end is used to irrigate the ostomy. The cone prevents the fluid that is being instilled from flowing back out of the stoma.

Acute liver failure

Acute Liver Failure Acute liver failure is a rare b ut serious condition that can develop rapidly, sometimes in just 2 days. When the liver is severely damaged, its many functions are impaired. The out- come of the disease may be decided within 48 to 72 hours of diagnosis. Possible outcomes are liver recovery, need for liver transplantation, or death. See Box 35-1 for causes. Box 35-2 ("Patient Education") teaches patients ways to prevent liver damage and possible liver failure. Acetaminophen Toxicity Acetaminophen (Tylenol) overdose is the most common cause of acute li ver failure. Acetaminophen should not exceed 3000 mg in a 24-hour period. Prescription drugs containing more than 325 mg of acetaminophen should not be prescribed or taken per Food and Drug Administra- tion (FDA) guidelines. Visit www.knowyourdose.org, an acetaminophen awareness program, for more informa- tion and a list of more than 600 medications containing acetaminophen. Review prescribed and o ver-the-counter medications to know which are combination drugs that contain acetaminophen to prevent excessive dosage. If overdose of acetaminophen is the cause, activated charcoal is given if it is within 4 hours of the overdose. N-acetylcysteine is then given to protect the liver. Aminoglycosides or nonsteroidal anti-inflammatory drugs (NSAIDS) are never given to patients with acetamin- ophen toxicity because nephrotoxicity can then be more severe. Signs and Symptoms BE SAFE! Many consequences of alcohol abuse such as cirrhosis can take years to develop but not acute alcohol toxicity. Ingesting a large quantity of ethanol (or a smaller quantity of alcohols not intended for beverages) in a short time can be fatal within a few hours. Alcohol poisoning is especially heartbreaking when it kills a young person whose companions let the victim "sleep it off" through ignorance or fear of retribution. Teaching young people about the hazards of alcohol and counseling adult patients about the responsible use of alcohol are appropriate health-teaching functions in all settings. Initial symptoms of liver failure—fatigue, gastrointestinal (GI) upset, and diarrhea—are vague and make detection difficult. As the condition w orsens, symptoms become more se vere: jaundice, hepatic encephalopathy, bleeding, and abdominal distention. The patient may suddenly lapse into an extremely serious illness, starting with confusion and progressing to coma. In a matter of hours, on x-ray , the liver shows a rapid reduction in size, a typical sign of onset of acute liver failure. In addition, there is a sudden elevation of liver enzymes, ALT, aspartate aminotransferase (AST), and bilirubin. Prothrombin time is elevated, with marked elevation being an ominous sign. Potassium and blood glucose levels drop. Therapeutic Measures Treatment is directed toward stopping and reversing the damage to the liver. The patient needs intensive amounts of supportive care. Maintaining the airway (head elevated 30°, NPO [nothing by mouth], nasogastric [NG] tube, endotracheal intubation) is important as encephalopathy progresses. An attempt is made to put the liver completely at rest. The patient is on bed rest. Stimulation is a voided. Most medications are discontinued because they are metabolized by the li ver. Dialysis may be ordered if the li ver damage results from an o verdose of a hepatotoxic substance to filter the substance from the blood. Nutrition may be pro vided via enteral or parenteral nutrition. Lactulose, neomycin, magnesium citrate, or sorbitol may be given to decrease ammonia levels (see later section on hepatic encephalopathy). If a liver transplant is needed, an otherwise healthy patient may be a priority organ recipient, depending on age and whether the patient is alcohol dependent. Nursing Process for the Patient With Acute Liver Failure Nursingcareofthepatientwithacuteliverfailureisthesame as for the patient with cirrhosis, which is discussed next.

ileostomy

An ileostomy is an end stoma formed by bringing the terminal ileum out to the abdominal wall following a total proctocolectomy. Two types of ileostomies can be formed: a conventional ileostomy and a continent ileostomy , such as a Kock pouch (sometimes called a Koch pouch) or Bar- nett's continent internal reservoir, which is a modification of a Kock pouch (Fig. 34.7). A conventional ileostomy has a small stoma in the right lo wer quadrant that requires a pouchatalltimesbecauseofthecontinuousflowofliquid effluent. Continent ileostomies are formed by taking a portion of the terminal ileum to construct an internal reservoir with a nipple valve. A stoma is created and the patient is taught to insert a catheter into the stoma three or four times a day to empty the reservoir. A continent ileostomy surgical proce- dure takes longer and requires additional instruction for the patient to be able to do self-care. It is important for the pa- tient to empty the pouch routinely to prevent pouch rupture. Complications can occur, especially for the K ock pouch, such as valve slippage or leaking, pouch rupture, or pouch- itis. Corrective surgery may be required. An ileoanal anastomosis connects the ileum to the anus and avoids the need for a stoma (Fig. 34.8). This is usually a two- step procedure. During the first surgery, the diseased bowel is removed. A reservoir (named by its shape: J [most common], S, W, or H pouch) is then formed from part of the ileum and connected to the anus. A temporary ileostomy is also formed to divert stool while the reservoir heals. After about 3 months, the temporary ileostomy is reversed and the patient can have bowel movements from the anus. Problems with perianal skin irritation resulting from frequent liquid stools may occur. An ileorectal anastomosis can also be performed, but this may not be a curative procedure for a patient with ulcerative colitis be- cause the rectum may still be diseased.

Appendicitis

Appendicitis Pathophysiology Appendicitis is the inflammation of the appendix, the small, finger-like appendage attached to the cecum of the lar ge in- testine (see Fig. 32.1). Because of the small size of the ap- pendix, obstruction may occur , causing inflammation and making it susceptible to infection. Signs and Symptoms Signs and symptoms of appendicitis include fever, increased WBCs,andgeneralizedpainintheupperabdomen. Within hours of onset, the pain usually becomes localized to the right lower quadrant at McBurney's point, midway between the umbilicus and the right iliac crest (Fig. 34.1). This is one of the classic symptoms of appendicitis. Nausea, vomiting, and anorexia are also usually present. Physical examination reveals slight abdominal muscular rigidity (guarding), normal bo wel sounds, and local rebound tenderness (intensification of pain when pressure is released after palpation) in the right lo wer quadrant of the abdomen. Sometimes there is pain in the right lower quadrant when the left lo wer quadrant is palpated (Ro vs- ing's sign). The patient may k eep the right le g flexed for comfort and e xperience increased pain if the le g is straightened. FIGURE 34.1 Pain at McBurney's point is a symptom of appendicitis. Diagnostic Tests A complete blood cell count (CBC) reveals elevated leukocyte (WBC) and neutrophil counts. An ultrasound or computed tomography (CT) scan reveals an enlargement in the area of the cecum. Therapeutic Measures The patient is kept NPO, and surgery is done immediately unless there is evidence of perforation or peritonitis.Applying ice to the site of pain and k eeping the patient in a semi- Fowler's position may help reduce pain while the diagnosis is being made. Laxatives and enemas are a voided because they may cause or complicate a rupture. The use of a heating pad on the abdomen is a voided because the w armth may in- crease inflammation and risk of rupture. If the appendix has ruptured, IV fluids and antibiotic therap y are started to treat infection and peritonitis. Sur gery may or may not be done right away. If infection is present, a drain may be inserted into the abdomen by a radiologist. Sur gery may then be delayed for up to several weeks while the infection is resolved. After surgery, the diet is adv anced as ordered and toler - ated. If the appendix has ruptured, the patient may ha ve an orogastric or nasogastric (NG) tube to decompress the stom- ach. Vital signs and abdominal data are collected to monitor for signs and symptoms of peritonitis. Pain control to promote early ambulation, coughing, deep breathing, and mo vement help prevent respiratory complications. Complications Perforation, abscess of the appendix, and peritonitis are major complications of appendicitis. With perforation, the pain is severe, and temperature is elevated to at least 100°F (37.7°C). An abscess is a localized collection of pus sepa- rated from the peritoneal cavity by the omentum or small bowel. This is usually treated with IV antibiotics and sur- gical drainage. An appendectomy is done about 6 weeks later.

Gallbladder disorders

Cholecystitis, Cholelithiasis, and Choledocholithiasis Gallstones and inflammations of the gallbladder and common bile duct are the most common disorders of the biliary system. Pathophysiology Cholecystitis is an acute or chronic inflammation of the gallbladder. It is most often a response to obstruction of the common bile duct resulting in edema and inflammation. Bacteria can invade stagnant bile and add to the inflamma- tion and irritation of the gallbladder. Chronic cholecystitis may be the result of repeated attacks of acute cholec ystitis or chronic irritation from gallstones. The gallbladder then becomes fibrotic and thickened and does not empty easily or completely. This is a risk factor for gallbladder cancer. Cholelithiasis is the formation of gallstones in the gall- bladder that are most often composed of cholesterol in the United States. They can be asymptomatic for decades. Chole- docholithiasis refers to gallstones within the common bile duct. Gallstones form when bile becomes supersaturated with a substance such as cholesterol, which then crystallizes, form- ing sludge with continued enlar gement to form stones. An- other type of gallstone is a pigment stone. Pigment stones are composed of calcium bilirubinate, which occurs when free bilirubin combines with calcium. Etiology and Incidence CHOLELITHIASIS. Gallstones occur most in w omen, from aging, obesity, pregnancy, stasis of bile, f asting, medica- tions, and heredity. Stasis may be caused by a decreased gallbladder-emptying rate, a partial obstruction in the common duct, or pregnancy. Excessive cholesterol intake combined with a sedentary lifestyle is link ed to an increased incidence of cholelithiasis, as are hemolytic blood disorders such as sickle cell disease and bo wel disorders such as Crohn's disease. After age 50, the rate of gallstones is about the same for men and women ("Cultural Considerations"). CHOLECYSTITIS. Cholelithiasisisresponsibleformostcases of cholecystitis, or inflammation of the gallbladder. Signs and Symptoms Signs and symptoms of cholecystitis and cholelithiasis are similar. Subjective symptoms include epigastric pain, RUQ tenderness, nausea, and indigestion, especially after eating foods high in f at. Objective symptoms include evidence of inflammation, such as an elevated temperature, pulse, and respirations; vomiting; and jaundice. The patient may have a positive Murphy's sign, which is the inability to take a deep breath when an examiner's fingers are pressed below the liver margin. Family history of either cholecystitis or cholelithiasis, dietary habits such as high f at intake or a recent lo w-fat diet, and reports of flatulence (gas), eructation (belching), nausea, v omiting, or abdominal discomfort after a high-f at meal are common e vidence of a gallbladder disorder. CHOLELITHIASIS. The epigastric pain caused by cholelithiasis may also be called biliary colic. The pain is a steady, aching, severe pain in the epigastrium and RUQ that may radiate back to behind the right scapula or to the right shoulder. The pain usually begins suddenly after a f atty meal and lasts for 1 to 3 hours. If the pain is caused by a stone in the common bile duct (choledocholithiasis), the pain may last until the stone has passed into the duodenum. Jaundice is more commonly present with acute choledocholithiasis because the common bile duct is blocked or inflamed. CHOLECYSTITIS. The biliary colic caused by cholecystitis typ- ically lasts 4 to 6 hours. The pain is made worse with move- ment such as breathing. The patient usually has nausea, vomiting, and a low-grade fever with the pain. Heartburn, in- digestion, and flatulence are more common with chronic cholecystitis. Patients often report repeated attacks of acute cholecystitis symptoms (Table 35.6). Complications Complications of cholecystitis include cholangitis (inflam- mation of the bile ducts), necrosis or perforation of the gallbladder, empyema (a collection of purulent drainage in the gallbladder), fistulas, and adenocarcinoma of the gall- bladder. A major complication of choledocholithiasis is acute pancreatitis if the pancreatic duct is obstructed. Diagnostic Tests An ultrasound of the gallbladder is the classic test done to detect stducts. An ERCP can be done to directly visualize the pancreatic ducts and bile ducts to determine the presence of stones in the common duct and allows the ability to remove stones from the common duct. Further examination may include a radionuclide scan, such as a hepatobiliary iminodiacetic acid scan. For this procedure, the patient will be gi ven an IV injection of a radioactive isotope that is metabolized by the liver and excreted in the bile. The scanning camera then traces the path of the isotope as it tra vels through the bile ducts, gallbladder , and intestines to identify blockages. The patient may ha ve an ele vated WBC count (normal: 5000-10,000 cells/mm3). If direct bilirubin is elevated (normal: 0.3-1.2 mg/dL), its cause is likely obstruction in the biliary or liver areas. Liver enzymes can rise from hepatic inflammation. Serum amylase and lipase may be ele vated if the pancreas is involved or if there is a stone in the common duct. ones, inflamed walls of the gallbladder, and dilated Therapeutic Measures Treatment of an acute episode of cholecystitis centers on pain control, prevention of infection, and maintenance of fluid and electrolyte balance. Pain control is achieved with analgesics. For itching relief if the patient is jaundiced from bile acid de- posits in the skin, colestipol (Colestid) or cholestyramine (Questran, LoCholest) is given. These drugs bind with the circulating bile acids for excretion in the stool. If the patient has nausea and vomiting, an antiemetic may be ordered (see Table 35.4). See "Nutrition Notes." SURGERY. Treatment for cholelithiasis typically in volves cholecystectomy (surgical removal of gallbladder) via laparoscopy. A laparoscopic cholecystectomy is done with a laparoscope through four small puncture wounds in the ab- domen. Patients are usually discharged in 24 hours or less, and recovery time is reduced with laparoscopic surgery. For large stones or an infected gallbladder , a traditional open cholecystectomy may be required. A T-tube may be inserted into the common duct to ensure that bile drainage is not obstructed (Fig. 35.7). T-tube drainage ranges from 500 to 1000 mL the first day and decreases to 200 mL by the third day. The patient with a traditional cholecystectomy has incisional pain that creates difficulty with coughing and deep breathing postoperatively because deep breathing causes the diaphragm to press on the operative site. Patients are hospi- talized for 2 to 3 days with a traditional cholecystectomy. EXTRACORPOREAL SHOCK-WAVE LITHOTRIPSY (ESWL). Extra- corporeal shock-wave lithotripsy is done less frequently now due to the availability of laparoscopic cholecystectomy. It uses shock waves to destroy stones in the gallbladder or biliary ducts. Patients who have few cholesterol stones that are not calcified are the most lik ely candidates for ESWL. After ESWL, the patient is usually put on a course of oral dissolution drugs to ensure complete removal of all stones and stone fragments. MEDICATION. Dissolution of small noncalcif ied stones (less than 2 centimeters) with the bile acid drugs ursodiol (Actigall) is used for those who are not sur gical candidates. Treatment with the dissolution drugs may tak e months and stones may return. Nursing Process of the Patient With a Gallbladder Disorder DATA COLLECTION. Monitor the patient frequently for pain, using the WHAT'S UP? questions. Take the patient's vital signs, particularly the temperature and pulse, frequently to monitor for signs of infection. Weigh the patient and inspect mucous membranes, skin turgor, and urinary output for signs of dehydration. Measure intak e and output, in- cluding any emesis or drainage from NG tubes or T-tubes. Removed gallbladder Observe stools and urine for color and consistenc y. Ob- struction of bile flow may result in stools that are clay col- ored or have a foul, greasy appearance or urine that is dark amber or tea colored. Report either ne w finding immedi- ately. Evaluate laboratory studies for elevation in the WBC count or abnormalities in electrolytes or serum bilirubin levels. NURSING DIAGNOSES, PLANNING, AND IMPLEMENTATION. Common nursing diagnoses for the patient with cholecysti- tis include pain and risk for def icient fluid volume. Addi- tional nursing diagnoses for the patient with cholelithiasis who has a surgical procedure include risk for impaired skin integrity related to surgical incision and T-tube drainage and risk for ineffective breathing pattern related to abdominal incision. Acute Pain related to biliary colic EXPECTED OUTCOME: The patient will rate pain as 2 or less on a 10-point scale. Assess the patient frequently for pain to guide treatment. • Administer analgesics as ordered to reduce pain. • Administer antispasmodics or anticholinergics as ordered for biliary colic. • Assist patient with positioning to assume whatever position provides the most comfort. Risk for Deficient Fluid Volume related to anorexia, nausea, vomiting, or excessive tube drainage EXPECTED OUTCOME: The patient will have adequate fluid volume as evidenced by stable vital signs, elastic skin turgor, and moist mucous membranes at all times. • Monitor intake and output, daily weights, and skin turgor to monitor fluid balance. • Monitor T-tube drainage. Carefully observe the T-tube drainage unit to prevent kinking of the tubing. Pressure in the biliary drainage system from poor drainage may greatly increase the patient's pain and the risk for infection. • Give antiemetics as needed to control nausea and vomiting. • Assist with administration of IV fluids and electrolytes as ordered while the patient is on restricted oral intake to maintain hydration. Risk for Impaired Skin Integrity related to surgical incision and T-tube drainage EXPECTED OUTCOME: The patient's skin will remain intact at all times. • Inspect the patient's skin and the sclerae of the eyes for jaundice, and report jaundice or pruritus, to provide treatment to reduce itching injury to skin. • Inspect the cholecystectomy incision for excessive drainage or evidence of infection such as redness, edema, or warmth, which can irritate and break down skin. • Change dressings frequently to protect the skin around the incision site from irritating drainage. • Protect the skin with a skin barrier product or bag such as those used with colostomies if bile is leaking around the T-tube site. An ostomy care nurse (if available) can be consulted for the best choice of dressing. A skin barrier can protect skin from breakdown due to contact with bile. Risk for Ineffective Breathing Pattern related to abdominal incision EXPECTED OUTCOME: The patient will have effective breath- ing pattern as evidenced by a respiratory rate of 16 to 20 per minute, even, unlabored, depth within normal limits at all times. • Monitor respiratory rate, depth, and effort, and ability to cough effectively. The high abdominal incision can cause pain with deep breathing and coughing. • After surgery, encourage the patient to cough and deep breathe at every encounter. Instruct the patient in the proper techniques before surgery and give the opportunity to practice. Deep breathing and coughing after any surgical procedure helps prevent atelectasis and respira- tory tract infections. TABLE 35.7 CHOLECYSTITIS SUMMARY Diagnostic Tests Ultrasound ERCP • If the patient is reluctant to cough because of pain, evaluate the pain medication regimen so that pain is controlled. • Assist the patient with splinting when coughing to make coughing less painful. • Encourage the patient to walk as soon as able to help mobilize secretions. EVALUATION. The plan of care for a patient with cholecys- titis or cholelithiasis is successful if the patient reports tol- erable pain not greater than 2 on a pain scale of 0 to 10, no weight loss, excessive thirst, urinary output greater than 50mL/hour;hasmoistmucousmembranes,elasticskintur- gor, intact skin with no w armth, redness, swelling, or pu- rulent drainage at the w ound site; no jaundice or itching; clear breath sounds; and a normal white blood cell count (Table 35.7). PATIENT EDUCATION. Discharge education focuses on diet. Patients are put on high-protein, lo w-fat diets. Encourage obese patients to lose weight. After a cholecystectomy, fat should be slo wly reintroduced into the diet. Once the duodenum becomes accustomed to a constant infusion of bile, the patient's individual tolerance for fat becomes the only restriction for diet.

chronic kidney disease

Chronic Kidney Disease Kidney disease is the eighth leading cause of death in the United States (U.S. Renal Data System, 2013), where CKD affects about 26 million people and the incidence is on the rise. This disease is a progressive, irreversible deterioration in renal function in which the body is unable to maintain meta- bolic, fluid, and electrolyte balance. It occurs with a gradual decrease in the function of the kidne ys over time. The result is accumulation of nitrogenous w aste products in the blood and uremia. CKD affects every body system (Table 37.8). Pathophysiology When a large proportion of the body's nephrons are damaged or destroyed, AKI or CKD occurs. As the nephrons die of f, the undamaged ones increase their w ork capacity and tak e over the w ork previously done by the dead ones, so the patient may experience significant kidney damage without showing symptoms. CKD is a progressi ve disease process. In the early , or silent, stage (decreased renal reserv e), the patient is usually without symptoms, even though up to 50% of nephron func- tion may have been lost (Table 37.9). This stage is often not diagnosed. The renal insufficiency stage occurs when the patient has lost75%ofnephronfunctionandsomesignsofmildkidne y disease are present. Anemia and the inability to concentrate urine may occur. BUN and creatinine levels are slightly ele- vated. These patients are at risk for further damage caused by infection, dehydration, drugs, heart failure, and use of diagnostic x-raydyes.Thegoalofcareistopreventfurtherdamage,ifpos- sible, by control of blood glucose levels and blood pressure. End-stage renal disease occurs when 90% of the nephrons are lost. Patients at this stage experience chronic and persistent abnormal kidney function. B UN and creatinine le vels are always elevated. These patients may make urine but not filter out the waste products, or urine production may cease. Dialysis or a kidney transplant is required to survive. Uremia (urea in the blood) is present in CKD. Patients even- tually develop problems in all body systems (Table 37.10). If left untreated, the patient with uremia dies, often within weeks. Etiology The causes of CKD are numerous. The most common include diabetes mellitus resulting in diabetic nephropathy , chronic high blood pressure causing nephrosclerosis, glomerulonephri- tis, and autoimmune diseases. Diabetes and hypertension account for close to 70% of all CKD (U.S. Renal Data System, 2013). Symptoms of Kidney Disease Patients in either AKI or CKD ha ve multiple symptoms. Figure 37.6 illustrates symptoms and some of the more com- mon ones are explained next. Disturbance in Water Balance Disturbances in the removal and regulation of water balance inthebodyoccurwithsignsoffluidaccumulation. Anearly symptom is edema (swelling) of the e xtremities, sacral area, and abdomen. Patients may report shortness of breath. Crackles and wheezes (signs of fluid accumulation) may be present on auscultation of the lungs. Blood vessels in the neck may be dis- tended, and the patient may be hypertensi ve. These patients may produce a large amount of dilute urine (polyuria), small amounts of urine (oliguria), or no urine (anuria). Disturbance in Electrolyte Balance As kidney function decreases, the kidne ys lose their ability to absorb and excrete electrolytes. Important electrolytes are sodium, potassium, and magnesium. When the kidneys are unable to maintain normal amounts of electrolytes in the blood, these substances accumulate at high le vels and may be life threatening. When the kidneys are unable to re gulate sodium levels adequately, the patient may sho w signs of hypernatremia (excessive sodium in the blood), which causes water reten- tion, edema, and hypertension. Hyponatremia (too little sodium) may occur when too much sodium is lost.This can occur when the patient has experienced prolonged episodes of vomiting or diarrhea or is urinating large amounts of di- luted urine. Patients with hyponatremia may show signs of confusion. The sodium may be normal or low due to being diluted from excess fluid. Hyperkalemia (potassium level exceeding 5 mEq/L) can be life threatening if the level goes above 7 mEq/L. The patient may have dysrhythmias and cardiac arrest if the potassium level is too high. P atients with hyperkalemia report muscle weakness, abdominal cramping, and diarrhea. The nurse may identify that the patient is confused or disinterested in care. These patients should be placed on a cardiac monitor and ob- served for cardiac dysrhythmias. A high potassium level in the patient with CKD may be caused by a diet high in potassium-rich foods, injuries, or blood transfusions. Monitoring daily laboratory v alues, re- stricting potassium intake, and reporting abnormalities are important. IV insulin with glucose, or calcium gluconate may be used as a temporary measure to dri ve excess potassium into the cells. Sodium polystyrene sulfonate (Kaye xalate) may be given either orally or as a retention enema; it causes potassium to be eliminated through the stool. The definitive treatment for hyperkalemia is hemodialysis, which remo ves potassium from the body. Dietary education is extremely im- portant. The patient is instructed to avoid foods that are high in potassium (Box 37-3). Calcium levels decrease because the kidneys are unable to produce the hormone that acti vates vitamin D, the vitamin needed for calcium absorption. Hypocalcemia exists when the calcium level falls below 8.5 mg/dL. Also associated with a low calcium level is hyperphosphatemia, a phosphorus le vel above 5 mg/dL. These imbalances cause the bones to release calcium, increasing the risk of fractures.These patients should ambulate regularly to prevent further calcium loss from the bone. Many patients who are on dialysis de velop hypercal- cemia due to hyperparathyroidism (excess release of parathy- roid hormone). Cinacalcet (Sensipar) reduces excess levels of parathyroid hormone, which then reduces calcium levels. Phosphates are also found in man y foods. Medication to bind phosphate, known as phosphate binders, is tak en by patients with high phosphate levels. Patients must take these medications with meals so they can bind with the phosphates and be eliminated in the stool. High phosphorus le vels may cause severe itching, and patients may have open sores from scratching, placing them at risk for infections. P atients also may have muscle cramps and aches. Disturbance of Removal of Waste Products With azotemia (rapid accumulation of toxic w astes in the blood), the patient may sho w signs of weakness and f atigue, confusion, seizures, twitching movements of extremities (as- terixis), nausea, vomiting, and lack of appetite and may report a metallic or bad taste in the mouth. There may be a smell of urine on the patient's breath. The patient may have yellowish pale skin and report itching due to urea crystals on the skin. Dialysis to remove excessive waste products in the blood is the only treatment for the underlying causes of these symptoms. Disturbance in Maintaining Acid-Base Balance Hydrogen ion excretion is affected, causing a disturbance in the acid-base balance that result in metabolic acidosis. Patients may report headache, f atigue, weakness, nausea, vomiting, and lack of appetite. As metabolic acidosis pro- gresses, the patient shows signs of lethargy, stupor, and coma. Respirations become fast and deep as the lungs attempt to blow off carbon dioxide to correct the acidosis (K ussmaul's respirations). See Chapter 6 for a more detailed discussion of acid-base balance. Disturbance in Hematologic Function Anemia is seen mainly in CKD, which causes disturbances in blood cells over time. Damaged kidneys do not produce adequate erythropoietin, the hormone that stimulates RBC production. Nutritional deficiencies and blood loss during dialysis also contribute to anemia. Regular injections of epo- etin (Epogen, Procrit), a synthetic form of erythropoietin, help restore RBC production and prevent anemia. A common side effect of erythropoietin is development of hypertension. Impaired WBC and immune functions contribute to an in- creased risk for infection. The patient should be protected from potential sources of infection. Impaired platelet function creates a risk for bleeding.The patient should be protected from injury, and signs of bleeding, such as blood in stool or emesis, are reported. Therapeutic Measures for Kidney Disease Kidney insufficiency and early kidne y disease are treated based on symptoms with a restricted diet and fluid intak e, medications, and careful monitoring for onset of serious problems that warrant initiation of dialysis. In later stages, dialysis is necessary to replace lost kidney function. A kidney transplant, when available, may return the patient to a nearly normal state of health. Diet Dietary recommendations are individualized by the dieti- tian and HCP based on the patient' s needs. Calories are high to maintain weight and energy needs. Protein is usu- ally restricted to limit nitrogen intake but is increased for a patient on dialysis because protein is lost during the dial- ysis process. Sodium is restricted to minimize sodium and fluid retention. Potassium is restricted, especially later in the disease when the kidne ys are unable to eliminate it. Calcium may be increased or supplemented because of poor absorption related to f aulty vitamin D acti vation. Phosphorus is restricted because of high blood le vels related to hypocalcemia. Saturated fat and cholesterol are restricted for patients with hyperlipidemia. Fluids are re- stricted to prevent overload. Most patients are given iron, folic acid, vitamins, and minerals to supplement the re- stricted diet ("Nutrition Notes"). Because restrictions are complex, the diet may be a source of frustration for patients. The nurse should assist the patient to identify foods that are palatable yet within the diet plan.The dietitian should be consulted for instruction and assistance. Medications Early in the disease, diuretics are gi ven to increase output, and ACE inhibitors, angiotensin receptor block ers, calcium channel blockers, or beta blockers may be used to control hy- pertension. Phosphate binders are given with meals to reduce phosphate levels. Calcium and vitamin D supplements are used to raise calcium levels. Both the active and storage forms of vitamin D should be considered to decrease fractures, can- cer, and infection rates and improve cardiac function. Agents to lower potassium levels are used if needed.All drug therapy is closely monitored because diseased kidneys are unable to effectively remove medications from the body . The patient with diabetes needs less insulin because one of the functions of the kidneys is to break do wn insulin. Because it is not being broken down, it remains in the body longer, and there- fore less is needed as the kidney disease progresses. Dialysis Dialysis is started when the patient develops symptoms of se- vere fluid overload, high potassium levels, acidosis, pericardi- tis, vomiting, lethargy, fatigue, or symptoms of uremia that are life threatening. Both peritoneal dialysis and hemodialysis involve the movement and diffusion of particles from an area of high concentration to an area of low concentration through a semipermeable membrane. Substances mo ve from blood through the semipermeable membrane into the dialysate. Fluid and electrolyte imbalances can be corrected with dial- ysis. Dialysis can also be used to treat drug overdoses. HEMODIALYSIS. Hemodialysis involves the use of an artificial kidney to remove waste products and excess water from the patient's blood. During the dialysis procedure, the patient' s blood and the dialyzing solution flow in opposite directions through the dialyzer across an enclosed semipermeable mem- brane. The dialysate contains electrolytes and water in a bal- anced mix that resembles blood plasma. On the other side is the patient's blood with metabolic w aste products, excess water, and electrolytes. The waste products from the patient's blood move into the dialysate by diffusion through the mem- brane because of the difference in their concentrations. The dialysate solution carries the w aste products away, and the cleansed blood is returned to the patient's body through an- other tube (Fig. 37.7). A hemodialysis treatment tak es 3 to 4 hours and is usually done three or four times a week. He- modialysis can be done at a hemodialysis center, at home, or in the hospital if the patient de velops a complication and needs hospitalization (Fig. 37.8). Hemodialysis provides a rapid and efficient way to remove waste products from the blood. It is also an excellent means to correct excessive fluid-overloaded states such as occur in heart failure. Hemodialysis is not without side ef fects. After a treat- ment, the patient normally feels weak and fatigued, some- times even too tired to eat. Sudden drops in blood pressure may cause the patient to become weak, dizzy , and nause- ated. Cardiac dysrhythmias and angina may occur . Fluid and electrolyte levels drop rapidly and cause the patient to feel lethargic and have muscle cramps. Patients are given large amounts of heparin, an anticoagulant, to k eep the blood from clotting while it is in the artificial kidney; this may cause bleeding from the puncture sites, GI tract, nose, or other sites if injury occurs. Box 37-4 re views nursing care for patients having hemodialysis. Vascular Access. Hemodialysis requires a permanent way to access the bloodstream for blood remo val and return to the body during dialysis. Typical permanent vascular access op- tions are an arteriovenous (AV) fistula (considered to be the gold standard) or a v ascular access graft. Fistulas or grafts are placed in the arm when possible. Early referral to a nephrologist can allow for the estab- lishment of vascular access so that it is matured (developed) before the need for dialysis. If this does not occur , then a temporary access is used until a fistula or graft is placed or usable. A central venous catheter with two or three ports (the third port can be used for medications by trained staff) is placed in a central v ein for temporary access. Central catheters should not be used long term because of the risk of infection. An AV fistula is made by sewing a vein and artery together under the skin (Fig. 37.9).AV fistulas may take several weeks to mature. The surgeon determines when the fistula is mature for use. An AV graft uses a tube of synthetic material to attach to an artery and a vein. Needles are inserted into the graft to ac- cess the patient's blood. Traditional graft material is not self- sealing and requires time for tissue growth to serve as a plug for the hole that the needle makes before it can be used. This may take 1 to 2 weeks. The Vectra® vascular access graft is self-sealing and does not require tissue gro wth so it can be used almost immediately after sur gical implantation. This self-sealing property also decreases postdialysis bleeding time and reduces the time required for the dialysis session. Vascular Access Care. AV fistulas and grafts are re gularly checked for patency by palpating for a thrill (a tremor) and auscultating for a bruit (swishing sound) at the site of the graft or fistula. Any decrease or cessation of bruit or thrill indicates occlusion. If a thrill or bruit is diminished or not present, the HCP is notified immediately. Special care of the access site must be taken because this is the patient's only way to elim- inate waste products (Box 37-5). It is important for the site to be carefully monitored per institution policy to detect any clotting or problems. Early detection of clotting allo ws the surgeon an opportunity to sa ve the access by performing a declotting procedure rather than a total revision. Postoperative Care. Initially, neurovascular checks are per - formed hourly for vascular surgery. Neurovascular checks in- clude extremity movement and sensation, presence of numbness or tingling, pulses, temperature, color, and capillary refill (nor- mally less than 3 seconds). Peripheral pulses are palpated to feel the thrill and auscultated to hear the bruit. If a pulse is absent or weak or the extremity is cool or dusky, the HCP is notified im- mediately. Dressings or incisions are checked, and any drainage, hematoma, or infection is documented and reported as needed. Vascular surgery pain is usually mild. Severe pain may indicate an occlusion of the graft. AV grafts can cause distal ischemia or "steal syndrome" because too much of the arterial blood is being "stolen" from the distal e xtremity. This is usually seen postoperatively and may require sur gical correction to restore blood flow to the extremity. Blood pressure readings and IVs should not be done in the extremity in which the access is placed. The extremity with the vascular access should be ele vated postoperatively. Range-of-motion exercises should be encouraged. P atients are taught care of the access PERITONEAL DIALYSIS. Peritoneal dialysis provides contin- uous dialysis treatment and is done by the patient or family in the home. The peritoneal membrane is used as a semiper- meable membrane across which e xcess wastes and fluids move from blood in peritoneal vessels into a dialysate solu- tion that has been instilled into the peritoneal cavity. A peri- toneal catheter is placed into the patient' s peritoneal space between the two layers of the peritoneum belo w the waist- line. This catheter is used to perform an e xchange. The ex- change process has three steps: (1) f illing, (2) dwell time, and (3) draining. The fill step involves instilling a bag of sterile dialyz- ing solution (dialysate) into the patient' s peritoneal cavity through the catheter. The amount of solution is individual- ized but is often 1000 mL. The solution is left to dwell in the abdomen for several hours, allowing time for the waste products from the blood to pass through the peritoneal membrane into the dialysate solution (Fig. 37.10). The solution is then drained out of the body and discarded. This process is repeated three or four times a day and is contin- uous for the patient. Several treatment plans use this exchange process. The treatment plan that best suits the patient's needs is determined by the patient and the dialysis team. Continuous ambulatory peritoneal dialysis is the most commonly used treatment plan. Usually three exchanges are done during the day and one before bedtime. Other treatment plans allow for the use of a computerized machine called a cycler to regulate the exchanges during sleeping hours. Some- times medications are added to the dialyzing solutions, such as heparin to prevent clotting of the catheter, insulin for the patient with diabetes, or antibiotics if there is infection. Patient and family education is extremely important for peritoneal dialysis to be successful. The patient must be taught and be able to demonstrate that he or she is able to do a successful exchange. Sterile technique while performing the exchanges is imperative, and the exchanges should be done in a clean en vironment. A major complication is peri- tonitis (infection of the peritoneum), which can be life threat- ening. The major cause of peritonitis is poor technique when connecting the bag of dialyzing solution to the peritoneal catheter. The first sign of peritonitis is usually abdominal pain. (See Chapter 34 for additional signs and symptoms of peritonitis.) If any symptoms of peritonitis occur, the patient must contact the HCP immediately so antibiotic treatment can begin. The patient should be taught to care for the e xit site (the site where the catheter comes out of the abdomen) and the need to inspect both the site and the dialysate solution for any signs of infection. Dietary education is also important. A dietitian can assist the patient in making appropriate choices for adequate calo- ries, protein, and potassium intak e. The peritoneal dialysis patient typically has fewer dietary and fluid restrictions than the patient on hemodialysis because peritoneal dialysis is continuous and maintains serum w aste levels. Proteins are lost through the peritoneal membrane into the dialysate fluid, so increased dietary protein is needed. This loss increases with peritonitis, which further increases permeability. Kidney Transplantation Kidney transplantation is another treatment for CKD and is extremely successful. An advantage of transplant compared with dialysis is that it re verses many of the physiological changes. The patient is also not dependent on dialysis and di- etary restrictions. A kidney transplant is a procedure in which a donor kidney is placed in the abdomen of a patient with CKD (Fig. 37.11). This healthy transplanted kidney functions as a normal kidney does. The donated kidney can come from a family member, a living, nonrelated donor, or a cadaver donor. Tissue and blood types must match so the body's immune system does not reject the donated kidney. Patients receive drugs to help prevent re- jection, which must be taken for the rest of the patient's life. Sometimes even with these drugs, the body rejects the kidney, and the patient must go back on dialysis ("Cultural Consider- ations" and "Patient Perspective"). Clinical trials that give the same donor's bone marrow at the time of the kidney transplant to reduce rejection and the need for lifelong antirejection medications are in progress. Patients in the studies have been able to stop or greatly reduce their antirejection medications. Nursing Process for the Patient With Kidney Disease Data Collection Kidney disease progressively affects all body systems. If AKI is short term, fewer effects may be seen because some effects will not develop. In CKD, more ef fects are seen because the disease has time to progress. Data should be collected for signs and symptoms in all body systems. F amily history of kidney disease and patient history of health problems such as hyper- tension, diabetes, systemic erythematous lupus, or urinary dis- orders are noted in the history. Also noted are medications the patient takes because they may be nephrotoxic and require adjustments. Recent changes in weight are documented. Signs and symptoms vary depending on the severity of CKD and its cause. Common signs are hypertension, abnor- mal laboratory values (creatinine, BUN), or changes in urine. See signs and symptoms section for other effects.

Chronic pancreatitis

Chronic Pancreatitis Chronic pancreatitis is ongoing pancreatic cellular damage and decreased pancreatic enzyme functioning often following repeated occasions of acute pancreatitis. Pathophysiology Chronic pancreatitis is a continuous, progressi ve disease that replaces functioning pancreatic tissue with f ibrotic tissue as a result of inflammation. Pancreatic ducts become obstructed, dilated, and finally atrophied. The acinar, or enzyme-producing, cells of the pancreas ulcerate in response to inflammation. The ulceration causes further tissue damage and tissue death, and it may cause cystic sacs filled with pancreatic enzymes to form on the surf ace of the pancreas. The pancreas becomes smaller and hardened, and progressively smaller amounts of pancreatic enzymes are produced. Etiology and Incidence The major cause of chronic pancreatitis in men is e xcessive alcohol ingestion that causes repeated attacks of acute pancreatitis. The major cause in women is chronic obstructive biliary disease, which leads to persistent inflammation of the pancreatic ducts. Other conditions kno wn to cause chronic pancreatitis are prolonged malnutrition, cancer of the pan- creas or duodenum, and prolonged use of enteral feedings, which can cause atrophy of the pancreas. The usual age for chronic pancreatitis to develop is between ages 45 and 60. The patient's mean life span is 25 years after the diagnosis of chronic pancreatitis is made. Death is often not related to pancreatic failure. Prevention Advise patients with acute pancreatitis from hea vy alcohol ingestion that abstinence could pre vent recurrence of the pancreatitis and prevent the possibility of chronic pancreatitis. Advise all patients with obstructi ve biliary disease to seek medical treatment for their condition to prevent the progres- sion from acute to chronic pancreatitis. Carefully monitor patients who are unable to feed themselv es for nutritionally adequate diets. Monitor routine laboratory values. Report any trend toward reduced functioning of the pancreas. Signs and Symptoms The signs and symptoms of chronic pancreatitis are less severe than for acute pancreatitis b ut are long term. The patient's history will show a pattern of remissions and exacerbations over years. The patient will report epigastric or lower upper quadrant (LUQ) pain, weight loss, and anorexia. Complications A variety of complications can result from chronic pancreatitis. Abscesses and fistulas may develop when cysts filled with pan- creatic enzymes burst into the abdominal cavity, causing severe inflammation and tissue necrosis. Pleural efusion may develop from inflammation just under the diaphragm. P ancreatic en- zymes are essential for normal absorption of nutrients from the intestines. Fat intolerance and malabsorption syndrome with fatty stools and diarrhea may develop in response to the limited amount of pancreatic enzymes produced. In addition, biliary obstruction may further complicate f at absorption. As the terminal third of the pancreas becomes in volved and the islets of Langerhans are destroyed, the patient exhibits symptoms of insulin-dependent diabetes mellitus (discussed in Chapter 40). Diagnostic Tests Serum amylase and serum lipase le vels elevate only in acute disease. In chronic pancreatitis, enzymes will be normal or below normal. Fecal fat analysis shows higher than normal amounts of f at. Both computed tomography (CT) and ultrasonography sho w characteristic pancreatic structural changes such as masses, calcif ication of ducts, cysts, and change in pancreatic size. ERCP can locate specific obstructions and detect ductal leaks. Therapeutic Measures Treatment is aimed at promoting comfort and maintaining adequate nutrition (see "Nutrition Notes: Nourishing the Patient With Pancreatitis"). Pain is managed with analgesics. Surgery may be necessary to treat biliary disease, repair fistulas, drain cysts, or repair other damage. Nursing Process for the Patient With Pancreatitis See the "Nursing Care Plan for the P atient With Acute and Chronic Pancreatitis."

cirhossis

Cirrhosis Cirrhosis is the progressi ve, irreversible replacement of healthy liver tissue with scar tissue. It is caused by chronic lvi er disease. In 2010, chronic li ver disease/cirrhosis was the 12th leading cause of death in the U.S. population (Murphy, Xu, & Kochanek, 2013). It occurs more commonly among men than women ("Cultural Considerations"). There are a v ariety of causes of cirrhosis (see Box 35-1). Chronic alcohol use is the most common cause of cirrhosis in the United States. Pathophysiology Signs and Symptoms Initially, symptoms are not usually seen with cirrhosis. As liver function becomes impaired, symptoms may begin to be seen. They include anorexia, nausea, vomiting, weight loss, and fatigue, which is due to decreased metabolic function of the liver. Jaundice may be present. The patient's skin may be dry from bile products deposited in the skin. The patient may report se vere pruritus (itching). The liver may be enlarged, firm, and tender . Laboratory v alues reflect progressive loss of liver function. As cirrhosis progresses, signs and symptoms of increasing loss of li ver function and complications related to the increasing loss of function develop (Fig. 35.2, Table 35.3). Complications Complications of cirrhosis include blood clotting defects, portal hypertension, ascites, hepatic encephalopathy , and hepatorenal syndrome. CLOTTING DEFECTS. Blood clotting defects may de velop because of impaired prothrombin and fibrinogen production in the liver. Furthermore, the absence of bile salts pre vents the absorption of fat-soluble vitamin K, which is essential for some blood clotting f actors. Patients with cirrhosis ha ve a tendency to bruise easily and can de velop disseminated intravascular coagulation or hemorrhage. PORTAL HYPERTENSION. Portal hypertension is persistent blood pressure ele vation in the portal circulation of the abdomen. Liver damage causes a blockage of blood flo w in the portal vein. Increased resistance from delayed drainage causes enlargement of the visible abdominal veins around the umbilicus (called caput medusae), rectal hemorrhoids, enlarged spleen (splenomegaly), and esophageal varices (dilated veins; Fig. 35.3). The most serious result of portal hypertension is bleeding esophageal varices. The walls of the esophageal veins are thin and tear easily. Varices usually develop from the fundus of the stomach upward and may extend into the upper esophagus.The blood-filled, thin-walled varices may tear easily from sudden excessive pressure, such as the intra-abdominal pressure that results from coughing, lifting, or straining, causing se vere bleeding.ASCITES. Ascites is an accumulation of serous fluid in the abdominal ca vity. The fluid accumulates from portal hypertension and low production of alb umin by the f ailing liver and aldosterone accumulation. An insufficient amount of albumin causes plasma to seep into the abdominal cavity. The kidneys respond to the decreased circulating blood volume by saving sodium and water. The accumulated fluid causes a markedly enlarged abdomen. The fluid may cause severe respiratory distress as a result of ele vation of the diaphragm. HEPATIC ENCEPHALOPATHY. Hepatic encephalopathy is caused by elevated ammonia, a byproduct of protein metabo- lism, which disrupts mental status. The damaged liver is unable to make the ammonia water soluble for excretion in the urine. Signs and symptoms of hepatic encephalopathy include pro- gressive confusion; asterixis, or flapping tremors in the hands caused by toxins at peripheral nerves; and fetor hepaticus, or foul breath caused by metabolic end products related to sulfu.r Stages of hepatic encephalopathy and signs and symptoms of the stages are as follows: • Early: The patient exhibits subtle changes in personality, fatigue, drowsiness, and changes in handwriting (the best assessment for the early stage). • Stupor and confusion: The patient is often belligerent and irritable and develops asterixis, muscle twitching, hyperventilation, and marked confusion. • Comatose: The patient gradually loses consciousness and becomes comatose. With treatment, if ammonia le vels decrease, the patient gradually regains consciousness. Hepatic encephalopathy represents end-stage liver failure and has a mortality rate as high as 90% once coma begins. HEPATORENAL SYNDROME. Hepatorenal syndrome is a sec- ondary failure of the kidneys in some patients with cirrhosis. Symptoms of hepatorenal syndrome include oliguria without detectable kidney damage, reduced glomerular filtration rate (GFR) with essentially no urine output or less than 200 mL per day, and nearly total sodium retention.Albumin and fresh frozen plasma to increase intravascular volume is given while avoiding diuretics. Diagnostic Tests Tests that show liver damage and functioning of the li ver are shown in Table 35.2. Abdominal radiographs of patients with cirrhosis may sho w ascites and enlar gement of the liver. An abdominal ultrasound may show liver enlargement early in cirrhosis or a small li ver later in the disease. An esophagogastroduodenoscopy (EGD) detects esophageal varices and bleeding (discussed later in the chapter).A liver biopsy may be done to determine the e xtent and nature of the liver damage (see Chapter 32). Therapeutic Measures Interventions for cirrhosis are to prevent advancement of the disease and treat complications. ASCITES. Ascites is treated with diuretics such as spironolactone (Aldactone) or furosemide (Lasix), sodium and fluid restriction (800-1000 mL/day), and albumin infusions for severe ascites. Paracentesis can be done to remove accumulated fluid from the peritoneal cavity when the fluid is compromising the patient's breathing, causing abdominal discomfort, or posing a threat of ruptured umbilical hernia. If large amounts of fluid are removed, albumin may be given to replace lost proteins to pre vent fluid shifting. Ascites can be treated by the placement of a shunt, called a transjugular intrahepatic portosystemic shunt , under fluoroscopy (Fig. 35.4). Access to place the shunt is gained through the jugular v ein. A stent is placed to connect the portal vein to the hepatic vein, in the middle of the liver. This reduces portal pressure by allowing blood to bypass the liver and be carried to the heart. It reduces fluid accumulation and aids in reducing the risk of bleeding.OPHAGEAL VARICES. The medical goals for managing bleeding from esophageal varices are to stop the bleeding im- mediately, maintain normal clotting, and treat infection. Bleeding varices can be treated with vasoconstrictors such as vasopressin, octreotide (Sandostatin), beta blockers or nitrates, and endoscopic variceal ligation (banding) or sclerotherapy to close the varices. Vitamin K, which is often deficient in liver disease, is given to assist with the clotting process.Antibiotic prophylaxis is given with hemorrhage because severe bacterial infection is a risk and can be a precursor to rebleeding varices. Banding of varices with rubber bands during endoscopy is done to stop the bleeding (Fig. 35.5). Sclerotherap y is another method of treatment during endoscopy. The varices are injected with a sclerosing agent that causes thickening and closing of the dilated vessels. Postprocedure the patient may report chest pain for up to 72 hours. Gi ve prescribed analgesics, and monitor the patient for relief of pain. Report severe pain unrelieved by the prescribed analgesic immediately because the patient may ha ve an esophageal perforation or ulceration, which is a complication of sclerotherapy. In emergency cases when other methods are not available, temporary tamponade (application of pressure) of the bleed- ing varices may be done with a multilumen esophagogastric tube that has a balloon on the end for inflation (Sengstaken- Blakemore tube or Minnesota tube). Complications of esoph- agogastric tamponade may include aspiration, erosion of the mucosa, perforation, and suffocation, so it is not often used. HEPATIC ENCEPHALOPATHY. Lactulose may be gi ven by mouth, NG tube, or enema (depending on ho w alert the pa- tient is) to make the colon contents more acidic. This creates an insoluble form of ammonia that is then e xcreted in the stool. Neomycin, an intestinal antibiotic, occasionally may be given to reduce colonic bacteria that change ammonium to ammonia. See "Nutrition Notes." Nutritional Care for Patients With Hepatic Encephalopathy Hepatic encephalopathy is associated with increased serum levels of ammonia caused by the liver's inability to degrade ammonia to urea. Ammonia is toxic to all cells, including those of the li ver and the brain. The goal of nutritional management of patients with hepatic encephalopathy is to promote protein synthesis by supplying ample amounts of amino acids. Only in cases of se vere protein intolerance should protein be restricted and then for as short a time as possible with supplemental branched-chain amino acids administered until normal protein intake is resumed. Complication of Alcoholic Liver Disease: Wernicke-Korsakoff Syndrome This disorder of the central nervous system, caused by thiamin deficiency, is diagnosed mainly in alcoholics b ut also occa- sionally in malnourished patients with no history of alcohol abuse, including women with hyperemesis gravidarum. Wernicke's encephalopathy is an acute neuropsychiatric condition caused by inadequate thiamin supplied to the brain. When caused by dietary deficiency, it can usually be successfully treated with oral or subcutaneous thiamin and rarely progresses to Korsakoff's psychosis, the result of damage to the brain tissue. Thiamin given at this stage will not re verse the effects. These patients display an abnormal mental state in which memory and learning are affected out of all proportion to other cogniti ve functions in an otherwise alert and responsive patient. Nursing Process for the Patient With Acute Liver Failure and Cirrhosis DATA COLLECTION. A complete history and physical assessment are done. Be alert to subjective symptoms of liver dysfunction, such as abdominal pain, anorexia, nausea, severe itching, and dull, aching RUQ pain. Note objective evidence of liver problems, such as jaundice, light-colored stools, ascites, ecchymosis (bruising) of the skin, GI bleeding, and any evidence of alterations in thought processes, such as confusion, disorientation, or inability to make decisions. NURSING DIAGNOSES, PLANNING, AND IMPLEMENTATION. Common nursing diagnoses for patient with cirrhosis include the following. Excess Fluid Volume related to portal hypertension (ascites) EXPECTED OUTCOME: Fluid volume will be controlled as evi- denced by stable weight and abdominal girth within normal limits for the patient. • Weigh the patient on admission and daily to measure fluid retention. • Measure and record the patient's abdominal girth (circum- ference) daily to monitor ascites. Mark the place where you measured so the same site will always be measured during subsequent assessments. • Report any weight gain or increase in girth promptly so treatment can be ordered and complications minimized. • Monitor the patient's vital signs and lung sounds; report changes and any evidence of difficulty breathing or changes in mental status promptly to detect fluid overload. • Measure all intake and output to accurately detect fluid overload. • Maintain a low-sodium diet and order fluid restrictions to reduce fluid retention. • Administer ordered diuretics as scheduled to reduce fluid volume. • If IV fluids or albumin have been ordered, assist in careful monitoring of the rate of infusion to prevent or detect fluid overload. Imbalanced Nutrition: Less Than Body Requirements related to anorexia and impaired metabolism of needed nutrients EXPECTED OUTCOME: The patient's (dry) weight will be within normal limits for height. • Monitor weight; report unexpected (nonfluid) weight loss so timely intervention can be implemented. • Monitor serum prealbumin, total protein, vitamin, and mineral levels because these may be better indicators of nutrition if nutritional status is masked by fluid overload in weight measurement. • Offer frequent mouth care to increase comfort and make food more palatable. Make sure that odors and other unpleasant stimuli are eliminated to prevent further worsening of appetite. • Offer the patient frequent, small, high-calorie meals to reduce feeling of fullness that can occur with larger meals. • Administer vitamins or supplements as ordered to correct deficiencies. Pain related to abdominal pressure EXPECTED OUTCOME: The patient will state pain level is acceptable. • Monitor pain level using a 10-point scale and WHAT'S UP? questions to guide treatment. • Give analgesics as ordered to control pain. Lower doses may be needed for the patient with liver dysfunction. • Encourage nondrug pain relief activities, such as distraction, imagery, and relaxation to possibly decrease the need for analgesics. Risk for Disturbed Thought Processes related to elevated ammonia levels The patient will remain alert and ori- ented to person, place, and time. • Assess the patient's level of consciousness and orientation often to allow prompt treatment. • Assess neuromuscular function by asking the patient to hold his or her arms out straight in front and steady. If asterixis, or liver flap, is present, the patient's hands will unwillingly dip and return to the horizontal position in a flapping motion due to elevated ammonia. • Look for changes in the patient's handwriting because changes can indicate altered neuromuscular function. • Give lactulose, neomycin, magnesium citrate, or sorbitol as scheduled to decrease serum ammonia levels. • Be aware that lactulose causes loose stools, and do not with- hold the medication when the patient develops diarrhea. Loose stools are a sign that the medication is working, not a reason to withhold it when treating ammonia levels. • Question giving medications such as sedatives, opioids, and tranquilizers because these can precipitate hepatic encephalopathy. • Reorient the patient to time and place as needed and helpful to reinforce reality. • Give simple, clear explanations of care, and give the patient time to understand the explanation because short, simple explanations are easier to process. • Provide a safe environment for the confused or unsteady patient to prevent injury. Risk for Ineffective Breathing Pattern related to excess fluid in the abdomen EXPECTED OUTCOME: The patient's respirations will be even and unlabored, 16 to 20 per minute. • Assess the patient's respiratory rate, rhythm, chest movement, skin color, and oxygen saturation frequently to determine if breathing pattern is effective. • Assist the patient to use an incentive spirometer and to cough gently every 2 to 4 hours to encourage deep breathing and keep airways clear. • Elevate the head of the patient's bed so that the patient's lungs have maximum room for expansion. • Administer analgesics carefully, as ordered, if pain is causing shallow respirations. Reducing pain with breathing allows for a more effective breathing pattern. • Reposition the patient at least every 2 hours to ventilate all areas of the lungs. • Assist with treatments to decrease ascites as ordered to increase room for lung expansion. Risk for Deficient Fluid Volume related to bleeding esophageal varices or gastrointestinal bleeding secondary to clotting dysfunction EXPECTED OUTCOME: Fluid volume will remain within normal limits without bleeding as evidenced by no signs and symptoms of bleeding, and vital signs within normal limits for the patient. • Monitor gastric secretions, stool, and urine at least every 8 hours, and report any signs of bleeding. Early identifica- tion of bleeding is essential to prompt treatment. • Monitor blood clotting laboratory studies such as pro- thrombin time and report any abnormal values to identify risk for bleeding. • Caution the patient to use a soft-bristle toothbrush and an electric rather than straight razor to avoid injury and bleeding. • Avoid suctioning the patient if possible because suctioning can cause esophageal varices to bleed. • Use a small-gauge needle for injections and apply direct pressure to all puncture sites to avoid bleeding. • Teach the patient to avoid hot, spicy, or irritating foods because these may irritate the esophageal mucosa and increase risk of bleeding. • Instruct the patient to avoid forceful coughing or nose blowing, straining, vomiting, or gagging if at all possible. Administer medications as ordered to prevent their occurrence. These can increase pressure and risk of bleeding varices. Risk for Infection related to impaired immune function EXPECTED OUTCOME: The patient will be free from infection as evidenced by WBC count within normal limit, afebrile. • Monitor for signs of infection and report promptly so treatment can begin. • Be aware that the earliest warning signs of infection may be subtle changes in the patient's behavior, such as sudden restlessness, an increase in confusion, or irritability. Early recognition is essential to prompt treatment. Carefully evaluate laboratory studies such as the WBC count. The WBC count may not elevate or may elevate slowly because the white cell activity is impaired. • Teach the patient careful hand hygiene and avoidance of people who are ill to prevent exposure to infection. EVALUATION. Nursing care has been effective if the patient is alert and oriented and has no signs of fluid retention, a stable weight appropriate for height, no abdominal pain or pain reported as tolerable using a 10-point scale, a respiratory rate between 16 and 20 respirations per minute with no cyanosis or changes in level of conscious- ness, no bleeding, no infection, no injuries, and an accurate knowledge of cirrhosis and proper disease management requirements. PATIENT EDUCATION. Teach patients how cirrhosis is affecting their bodies. In particular, patients need to know about portal system hypertension and hepatic encephalopathy. In addition, teach: How to observe for and report any confusion, tremors, or personality changes • The importance of adequate rest and avoidance of strenuous activity • See "Nutrition Notes" • The need to use opioids, sedatives, and tranquilizers cau- tiously due to potential mental function impairment • The need to promptly report any bleeding; any sign of low potassium, such as muscle cramps, nausea, or vomiting caused by diuretics; changes in mental status, such as confusion or personality changes; changes in weight; and any increase in current symptoms • The importance of avoiding alcohol • The importance of frequent follow-up care and laboratory studies Liver Transplantation The patient with end-stage liver failure from cirrhosis, hepatitis, biliary disease, metabolic disorders, or hepatic vein obstruction might be evaluated for a liver transplant. The patient will be evaluated for emotional and physical stability and must accept that he or she will be on daily medications for life ("Cultural Considerations"). After the surgical implantation of a donor liver, the patient must be closely observed for evidence of donor organ rejection. The patient will be on drugs to suppress immune system responses and prevent tissue rejection. Observe the patient for the following signs of impending rejection: • Pulse greater than 100 beats per minute • Temperature greater than 101°F (38°C) • Reports of RUQ pain • Increased jaundice • Decrease in bile from the T-tube or change in bile color. In addition, laboratory studies may show increased serum transaminases (ALT and AST), serum bilirubin, alkaline phosphatase, and prothrombin time. Symptoms of acute tissue rejection usually develop between the 4th and 10th postoper- ative days. The patient who has received an organ transplant needs extended medical follo w-up. Teach the patient to promptly report to the physician an y symptoms of infection, bleeding episodes, or RUQ pain. As a short-term bridge to li ver transplant, bioartificial livers with filtering membranes have been used. Under study, for longer term support is hepatoc yte transplantation via a splenic artery catheter. Cancer of the Liver Cancer of the liver usually results from metastasis from a primary cancer at a distant location.The liver is a likely area of involvement if cancer originated in the esophagus, lungs, breast, stomach, colon, pancreas, kidne y, bladder, or skin. For some patients, liver cancer is the primary tumor site. Patients with a history of chronic hepatitis B or C infection, nutritional deficiencies, heavy alcohol use or smoking, and exposure to hepatotoxins have an increased risk for cancer of the liver. Symptoms of cancer of the liver include encephalopathy, abnormal bleeding, jaundice, and ascites. Laboratory tests show elevated serum alkaline phosphatase. Radiologic exam- inations may include abdominal radiographs or radioisotope scans, which show tumor growth. Liver cancer is definitively diagnosed with a positive needle biopsy combined with an ultrasound exam of the liver. Liver cancer is staged upon diagnosis. If found early , surgery can be curati ve. Rarely, though, is it found early. Care of the postsur gical patient is similar to other abdominal surgery patients. If surgery is not an option, the patient may receive chemotherapeutic drugs by injection directly into the affected lobe of the liver or into the hepatic artery; sorafenib, which, slo ws the spread of cancer cells; or radiation therapy. The overall survival rate for liver cancer is low. (See Chapter 11 for care of patients with cancer.)

UTI's

Disorders of the urinary tract include a v ariety of problems involving the kidneys, ureters, bladder, and urethra. These problems may arise from infection, obstructions, cancer , hereditary disorders, and metabolic, traumatic, or chronic dis- eases. Some may lead to chronic kidney disease (CKD) if not treated or controlled. Infection may be found in three anatomic parts of the urinary tract: the urethra, resulting in urethritis; the bladder, with a diagnosis of cystitis; or the kid- neys, with a diagnosis of p yelonephritis. When problems occur with the kidney, homeostasis of the body is affected. URINARY TRACT INFECTIONS Urinary tract infection (UTI) refers to invasion of the urinary tract by bacteria. Normally, the urinary tract is sterile above the urethra. UTI is the second most common bacterial dis- ease. In the hospital, UTIs are the most common hospital- acquired infection (HAI). Lower UTIs include urethritis, pro- statitis, and cystitis. Upper UTIs include pyelonephritis and ureteritis. Infections may result in sepsis or CKD. Risk Factors for Urinary Tract Infections UTIs are caused most often by an ascending infection, start- ing at the external urinary meatus and progressing toward the bladder and kidneys. Most UTIs are caused by the bacterium Escherichia coli, which is commonly found in feces. Other less common pathogens include Staphylococcus saprophyti- cus, Klebsiella spp., and Enterobacter. Risk factors for UTI include (a) incomplete emptying of the bladder; (b) contam- ination in the perineal and urethral area; (c) instruments or tubes inserted into the urinary meatus; (d) reflux of urine be- cause of faulty valves; previous UTIs; (e) anatomical and genetic aspects of females; (f) pregnancy and asymptomatic bacteriuria; and aging. Incomplete Bladder Emptying Stasis of urine in the bladder can result from obstruction or simply from not voiding frequently enough. Urine overdistends the bladder, decreasing the blood supply to the w all of the bladder, which keeps white blood cells (WBCs) from fighting contamination that may have entered the bladder. The standing urine then serves as a culture medium for bacterial growth. In- complete emptying of the bladder prevents flushing out of the bacteria and allows bacteria to ascend to higher structures. Contamination in Perineal and Urethral Areas Contamination in the perineal and urethral areas can be from fecal soiling, from se xual intercourse in which bacteria are massaged into the urinary meatus, or from infection in the area, such as vaginitis, epididymitis, or prostatitis. Instrumentation Infection Having instruments or tubes inserted into the urinary meatus can cause infection. The most common cause of instrumen- tation infection is urinary catheterization. Bacteria ascend around or within the catheter , causing infection. Within 48 hours of catheter insertion, bacterial colonization begins. Many patients develop a UTI within 2 weeks of placement of an indwelling urinary catheter. Faulty Valves Causing Reflux of Urine Faulty valves that do not maintain one-w ay flow can cause reflux of urine from the urethra to the bladder or the bladder to the ureter. Reflux can be congenital, or it may be acquired as a result of previous infections. Previous Urinary Tract Infections Previous UTIs are thought to provide a reservoir of persistent bacteria that cause reinfection. Incomplete bladder emptying can precipitate infections as well. Female Anatomic and Genetic Differences Women are more susceptible to UTIs than men because of the short length of the female urethra and its proximity to the anus and vagina. Some women with recurrent UTIs ha ve a shorter mean distance from the urethra to anus. This can facilitate colonization of the urinary tract. Genetic f actors have been found that may play a role in w omen who have a certain phenotype for developing UTIs. Pregnancy Pregnant women may have asymptomatic bacteriuria. Untreated, 40% to 50% will de velop pyelonephritis. Pregnant women may be prone to infection with group B streptococci. Most commonly, infection occurs in the second and third trimesters. Aging and the Urinary Tract Older adults have an increased incidence of UTIs due to di- minished immune function, diabetes, and neurogenic bladder which fails to completely empty. Aging increases the risk of lower UTIs and may also mask symptoms. UTI is the most common cause of acute bacterial sepsis in patients over age 65. Older men are predisposed to infection because an enlar ged prostate obstructs urine flow. In older women, the decline in estrogen can also contribute to the risk of UTI. Signs and Symptoms UTIs are characterized by common symptoms of dysuria, ur - gency, frequency, incontinence, nocturia, hematuria, back pain, and cloudy, foul-smelling urine (Table 37.1). In the older adult, the most common presenting symptom of UTI is generalized fatigue. Atypical symptoms or a change in cognitive function- ing, especially noted in patients without dementia, can be seen. A decline in mental status and fever in any patient with an in- dwelling catheter meets the diagnostic criteria for a UTI. Types of Urinary Tract Infections Urethritis Urethritis is inflammation of the urethra that may result from a chemical irritant, bacterial infection, trauma, or e x- posure to a sexually transmitted infection (STI). Posttrau- matic urethritis can occur with intermittent catheterization or instrumentation of the urethra. Bubble bath and bath salts are common urethral irritants and should not be used by any- one with a history of UTIs. Urethritis can also be caused by spermicidal agents. Gonorrhea and chlamydiosis are STIs that can cause urethritis in men. It is common to have some degree of urethritis in association with bladder or prostatic infections. Symptoms of urethritis include urinary frequenc y, ur- gency, and dysuria. The male patient may ha ve discharge TABLE 37.1 URINARY TRACT INFECTION (URETHRITIS, CYSTITIS, PYELONEPHRITIS) SUMMARY from the penis. A urinalysis or urine culture is done to di- agnose urethritis. The treatment of urethritis is based on the cause. If it is a chemical irritant, it is avoided. If urethritis is caused by bacte- ria, an antibiotic is prescribed based on the results of a culture. Phenazopyridine (Pyridium), a urinary analgesic, is often used to treat dysuria. The patient should be forewarned that urine will turn orange while taking phenazopyridine. If ure- thritis was sexually transmitted, it is important that the sexual partner also be treated. Cystitis is inflammation and infection of the bladder wall. It can be due to bacteria, viruses, fungi, or parasites.About 90% of UTIs are caused by Escherichia coli. In most cases, the causative organisms first grow in the perineal area and then ascend into the bladder. Symptoms include dysuria, frequenc y, urgency, and cloudy urine. Cystitis acquired outside the hospital is diag- nosed with a routine urinalysis collected as a midstream, clean-catch specimen. Changes seen in the urinalysis include cloudy urine and the presence of WBCs, bacteria, and some- times red blood cells (RBCs) in the specimen. Nitrites are usually positive. Some laboratories also examine for leuko- cyte esterase, which is positi ve if infection is present in the urine. In complicated UTIs, such as one acquired in the hos- pital or a repeat infection, a urine culture and sensiti vity should be done. Hospital-acquired UTIs are often caused by bacteria that are resistant to the usual antibiotics used for UTIs. A sensitivity test can identify which antibiotics will be effective against the offending organism. Treatment of uncomplicated c ystitis is most often a combination of sulfa medication, such as sulf amethoxa- zole and trimethoprim (Bactrim, Septra), or nitrofurantoin (Macrodantin). Complicated cystitis is often treated with ciprofloxacin (Cipro). Other antibiotics may be prescribed depending on the results of the urine culture and sensitivity. Estrogen used as an intravaginal cream may prevent recurrent UTIs in post- menopausal women. The patient is told to f inish all pre- scribed medications, force fluids unless contraindicated, and return for a follow-up urinalysis or culture after the antibiotic course is complete to ensure that the infection is gone. Pyelonephritis PATHOPHYSIOLOGY. Pyelonephritis is infection of the renal pelvis, tubules, and interstitial tissue of one or both kidneys. Pyelonephritis usually begins with colonization and infection of the lower urinary tract by means of the ascending urethral route. A preexisting condition is usually present, such as ob- struction, strictures, stones, or vesicoureteral reflux. Risk fac- tors include urological surgery, lymphatic infection, urinary stasis, and decreased immunity. Acute pyelonephritis begins in the renal medulla and spreads to the adjacent cortex. Pathophysiology includes formation of small abscesses throughout the kidney and gross enlargement of the kidney. On occasion, kidney infection is caused by bacteria spreading from a distant site through the bloodstream and entering the kidney through the glomerulus. Urosepsis is a severe infec- tion of the urinary tract with systemic inflammatory response syndrome. Prompt diagnosis and treatment are essential to prevent septic shock and death. SIGNS AND SYMPTOMS. Symptoms include fatigue, urgency, frequency, dysuria, flank pain, fever, and chills. Costoverte- bral tenderness on the right or left side (tenderness posteriorly at angle where rib and vertebrae join when struck gently with heel of examiner's closed fist), which is associated with renal disease, is noted. The urine is cloudy with increased WBCs, bacteria, casts, RBCs, and positi ve nitrites. In contrast to cystitis, the patient with p yelonephritis is much sick er and shows signs of systemic disease. In acutely ill patients, blood cultures may be obtained. DIAGNOSTIC TESTS. Several tests are helpful to dif ferentiate pyelonephritis from cystitis. With kidney infection, the urinal- ysis will show casts. Casts are microscopic particles formed in the kidney from abnormal constituents in the urine such as WBCs, RBCs, or pus. The urine specimen will have more than 100,000 colonies of bacteria per milliliter . The presence of casts always indicates a problem in the kidneys. The complete blood cell (CBC) count will sho w an elevated WBC count. There will also be an increase in sedimentation rate. THERAPEUTIC MEASURES. Treatment of pyelonephritis includes administration of antibiotics based on the results of the culture and sensitivity (Table 37.2). With severe Gram-negative infec- tions, the patient is hospitalized for intravenous (IV) antibiotics. The patient with acute p yelonephritis generally heals com- pletely after treatment and has no lasting kidney damage. COMPLICATIONS. Repeated kidney infections can result in scarring and loss of kidney function, leading to CKD. Nursing Process for the Patient With a Urinary Tract Infection Data Collection Listen to the patient' s concerns about the diagnosis. Ask about pain on urination, flank pain, or general symptoms of infection, such as fe ver, chills, and malaise. The patient's usual pattern of voiding and any urinary frequency, burning, or pain on urination is documented. Note presence of pain in the lower abdomen, flank, or costovertebral angle. Document the presence of a catheter, recent instrumentation, surgery, or other predisposing f actors. Inspect the urine for v olume, color, concentration, cloudiness, blood, or foul odor. Review urinalysis and culture results. Nursing Diagnoses, Planning, and Implementation Acute Pain related to inflammation of the urethra, bladder, and other urinary structures EXPECTED OUTCOME: The patient will report relief from pain and discomfort. • Administer antimicrobial therapy as ordered to relieve pain and discomfort from inflammation and infection. • Administer antispasmodic agents as ordered to relieve bladder irritability and pain. • Encourage fluids at 2 to 3 L per day to flush bacteria from urinary tract and promote renal blood flow. • Apply heat to suprapubic area to relieve discomfort. • Encourage voiding every 3 hours to empty the bladder, lower bacterial counts, reduce stasis, and prevent reinfection. • Suggest consuming cranberry juice or capsules to prevent bacteria from sticking on the walls of the bladder (see "Evidence-Based Practice"). • Teach patient to finish all prescribed medications to pre- vent recurrent infection. • Teach patient to avoid cola, coffee, tea, and alcohol be- cause they are urinary irritants. • Teach patient to empty bladder as soon as urge is felt and after sexual intercourse to flush bacteria out of the body. • Teach patient to avoid substances such as bubble bath and scented toilet paper, which can be irritants. • Teach patient to wear cotton underwear to reduce perineal moisture. Impaired Urinary Elimination related to frequency, nocturia, dysuria, and incontinence EXPECTED OUTCOME: The patient will return to previous voiding patterns. • Monitor urinary elimination, including frequency, consis- tency, volume, and color, to identify signs and symptoms of UTI. • Administer antimicrobial drugs as ordered to eliminate symptoms produced by microbial growth. • Encourage adequate fluids to prevent infection and dehydration. • Encourage women to void after sexual intercourse to flush bacteria out of the urethra. • Teach patient to recognize signs and symptoms of UTI to monitor effectiveness of treatment and detect recurrence. Risk for Injury related to sepsis, kidney disease, or kidney injury EXPECTED OUTCOME: The patient will be free from injury due to sepsis or recurrent infection. • Administer antimicrobial drugs as prescribed to prevent recurrent infection or complications. • Monitor intake and output to ensure adequate intake and normal output. • Monitor patient for signs and symptoms of bacteriuria and bacteremia such as fever, chills, recurrent pain. • Explain need for follow-up urine culture and imaging studies when indicated by recurrent symptoms. • Teach need for adequate fluid intake to prevent dehydra- tion and renal impairment. • Teach signs and symptoms of UTI so patient can detect recurrence or complications. The outcomes have been met if the patient v erbalizes relief of pain and discomfort, returns to previous voiding patterns, and is free from injury related to sepsis, CKD, or recurrent infectionPatient Education It is very important that patients be advised to tak e the entire prescribed antibiotic until it is gone. It is not un - common for patients to tak e medication for se veral days until symptoms are gone, and then stop. Stopping the an- tibiotic too early allows the infection to continue. It may become chronic and resistant to antibiotics as a result. In addition to encouraging fluids, cranberry products may be helpful. Patients who have one UTI commonly develop repeat in- fections. It is important that such patients recei ve education to prevent repeated infections of the urinary tract (Box 37-1 and "Nutrition Notes")

gastritis

Gastritis is inflammation of the stomach mucosa and can be acute or chronic. Causes are listed in Box 33-2. Acute Gastritis Pathophysiology Gastritis results when the protective mucosal barrier is bro- ken down and allows autodigestion from hydrochloric acid and pepsin to occur. This results in edema of the tissue and possible hemorrhage. With severe gastritis, the gastric mu- cosa can become gangrenous and perforate, which can lead to peritonitis (infection of the peritoneum). Scarring may also occur, resulting in pyloric obstruction. Causes of Gastritis Diet • Alcohol • Spicy foods Microorganisms • Helicobacter pylori • Salmonella Medications • Aspirin • Nonsteroidal anti-inflammatory drugs • Corticosteroids • Digitalis • Chemotherapy drugs Stress • Physiological • Psychological Trauma Other Factors • Reflux of bile • Smoking • Radiation • Nasogastric suctioning Endoscopic procedures Signs and Symptoms The major symptom of gastritis is abdominal pain, which is often accompanied by nausea and anorexia. The patient may also experience abdominal tenderness, a feeling of fullness, reflux, belching, and hematemesis. If the cause of the gastritis is contaminated food, symptoms including diarrhea usually start within 5 to 6 hours. Therapeutic Measures Treatment of gastritis is remo val of the irritating substance and provision of a bland diet of liquids and soft foods along with antacids. Medication therap y may include antiemetics to control vomiting and antacids and/or histamine receptor antagonists to control pain. With a bland diet, the patient usu- ally recovers in a short period of time. Chronic Gastritis Chronic gastritis occurs over time and is classified as type A or type B. Type A Type A chronic gastritis is often referred to as autoimmune gastritis and occurs in the fundus (body of stomach). Chronic gastritis type A is diagnosed by endoscopy, upper GI x-ray examination, and gastric aspirate analysis (see Chapter 32). Type A gastritis is often asymptomatic. P a- tients with type A gastritis usually do not secrete enough in- trinsic factor from their stomach cells and as a result ha ve difficulty absorbing vitamin B12, which leads to pernicious anemia (discussed later). Type B Type B chronic gastritis affects the antrum and pylorus (lower end of the stomach near the duodenum) and is associated with Helicobacter pylori bacterial infection. Type B is the most common type of chronic gastritis. Signs and symptoms in- clude poor appetite, heartburn after eating, belching, a sour taste in the mouth, and nausea and vomiting. Type B gastritis can also be diagnosed by endoscopy, upper GI x-ray exami- nation, and gastric aspirate analysis. H. pylori infection is treated with antibiotics. Stress-Induced Gastritis A small number of patients who are critically ill may develop GI mucosal damage from ischemia.The stress response to the illness causes reduced blood flo w to the stomach and small intestine, resulting in ischemia and damage to the mucosa.The damaged mucous barrier then allows acid secretions to create ulcerations. Preventive treatment has dramatically reduced stress ulceration, which can have a high mortality rate because of the multiple bleeding ulcer sites. This treatment includes trauma care that quickly restores oxygen to the stomach, as well as early feeding within 24 hours of the trauma and pro- phylactic sucralfate (forms a gel that binds to the base of an ulcer), antacids, or histamine blockers.

HEmorrhoids

Hemorrhoids Hemorrhoids are enlarged veins within the anal tissue. They are caused by an increase in pressure in the veins, often from increased intra-abdominal pressure. Internal hemorrhoids occur above the internal sphincter, and external hemorrhoids occur below the external sphincter. Most hemorrhoids are caused by straining during bowel movements. They are com- mon during pregnancy. Prolonged sitting or standing, obesity, and chronic constipation also contribute to hemorrhoids. Por- tal hypertension related to liver disease may also be a factor. Internal hemorrhoids are usually not painful unless the y prolapse. They may bleed during bowel movements. External hemorrhoids cause itching and pain when inflamed and filled with blood (thrombosed). Inflammation and edema occur with thrombosis, causing severe pain and possibly infarction of the skin and mucosa over the hemorrhoid. Treatment is aimed at pre venting constipation, avoiding straining during defecation, maintaining good personal hy- giene, and making lifestyle changes to relie ve hemorrhoid symptoms and discomfort. Increased fluid intak e and stool softeners can be used to reduce the need for straining. Daily sitz baths increase circulation to the area and aid in comfort and healing. Prolonged standing and sitting are avoided. As- tringents, such as witch hazel, can be used for symptom re- lief. Anti-inflammatory medications may be tried, such as steroid creams or suppositories. Alternating ice and heat helps relieve edema and pain for thrombosed hemorrhoids. The blood clot will be removed by a HCP. If surgery is required for internal hemorrhoids methods in- clude rubber-band ligation using a rubber band around the hemorrhoid that cuts off the blood supply, causing the hem- orrhoid to slough off into the stool; infrared coagulation that burns off the hemorrhoid; sclerotherapy that shrinks the hem- orrhoid with a chemical solution; hemorrhoidectomy to sur- gically remove the hemorrhoid. Patient education includes prevention and self-care. The patient should be instructed to consume a high-fiber diet and 2 to 3 L of fluid a day to promote regular bowel movements. The effects and side effects, proper dosage, and frequency of local or topical medications should be explained. If the patient has surgery, analgesics are given as needed because the many nerve endings in the anal canal can cause severe pain. Comfort measures such as a side-lying position and fresh ice packs can be used to relieve pain. After the first postoperative day, sitz baths may be ordered. Unfortunately, a side effect of opioid analgesics is constipation, which needs to be avoided, especially in the immediate postoperative pe- riod. Because the first bowel movement can be painful and anxiety provoking, stool softeners are gi ven and analgesics administered before the first bowel movement.

bowel obstruction

Intestinal obstructions occur when the flow of intestinal con- tents is blocked. The two types of intestinal obstruction are mechanical and nonmechanical, both of which can be either partial or complete. Mechanical obstruction occurs when a blockage occurs within the intestine from conditions causing pressure on the intestinal walls such as adhesions, twisting of the bo wel, or strangulated hernia. Nonmechanical obstruction occurs when peristalsis is impaired and the intestinal contents cannot be propelled through the bowel. Nonmechanical obstruction is seen following abdominal surgeries, trauma, mesenteric is- chemia, or infection. The severity of the obstruction depends on the area of bowel affected, the amount of occlusion within the lumen, and the amount of disturbance in the blood flo w to the bowel (Table 34.8). Small-Bowel Obstruction Pathophysiology When obstruction occurs in the small bowel, a collection of intestinal contents, gas, and fluid occurs proximal to the ob- struction. The distention that results stimulates gastric secre- tion but decreases the absorption of fluids. As distention worsens, the intraluminal pressure causes a decrease in v e- nous and arterial capillary pressure, resulting in edema, necrosis, and eventually perforation of the intestinal wall. Etiology Following abdominal surgery, loops of intestine may adhere to areas in the abdomen that are not healed. This may cause a kink in the bowel that occludes the intestinal flow. These ad- hesions, or bands of scar tissue, are the most common cause of small-bowel obstruction and are usually acquired from pre- vious abdominal surgery or inflammation. Hernias and neo- plasms are the ne xt most common causes, follo wed by inflammatory bowel disease, foreign bodies, strictures, volvu- lus, and intussusception. A volvulus occurs when the bowel twists, occluding the lumen of the intestine. Intussusception TABLE 34.8 BOWEL OBSTRUCTION SUMMARY occurs when peristalsis causes the intestine to telescope into itself (Fig. 34.5). These conditions are mechanical obstructions. Paralytic, or adynamic, ileus is a nonmechanical obstruction that occurs when the intestinal peristalsis decreases or stops because of a vascular or neuromuscular pathological condition. Box 34-1 lists causes of nonmechanical obstructions. Signs and Symptoms The patient initially reports wavelike abdominal pain and vom- iting. Initially, flatus and feces that are lo w in the bo wel and blood and mucus may be passed, but this stops as the obstruc- tion becomes worse. The symptoms progress as the obstruction worsens or becomes complete. As the obstruction becomes more extreme, peristaltic waves reverse, propelling the intes- tinal contents toward the mouth, eventually leading to fecal vomiting. Peristaltic waves may be visible in a thin person. Pain and abdominal distention are present. P ain that is sharp and sustained may indicate perforation. In mechanical obstruc- tions, high-pitched, tinkling bowel sounds are heard proximal causes of nonmechanical bowel obstruction• Abdominal surgery and trauma • Pneumonia • Spinal injuries • Hypokalemia • Myocardial infarction • Peritonitis • Vascular insufficiencyto the obstruction and are absent distal to it. If the obstruction is nonmechanical, there is an absence of bowel sounds. Loss of fluid and electrolytes leads to dehydration, with its associated symptoms of e xtreme thirst, dro wsiness, aching, and general malaise. The lower in the GI tract the ob- struction is, the greater the abdominal distention. An uncor- rected obstruction can lead to shock and possibly death. Diagnostic Tests Dilated loops of bowel are evident in radiographic studies and CT scans. If strangulation or perforation occurs, leuk o- cytosis is evident. Hemoglobin and hematocrit le vels are elevated if the patient is dehydrated, and serum electrolyte levels are decreased. Therapeutic Measures In most cases, the patient is NPO and the bo wel is decom- pressed using a NG (or, rarely, a tungsten-weighted intestinal) tube, which relieves symptoms and may resolve the obstruc- tion. An IV solution with electrolytes is initiated to correct the fluid and electrolyte imbalance. Sometimes IV antibiotics are begun. Complete mechanical obstruction requires surgical intervention, such as removal of tumors, release of adhesions, or bowel resection with anastomosis. Large-Bowel Obstruction Pathophysiology Obstruction in the large bowel is less common and not usu- ally as dramatic as small-bowel obstruction. Dehydration oc- curs more slowly because of the colon's ability to absorb fluid and distend well beyond its normal full capacity. If the blood supply to the colon is cut off, the patient's life is in jeopardy because of bowel strangulation and necrosis. Etiology Most large-bowel obstructions occur in the sigmoid colon and are caused by carcinoma, inflammatory bowel disease, diver- ticulitis, or benign tumors. Impaction of stool may also cause obstruction. Signs and Symptoms Symptoms of large-bowel obstruction develop slowly and de- pend on the location of the obstruction. If the obstruction is in the rectum or sigmoid, the only symptom may be consti- pation. As the loops of bowel distend, the patient may report crampy lower abdominal pain and abdominal distention. Vomiting, if it occurs, is a late sign and may be fecal. High- pitched tinkling bowel sounds may be heard.A localized ten- der area and mass may be felt on palpation. Lar ge-bowel obstructions, if not diagnosed and treated, can lead to gan- grene, perforation, and peritonitis. Therapeutic Measures Radiological examination reveals a distended colon. If im- paction is present, enemas and manual disimpaction may be effective. Other mechanical blockages may require sur gical intervention. Surgical resection of the obstructed colon may be neces- sary. A temporary colostomy may be indicated to allo w the bowel to rest and heal. Sometimes an ileoanal anastomosis is done. A patient who is a poor surgical risk may have a cecos- tomy (an opening from the cecum to the abdominal w all) to allow diversion of stool. Nursing Process for the Patient With a Bowel Obstruction DATA COLLECTION. Each quadrant of the abdomen is auscul- tated for bowel sounds to identify the location of the obstruc- tion. The abdomen is palpated for distention, f irmness, and tenderness. The amount and character of stool, if any, are doc- umented. Pain is assessed using the institution' s pain scale and described according to location and character , such as crampy or wavelike. Vital signs are monitored for signs of in- fection or shock. Daily weight and intake and output are mon- itored. Skin turgor is assessed for fluid deficit. If a nasogastric or nasointestinal tube is in place, the amount, color, and char- acter of drainage are documented. NURSING DIAGNOSES, PLANNING, AND IMPLEMENTATION. Acute Pain related to abdominal distention EXPECTED OUTCOME: The patient will state pain is relieved or at an acceptable level within 30 minutes of report of pain. • Assess pain level using rating scale to consistently com- municate patient level. • Give medications ordered for pain cautiously because they may mask symptoms of perforation and decrease intestinal motility. • Position patient in semi-Fowler's position to reduce ten- sion on the abdomen. Risk for Deficient Fluid Volume related to vomiting EXPECTED OUTCOME: The patient will maintain vital signs and urine output within normal limits at all times. • Accurately monitor intake and output and note trends to identify fluid deficit. • Maintain fluid replacement as ordered to prevent dehydration. Risk for Electrolyte Imbalance related to suctioning EXPECTED OUTCOME: The patient will maintain vital signs and urine output within normal limits at all times. • Monitor electrolyte values to identify imbalances. • Monitor vital signs, and watch for signs of electrolyte im- balances such as weakness accompanied by low potas- sium levels to identify imbalances for prompt treatment. • Give ice chips sparingly if ordered by the HCP. Melted ice increases electrolyte and hydrochloric acid removal when suctioned from the stomach, and electrolyte imbalance and metabolic alkalosis occur. Risk for Dysfunctional Gastrointestinal Motility EXPECTED OUTCOME: The patient will maintain passage of flatus and stool. • Monitor GI function for presence of flatus and bowel movements to detect problems. • Maintain orogastric, NG, or nasointestinal tube on low in- termittent suction as ordered to relieve discomfort from distention. • Maintain NPO status to rest the bowel and promote comfort. EVALUATION. Goalsaremetifthepatientstatesthatpainis controlled, fluid is balanced, electrolytes are within normal limits, and GI motility is normal.

Renal failure

Polycystic kidney disease is a hereditary disorder that can re- sult in CKD. The disease affects men and women equally. Polycystic kidney disease is characterized by formation of multiple cysts in the kidney that can eventually replace nor- mal kidney structures. The cysts are grapelike and contain serous fluid, blood, or urine.The patient typically first shows signs of the disease in adulthood. The initial symptoms include a dull heaviness in the flank or lumbar re gion and hematuria. Other symptoms include hypertension and UTIs. People with inherited polyc ystic kidney disease may also experience aneurysms in the brain and di verticulosis in the colon. As the disease progresses, the patient develops symp- toms of CKD (discussed later). The renal cysts are usually diagnosed with ultrasound imaging. Ultrasound uses no dyes or radiation, so it is safe for all patients, including pre gnant women. Often there is a strong f amily history of polycystic kidney disease. There is no treatment to stop the progression of polycystic kidney disease. Complications such as UTIs are treated as needed. Headaches that are se vere due to hypertension or seem to feel different might be caused by aneurysms in the brain. A patient with severe or recurring headache should see a HCP. As the disease progresses, treatment for hypertension and eventual CKD may be needed. Because polyc ystic dis- ease is hereditary, patients should be counseled about the risks of children inheriting it. CHRONIC RENAL DISEASES Diabetic Nephropathy Diabetic nephropathy is the most common cause of CKD. It is a long-term complication of diabetes mellitus in which the effects of diabetes result in damage to the small blood vessels in the kidne ys. Microalbuminuria may be detected within 5 years of the onset of type 1 diabetes and 10 to 15 years after the onset of type 2 diabetes. Renal damage appears about 15 to 20 years after onset of type 1 diabetes, but it may also be a complication of type 2 diabetes. Risk factors for development of diabetic nephropathy include hypertension, genetic predis- position, smoking, and chronic hyperglycemia. Careful control of blood glucose le vels reduces the risk of nephropathy in patients with diabetes. Pathophysiology Multiple factors contribute to diabetic nephropathy. It begins with increased osmotic pressure from hyper glycemia, in- creased diuresis and compensatory cell growth and expansion, and increased glomerular filtration rate (GFR). Widespread atherosclerotic changes occur in the blood v essels of patients with diabetes, decreasing the blood supply to the kidne y. Ab- normal thickening of glomerular capillaries damages the glomerulus, allowing protein to leak into urine. P atients with diabetes also commonly develop pyelonephritis and renal scar- ring. Another complication of diabetes, neurogenic bladder , causes incomplete bladder emptying. This results in urine re- tention, which can cause infection or obstruction of urine, fur- ther damaging the kidneys. Initially, patients lose only small amounts of protein in their urine (microalbuminuria); this disease can be detected only with careful w atching by the HCP , using frequent examinations of the urine. As the disease progresses, high- output CKD (nonoliguria) can de velop, in which a lar ge amount of diluted urine is e xcreted without the usual amounts of w aste products dissolv ed in the urine. The patient can lose large amounts of protein in the urine and develop nephrotic syndrome, which causes massive edema because of low levels of albumin in the blood. As renal function decreases, the patient needs smaller doses of in- sulin because the kidney normally degrades insulin. Be- cause the kidney is no longer able to break do wn insulin and excrete it, small doses of insulin circulate in the body for long periods. Symptoms The progression of nephropathy is marked by microalbumin- uria advancing to proteinuria. Hypertension accelerates the renal damage. As diabetic nephropathy progresses, urine out- put decreases, toxic w astes accumulate, and the patient de- velops CKD. For symptoms, see the discussion of CKD in a later section. Complications Patients with diabetic nephropathy often have a guarded prog- nosis because they are vulnerable to all the complications of long-term diabetes in addition to kidney disease. The risk of cardiovascular disease is significant with the progression of protein spilling in the urine. Diagnostic Tests Diabetic nephropathy is diagnosed by carefully watching the patient with diabetes for onset of protein spillage or microal- buminuria in the urine, which is an early sign of the disease. Serum creatinine levels and 24-hour creatinine clearance tests are then done to confirm the presence and extent of diabetic nephropathy. Therapeutic Measures In the early stages of diabetic nephropathy , strict control of blood glucose levels and blood pressure can help slo w the progress of the disease and reduce symptoms. Angiotensin- converting enzyme (ACE) inhibitors or angiotensin II recep- tor blockers (ARBs) may be given to slow the decline of the GFR and microalbuminuria. As the disease progresses, the patient needs dialysis to maintain life. Unfortunately , other complications related to diabetes cause patients to tolerate dialysis less well than patients with CKD from other causes. Kidney or kidney-pancreas transplant, when available, is the treatment of choice for the patient with diabetic nephropathy and often improves the patient's chance for a healthier life. Nephrotic Syndrome Nephrotic syndrome is the excretion of 3.5 g or more of protein in the urine per day. Nephrotic syndrome may occur as a result of other disease processes. In nephrotic syndrome, large amounts of protein are lost in the urine from increased glomerular mem- brane permeability. As a result, serum albumin and total serum protein are decreased. Normally, albumin and other serum pro- teins maintain fluid within the v ascular space. When levels of these proteins are low, fluid leaks from the blood vessels into tis- sues, resulting in edema. With very low levels of protein, ascites and massive widespread edema (anasarca) occur. In response to the low protein levels, the liver produces lipoproteins. As a result, serum cholesterol, low-density lipoproteins, and triglyceride lev- els are elevated. Urine may appear foamy from lipoproteinemia. Loss of immunoglobulins may lead to increased susceptibility to infection. Elevated blood pressure readings are noted. Treatment is focused on the cause and symptoms of nephrotic syndrome. To control edema, sodium intake is restricted. Protein intake is based on the severity of urinary protein loss. Diuretics may be used. Lipid-lowering drugs may be tried.Anticoagulants are given for thrombosis prevention. In some cases, corticos- teroids may be used to reduce inflammation. Complications of nephrotic syndrome include impaired im- mune function, nutritional imbalances, and, most importantly, increased blood coagulation, which is due to urinary loss of clotting inhibitors such as antithrombin III and plasminogen. Nursing care focuses on the edema and pre venting infec- tion. For edema, daily weights, careful measurements of intake and output, and abdominal girth measurements are performed and documented. Edematous tissue must be protected from in- jury. Preventing malnutrition is challenging b ut important in maintaining normal body functions. Nephrosclerosis Hypertension damages the kidneys by causing sclerotic changes in the small arteries and arterioles, such as arteriosclerosis with thickening and hardening of the renal blood v essels (nephrosclerosis). Arteriosclerotic changes in the kidney blood vessels result in a decreased blood supply to the kidne y (is- chemia of the kidney) and can eventually destroy the kidney. The remaining nephrons try to compensate with vasodilation to increase blood flow to the glomeruli. This results in increased glomerular pressure and filtration, which thickens the blood ves- sels. High pressure in the kidneys causes the vessels to weaken and hemorrhage. Large areas of the kidney become damaged. Symptoms of nephrosclerosis include proteinuria, hyaline casts in the urine, and, as it progresses, symptoms of CKD. The treatment for nephrosclerosis is to reduce blood pres- sure and treat the hypertension. The patient is placed on anti- hypertensive medications or, if already on these, changed to stronger antihypertensive medications. The patient is placed on a low-sodium diet. Dialysis may be used to maintain life. The prognosis is often poor because by the time the patient has developed nephrosclerosis, there is widespread arterioscle- rosis throughout the body. Arteriosclerosis makes the patient prone to myocardial infarctions or cerebrovascular accidents. The major nursing diagnosis that is rele vant when the pa- tient develops nephrosclerosis is Ineffective Health Mainte- nance. The priority is to help the patient learn as much about the control of hypertension as possible.The patient should also be taught the symptoms of CKD. Once the patient has lost renal function, the nursing care plan for CKD is appropriate. GLOMERULONEPHRITIS Pathophysiology Glomerulonephritis is an inflammatory disease of the glomeru- lus. It can be caused by a v ariety of factors including immuno- logical abnormalities, toxins, v ascular disorders, and systemic diseases. Inflammation occurs as a result of the deposition of antigen-antibody complexes in the basement membrane of the glomerulus or from antibodies that specifically attack the base- ment membrane. The resulting immune reaction in the glomeru- lus causes inflammation, which in turn causes the glomerulus to be more porous, allowing proteins, WBCs, and RBCs to leak into the urine. Etiology Acute Poststreptococcal Glomerulonephritis Glomerulonephritis is most commonly associated with a group A beta-hemolytic streptococcal infection following a strepto- coccal infection of the throat or skin.This is the most common cause in children and young adults.Antibodies form complexes with the streptococcal antigen and are deposited in the base- ment membrane of the glomerulus, inducing damage from in- flammation. Damaged glomeruli become unable to filter blood correctly, and protein leaks into the urine. Edema, oliguria, and hypertension result. Glomerulonephritis typically de velops about 6 to 10 days after the preceding infection. The disease has an abrupt onset. Other kinds of bacteria and viruses can also be the offending infectious agent. Goodpasture's Syndrome Occasionally glomerulonephritis is caused by an autoimmune response, in which the person, for unkno wn reasons, forms antibodies against his or her own glomerular basement mem- brane. Glomerulonephritis caused by an autoimmune response usually progresses rapidly and often leads to CKD. Chronic Glomerulonephritis Chronic glomerulonephritis occurs o ver years as a result of glomerular inflammatory disease. There may be no history of renal disease before the diagnosis. Often, proteinuria and hema- turia may have been noted previously before the diagnosis. Sys- temic lupus erythematosus and insulin-dependent diabetes mellitus may precede chronic glomerular injury. It is often dis- covered during an examination for another concern. Ultrasound, CT scan, or renal biopsy is used to diagnose the cause. Symptoms Symptoms of glomerulonephritis include fluid overload with oliguria, hypertension, electrolyte imbalances, and edema Edema may begin around the eyes (periorbital edema) and face and progress to the abdomen (ascites), lungs (pleural effusion), and extremities. Flank pain may be pres- ent. Blood urea nitrogen (BUN) and creatinine levels may be elevated. Urinalysis shows RBCs, WBCs, albumin, and casts. The urine is dark or cola colored from old RBCs and may be foamy because of proteinuria. Complications The prognosis is good for acute glomerulonephritis acquired in childhood, and most children reco ver completely. Adults who develop glomerulonephritis may recover renal function or progress to chronic glomerulonephritis. Some patients de- velop rapidly progressi ve glomerulonephritis, which can quickly lead to acute renal injury. Chronic glomerulonephritis is a slow process characterized by hypertension, gradual loss of renal function, and eventual CKD. Diagnostic Tests Glomerulonephritis is diagnosed with urinalysis, which shows protein, casts, or RBCs and ele vated serum levels of nitrogenous wastes (creatinine, urea). Hypertension may be present. Kidney ultrasound, x-ray, or biopsy may be done to determine abnormal kidney shape, size, blood flow, inflam- mation, or scarring of the glomeruli. TABLE 37.6 GLOMERULONEPHRITIS SUMMARY Therapeutic Measures Most cases of acute glomerulonephritis resolve spontaneously in about a week, but some progress to CKD. Treatment is pri- marily symptomatic. Sodium and fluid restrictions may be or - dered, along with diuretics to treat fluid retention. Medications may be given to control hypertension. If associated with a strep- tococcal infection, antibiotics are given to treat any remaining infection. If fluid overload is severe, dialysis may be done. Nursing Care Nursing care for a patient with glomerulonephritis focuses on symptom relief. Vital signs are monitored because the pa- tient may be critically ill. During the acute phase, rest is en- couraged. Edema is controlled with fluid and sodium intake restrictions. Protein intake may be limited if the kidneys are not filtering protein waste products (as seen by increased serum BUN and creatinine levels). Other care is discussed in the next section on CKD. Teaching the patient about pre- venting glomerulonephritis is important. Antibiotics for di- agnosed streptococcal throat infections should be tak en for prevention. ACUTE KIDNEY INJURY OR CHRONIC KIDNEY DISEASE Kidney disease is diagnosed when the kidneys are no longer functioning adequately to maintain normal body processes. This results in dysfunction in almost all other parts of the body as a result of imbalances in fluid, electrolytes, and cal- cium levels, as well as impaired RBC formation and de- creased elimination of waste products. It can be acute (acute kidney injury) with sudden onset of symptoms, or it can be chronic (CKD), occurring gradually over time. For more in- formation on kidne ys, visit the American Kidney Fund (www.kidneyfund.org), the National Kidne y Foundation (www.kidney.org), and the American Association of Kidney Patients (www.aakp.org). Acute Kidney Injury Acute kidney injury (AKI) is the sudden (hours to days) loss of the kidneys' ability to clear w aste products and re gulate fluid and electrolyte balance. Rapid accumulation of toxic wastes from protein metabolism in the blood (azotemia) oc- curs. In azotemia, the serum urea level (measured by BUN) and creatinine level are elevated. Potassium imbalances may lead to tachycardia. Most types ofAKI are reversible if diag- nosed and treated early; however, AKI can lead to CKD. It is often associated with a urine output of less than 30 mL/hr or 400 mL/day. It may be caused by hypotension, dehydration, vascular obstruction, glomerular disease, or acute tub ular necrosis, in which the tubules are damaged. This may occur after administration of diagnostic contrast agents (contrast- induced nephropathy). There are three major mechanisms of injury in mechanisms are hypoperfusion, direct tissue injury, and hyper- sensitivity reactions causing renal inflammation. InAKI, rapid damage to the kidney causes waste products to accumulate in the bloodstream, resulting in signs and symptoms.The patient becomes oliguric, with urine output decreasing to less than 20 mL/h. Treatment is directed toward correcting the cause, supporting the patient with dialysis, and preventing complica- tions that may lead to permanent damage. Many patients with AKI recover completely. About 40% to 50% of patients hos- pitalized with intrarenal AKI die from complications, such as infection, pneumonia, or sepsis (AKI can progress through four stages, with an intrarenal cause taking a longer reco very time because there is actual renal damage. Once an event causes AKI in the initial phase, symptoms occur in hours to days. OLIGURIC PHASE. In the oliguric phase, less than 400 mL of urine is produced in 24 hours. Fifty percent of those withAKI experience this phase, which occurs from 24 hours to 7 days after the initial phase. This phase can last up to 2 weeks to several months. Prognosis for renal recovery is decreased the longer this phase lasts. In the oliguric phase, fluid is retained, electrolytes become imbalanced, and waste products are not excreted as urine out- put decreases. Signs of fluid overload arise. Serum potassium rises while sodium is lost in the urine, creating a normal or low serum sodium level. The longer this phase lasts, the more effects that are seen. These may include metabolic acidosis from reduced hydrogen ion excretion and sodium bicarbonate levels, increased phosphate and decreased calcium levels, ab- normal blood cells (RBCs, WBCs, platelets), neurologic ef- fects ranging from confusion to seizures to coma, and finally effects on all body systems as is seen in chronic renal failure (discussed later). DIURETIC PHASE. As the kidneys begin to excrete waste prod- ucts again, 1 to 3 L/day of urine is produced. Osmotic diuresis occurs from the elevated waste products (urea), which the body is attempting to eliminate. The kidneys are not yet able to concentrate urine, so dehydration and hypotension are a concern. It is important for the nurse to monitor for hypo v- olemia, hyponatremia, hypokalemia, and hypotension in this phase. Serum BUN and creatinine levels are high until the end of this phase, when they begin to return to normal. This phase may last 1 to 3 weeks. RECOVERY PHASE. In this final phase, recovery begins as the glomerular filtration rate rises. Waste product levels (BUN, creatinine) decrease greatly within the f irst 2 weeks of this phase. However, recovery can take up to 1 year. Those who do recover usually do so without complications. Older adults are more at risk for reduced reco very of renal function. In those who do not recover renal function, CKD occurs. Etiology AKI is often classified as prerenal, intrarenal, or postrenal. These categories relate to the causes leading to the injury . Each category is associated with the location of the cause in the kidney. Understanding the cause can point to the direction of treatment plans helpful to the patient. PRERENAL INJURY. Prerenal (before the kidne y) injury, the most common cause of AKI, is associated with a decrease or interruption of blood supply to the kidne ys. Causes may in- clude decreased blood pressure from dehydration, blood loss, shock, or trauma to or blockage in the arteries that carry blood to the kidne ys. When the nephrons recei ve an inadequate blood supply, they are unable to make urine, and waste prod- ucts are not adequately remo ved. Use of nonsteroidal anti- inflammatory drugs (NSAIDs) and cyclooxygenase-2 (COX) inhibitors can also lead to prerenal injury. These drugs impair the autoregulatory responses of the kidne y by blocking prostaglandin, which is needed for renal perfusion. Prerenal injury can be diagnosed by e valuating possible causes. If dehydration is the cause, then an IV fluid challenge may be given. With increased IV fluid, more blood flows to the kidneys for filtering, which increases urine output and waste product filtering. An arteriogram of the renal arteries is helpful to determine if the blood supply to the kidne ys is decreased or blocked; angioplasty may be used to open the blockage. Serum creatinine increases and creatinine clearance decreases. Urinalysis may be helpful in determining the cause as well. Newer biomarkers such as interleukin 18, neutrophil gelatinase-associated lipocalin (NGAL), and kidne y injury molecule-1 (KIM-1) might be able to provide more informa- tion on the type of kidne y injury. These markers are under ongoing study. INTRARENAL INJURY. Intrarenal (inside the kidne y) injury occurs when there is damage to the nephrons inside the kid- ney. The most common causes are ischemia, reduced blood flow, and toxins. Other causes are infectious processes lead- ing to glomerulonephritis, trauma to the kidney, exposure to nephrotoxins, allergic reactions to contrast agents, and se- vere muscle injury, which releases substances that are harm- ful to the kidneys. A number of substances can be toxic to the kidne ys (nephrotoxic) when they enter the body (Table 37.7). Kidney damage is most likely to occur when these substances enter TABLE 37.7 COMMON NEPHROTOXINS the body in high concentrations or when pree xisting kidney damage is present for some other reason. Man y commonly administered medications can be nephrotoxic. Aminoglyco- sides are nephrotoxic antibiotics; when they are administered, blood levels of the drugs are carefully monitored to a void toxic levels. CONTRAST-INDUCED NEPHROPATHY. Contrast agents used during tests such as IV pyelograms and CT scans can cause kidney damage, especially when the patient is dehydrated and has preexisting renal damage. The incidence increases with age greater than 60 years, decreased renal function, poor renal perfusion, or exposure to nephrotoxic drugs. Contrast media has the potential to cause renal vasoconstriction, hypoxia, and alteration of renal blood flow (Jorgensen, 2013). Loss of reg- ulation of renal blood flow causes decreased oxygen transport with causes increasing renal medullary hypoxia, necrosis and renal cell tubular collapse (Isaac, 2012). Before administra- tion of contrast media, patients should be assessed for risk factors: diabetes mellitus, hypertension, dyslipidemia, ad- vanced age over 70, renal surgery. Anemia, proteinuria, hy- peruricemia, and the use of diuretics and other nephrotoxic drugs increases the likely hood of contrast-induced nephropa- thy. Prevention strategies should focus on screening patients for dehydration and risk f actors. IV hydration with normal saline is most effective. Hydration is inexpensive and usually without risks. Studies are being done on the use of sodium bicarbonate infusion as well as the use of N-acetylc ysteine to prevent contrast-induced nephropathy. (Jorgensen, 2013). POSTRENAL INJURY. Postrenal (after the kidney) injury is as- sociated with an obstruction that blocks the flow of urine out of the body. Only 5% of acute kidney injuries are classified as postrenal. In this case, the blood supply to the kidneys and nephron function initially may be normal, but urine is unable to drain out of the kidne y, resulting in the backup of urine and impaired nephron function. Common causes are kidne y stones, tumors of the ureters or bladder , and an enlar ged prostate that blocks the flow of urine. Diagnosis of causes can be done with x-ray e xamination of the kidneys, ureters, and bladder. Cystoscopy will show tumors, stones, or prostate enlargement. Renal ultrasound can measure kidney size, detect tumors and blockages, and reveal cystic disease. Surgical intervention may be needed to correct the problem. Measures AKI is treated by relieving the cause. Prevention of perma- nent damage is the goal of treatment. Signs and symptoms are managed as they develop, and supportive care is given. Treatment may include restoring fluid and electrolyte bal- ance, discontinuing nephrotoxic drugs that may have caused the problem, bypassing urinary tract obstructions with catheters, or using short-term continuous renal replacement therapy to filter blood and restore potassium and other elec- trolytes to normal. Some symptoms, such as anemia, may not have time to develop in the patient with AKI as they do in CKD. The care of the patient with AKI is similar to care of the patient with CKD. CONTINUOUS RENAL REPLACEMENT THERAPY. Continuous renal replacement therapy (CRRT) is used to remo ve fluid and solutes in a controlled, continuous manner in unstable patients with AKI. Unstable patients may not be able to tol - erate the rapid fluid shifts that occur in hemodialysis, so CRRT provides an alternative therapy that results in less dra- matic fluid shifting. CRRT can be used with hemodialysis, which is needed if se vere symptoms of uremia (hyper- kalemia) are present. CRRT is not as complex as hemodialysis and can be done for more than a month, if needed, via tem- porary vascular access. During CRRT, a permeable hemof ilter is attached to the vascular access. Blood flows through the hemofilter and ex- cess fluids and solutes mo ve into a collection bag. The re- maining blood returns to the patient via the venous access. If desired, replacement fluid and electrolytes can be gi ven through the vascular access. Monitoring intake and output, fluid and electrolytes, daily weights, hourly vital signs, and vascular access is important.

Nausea and vomiting

Nausea is the subjective feeling of the urge to vomit. Vomit- ing is the act of e xpelling stomach contents from the body through the esophagus and mouth. It is a protective function to rid the body of harmful substances from the gastrointesti- nal (GI) tract. This reflex is controlled by the vomiting center of the brain. Stimuli and conditions that are directly related to the GI tract or independent of it can trigger nausea and vomiting. Viral GI infection and other infections, motion sickness, stress, pregnancy, medications (narcotics), myocar- dial infarction, uremia, and other conditions may cause nau- sea and vomiting. Therapeutic Measures Nausea and vomiting may be self-limited and require no in- tervention. If it is prolonged, however, dehydration and elec- trolyte imbalances can occur. The loss of hydrochloric acid from the stomach can result in metabolic alkalosis. Emesis that looks lik e coffee grounds (dark bro wn) occurs from bleeding in the stomach and requires further assessment. Nursing Process for the Patient With Nausea and Vomiting Data Collection The characteristics of the episodes of the nausea and vomiting are noted. Medical conditions, medications, and treatments are documented to aid in diagnosing the cause. Signs of early fluid deficit, such as weakness, headache, muscle cramps, rest- lessness, inability to concentrate, and postural hypotension, are reported for treatment. Later signs include confusion, olig- uria, cold clammy skin, and chest or abdominal pain. Nursing Diagnoses, Planning, and Implementation Nausea related to various causes EXPECTED OUTCOME: Patient will report no nausea or relief from nausea within 30 minutes of reporting nausea. • Provide quiet, odor-free, visually clean environment to avoid triggering stimuli. • Give antiemetics as ordered to relieve nausea. • Provide frequent oral care to remove emesis taste and en- hance patient comfort. • Teach patient to avoid triggering fluids or foods to prevent nausea and vomiting. Risk for Aspiration related to decreased gag reflex or unconsciousness EXPECTED OUTCOME: Patient's airway and lung sounds will remain clear at all times. • Identify patients who are nauseated and at risk of aspira- tion to plan preventive care. • Turn patient onto side if nauseated and vomiting to protect airway and prevent aspiration. Deficient Fluid Volume EXPECTED OUTCOME: Patient's vital signs will remain within normal limits. Monitor for early signs of hypovolemia in patients with vomiting to allow treatment and prevent complications. • Obtain daily weight on same scale, at same time of day, with same type of clothing to detect fluid losses. (A 1-pound weight loss reflects a fluid loss of 500 mL.) • Monitor intake and output and vital signs including ortho- static blood pressure per shift or daily or more frequently as patient's condition indicates to report changes for prompt treatment. • Provide fluids as ordered to hydrate patient. IV fluids allow the GI tract to rest. Slightly chilled sports replace- ment drinks or ginger ale may be given in small amounts at frequent intervals. Monitor older adults for excess fluid volume during treat- ment of deficient fluid volume to prevent and detect fluid overload, which may occur quickly in the older adult. The patient's goals are met if nausea is not present, lung sounds remain clear, and vital signs remain within normal limits.

Pancreatitis

Pancreatitis Pancreatitis, inflammation of the pancreas, may be either acute or chronic. The two forms of pancreatitis have different courses and are considered two different disorders. Acute Pancreatitis Pathophysiology Inflammation of the pancreas appears to be caused by a process called autodigestion. Recall that the pancreas normally secretes digestive enzymes. For reasons not fully understood, pancreatic enzymes can be activated while they are still in the pancreas and be gin to digest the pancreas. In addition, large amounts of enzymes are released by inflamed cells. As the pancreas digests itself, chemical cascades occur. Trypsin destroys pancreatic tissue and causes v asodilation. As capillary permeability increases, fluid is lost to the retroperitoneal space, causing shock. In addition, trypsin appears to set off another chain of events that causes the con- version of prothrombin to thrombin, so that clots form. The patient may develop disseminated intravascular coagulation (see Chapter 28). Etiology Acute pancreatitis is most commonly associated with heavy alcohol consumption or gallstones. Alcohol appears to act directly on the acinar cells of the pancreas and the pancreatic ducts to irritate and inflame the structures. Cholelithiasis (gallstones) or cholangitis (inflammation of the bile ducts) can also trigger pancreatitis. Gallstones may plug the pancreatic duct and cause inflammation from excessive fluid pressure on sensiti ve ducts. The irritant effect of bile itself may cause inflammation. Ele vated triglycerides, pancreatic tumors, or, rarely, medications can cause pancreatitis. Prevention Caution patients who drink alcohol to stop. P atients with biliary disease need to seek medical treatment for these to occur from secondary causes. From the onset of symptoms, cardiovascular, pulmonary (including acute respiratory dis- tress syndrome), and renal failure are the most likely causes of death. Hemorrhage, peripheral v ascular collapse, and in- fection are also major concerns. A purplish discoloration of the flanks (Turner's sign) or a purplish discoloration around the umbilicus (Cullen's sign) may occur with e xtensive he- morrhagic destruction of the pancreas. Diagnostic Tests Diagnosis of acute pancreatitis is made when tw o of these are present: abdominal pain, serum amylase (normal: 8 0- 180 units/dL) and/or serum lipase (normal: 0 to 160 units/L) more than 3 times normal, abdominal imaging is indicative of it. Serum amylase rises quickly and then returns to normal in 3 to 5 days. Serum lipase is thought to be more specific for acute pancreatitis and ele vates and stays ele- vated for a longer period of time. Glucose, bilirubin, alkaline phosphatase, lactic dehydrogenase, ALT, AST, cholesterol, and potassium are all ele vated. Decreases are seen in serum albumin, calcium, sodium, and magnesium. Ultrasonography may sho w pleural ef fusion from local inflammatory reaction to pancreatic enzymes or a change in the size of the pancreas. Therapeutic Measures Early aggressive IV hydration during the first 24 hours for hypovolemia treatment is recommended. In asymptomatic mild acute pancreatitis, oral nutrition is gi ven ("Nutrition Notes"). In severe cases, enteral feeding is maintained (see "Evidence-Based Practice"). A histamine (H2) antagonist can help decrease acid stimulation of pancreatic secretions (Table 35.4). Additional drug orders include electrolytes such as calcium and magnesium to replace losses, short- acting insulin to combat hyperglycemia, and antibiotics to treat sepsis (T able 35.5). Sur gery may be needed for debriding necrotic tissue. Abscesses or pseudocysts may need to be drained. Pain relief is essential, and opioids such as morphine or hydromorphone (Dilaudid) are ordered for pain. The patient may be given antianxiety agents to decrease oxygen demand. Supplemental oxygen may be required if abdominal pressure, pleural effusion, or acidosis cause impaired gas exchange or an ineffective breathing pattern.

Gerd

Pathophysiology GERD is a condition in which gastric secretions reflux into the esophagus. The esophagus can be damaged by acidic gastric secretions and exposure to digestive enzymes. GERD is caused primarily by conditions that afect the ability of the lower esophageal sphincter to close tightly , such as hiatal hernia. Signs and symptoms of GERD include heartburn, regurgita- tion, dysphagia, and bleeding (Table 33.1). Aspiration is a concern. Scar tissue can develop from the inflammation. Diagnostic Tests Diagnostic tests include a barium sw allow, esophagoscopy (an endoscopic procedure), or pH monitoring of the normally alkaline esophagus. Complications Complications of GERD can result in esophagitis (inflamma- tion of the esophagus) due to acid reflux. Over time this can lead to changes in the epithelium of the esophagus and lead to Barrett's esophagus. This is a precancerous lesion that puts the patient at risk of developing esophageal cancer. Barrett's tissue can be remo ved during a 30-minute outpatient endo- scopic procedure using radiofrequency ablation (the BARRx system). Normal tissue returns, and the risk of cancer is re- duced. Respiratory complications such as bronchospasm, laryngospasm, and aspiration pneumonia can also occur owing to aspiration of gastric contents. There is the potential for asthma, chronic bronchitis, or pneumonia due to the as- piration of gastric contents. Therapeutic Measures Lifestyle changes are recommended along with medications. Obese patients are encouraged to lose weight.A low-fat, high- protein diet is recommended because f at causes decreased functioning of the lower esophageal sphincter. See "Nutri- tional Notes" for additional things to a void. Patient teaching includes eating small meals often during the day, drinking flu- ids between meals instead of with meals, avoiding late evening meals, snacking, and fluids 2 to 3 hours before bedtime. Med- ications may include nonprescription antacids for mild symp- toms. Histamine (H2) receptor antagonists (acid reducers) that are available in nonprescription and prescription strengths are used for mild to moderate symptoms. Proton pump inhibitors (PPIs) reduce acid in the stomach and are used for frequent, severe symptoms and Barrett's esophagus. (Table 33.4 later Diagnostic Tests Complications X-ray studies Endoscopy Fluoroscopy Esophagitis Barrett's syndrome Respiratory symptoms Priority Acute Pain Nursing Deficient Knowledge Diagnoses in this chapter provides information on PPIs.) There are sus- pected risks associated with PPI use that includes a possible increased risk of osteoporosis and Clostridium difficile infec- tion. If diarrhea occurs that does not stop, patients should con- tact a health care pro vider (HCP; Janarthanan, Ditah, Adler, & Ehrinpreis, 2012). Surgery can be done if necessary to alleviate symptoms. A fundoplication or endoscopic procedures can be done. As you read, what do you think the benefit of the following procedure is over fundoplication surgery? A minimally in- vasive procedure, transoral incisionless fundoplication (TIF) is performed through the mouth without incisions. It employs the EsophyX device to create an esophagogas- tric fundoplication that is up to 270° and 2 to 3 cm in length. EsophyX, uses an endoscope to tighten the lo wer esophageal sphincter, which aids in improving or eliminat- ing gastroesophageal reflux with good success ( www .endogastricsolutions.com/TIF.aspx). If you thought that the benefit of TIF is that it's minimally invasive and, there- fore, has a speedier recovery, you would be correct. Other endoscopic procedures that use radiofrequency waves, such as the Stretta, can be done. The radiofrequency waves are injected into the lower esophageal sphincter muscle to form collagen contraction, which leads to a barrier against reflux. Nursing Process for the Patient With GERD Data Collection Assessment of the patient with GERD includes evaluation of reports of heartburn. The onset, duration, characteristics, and precipitating or relieving factors are noted. Nursing Diagnoses, Planning, and Implementation Acute Pain related to inflammation of esophageal tissues EXPECTED OUTCOME: The patient will state a reduction of pain to an acceptable level or total relief of pain within 30 minutes of report of pain. • Identify factors that increase pain to develop teaching plan. • Monitor pain level using pain rating scale to identify pain level. • Instruct patient regarding factors that aggravate pain to en- hance management of condition. • Instruct patient to sleep with head of bed elevated 4 to 6 inches, eat small meals, and avoid lying down for 2 hours after eating to prevent reflux of gastric contents into esophagus. Instruct patient to avoid smoking and alcohol because they decrease functioning of the lower esophageal sphincter. • Instruct patient to avoid foods that cause discomfort to avoid pain. • Review medication schedule and teach patient to take medications even if symptoms are relieved because the underlying pathology still exists. • Provide pain medications on routine schedule, especially postoperatively, to provide optimum pain relief and control. Evaluation The goals are met if the patient is able to manage medica- tions, pain is controlled, and symptoms are relieved.

Ibs

Pathophysiology Irritable bowel syndrome (IBS) is not a disease b ut rather a functional problem. The colon mucosa is not damaged by the condition, and there is no increased risk of colorectal cancer. IBS is a disorder of altered intestinal motility in which the colon muscle contracts more easily . It contracts in a disor - derly way that can be violent and last for long times or , at times, it may not contract at all. The abnormal contractions lead to changes in bowel patterns. Thus, the disorder may be classified as IBS with diarrhea, IBS with constipation, or IBS with mixed diarrhea and constipation. Additionally, patients experience increased abdominal discomfort or pain. Local- ized prolonged contractions may cause stool to be retained for a long time, causing it to become hardened as water is ab- sorbed from it. Bloating may also occur because air is unable to be expelled. Mucus may be seen in the stool, although this is not abnormal and does not typically cause a problem. Symptoms may be exacerbated by psychological stress or food intolerances. The nerves in the bowel are overly sensi- tive in people with IBS. At times of stress in daily li ving, abnormal contractions may result. Etiology There is a hereditary tendency for IBS. IBS is more common in women than men and in those who are young to middle- aged. Flare-ups can be caused by other illnesses, infections, or the menstrual cycle. Signs and Symptoms IBS is characterized by reports of gas, bloating, constipa- tion, diarrhea, or alternating constipation and diarrhea.The patient also has feelings of abdominal bloating, with or without visible abdominal distention. Other symptoms include the rectal passage of mucus, a feeling of incom- plete evacuation, abdominal pain, depression, anxiety, and palpitations. Diagnostic Tests Diagnosis of IBS is made based on history and physical examination along with stool e xamination, colonoscopy, and sigmoidoscopy to rule out other disorders. Avoiding milk products for a time may be advised to rule out lactose intolerance. Therapeutic Measures IBS is a chronic condition, but symptoms can generally be controlled through lifestyle, diet, stress management, and medication. See "Nutrition Notes" for diet. A high-fiber and high-bran diet (psyllium [Metamucil] or methylcellu- lose [Citrucel]) may help to form softer , larger stools but may increase other symptoms in some people. Eating smaller, frequent meals can be helpful in reducing bo wel contractions. Patients can k eep a diary of foods eaten, stressors, and symptoms. This can help the HCPs identify flare-up triggers. Stress management, beha vioral therapy (biofeedback, hypnosis, psychotherapy), and exercise are helpful in relaxing the bo wel as well as contrib uting to overall health. Various medications are used depending on the type of IBS. Antidepressants are given to block the brain's percep- tion of abdominal pain. For IBS with constipation, selective serotonin reuptake inhibitors (SSRIs) such as parox etine HCl (Paxil) are gi ven. Tricyclic antidepressants (such as amitriptyline HCl [Elavil]) are used for IBS with diar - rhea because they tend to cause constipation.Antispasmod- ics such as hyoscyamine (Levbid) or dicyclomine (Bentyl) are used in IBS for diarrhea to relie ve the painful colon spasms. For women in whom treatment for IBS with constipation has not been successful, lubiprostone (Amitiza) may be used. It is a chloride channel activator that increases fluid secretion in the small intestine to help pass stool. Nursing Process for the Patient With IBS Data Collection Height, weight, and data on the symptoms, including pain that the patient e xperiences, are collected. Timing of thon self-esteem, socialization, and personal and f amily roles are explored because IBS is a signif icant cause of missed work and school and also causes social withdra wal and em- barrassment for people with it. Knowledge of the syndrome and its treatment are determined. Readiness for managing the syndrome is determined to plan care. Nursing Diagnoses, Planning, and Implementation Constipation related to irregular motility of GI tract EXPECTED OUTCOME: The patient will maintain passage of soft, formed stool every 1 to 3 days without straining. • Assess normal pattern of defecation, diet and fluid intake, and medications to help identify factors contributing to constipation for planning care. • Increase fluid intake, if not contraindicated, to 2 to 3 L per day to prevent hard stools. • Teach patient about the benefits of increasing fiber and bran in the diet to promote soft, larger stools that are easier to pass. • Give medication as ordered to control symptoms. Diarrhea related to irregular motility of GI tract EXPECTED OUTCOME: The patient will maintain formed, soft stool every 1 to 3 days. • Obtain history including medications regarding diarrhea episodes to help identify cause. • Monitor and record stool characteristics, amount, and fre- quency to plan care. • Give antidiarrheal medications as ordered. Controlling di- arrhea controls comfort and fluid balance. • Limit caffeine intake because it stimulates intestinal motility. • Keep skin clean, dry, and protected with a moisture bar- rier, such as petrolatum or medicated ointment, after each bowel movement to protect perianal skin from contact with liquid stools and their enzymes. Readiness for Enhanced Self Health Management related to desire to manage symptoms of IBS EXPECTED OUTCOME: The patient will state understanding and ability to carry out preventive measures to control symptoms before discharge. • Explain IBS including symptoms, aggravating factors, and treatments to promote understanding, which will aid abil- ity to follow therapeutic regimen. • Encourage use of food diary documenting foods eaten and timing of symptom occurrence to identify food triggers for symptoms including lactose intolerance. Consult registered dietitian and share food diary to allow identification of food connection with symptoms and meal planning to prevent symptoms. • If lactose intolerant, teach patient to avoid dairy products and substitute yogurt to reduce symptoms. Evaluation The plan has been ef fective if the patient has re gular bowel function pattern, verbalizes understanding of self-care meas- ures, and expresses satisfaction with the outcomes.

Ulcers

Pathophysiology Peptic ulcer disease (PUD) is a condition in which the lining of the stomach, p ylorus, duodenum, or the esophagus is eroded, usually from infection with H. pylori. The erosion may extend into the muscular layers or the peritoneum. Peptic ulcers occur in the portions of the GI tract that are e xposed to hydrochloric acid and pepsin. The erosion is due to an in- crease in the concentration or acti vity of hydrochloric acid and pepsin. The damaged mucosa is unable to secrete enough mucus to act as a barrier against the hydrochloric acid. Some individuals have more rapid gastric emptying, which, com- bined with hypersecretion of acid, creates a large amount of acid moving into the duodenum. As a result, peptic ulcers occur more often in the duodenum. Ulcers are named by their location: esophageal, gastric, or duodenal. Duodenal ulcers are more common than gastric ulcers. Etiology Until 1982, the cause of peptic ulcers was poorly understood and thought to be related to stress, diet, and alcohol or caf- feine ingestion. However, research results ha ve found that PUDisprimarilycausedbyinfectionwiththeGram-negative bacterium H. pylori. This bacterium is responsible for 80% of gastric ulcers and more than 90% of duodenal ulcers.Two- thirds of all people are infected with H. pylori, and it is most common in those who are older adult Hispanics, African Americans, or in lower socioeconomic groups in the United States. The discovery of H. pylori has led to changes in treat- ing and curing peptic ulcers.It is not known how H.pyloriis transmitted, although the oral-oral or fecal-oral route is likely. Contaminated water may also play a role.Vaccines to prevent peptic ulcers are being developed. Signs and Symptoms Symptoms vary with the location of the ulcer (Table 33.2). Symptoms, including pain, may not be e xperienced with gastric or duodenal ulcers until complications such as hem- orrhage, obstruction, or perforation de velop. If pain does occur, patients with gastric ulcers commonly experience a burning and gnawing pain in the high left epigastric region, and may increase with food ingestion or 1 to 2 hours after a meal. Duodenal ulcers produce cramping or burning pain in the midepigastric or upper abdominal area, which occurs 2 to 4 hours after meals or in the middle of the night. This intermittent pain may be relieved by the ingestion of food or antacids. Anorexia and nausea and v omiting may also occur with either ulcer location. Bleeding may occur with massive hemorrhaging or slow oozing. Patients often have low hematocrit and hemoglobin levels, and gastric or fecal occult blood may be found, depending on where the ulcers are located. Signs and Symptoms Gastric ulcer Duodenal ulcer Intermittent high left epigastric or upper abdominal burning or gnawing pain, increased 1-2 hours after meals or with food Variable pain pattern possibly made worse by food Antacids ineffective Can lead to gastric cancer Patient may be malnourished Hematemesis more common than melena Intermittent midepigastric or upper abdominal burning or cramping pain, increased 2-4 hours after meals or in the middle of the night Relieved by food or antacids Patient usually well nourished Melena more common than hematemesis Anorexia Nausea and vomiting Bleeding (stomach secretions or stool positive for occult blood) Diagnostic Tests H. pylori Peptic ulcer Urea breath test Immunoglobulin G antibody detection test for H. pylori Biopsy Culture Upper GI series (barium swallow) Esophagogastroduodenoscopy erapeutic Measures Antibiotics Proton pump inhibitors H2 antagonists Bismuth subsalicylate Sucralfate (Carafate) Antacids Bland diet Avoiding irritants, such as smoking, caffeine, alcohol, trigger foods Complications Complications Bleeding Perforation Obstruction Priority Nursing Acute Pain Diagnoses Risk for Injury Deficient Knowledge Major complications can result from PUD. These include bleeding, perforation, and obstruction. Bleeding can occur in varying degrees from occult blood in stool and emesis to mas- sive bright red bleeding. Hemorrhage tends to occur more often with gastric ulcers in older adults. The patient may ex- perience signs and symptoms of shock. Treatment includes stopping the bleeding, replacing fluid and electrolytes, and possibly administering vasopressin to stop the bleeding. Diagnostic Tests H. pylori can be diagnosed with several tests. The urea breath test is performed by having the patient drink carbon-labeled urea. The urea is metabolized rapidly if H. pylori is present, allowing the carbon to be absorbed and measured in exhaled carbon dioxide. An immunoglobulin G antibody detection test for H. pylori identifies whether the patient is infected with H. pylori. These are both noninvasive detection tests. Biopsy specimens for the Campylobacter-like organism (CLO) biopsy urease test and a histological examination can be obtained during EGD. Biopsy is the most conclusi ve test for H. pylori. Cultures of the biopsy specimen may also be done to determine antimicrobial susceptibility. Therapeutic Measures Several treatment options are used to cure H. pylori without recurrence (Table 33.3). For better effectiveness, triple therapy with two antibiotics to decrease resistance of the bacteria and a PPI or H2 antagonist is used. Treatment lasting 14 days has better eradication rates than 10-day treatments. Bismuth sub- salicylate (e.g., in Pepto-BismolTM) may also be used for its antibacterial effects. PPIs are powerful agents that stop the final step of gastric acid secretion to reduce mucosa erosion and aid in healing ulcers (Table 33.4). H2 antagonists block H2 receptors to de- crease acid secretion, although the y are not as po werful as gastric acid pump inhibitors. A bland diet may also be rec- ommended, and foods kno wn to cause discomfort to the patient, such as spicy foods, carbonated drinks, and caffeine, should be avoided until the ulcer heals. Alcohol should also be avoided during the healing period. Hyposecretory Agents H2 receptor blocking agents: Inhibit gastric acid secretion by blocking H2 receptors on gastric parietal cells. Examples cimetidine (Tagamet) ranitidine (Zantac) famotidine (Pepcid) nizatidine (Axid) Nursing Implications Monitor mental status of older adults. Do not give antacids within 1 hour of Tagamet. Give with meals and at bedtime. Interacts with theophylline, phenytoin, warfarin, and beta blockers. Give antacids at least 1 hour before or 2 hours after Zantac. Can be given in single bedtime dose. May be given with antacids. Can be given in single bedtime dose. Give antacids at least 1 hour before or 2 hours after Axid. Can be given in single bedtime dose or, if given twice a day, one dose at bedtime. Monitor for excessive drowsiness and monitor and record stools. Proton pump inhibitors: Bind to an enzyme in the presence of acidic gastric pH, preventing final transport of hydrogen ions into the gastric lumen. dexlansoprazole (Dexilant) omeprazole (Prilosec) lansoprazole (Prevacid) rabeprazole (Aciphex) Delayed release. Capsule swallowed whole. Give before meal in morning. Capsule swallowed whole. Assess for abdominal pain and bleeding. Monitor CBC and liver enzymes.Notify physician of bleeding, diarrhea, headache, or abdominal pain. Give before meals. Capsule not to be crushed or chewed. May be sprinkled on applesauce and taken immediately. Packet mixed as liquid, but not for nasogastric (NG) tube because it sticks to tube. Sublingual tablet may be dissolved and given through NG tube. Notify physician of bleeding, diarrhea, headache, or abdominal pain. Tablets to be swallowed whole. Antacids Increase gastric pH to reduce pepsin activity; strengthen gastric mucosal barrier and esophageal sphincter tone. aluminum-magnesium combinations (Riopan, Maalox, Mylanta, Gelusil) Do not give to patients with renal disease. Monitor bowel movements and signs of hypermagnesemia. Riopan low in sodium.

Hernia

Pathophysiology The esophagus passes through an opening in the diaphragm called the hiatus. A hiatal hernia is a condition in which the stomach slides up through the hiatus of the diaphragm into the thorax (Fig. 33.4). A sliding hiatal hernia is the most com- mon type in which the junction of the stomach and esophagus slides up into the thoracic cavity when a patient is supine and then usually goes back into the abdominal ca vity when the patient stands upright. A paraesophageal hernia is rarer b ut serious as part of the stomach squeezes through the hiatus and is at risk for strangulation (blood supply is cut of). Hiatal hernia occurs most commonly in smok ers, those who are older than age 50, obese, or pregnant. People with hiatal her- nia often have gastroesophageal reflux disease (GERD) as well (discussed later). Signs and Symptoms A small hernia may not produce an y discomfort or require treatment. However, a large hernia can cause pain, heartburn, a feeling of fullness, or reflux, which can injure the esopha- gus with possible ulceration and bleeding. Diagnostic Tests Hiatal hernias are diagnosed by x-ray studies and fluoroscopy. Therapeutic Measures Lifestyle changes for symptomatic hiatal hernia include los- ing weight, taking antacids, eating small meals that pass eas- ily through the esophagus, not reclining for 3 to 4 hours after eating, elevating the head of the bed 6 to 12 inches to prevent reflux, and avoiding bedtime snacks, spicy foods, alcohol, caffeine, and smoking (see "Nutrition Notes"). Surgical Management Surgery is done for symptomatic hiatal hernia when GERD, strangulation, or obstruction is present. Fundoplication, in which the stomach fundus is wrapped around the lower part of the esophagus, is the most common surgical procedure per- formed (Nursing Care The patient is taught lifestyle interv entions to reduce the symptoms of hiatal hernia. If the patient under goes surgery, general postoperative nursing care is pro vided. In addition, following fundoplication, patients are assessed for dysphagia during their first postoperative meal. If dysphagia occurs, the physician should be notif ied because the repair may be too tight, causing obstruction of the passage of food. Pathophysiology and Etiology A hernia is an abnormal protrusion of an organ or structure through a weakness or tear in the wall of the cavity normally containing it, which in this case is the abdominal w all. Her- nias are caused by a weakness in the abdominal w all along with increased intra-abdominal pressure, such as the pressure from coughing, straining, and hea vy lifting. Obesity, preg- nancy, and poor wound healing are also risk factors. The her- nial sac is formed by the peritoneum protruding through the weakened muscle wall. Contents of the hernia can be small or large intestine or the omentum. Indirect hernias are caused by a defect of structural closure. Direct hernias are acquired and arise from a weakness in the abdominal w all, usually at old incisional sites. Figure 34.4 illustrates the v arious types of hernias. In- guinal hernias are located in the groin where the spermatic cord in males or the round ligament in females emerges from the abdominal wall. This common hernia is an example of an indirect hernia and is usually seen in males. Umbilical hernias are seen most often in obese women and in children. They are caused by a failure of the umbilical ori- fice to close. Ventral (incisional) hernias usually result from a weakness in the abdominal w all after abdominal sur gery, especially in the obese patient, if a drainage system was used, the patient experienced poor wound healing, or the patient received inadequate nutrition. Prevention Congenital defects cannot be prevented. However, reducing strain on abdominal muscles is helpful. Those who do heavy lifting, tugging, or pushing should wear a support binder or avoid the lifting. A healthy lifestyle of maintain- ing normal weight, not smoking, and eating high-fiber foods is recommended. Signs and Symptoms Unless complications occur, few symptoms are associated with hernias. An abnormal bulging can be seen in the afected area of the abdomen, especially when straining or coughing. The patient may have some discomfort due to tension on tis- sues around the hernia. The herniation may disappear when the patient lies down. If the intestinal mass easily returns to the abdominal cavity or can be manually placed back in the abdominal cavity, it is called a reducible hernia. When adhe- sions or edema occur between the sac and its contents, the hernia becomes irreducible or incarcerated. Complications An incarcerated hernia may become strangulated if the blood and intestinal flow are completely cut off in the trapped loop of bowel. Strangulated hernias do not develop in adults very often. Incarceration leads to an intestinal obstruction and pos- sibly gangrene and bowel perforation. Symptoms are pain at the site of the strangulation, nausea and vomiting, and colicky abdominal pain. Therapeutic Measures Hernias are diagnosed by physical examination. Treatment op- tions include no treatment, observing the hernia, using short- term support devices, or surgery to cure the hernia.A supportive truss or brief applies pressure to k eep the reduced hernia in place. Emergency surgery is needed for strangulation or the threat of bowel obstruction. Surgical repair is recommended for inguinal hernias. Surgical procedures are most often done la- paroscopically and include hernioplasty (open or laparoscopi- cally) or herniorrhaphy (open hernia repair). Herniorrhaphy involves making an incision in the abdominal w all, replacing the contents of the hernial sac, sewing the weakened tissue, and closing the opening. Hernioplasty involves replacing the hernia into the abdomen and reinforcing the weak ened muscle wall with wire, f ascia, or mesh. Bo wel resection or a temporary colostomy may be necessary if the hernia is strangulated. The patient is instructed to avoid activities that increase intra- abdominal pressure, such as lifting heavy objects. The patient is taught to recognize signs of incarceration or strangulation and the importance of notifying the HCP immediately . If a support truss or brief has been ordered, the patient is taught to apply it before arising from bed each morning while the hernia is not protruding. Special attention should be paid to maintenance of skin integrity beneath the truss. Postoperative Care Care following inguinal hernia repair is generally similar to any abdominal postoperative care (see Chapter 12). Patients can perform deep breathing to keep lungs clear postopera- tively but should avoid coughing. Coughing increases ab- dominal pressure and could af fect the hernia repair . The male patient may experience swelling of the scrotum. Ice packs and elevation of the scrotum may be ordered to reduce the swelling. Because most patients are discharged the same day of surgery, they are taught to change the dressing and report difficulty urinating, bleeding, and signs and symp- toms of infection, such as redness, incisional drainage, fever, or severe pain. The patient is also instructed to avoid lifting, driving, or sexual activities for 2 to 6 weeks as spec- ified by the HCP. Most patients can return to nonstrenuous work within 2 weeks.

colorectal cancer

Pathophysiology and Etiology Colorectal cancer is one of the most common types of inter- nal cancer in the United States. It originates in the epithelial lining of the colon or rectum and can occur anywhere in the large intestine. People with a personal or f amily history of ulcerative colitis, colon cancer, or polyps of the rectum or large intestine are at higher risk for developing cancer. Col- orectal cancer has also been linked with previous gallbladder removal and dietary carcinogens. A major causative factor is lack of fiber in the diet, which prolongs fecal transit time and in turn prolongs exposure to possible carcinogens. Also, bacterial flora is believed to be altered by excess fat, which converts steroids into compounds having carcinogenic prop- erties. Lifestyle factors such as obesity, smoking, alcohol in- take, and a large amount of red meat in the diet increase the risk of colon cancer. Signs and Symptoms Manifestations of colorectal cancer v ary according to the type of tumor and the location. A change in bowel habits is the most common symptom (Table 34.9). Blood or mucus in stools may occur. Although all tumors cause varying de- grees of obstruction, those in the descending colon and rec- tum generally do not cause anemia, weight loss, nausea, or vomiting. Diagnostic Tests Screening for colorectal cancer in those o ver age 50 is the best prevention, but screening rates could be higher. Screen- ing guidelines can be found in Chapter 11 or on theAmerican Cancer Society's website at www.cancer.org. Home screening for blood in the stool can be done with a home colon cancer test kit. Immunological tests look for small amounts of blood. If blood is found, a HCP should be contacted for follow-up. Most colorectal cancers are iden- tified by biopsy done at the time of endoscop y (proctosig- moidoscopy, sigmoidoscopy, or colonoscopy). A CT scan can perform a virtual colonoscopy to view the inside of the colon. The carcinoembryonic antigen blood test is used to assess response to treatment of GI cancer. Carcinoembryonic antigen is present when epithelial cells rapidly di vide and provides an early warning that the cancer has returned. Therapeutic Measures Small, localized tumors may be e xcised and treated during endoscopy or laparoscopy. These procedures can also be used as palliative care for patients with advanced tumors who can- not tolerate major surgery. If a tumor is causing obstruction, TABLE 34.10 INTESTINAL SURGERIES a stent can be placed to keep the colon open for bowel func- tion until surgery. Surgery is performed either to resect lar ger tumors and anastomose the remaining bowel or to create a fecal diversion by forming an ostomy. A variety of surgical procedures can be done depending on the location and e xtent of the cancer (Table 34.10 and Fig. 34.6). Medical management can in- clude radiation therapy, chemotherapy, and monoclonal anti- body therapy. When used, along with sur gery, increased survival rates have been demonstrated. Monoclonal antibody therap y uses antibodies that are made in a laboratory and w ork like normal antibodies do. They can enhance immune system function, interfere with the cancer cell's growth, or even carry treatment such as drugs or radiation to cancer cells. The antibody is designed to attach tocancercellstoflagthemfortheimmunesystemsothe y can be destroyed. Bevacizumab (Avastin) blocks the making of new blood vessels to deprive cancer cells of nourishment. Cetuximab (Erbitux) blocks the cell's growth signal to stop it from growing. Complications Complications include bleeding, complete obstruction of the colon, perforation, anastomosis leaking leading to peritoni- tis, and extension of the tumor to adjacent organs. Colorectal cancer can metastasize to the lymphatic system and liver. If the patient has an anastomotic leak, the location of the leak determines the effects that are seen. The patient may need to be NPO for up to 4 weeks to rest the GI tract and prevent more leakage and also receive high-dose antibiotic therapy such as ciprofloxacin (Cipro) or metronidazole (Flagyl). Ongoing monitoring includes WBCs, sedimenta- tion rate, and fe ver. The patient will lik ely go home with special home care needs. A peripherally inserted central catheter line is placed to continue the antibiotic therapy. Nursing Process for the Patient With Colorectal Cancer Data Collection Risk factors for colorectal cancer are identif ied by asking questions about the patient' s personal and f amily history: Is there a history of inflammatory bowel disease? What were the patient's dietary habits? What foods were usually eaten, and how much fluid w as usually consumed? Prior to diagnosis, did the patient experience constipation or diarrhea? Has there been a change in bo wel habits? Has mucus or blood been noted in the stools? What social habits does the patient have? Did the patient smok e, drink alcoholic be verages, exercise? Has there been a recent weight loss? If so, how much and over what period of time? Does the patient admit to unusual fatigue or insomnia? Stool should be checked for mucus or blood. If the patient has sur gery, postoperative assessment in- cludes monitoring vital signs and the return of flatus and bowel movements. Lung sounds are monitored for response to coughing and deep breathing and early ambulation. Dress- ings are observed for drainage. Large amounts of drainage or bleeding are reported. If a drain is inserted in the perineal wound, moderate amounts of serosanguineous (light pink) drainage are expected. If the patient has an ostomy, it is mon- itored (see ostomy section later in the chapter). Nursing Diagnoses, Planning, and Implementation Acute Pain related to tissue compression from the tumor EXPECTED OUTCOME: The patient will report pain relieved or at an acceptable level. • Have patient identify pain using a rating scale to identify pain level consistently. • Administer analgesics as prescribed postoperatively to relieve pain. Fear related to serious threat to well-being EXPECTED OUTCOME: The patient will state fear is reduced after information is given related to patient's condition. • Assist patient in identifying fears to develop plan for reducing fears. • Set aside time to allow the patient who so desires to talk, cry, or ask questions about the diagnosis and planned surgery to help reduce fear. • Answer questions accurately to provide a trusting relationship.

Oral cancer

Pathophysiology and Etiology Oral cancer can occur anywhere in the mouth or throat. If de- tected early enough, it is curable. Oral cancer is found most commonly in patients who use alcohol or an y form of to- bacco. The highest incidence of oral cancer is found in the pharynx (throat), with the lowest incidence being on the lips. Signs and Symptoms Any oral sore that does not heal in 2 weeks should be assessed by the patient's physician. Cancerous ulcers are often painless but may become tender as the cancer progresses. In the later stages, the patient may report dificulty chewing, swallowing, or speaking or may have swollen cervical lymph glands. Diagnostic Tests Biopsy specimens are taken to determine the presence of cancer. Therapeutic Measures Oral cancer treatment varies depending on the individualized diagnosis. Radiation, chemotherapy, and surgery are used alone or in combination to treat oral cancer. Radical or mod- ified neck dissection is often performed because this type of cancer frequently has metastasized to cervical lymph nodes by the time it is diagnosed (Fig. 33.3).The tumor is removed along with lymph nodes, muscles, blood vessels, glands, and part of the thyroid, depending on the e xtent of the cancer. Drains are inserted into the incision to prevent fluid accumu- lation. A tracheostomy is usually performed to protect the air- way and prevent obstruction. Nursing Care Preoperative and postoperative nursing care is discussed in Chapter 12. Preoperatively, the use of alcohol or tobacco is addressed and referrals to cessation programs and support groups offered. Preoperative teaching includes how the patient will communicate if a tracheostomy is placed. Postoperatively, major concerns are airway patency, communication, and nutri- tional needs. Nursing care for the patient with a tracheostomy is discussed in Chapter 29. The airway must be monitored and secretions controlled to prevent aspiration. Determining that the methods the patient is using for communication are satisfactory is evaluated. Tube feedings (see Chapter 32) are usually gi ven to meet the patient's nutritional needs because sw allowing is difficult.

Peritonitis diverticulosis and litis

Peritonitis is inflammation of the peritoneum that occurs from a variety of causes. It is a serious condition that can be life threatening. Pathophysiology and Etiology Diverticulosis and Diverticulitis Pathophysiology A diverticulum is a herniation or outpouching of the bowel mucous membrane caused by increased pressure within the colon and weakness in the bowel wall. Diverticulosis is a condition in which multiple diverticula are present without evidence of inflammation (Fig. 34.2). Man y people have diverticulosis without knowing it because it develops grad- ually. When food and bacteria are trapped in a di verticu- lum, inflammation and infection de velop. This is called diverticulitis. Etiology Chronic constipation usually precedes the development of di- verticulosis by many years. When the patient is chronically constipated, pressure within the bowel is increased, leading to development of diverticula. A major cause of the disease is a decreased intake of dietary fiber. Diverticulosis is most com- mon in the sigmoid colon.A small percentage of patients with diverticulosis develop diverticulitis. People older than age 60 are the most common group to experience diverticulitis. • WORD • BUILDING • peritonitis: periton—pertaining to peritoneum + itis—inflammation diverticulosis: diverticul—blind pouch + osis—condition diverticulitis: diverticul—blind pouch + itis—inflammation Diverticula FIGURE 34.2 A diverticulum is a herniation or outpouching of the bowel mucous membrane. Having multiple diverticula is a condition called diverticulosis. If they become inflamed or in- fected, the condition is called diverticulitis. y abdominal Generalized abdominal pain evolves into localized pain at the site of the perforation or leakage. The area of the abdomen that is affected is extremely tender and aggravated by move- ment. Rebound tenderness and abdominal rigidity are present. Decreased peristalsis results in nausea and vomiting. Infection causes fever, increased WBCs, and an elevated pulse. Diagnostic Tests Rapid diagnosis is essential in pre venting complications. Tests include an abdominal x-ray or computed tomography (CT) scan to show distention or perforation, WBCs signifi- cantly elevated, paracentesis and laboratory studies to identify a causative organism, or exploratory surgery to identify the cause. Therapeutic Measures The patient is NPO because of impaired peristalsis. Fluid and electrolyte replacement is crucial to correct hypo volemia and prevent or treat shock. Abdominal distention is relieved through insertion of an orogastric (or NG) tube with low in- termittent suction. Antibiotics are used to treat or prevent sep- sis. Depending on the cause of the peritonitis, sur gery may be performed to excise, drain, or repair the cause.An ostomy may be formed to divert stool, allowing resolution of the in- fection. After surgery, the patient usually has a wound drain, a NG tube, and a urinary catheter. Pain control is essential to overall recovery. Severely compromised patients may receive parenteral nutrition (PN) to meet nutritional needs. Complications Wound dehiscence (separation of layers of a surgical wound) or evisceration (protrusion of abdominal viscera) can occur if the patient has had abdominal sur gery. Complications of peritonitis are intestinal obstruction (discussed later), hypo- volemia caused by the shift of fluid into the abdomen, and septicemia from bacteria entering the bloodstream. Shock and ultimately death may result. Trauma, ischemia, or tumor perforation in an organ causes leakage of the organ's contents into the peritoneal cavity. The most common cause of peritonitis is a ruptured ap- pendix, but it can also occur after perforation of a peptic ulcer, gangrenous gallbladder, intestinal diverticula, incarcerated her- nia, or gangrenous small bowel. It may also be a complication of peritoneal dialysis. Peritonitis results from the inflammation or infection that is caused by the leakage. The tissues become edematous and be gin leaking fluid containing increasing amounts of blood, protein, cellular debris, andWBCs. Initially, the intestinal tract responds with hypermotility, but this is soon followed by paralysis (paralytic ileus). Prevention Gerontological Issues With aging, the incidence of diverticular disease increases. Clinical manifestation of this condition may include ab- dominal pain, rectal bleeding, nausea, and v omiting. Patients may not notice the abdominal pain until infection is present. Many times the symptoms are not reported early because patients fear it may be cancer. Blood in the stool, which can be an indication of di verticulitis, may not be seen by the older adult due to impaired vision. Diverticulitis can be prevented by increasing dietary fiber to prevent constipation and onset of diverticulosis. Signs and Symptoms The patient with diverticulosis is generally asymptomatic. When diverticulitis is present, the patient e xhibits bowel changes, possibly alternating between constipation and di- arrhea (Table 34.4). Steady or crampy pain in the left lower quadrant of the abdomen is the most common symptom.As the condition w orsens, bleeding may occur , along with weakness, fever, fatigue, and anemia. Guarding and rebound tenderness may be present. If an abscess de velops, the di- verticulum may rupture, leading to peritonitis ("Geronto- logical Issues"). Diagnostic Tests Diverticulosis is confirmed with sigmoidoscopy, colonoscopy, or barium enema. The diverticula and specific areas of inflam- mation can be seen during a colonoscop y or sigmoidoscopy. If an abscess is suspected, a CT scan may be done. Barium enema may show irregular narrowing of the colon and thick- ened muscle walls. A stool specimen may show occult blood. An abdominal x-ray e xamination may be done to identify a perforated diverticulum. TABLE 34.4 SYMPTOMS ASSOCIATED WITH DIVERTICULITIS Therapeutic Measures Diverticulosis is managed by pre venting constipation. With acute diverticulitis, the patient may be hospitalized for ad- ministration of IV antibiotics and pain control. An NG tube, IV fluids, and NPO status may be ordered until pain, nausea or vomiting, fever, and inflammation decrease. When the acute period is over, a progressive diet is started. Whether or not perforation occurs, surgical resection with anastomosis or a temporary colostomy (discussed later) may be done to allow the inflammation to subside and the diseased portion of the colon to rest. Dietary considerations for a patient with di verticulosis (without evidence of inflammation) include foods that are soft but high in fiber, such as prunes, raisins, and peas. Unprocessed bran can be added to soups, cereals, and salads to gi ve added bulk to the diet. Fiber should be increased in the diet slowly to prevent excess gas and cramping. Some health care providers recommend avoiding nuts or foods with small seeds that can get caught in diverticula, such as tomatoes and raspberries, but this has not been shown to prevent diverticulitis. If the patient is overweight, he or she is encouraged to lose weight. Surgery may be needed for ruptured di verticula. Laparo- scopic surgery can be used to decrease the morbidity and mortality associated with this emergency surgery. Nursing Process for the Patient With an Inflammatory or Infectious Disorder Data Collection Assessment of pain is essential for patients with inflammation or infection. Monitor the patient closely and notify the HCP immediately if pain increases, especially if associated with abdominal rigidity. Increased pain may indicate that the bowel has ruptured and peritonitis is developing. Abdominal distention is monitored and recorded. With diverticulitis, a firm mass may be palpated in the sigmoid area. Vital signs are monitored for fever or signs of septic shock. Intake and output are monitored and recorded accurately so that appropriate fluid replacement therapy is ordered. Moni- toring for reduced urinary output, dropping blood pressure, and rising pulse rate can sho w fluid volume imbalance. If a fever is noted, the patient may be de veloping sepsis. All symptoms are reported to the HCP promptly. Nursing Diagnoses, Planning, and Implementation Acute Pain related to inflammatory process EXPECTED OUTCOME: The patient will report pain is at an acceptable level within 30 minutes of report of pain. • Have patient rate pain on objective scale such as 0 to 10 to determine pain level. • Give analgesics or antispasmodic drugs as ordered to relieve pain. • Use position changes, diversion, and relaxation exercises to help relieve pain. Semi-Fowler's position may reduce tension on the abdomen. • Provide frequent mouth care if an NG tube is in place to increase comfort. Risk for Deficient Fluid Volume related to diarrhea or fluid shifting from the circulation to the peritoneal cavity EXPECTED OUTCOME: The patient will maintain vital signs and urine output within normal limits at all times. • Record intake and output to determine fluid balance. • Weigh patient daily to determine fluid loss. • Monitor vital signs and urine output and report changes to detect changes from within normal limits. • Maintain IV fluid replacement as ordered to maintain fluid balance if output is greater than intake. For constipation related to a low-fiber diet, see the earlier section on constipation.

urological obstruction

Urinary tract obstruction is an interference with the flo w of urine at any location along the urinary system. It is always a significant problem. The obstruction of urine flow causes di- lation and thinning of the renal tubules with eventual atrophy of renal tissues. Renal blood flow is compromised. Eventu- ally renal tissue is destroyed by the compression. Urethral Strictures A urethral stricture is a narrowing of the lumen of the urethra caused by scar tissue. Urethral strictures are becoming more prevalent due to the rising incidence of STIs in young adults. Most strictures are acquired from injury or infection. Some strictures are a result of trauma from insertion of catheters or surgical instruments, untreated gonorrhea, and congenital abnormalities. The patient with a urethral stricture has a diminished uri- nary stream and is prone to developing UTIs because of ob- struction of urine flow. Urethral strictures are often seen in older men. The problem becomes more apparent when at- tempts to insert a urinary catheter are unsuccessful because of the narrowed lumen. Initially the treatment of a urethral stricture is mechanical dilation by the urologist, who inserts instruments to stretch open the urethra and then inserts a urinary catheter . If the stricture continues to be a problem after dilation, the area can be surgically repaired (urethroplasty) and a stent inserted. The dilation process can be done at the bedside. This is a painful experience for the patient, and it is helpful and caring to administer pain medication before the procedure.The nurs- ing diagnosis of Acute Pain is very relevant. An indwelling catheter is typically inserted after the dilation, so the nursing diagnosis of Risk for Infection is also present. Patients are taught about UTI prevention Renal calculi (kidney stones; one stone is a calculus) are hard, usually small stones that form somewhere in the renal structures (Table 37.3). The stones are masses of crystals and protein that form when the urine becomes supersaturated with a salt capable of forming solid crystals. Diet and lifestyle can account for the prevalence of stones in some patients. Symp- toms occur when the stones become impacted in the urinary tract. When stones are found in the kidneys, the condition is called nephrolithiasis (Fig. 37.1). Pathophysiology Normally, substances dissolved in urine, including urinary salts, are diluted and readily excreted from the body. Calculi are formed when urinary salts are concentrated enough to set- tle out; the salts often collect and deposit around a nucleus (see Table 37.3). Substances that can serv e as a nucleus in- clude pus, blood, dead tissue, a catheter, and crystals. Stones usually grow on the papillae or in the renal tubules, calyces, or renal pelvis. Stones may also form in the ureter or bladde.r Stones less than 5 mm are readily passed in the urine. Etiology Causes of calculi formation include a family history of stones, chronic dehydration (causing more concentrated urinary salts),andinfection,becausethelatterprovidesanucleusfor stone formation. Additional contributing causes of calcium stones include dietary factors ("Nutrition Notes") and med- ications (Table 37.4). Excessive amounts of calcium in the water in some geographic areas may also be a factor. Immo- bility causes stone formation because of the resulting urinary stasis; in addition, calcium leaves the unstressed bones during immobility, so more calcium is in the blood, which is then filtered through the kidneys. Stones are more common in men than women. A diet high in sodium and animal protein in- creases the amount of calcium in the urine (hypercalciuria) and may contribute to the formation of stones.The risk peaks between ages 30 and 50. Signs and Symptoms Symptoms of renal calculi include e xcruciating flank pain and renal colic. When a stone is lodged in the ureter , it is common to have pain radiate down to the genitalia. The pain results when the stone pre vents urine from draining. Addi- tional symptoms include hematuria from irritation by the stone, dysuria, frequency, urgency, and enuresis. The patient also may ha ve costovertebral tenderness. Some people develop nausea, vomiting, and diarrhea because of the prox- imity of the GI structures. Table 37.5 summarized the dis- cussion of renal calculi. Prevention Consult with the HCP and dietitian to determine if an y foods should be avoided, depending on the type of stone found. "Nutrition Notes: Renal Calculi" discusses foods that may contribute to calculi development (see also "Cul- tural Considerations"). Encourage fluid intak e to prevent dehydration. Encourage the patient to w alk, which pro- motes the excretion of stones and reduces bone calcium re- sorption (release). Urocit(r)-K (potassium citrate), which restores chemicals in the urine that pre vent crystals from forming to decrease calcium oxalate and uric acid stones, might be prescribed. Complications The presence of renal calculi increases the risk for UTIs be- cause of obstruction of the free flow of urine. Untreated ob- struction of a stone in a ureter or the urethra can also result in retention of urine and damage to the kidney. This process is called hydronephrosis (discussed later). Diagnostic Tests Helical computed tomography (CT) without contrast is the preferred diagnostic test. It requires no contrast agent and has the ability to detect stones in the distal ureters as well as small stones less than 1 to 2 mm. Other tests include an abdominal x-ray or an IV p yelogram, which will identify the anatomic location of the stone. Renal ultrasound may be done to identify a stone in the renal pelvis, calyx, or ureter. This is the preferred test for pregnant women suspected of having a kidney stone. Urinalysis may indicate gross or microscopic hematuria and could indicate abrasion of the urinary tract. The presence of crystals or urinary pH may indicate calculus type. Two con- secutive 24-hour urine collections should be done while the patient follows his or her usual diet. The 24-hour urine col- lection should measure total urine v olume, calcium, oxalate, citrate, uric acid, sodium, potassium, phosphorus, pH, and cre- atinine as well as cystine and magnesium. Therapeutic Measures Renal calculi are treated medically if possible. Most small stones are flushed out of the body during urination. P atients can pass stones in the urine if the y are 5 mm or smaller . Drinking 2 to 3 quarts of fluids, taking analgesics such as Tylenol or ibuprofen, and perhaps a prescribed alpha-blocker medication (such as tamsulosin [Flomax]) to relax ureter muscles will help pass a small stone. Patients who develop severe renal colic are usually admit- ted to the hospital. IV fluids are given to hydrate the patient and help flush the stone out of the body. All urine is strained to detect passage of stones, and pain medication is gi ven. If the patient is unable to pass the stone and infection, impaired renal function, or se vere pain continues, interv ention is needed. The solubility of stone-forming substances can be changed by altering the pH of the urine. Calcium stones may be treated with thiazide diuretics and allopurinol (Aloprim, Zyloprim). Surgical removal may be required for large stones, obstructions, or intractable pain. LITHOTRIPSY. Lithotripsy is the use of sound, laser, or dry shock- waveenergiestobreakthestoneintosmallfragments. Types of lithotripsy include e xtracorporeal shock-wave lithotripsy (ESWL), electrohydraulic lithotripsy, laser lithotripsy, and per- cutaneous ultrasonic lithotripsy. With ESWL, a form of lithotripsy , sedated or anesthetized patients lie down on the lithotriptor with a w ater-filled device supporting their back. Ultrasonic shock waves are used to break up the stone into sand particles, which are then urinated out over a week with small discomfort or be small enough to be re- moved. Some lithotripsy procedures do not require submersion and use other means of initiating shock waves (Fig. 37.2). Oc- casionally, a stent is placed in the ureter to facilitate the passage of the stone fragments. After the procedure, the patient is usually discharged home after being told to increase fluid intake to help flush the sand particles out, strain the urine to catch stone frag- ments for analysis, and notify the urologist if there are any prob- lems. Blood in the urine is common after lithotripsy. ESWL is most effective with stones that are in the kidne y. ESWL may increase the risk of kidney disease or hypertension later in life. SURGERY FOR RENAL CALCULI. Some patients may need sur- gery for stone remo val. The particular procedure chosen— endoscopic or open surgery—depends on the location of the stone. Endoscopic procedures for the bladder include cystoscopy for small stones and c ystolitholapaxy for larger stones. For cystolitholapaxy, an instrument is inserted through the urethra tothebladdertocrushthestone. Thestoneisthenwashed out with an irrigating solution. If the stone is lodged in a ureter, the urologist may insert an instrument into the ureter through a cystoscope to crush the stone or use an ultrasonic lithotripsy instrument to break the stone into fragments. Post- operative care following these procedures is similar to care following any cystoscopy (see Chapter 36). The open surgery procedure for stones in the bladder is a cystotomy and for the ureter an ureterolithotomy. Monitors Ellipsoidal reflector For kidney stones, a percutaneous nephrolithotomy is performed in which a scope is inserted through the skin into the kidney to aid in breaking up the stone and to irrigate the renal pelvis. A nephrostomy tube is often left in place at first to prevent stone fragments from passing through the urinary system. If the stone is very large, a nephrolithotomy may be needed, which involves a surgical incision into the kidney to remove the stone. A pyelolithotomy is done to remove stones lodged in the renal pelvis. Nursing Process for the Patient With Renal Calculi DATA COLLECTION. Patients with stones are often in e x- treme pain and should be monitored for pain. Patients over age 60 should have an abdominal aneurysm ruled out. A health history may identify a f amily or patient history of previous stone formation. People who have had stones usu- ally have a recurrence. Why would renal colic usually begin suddenly, progress rapidly, and peak over a 30-minute pe- riod? Because it occurs as urine attempts to pass the stone. Flank pain may radiate to the genitals. Diminished or absent bowel sounds may progress to an ileus.The patient may also be restless, pale, and lightheaded. Nursing care of a patient with a renal calculus in volves careful measurement of intake and output and observation of urineforabnormalitiessuchashematuria,pyuria,orpassage of a stone. Obstruction may occur at the bladder neck or ure- thra. With obstruction, anuria (less than 50 mL of urine out- put daily) or oliguria (less than 400 mL of urine output daily) is noted. This is an emergency situation and must be treated immediately to preserv e kidney function. Temperature is monitoredforonsetoffever,whichwouldindicateinfectionBlood pressure may decrease if severe pain causes shock. A special strainer is used to strain all urine for stones. If a stone is found, it is saved for analysis in the laboratory. The patient is also asked about a recent history of infection, diet or actvi - ity changes, or other risk factors for renal calculi. If the cause can be identified, teaching can be done to help prevent recur- rent calculi. NURSING DIAGNOSIS, PLANNING, AND IMPLEMENTATION. Acute Pain related to the presence of, obstruction, or movement of a stone within the urinary system EXPECTED OUTCOME: The patient will verbalize the relief of pain or ability to tolerate pain. • Ask severity, location, and duration of pain using a pain scale. Pain is typically in the flank or costovertebral angle and may radiate to the pelvic, groin, or abdominal area. • Monitor patency of drains, and catheters. Obstruction of urine flow will increase pain. • Encourage fluid intake, unless contraindicated, to promote the passage of stone, dilute the urine, and reduce the risk of further stone formation. • Administer pain medication as ordered to promote comfort. • Apply heat to flank area to reduce pain and promote comfort. • Ambulate if possible to facilitate the passage of the stone through the urinary system. • Strain urine through gauze or strainer to identify stones that may have been passed providing pain relief. Risk for Infection related to the introduction of bacteria from obstructed urinary flow and instrumentation EXPECTED OUTCOME: The patient will remain infection free. • Monitor vital signs, and observe for chills, cloudy, foul- smelling urine, or bleeding. Abnormalities may indicate an infection. • Monitor urine amount, color, clarity, and odor to ensure patency of urinary system or tubes. Foul-smelling or cloudy urine may indicate an infection. • Encourage fluid intake to flush bacteria and stones and prevent further stone formation. Deficient Knowledge related to lack of knowledge about pre- vention of recurrence, diet, and symptoms of renal calculi EXPECTED OUTCOME: The patient will verbalize an under- standing of the factors related to the recurrence of renal calculi, infection, and treatment options. • Note recurrence of renal stones. Recurrence may indicate knowledge deficit. • Note family history of renal stones and explain relevance to patient. Stones have a higher incidence in patients with a positive family history. • Determine the relationship between activity and stones. Sedentary lifestyle or limited mobility may increase risk of stone formation. • Ask the patient's understanding of possible courses of ther- apy to treat renal stones to establish baseline knowledge. • Teach the importance of maintaining a fluid intake of 2 to 3 quarts per day. Low-solute (dilute) urine helps prevents stone formation. • Teach patient about medications used to prevent recur- rence of renal stones: • Diuretics (thiazide type) increase tubular reabsorption of calcium, making it less available for calculi formation in the urinary tract. • Allopurinol (Zyloprim) reduces uric acid production. • Antibiotics prevent chronic UTI, which may precede renal calculus formation. • As applicable, teach patient about management of stones. Most stones pass spontaneously. There may be pain, nau- sea, and vomiting. Medical management consists of fluids, pain management, and antibiotics. Mechanical interven- tions with percutaneous catheters and nephroscopic pro- cedures, lithotripsy, or surgery can be used to eliminate stones. • Teach patient to strain all urine. Stone fragments may con- tinue to pass for weeks after stone crushing or lithotripsy. • Teach patient to report signs of infection, pain not relieved by medication, nausea, chills, or the appearance of foul- smelling urine for treatment. EVALUATION. Outcomes have been achieved if the patient remains comfortable, free from infection, and gains under - standing about prevention of the reoccurrence of renal stones. .