MED SURG 2

47.4 Compare Crohn's disease and ulcerative colitis with regard to their pathophysiology; clinical manifestations; diagnostic evaluation; and medical, surgical, and nursing management

(IBD IS A TERM USED FOR A GROUP OF CHRONIC DISORDERS - CROHNS AND UC CROHN'S (Regional Enteritis) - characterized by periods of remission and exacerbation - The results of a barium series (the most conclusive diagnostic aid) will show regional, discontinous lesions, narrowing of the colon, thickening of the bowel wall, and mucosal edema - initial lesions then deepen into longitudinal and transverse ulcers, separated by edematous patches, creating a characteristic cobblestone appearance to the affected bowel. Clinical Manifestations The onset of symptoms is usually insidious in Crohn's disease, with prominent *right lower quadrant* abdominal pain and diarrhea unrelieved by defecation. - Scar tissue and the formation of granulomas interfere with the ability of the intestine to transport products of upper intestinal digestion through the constricted lumen, resulting in crampy abdominal pain. - There is abdominal tenderness and spasm. - Because eating stimulates intestinal peristalsis, the crampy pains occur AFTER meals. - To avoid these bouts of crampy pain, the patient tends to limit food intake, reducing the amounts and types of food to such a degree that normal nutritional requirements are often not met. As a result, weight loss, malnutrition, and secondary anemia occur - Disrupted absorption causes chronic diarrhea and nutritional deficits. The result is a person who is thin and emaciated from inadequate food intake and constant fluid loss. - Chronic symptoms include diarrhea, abdominal pain, steatorrhea (i.e., excessive fat in the feces), anorexia, weight loss, and nutritional deficiencies. UC (Ulcerative Colitis) - Ulcerative colitis is a chronic ulcerative and inflammatory disease of the mucosal and submucosal layers of the colon and rectum that is characterized by unpredictable periods of remission and exacerbation with bouts of abdominal cramps and bloody or purulent diarrhea. The inflammatory changes typically begin in the rectum and progress proximally through the colon - The results of a barium series will show diffuse involvement, shortening of the colon, but no narrowing of the colon or mucosal edema UC PATHO - Ulcerative colitis affects the superficial mucosa of the colon and is characterized by multiple ulcerations, diffuse inflammations, and desquamation or shedding of the colonic epithelium. Bleeding occurs as a result of the ulcerations. The mucosa becomes edematous and inflamed. The lesions are contiguous, occurring one after the other. Eventually, the bowel narrows, shortens, and thickens because of muscular hypertrophy and fat deposits. Because the inflammatory process is not transmural (i.e., it affects the inner lining only), abscesses, fistulas, obstruction, and fissures are uncommon in ulcerative colitis Clinical Manifestations OF UC The clinical course is usually one of exacerbations and remissions. - symptoms of ulcerative colitis include diarrhea, with passage of mucus, pus, or blood; *left lower quadrant* abdominal pain; and intermittent tenesmus. The bleeding may be mild or severe, and pallor, anemia, and fatigue result. - The patient may have anorexia, weight loss, fever, vomiting, and dehydration, as well as cramping, tenesmus (the feeling that you need to pass stools, even though your bowels are already empty), and the passage of six or more liquid stools each day. - The disease is classified as mild, severe, or fulminant, depending on the severity of the symptoms. - Hypoalbuminemia, electrolyte imbalances, and anemia frequently develop. - Extraintestinal manifestations include skin lesions (e.g., erythema nodosum), eye lesions (e.g., uveitis), joint abnormalities (e.g., arthritis), and liver disease - Colonoscopy is the definitive screening test that can distinguish ulcerative colitis from other diseases of the colon with similar symptoms. Complications - toxic megacolon, perforation, and bleeding as a result of ulceration, vascular engorgement, and highly vascular granulation tissue. In toxic megacolon, the inflammatory process extends into the muscularis, inhibiting its ability to contract and resulting in colonic distention. - Symptoms include fever, abdominal pain and distention, vomiting, and fatigue. - If the patient with toxic megacolon does not respond within 72 hours to medical management with NG suction, IV fluids with electrolytes, corticosteroids, and antibiotics, surgery is required. - A subtotal colectomy may be performed if bowel perforation has not occurred. - Otherwise, colectomy is indicated; it is ultimately needed in up to one third of patients with severe ulcerative colitis - For many patients, surgery becomes necessary to relieve the effects of the disease and to treat these serious complications; an ileostomy usually is performed. Medical Management of Chronic Inflammatory Bowel Disease - for both Crohn's disease and ulcerative colitis is aimed at reducing inflammation, suppressing inappropriate immune responses, providing rest for a diseased bowel so that healing may take place, improving quality of life, and preventing or minimizing complications. Most patients have long periods of well-being interspersed with short intervals of illness. Management depends on the disease location, severity, and complications Nutritional Therapy - Oral fluids and a low-residue, high-protein, high-calorie diet with supplemental vitamin therapy and iron replacement are prescribed to meet nutritional needs, reduce inflammation, and control pain and diarrhea. - Fluid and electrolyte imbalances from dehydration caused by diarrhea are corrected by IV therapy as necessary if the patient is hospitalized or by oral fluids if the patient is managed at home. - Any foods that exacerbate diarrhea are avoided. Milk may contribute to diarrhea in those with lactose intolerance. - Cold foods and smoking are avoided because both increase intestinal motility. - Parenteral nutrition may be indicated Pharmacologic Therapy - Sedatives and antidiarrheal and antiperistaltic medications are used to minimize peristalsis in order to rest the inflamed bowel. They are continued until the patient's stools approach normal frequency and consistency. - Aminosalicylates such as sulfasalazine (Azulfidine) are often effective for mild or moderate inflammation and are used to prevent or reduce recurrences in long-term maintenance regimens. - Sulfa-free aminosalicylates (e.g., mesalamine [Asacol, Pentasa]) are effective in preventing and treating recurrence of inflammation. - Antibiotics (e.g., metronidazole [Flagyl]) are used for complications such as abscesses or fistula formation - Corticosteroids are used to treat severe and fulminant disease and can be given orally (e.g., prednisone) in outpatient treatment or parenterally (e.g., hydrocortisone [Solu-Cortef]) in hospitalized patients. - Topical (i.e., rectal administration) corticosteroids (e.g., budesonide [Entocort]) are also widely used in the treatment of distal colon disease. - Immunomodulators (e.g., azathioprine [Imuran], mercaptopurine [6-MP], methotrexate [MTX], cyclosporine [Neoral]) have been used to alter the immune response. COMPARISON UC- starts in rectum & works up left colon (descening) primarily mucosal layer Crohn's- primarily in the ileum (middle part of small intestine), secondarily in the colon transmural (all 4 layers) & segmental (patchy lesions), may occur anywhere in the GI tract LESIONS UC- continuous Crohn's- patchy (cobblestone/skip lesions) STOOL UC- severe watery diarrhea, bloody stools, diarrhea Crohn's- less severe diarrhea, steatorrhea, stool is soft or semi formed - melena Fistula, fissure, or abscess UC- rare Crohn's- more common in crohn's Malabsorption/malnutrition UC-doesn't occur because it starts in the rectum Crohn's- small intestinal malabsorption Age of onset UC-all ages but usually in the 20's-30's Crohn's-occurs at all ages, most often in 3rd decade of life Clinical manifestations for UC rectal bleeding & bloody stool are common, frequent diarrhea, 10-20 BM per day, urgency, continuous cramping pain in the LLQ, fever, tachycardia, fluid & electrolyte imbalances Clinical manifestations for Crohn's less frequent diarrhea usually not bloody, colicky pain LRQ- mild to severe, abdominal tenderness, spasms, weight loss, malaise, crampy pain after meals lower grade fever Complications UC- colon cancer, toxic megacolon, anal fissures, abdo abcesses, hemorrhoids, chronic blood loss (leads to hypotension), infections, anemia, dehydrations, malnutrition Crohn's- Fistula's, abscesses, obstructions, infections, anemia, dehydration, malnutrition, thickened intestinal wall (fibrous) UC complications -hemorrhage Toxic megacolon -dilated and leaky colon, leads to peritonitis and sepsis -acute motor paralysis -acute dilation of colon -symptoms: fever, tachycardia, hypotension, dehydration, abdominal tenderness, and cramping, change in the number of stools per day -other causes: use of laxatives, narcotics, and electrolyte imbalance and infections -colorectal cancer -after 8-15 years after diagnosis of UC, yearly colonoscopies CD complications -intestinal obstruction -abscess -fistula: abnormal connection -fissures: crack -ulcers-increase cancer risk -perforation -hemorrhage Diagnostics UC- medical hx, presence of symptoms., colonoscopy, barium enema, xray, blood work (CBC, hct, Hgb, ESR) to rule out other things Crohn's - same as UC but instead of colonoscopy - they do a sigmoidoscopy Treatment UC- if entire colon is removed UC is cured = permanent ileostomy Crohn's- surgery is not a cure because disease will reappear. Tx is pharmacological

47.6 Identify the responsibilities of the nurse in meeting the needs of the patient with an intestinal diversion.

) 1337 HOME CARE CHECKLIST 47-6 EDUCATION FAMILIAR WITH NORMAL STOMA, ANTICIPATED FINDINGS IN POST OP EMOTIONAL 1433 47-8 MANAGING OSTOMY CARE, EDUCATION THAT MUST BE PROVIDED An ileostomy is the surgical creation of an opening into the ileum or small intestine. A colostomy is the surgical opening into the colon by means of a stoma to allow drainage of contents of the colon. Providing Preoperative Care - A period of preparation with replacement of fluid, blood, and protein is necessary prior to surgery. - Antibiotics may be prescribed. - If the patient has been taking corticosteroids (i.e., to treat IBD), they will be continued during the surgical phase to prevent steroid-induced adrenal insufficiency. - patient is given a low-residue diet, provided in frequent, small feedings. - All other preoperative measures are similar to those for general abdominal surgery. The abdomen is marked for the proper placement of PREOPERATIVE CARE OF NURSE - INTERVENTIONS 1) Ascertain whether the patient has had a previous surgical experience, and ask for recollections of positive and negative impressions. 2) Determine what information the surgeon gave the patient and family and whether it was understood. Clarify and elaborate as necessary. Determine whether the stoma is permanent or temporary. Be aware of the patient's prognosis if carcinoma exists. 3) Use pictures, drawings, or websites to illustrate the location and appearance of the surgical wounds (abdominal, perineal) and the stoma if the patient is receptive. 4) Explain that oral/parenteral antimicrobial agents will be given to cleanse the bowel preoperatively. Mechanical cleansing may also be required. 5) Assist the patient during nasogastric/nasoenteric intubation, if indicated. Measure drainage from the tube. 6) Encourage the patient to verbalize feelings about the stoma. Offer to be present when the stoma is first viewed and touched. Providing Postoperative Care - As with other patients undergoing abdominal surgery, the nurse encourages those with an ostomy to engage in early ambulation. - It is important to administer prescribed pain medications as required. - The nurse observes the stoma for color and size. It should be pink to bright red and shiny. - Typically, a temporary clear or transparent plastic bag (i.e., appliance or pouch) with an adhesive facing is placed over the ostomy in the operating room and firmly pressed onto the surrounding skin. - The nurse monitors the ostomy for fecal drainage, which should begin about 24 to 48 hours after surgery for an ileostomy and within 3 to 6 days after surgery for a colostomy. - The drainage from an ileostomy is a continuous liquid from the small intestine because the stoma does not have a controlling sphincter. The contents drain into the pouch and are thus kept from coming into contact with the skin. They are collected, measured, and discarded when the pouch becomes full. - If a continent ileal reservoir was created, as described for the Kock pouch, continuous drainage is provided by an indwelling reservoir catheter for 2 to 3 weeks after surgery. This allows the suture lines to heal. - Stool drainage from transverse colostomies may be soft and unformed; whereas, stool from descending and sigmoid colostomies is more solid - Because patients lose large fluid volumes in the early postoperative period, an accurate record of fluid I&O, including fecal discharge, is necessary to help gauge each patient's fluid needs. - There may be 1,000 to 2,000 mL of fluid lost each day in addition to expected fluid loss through urine, perspiration, respiration, and other sources. - With this loss, sodium and potassium are depleted. The nurse monitors laboratory values and administers electrolyte replacements as prescribed. - Fluids are given IV for 4 to 5 days to replace lost fluids. - NG suction may be a part of the immediate postoperative care, with the tube requiring frequent irrigation, as prescribed. - purpose of NG suction is to prevent a buildup of gastric contents while the intestines are not functioning. - After the tube is removed, the nurse offers sips of clear liquids and gradually progresses the diet. - Nausea and abdominal distention, which may indicate intestinal obstruction, must be reported immediately. POSTOPERATIVE CARE OF NURSE - INTERVENTIONS 1) Provide information about expected bowel function: - Characteristics of effluent - Frequency of discharge 2) Explain how to prepare the appliance for an adequate fit. A) Choose the drainage appliance that will provide a secure fit around the stoma. Measure the stoma size with a measuring guide provided by the ostomy equipment manufacturer and compare with the opening on the pouch. The barrier opening should be sized to "hug" the stoma and cover the peristomal skin; wafer barriers can be pulled or molded to the size of the stoma. B) Remove any plastic covering that protects the appliance adhesive. Note: The pouch is applied by pressing the adhesive for 30 seconds to the skin barrier. 3) Demonstrate how to change the appliance or empty the pouch before leakage occurs. Be aware that the older adult may have diminished vision and difficulty handling equipment. 4) If appropriate, demonstrate how to irrigate the colostomy (usually on the 4th or 5th day). Recommend that irrigation be performed at a consistent time, depending on the type of colostomy. 5) Provide information about signs and symptoms of irritated or inflamed skin. Use pictures if possible. (Peristomal skin should be slightly pink without abrasions and similar to that of the entire abdomen.) 6) Instruct patient how to cleanse the peristomal skin gently. 7) Demonstrate how to apply a skin barrier (e.g., wafer). 8) Demonstrate how to remove the pouch. (never pull) 9) Conduct a complete nutritional assessment to identify any foods that may increase peristalsis by irritating the bowel. 10) Advise the patient to avoid food products with a cellulose or hemicellulose base (nuts, seeds) bc Cellulose food products are the nondigestible residue of plant foods. They hold water, provide bulk, and stimulate elimination. 11) Recommend moderation in intake of certain irritating fruits such as prunes, grapes, and bananas. (may increase effluent) 12) Encourage the patient to verbalize concerns and fears. The sexual partner is welcomed to participate in the discussion and recommend alternative sex positions. 13) Estimate fluid intake and output (I&O): - Record I&O - Daily weights An early indicator of fluid imbalance is a daily, significant difference between I&O. The average person ingests (food, fluids) and loses (from urine, feces, lungs) about 2 L of fluid every 24 hours. A gain/loss of 1 L of fluid is reflected in a body weight change of 1 kg (2.2 lb). 14) Assess serum and urinary values of sodium and potassium. Sodium is the major electrolyte regulating water balance. Vomiting results in decreased urinary and serum sodium levels. Urinary sodium values, in contrast to serum values, reflect early, sensitive changes in sodium balance. Sodium works in conjunction with potassium, which is also decreased with vomiting. A significant deficiency in potassium is associated with a decrease in intracellular potassium bicarbonate, which leads to acidosis and compensatory hyperventilation. 15) Observe and record skin turgor and the appearance of the tongue. Providing Emotional Support The patient may think that everyone is aware of the ostomy and may view the stoma as a mutilation compared with other abdominal incisions that heal and are hidden. Because there is loss of a body part and a major change in anatomy and function, the patient often goes through the phases of grief—denial, anger, bargaining, depression, and acceptance. Nursing support through these phases is important, and understanding of the patient's emotional state should determine the approach taken. Conversely, a surgical procedure to create an ileostomy can produce dramatic positive changes in patients who have suffered from IBD for several years. After the discomfort of the disease has decreased and the patient learns how to take care of the ileostomy, he or she often develops a more positive outlook. Until the patient progresses to this phase, an empathetic and tolerant approach by the nurse plays an important part in recovery. The sooner the patient masters the physical care of the ostomy, the sooner he or she will psychologically accept it. Strong self-care skills are associated with better outcomes and adjustment for patients support groups may be helpful as well Managing Skin and Stoma Care - patient with an ileostomy cannot establish regular bowel habits because the contents of the ileum are fluid and are discharged continuously. The patient must wear a pouch at all times. - Stomal size and pouch size vary initially; the stoma should be rechecked 3 weeks after surgery, when the edema has subsided. The final size and type of appliance is selected in 3 months, after the patient's weight has stabilized and the stoma shrinks to a stable shape. - The incidence of complications related to a colostomy is usually less than that of an ileostomy. - Postoperatively, the stoma is examined for swelling (slight edema from surgical manipulation is normal), color (a healthy stoma is pink or red), discharge (a small amount of oozing is normal), and bleeding (an abnormal sign if bright red or more than trace amounts) - Skin excoriation around the stoma can be a persistent problem, particularly for ileostomies. - Peristomal skin integrity may be compromised by several factors, such as an allergic reaction to the ostomy appliance, skin barrier, or paste; chemical irritation from the effluent; mechanical injury from the removal of the appliance; and infection. - If irritation and yeast growth occur, nystatin powder (Mycostatin) is dusted lightly on the peristomal skin and a pouch with skin barrier is applied over the affected area Changing an Appliance - The amount of time a person can keep the appliance sealed to the body surface depends on the location of the stoma and on body structure. - The usual wearing time, which also depends on the type of skin barrier, is 5 to 10 days. - The appliance is emptied every 4 to 6 hours, or at the same time the patient empties the bladder. - An emptying spout at the bottom of the appliance is closed with a special clip or Velcro closure made for this purpose. - If the patient wishes to bathe or shower before putting on a clean appliance, micropore tape applied to the sides of the pouch keeps it secure during bathing. - Most pouches are disposable and odor proof. - Foods such as spinach and parsley act as deodorizers in the intestinal tract; foods that cause odors include asparagus, cabbage, onions, and fish. - Bismuth subcarbonate tablets, which may be prescribed and taken orally three or four times each day, are effective in reducing odor. Irrigating a Colostomy - purpose of irrigating a colostomy is to empty the colon of gas, mucus, and feces so that the patient can go about social and business activities without fear of fecal drainage. - A stoma does not have voluntary muscular control and may empty at irregular intervals. - Regulating the passage of fecal material is achieved by irrigating the colostomy or allowing the bowel to evacuate naturally without irrigations. This choice depends on the person and the type of the colostomy (i.e., descending or sigmoid colostomies). - By irrigating the stoma at a regular time, there is less gas and retention of the irrigant. - The time for irrigating the colostomy should be consistent with the schedule that the person will follow after leaving the hospital. Managing Dietary and Fluid Needs - A low-residue diet is followed for the first 6 to 8 weeks. - Strained fruits and vegetables are ingested. These foods are important sources of vitamins A and C. - Later, there are few dietary restrictions, except for avoiding foods that are high in fiber or hard-to-digest kernels, such as celery, popcorn, corn, poppy seeds, caraway seeds, and coconut, which may result in a stomal obstruction (food blockage) for the person with an ileostomy. Foods are reintroduced one at a time. - Getting enough fluids during the summer may be a challenge, when fluid lost through perspiration adds to the fluid loss through the ileostomy. - Fluids such as sports drinks (Gatorade) are helpful in maintaining electrolyte balance. - If the fecal discharge is too watery, fibrous foods (e.g., whole-grain cereals, fresh fruit skins, beans, corn, nuts) are restricted. - If the effluent is excessively dry, salt intake is increased. - Increased intake of water or fluid does not increase the effluent, because excess water is excreted in the urine. Gerontologic Considerations - Some older adults may require an ostomy but have difficulty managing care due to decreased vision, impaired hearing, and difficulty with fine motor coordination. - It may be helpful for patients to handle ostomy equipment and simulate cleaning the peristomal skin and irrigating the stoma before surgery. - Skin care is a major concern in older patients with an ostomy because of the skin changes that occur with aging—the epithelial and subcutaneous fatty layers become thin, and the skin is irritated easily - To prevent skin breakdown, special attention is paid to skin cleansing and the proper fit of an appliance. Stoma skin barriers should be molded into shape around the stoma Preventing Complications - Monitoring for complications is an ongoing activity for the patient with an ostomy. Peristomal skin irritation, which results from leakage of effluent, is the most common complication of an ileostomy. - A drainable pouching system that does not fit well is often the cause. - Other common complications include diarrhea, stomal stenosis, urinary calculi, and cholelithiasis. Even in the presence of a properly fitted drainable pouching system, diarrhea can be problematic. Diarrhea, manifested by very irritating effluent that rapidly fills the pouch (every hour or sooner), can quickly lead to dehydration and electrolyte losses. Supplemental water, sodium, and potassium are given to prevent hypovolemia and hypokalemia. Antidiarrheal agents are given. Stenosis is caused by circular scar tissue that forms at the stoma site. The scar tissue must be surgically released. Urinary calculi may occur in patients with ileostomies and are at least partly attributed to dehydration from decreased fluid intake. Crohn's disease is a risk factor for cholelithiasis (i.e., gallstones) due to altered absorption of bile acids

49.6 Use the nursing process as a framework for care of the patient with cirrhosis of the liver.

)Cirrhosis is a chronic disease characterized by replacement of normal liver tissue with diffuse fibrosis that disrupts the structure and function of the liver. There are 3 types of cirrhosis or scarring of the liver: - Alcoholic cirrhosis, in which the scar tissue characteristically surrounds the portal areas. This is most frequently caused by chronic alcoholism and is the most common type of cirrhosis. - Postnecrotic cirrhosis, in which there are broad bands of scar tissue. This is a late result of a previous bout of acute viral hepatitis. - Biliary cirrhosis, in which scarring occurs in the liver around the bile ducts. This type of cirrhosis usually results from chronic biliary obstruction and infection (cholangitis); it is much less common. PATHO Nutritional deficiency with reduced protein intake contributes to liver destruction in cirrhosis, but excessive alcohol intake is the major causative factor in fatty liver and its consequences. However, cirrhosis can occur in people who do not consume alcohol and in those who consume a normal diet and have a high alcohol intake. - exposure to certain chemicals (carbon tetrachloride, chlorinated naphthalene, arsenic, or phosphorus) or infectious schistosomiasis. - Twice as many men as women are affected, although, for unknown reasons, women are at greater risk for development of alcohol-induced liver disease. Most patients are between 40 and 60 years of age. - Alcoholic cirrhosis is characterized by episodes of necrosis involving the liver cells, which sometimes occur repeatedly throughout the course of the disease. The destroyed liver cells are gradually replaced by scar tissue. Eventually, the amount of scar tissue exceeds that of the functioning liver tissue. CLINICAL MANIFESTATIONS liver enlargement, portal obstruction, ascites, infection and peritonitis, varices, GI varices, edema, vitamin deficiency, anemia, mental deterioration Compensated cirrhosis, with its less severe, often vague symptoms, may be discovered secondarily at a routine physical examination. The hallmarks of decompensated cirrhosis result from failure of the liver to synthesize proteins, clotting factors, and other substances and manifestations of portal hypertension Compensated - Abdominal pain - Ankle edema - Firm, enlarged liver - Flatulent dyspepsia - Intermittent mild fever - Palmar erythema (reddened palms) - Splenomegaly - Unexplained epistaxis - Vague morning indigestion - Vascular spiders Decompensated - Ascites - Clubbing of fingers - Continuous mild fever - Epistaxis - Gonadal atrophy - Hypotension - Jaundice - Muscle wasting - Purpura (due to decreased platelet count) - Sparse body hair - Spontaneous bruising - Weakness - Weight loss - White nails Liver Enlargement Early in the course of cirrhosis, the liver tends to be large, and the cells are loaded with fat. The liver is firm and has a sharp edge that is noticeable on palpation. Abdominal pain may be present because of recent, rapid enlargement of the liver, which produces tension on the fibrous covering of the liver (Glisson capsule). Later in the disease, the liver decreases in size as scar tissue contracts the liver tissue. The liver edge, if palpable, is nodular. Portal Obstruction and Ascites Portal obstruction and ascites—late manifestations of cirrhosis—are caused partly by chronic failure of liver function and partly by obstruction of the portal circulation. Almost all of the blood from the digestive organs is collected in the portal veins and carried to the liver. Because a cirrhotic liver does not allow free blood passage, blood backs up into the spleen and the GI tract, and these organs become the seat of chronic passive congestion—that is, they are stagnant with blood and therefore cannot function properly. Indigestion and altered bowel function result. Fluid rich in protein may accumulate in the peritoneal cavity, producing ascites. This can be detected through percussion for shifting dullness or a fluid wave Infection and Peritonitis Bacterial peritonitis may develop in patients with cirrhosis and ascites in the absence of an intra-abdominal source of infection or an abscess. Gastrointestinal Varices The obstruction to blood flow through the liver caused by fibrotic changes also results in the formation of collateral blood vessels in the GI system and shunting of blood from the portal vessels into blood vessels with lower pressures. As a result, the patient with cirrhosis often has prominent, distended abdominal blood vessels, which are visible on abdominal inspection (caput medusae) and distended blood vessels throughout the GI tract. The esophagus, stomach, and lower rectum are common sites of collateral blood vessels. These distended blood vessels form varices or hemorrhoids, depending on their location. Because these vessels were not intended to carry the high pressure and volume of blood imposed by cirrhosis, they may rupture and bleed. Therefore, assessment must include observation for occult and frank bleeding from the GI tract. Edema Another late symptom of cirrhosis is edema, which is attributed to chronic liver failure. Vitamin Deficiency and Anemia Because of inadequate formation, use, and storage of certain vitamins (notably vitamins A, C, and K), signs of deficiency are common, particularly hemorrhagic phenomena associated with vitamin K deficiency. Chronic gastritis and impaired GI function, together with inadequate dietary intake and impaired liver function, account for the anemia that is often associated with cirrhosis. Mental Deterioration Additional clinical manifestations include deterioration of mental and cognitive function with impending hepatic encephalopathy and hepatic coma, as described previously. Serial neurologic assessment is indicated, including assessment of the patient's general behavior, cognitive abilities, orientation to time and place, and speech patterns. INTERVENTIONS Nursing interventions are directed toward - promoting patient's rest - improving nutritional status - providing skin care - reducing risk of injury - monitoring and managing potential complications PROMOTING REST - Rest and supportive measures - Positioning for respiratory efficiency - Oxygen - Planned mild exercise and rest periods - Address nutritional status to improve strength - Measures to prevent hazards of immobility *decreased demand on liver, will increase liver blood supply IMPROVING NUTRITIONAL STATUS - I&O - Encourage small frequent meals - High-calorie diet, sodium restriction (Reduces edema and ascites formation) - Protein modified or restricted if patient is at risk for encephalopathy - Supplemental vitamins, minerals, B complex, provide water-soluble forms of fat-soluble vitamins if patient has steatorrhea (fatty stools) - Consider patient preferences - Provide diet high in carbohydrates with protein intake of 1.2-1.5 g/kg/day. PROVIDING SKIN CARE - Frequent position changes - Gentle skin care - Reduce scratching related to pruritus REDUCING RISK OF INJURY - Prevent falls, trauma related to risk for bleeding - bleeding precautions - raised side rails COMPLICATIONS Bleeding and Hemorrhage The patient is at increased risk for bleeding and hemorrhage because of decreased production of prothrombin and decreased ability of the diseased liver to synthesize the necessary substances for blood coagulation (see the Esophageal Varices section). Hepatic Encephalopathy Hepatic encephalopathy and coma, which are complications of cirrhosis, may manifest as deteriorating mental status (delirium) or as physical signs such as abnormal voluntary and involuntary movements. - Monitoring is essential to identify early deterioration in mental status. The nurse monitors the patient's mental status closely and reports changes so that treatment for encephalopathy can be initiated promptly. An extensive baseline and ongoing neurologic evaluation is key to identify progression through the four stages of encephalopathy Fluid Volume Excess Patients with advanced chronic liver disease develop cardiovascular abnormalities. These occur due to an increased cardiac output and decreased peripheral vascular resistance, possibly resulting from the release of vasodilators. A hyperdynamic circulatory state develops in patients with cirrhosis, and plasma volume increases. This increase in circulating plasma volume is probably multifactorial, but some studies have implicated excess production of nitrous oxide, such as that seen in sepsis, as one causative factor (Nusrat et al., 2014). The greater the degree of hepatic decompensation, the more severe the hyperdynamic state. Close assessment of cardiovascular and respiratory status is of key importance for the care of patients with this disorder. Pulmonary compromise is always a potential complication of ESLD because of plasma volume excess; consequently, the nurse has an important role in preventing pulmonary complications. Administering diuretic agents, implementing fluid restrictions, and enhancing patient positioning can optimize pulmonary function. Fluid retention may be noted in the development of ascites, lower extremity swelling, and dyspnea. Monitoring of I&O, daily weight changes, changes in abdominal girth, and edema formation is part of nursing assessment in the hospital or in the home setting. Patients are also monitored for nocturia and, later, for oliguria, because these states indicate increasing severity of liver dysfunction PT EDUCATION AT DISCHARGE - Of greatest importance is the exclusion of alcohol from the diet. - patient should avoid the consumption of raw shellfish. - Sodium restriction will continue for a considerable time, if not permanently. - ALSO, rest, lifestyle changes, adequate dietary intake, and the elimination of alcohol. The nurse also instructs the patient and family about symptoms of impending encephalopathy, possible bleeding tendencies, and susceptibility to infection.

55.5 Identify potential causes of an obstruction of the urinary tract along with the medical and surgical management of the patient with this condition.

- Bladder or prostate tumors, strictures, benign prostatic hyperplasia, and urinary stones are some potential causes of obstruction that can lead to infections.

16.7 Apply skills for communicating with seriously ill patients and their families.

- Develop level of comfort and expertise in communicating with seriously/terminally ill patients/families - Communication should be tailored to the level of understanding and values - Arrangements should be made to have the discussion at a time that is best for everyone - Create the right setting - Space should be conducive to seating all at eye level Keys to effective listening include the following: - Resist the impulse to fill the "empty space" in communication with talk. - Allow the patient and the family sufficient time to reflect and respond after asking a question. - Prompt gently: "Do you need more time to think about this?" - Avoid distractions (noise, interruptions). - Avoid the impulse to give advice. - Avoid canned responses: "I know just how you feel." - Ask questions. - Assess understanding—your own and the patient's—by restating, summarizing, and reviewing.

55.2 Use the nursing process as a framework for care of the patient with a lower UTI.

1617 uti most common with older adults 1618 additional factors that contribute to older adults -urine cultures urinalysis ct scan antibiotics 1619 med management interventions 1620 65-5 preventative technqies to prevent recurrence of utis CLINICAL MANIFESTATIONS: Upper UTI -Involves the Kidney, pelvis, & ureters. -Typically causes fever, chills, flank pain (the pt is sick) Lower UTI -Involves lower urinary tract (bladder, urethra) -Usually no systemic manifestations (asymptomatic) -The infection is localized & doesn't go to other body systems. S/S of a UTI -Urinary frequency -Urgency -Incontinence -Nocturia -Nocturnal enuresis -Weak stream -Hesitancy -Dysuria -Pain on urination UTI clinical manifestations -Urine may contain visible blood or sediment, giving cloudy appearance. -Flank pain, chills, & fever indicate infection of upper tract -Pyelonephritis FROM TEXT Clinical Manifestations - Signs and symptoms of an uncomplicated lower UTI include burning on urination, urinary frequency (voiding more than every 3 hours), urgency, nocturia (awakening at night to urinate), incontinence, and suprapubic or pelvic pain. - Hematuria and back pain may also be present. In older adults, these symptoms are less common - In patients with complicated UTIs, manifestations can range from asymptomatic bacteriuria to gram-negative sepsis with shock. - Complicated UTIs often are caused by a broader spectrum of organisms, have a lower response rate to treatment, and tend to recur. - Many patients with catheter-associated UTIs are asymptomatic; however, any patient with a catheter who suddenly develops signs and symptoms of septic shock should be evaluated for urosepsis (the spread of infection from the urinary tract to the bloodstream that results in a systemic infection). NURSING PROCESS - LOWER UTI ASSESSMENT - A history of pertinent signs and symptoms is obtained from the patient with a suspected UTI. - The presence of pain, frequency, urgency, hesitancy, and changes in urine are assessed, documented, and reported. - The patient's usual pattern of voiding is assessed to detect factors that may predispose him or her to UTI. - Infrequent emptying of the bladder, the association of symptoms of UTI with sexual intercourse, contraceptive practices, and personal hygiene are assessed. - The patient's knowledge about prescribed antimicrobial medications and preventive health care measures is also assessed. - urine is assessed for volume, color, concentration, cloudiness, and odor—all of which are altered by bacteria in the urinary tract. - Patients need to be asked specifically about the use of complementary and alternative therapies. Researchers in one study reported that women with interstitial cystitis (inflammation of the bladder wall) used both complementary and conventional therapies. The most common complementary therapies reported included diet, biofeedback, dietary supplements, meditation, yoga, and massage DIAGNOSIS - Acute pain related to infection within the urinary tract - Deficient knowledge about factors predisposing the patient to infection and recurrence, detection and prevention of recurrence, and pharmacologic therapy POSSIBLE COMPLICATIONS - Sepsis (urosepsis) - Acute kidney injury and/or chronic kidney disease may occur as the long-term result of either an extensive infective or inflammatory process PLANNING/GOALS - Major goals for the patient may include relief of pain and discomfort, increased knowledge of preventive measures and treatment modalities, and absence of complications. INTERVENTIONS RELIEVING PAIN - pain associated with a UTI is quickly relieved once effective antimicrobial therapy is initiated. - Antispasmodic agents may also be useful in relieving bladder irritability and pain. - Analgesic agents and the application of heat to the perineum help relieve pain and spasm. - patient is encouraged to drink liberal amounts of fluids (water is the best choice) to promote renal blood flow and to flush the bacteria from the urinary tract. - Urinary tract irritants (e.g., coffee, tea, citrus, spices, colas, alcohol) should be avoided. - Frequent voiding (every 2 to 3 hours) is encouraged to empty the bladder completely, because doing so can lower urine bacterial counts, reduce urinary stasis, and prevent reinfection MONITORING AND MANAGING POTENTIAL COMPLICATIONS The goal of treatment is to prevent infection from progressing and causing permanent kidney damage and injury. - Appropriate antimicrobial therapy, liberal fluid intake, frequent voiding, and hygienic measures are commonly prescribed for managing UTIs. - Patient is instructed to notify the primary provider if fatigue, nausea, vomiting, fever, or pruritus occurs. - Periodic monitoring of renal function and evaluation for strictures, obstructions, or stones may be indicated for patients with recurrent UTIs. Patients with UTIs are at increased risk for gram-negative sepsis. For each day a urinary catheter is in place, the risk of developing catheter-associated urinary tract infection (CAUTI) increases. CAUTI: interventions to prevent infection + urosepsis - Using strict aseptic technique during insertion of the smallest catheter possible - Securing the catheter to prevent movement - Frequently inspecting urine color, odor, and consistency - Performing meticulous daily perineal care with soap and water - Maintaining a closed system - Following the manufacturer's instructions when using the catheter port to obtain urine specimens Careful assessment of vital signs and level of consciousness may alert the nurse to kidney involvement or impending sepsis. Positive blood cultures and elevated WBC counts must be reported immediately. At the same time, appropriate antibiotic therapy and increased fluid intake are prescribed (IV antibiotic therapy and fluids may be required). Aggressive early treatment is the key to reducing the mortality rate associated with CAUTI especially in older patients, those with anemia, and those with elevated blood sugar levels PROMOTING HOME, COMMUNITY-BASED, AND TRANSITIONAL CARE Health-related behaviors that help prevent recurrent UTIs include practicing careful personal hygiene, increasing fluid intake to promote voiding and dilution of urine, urinating regularly and more frequently, and adhering to the therapeutic regimen. Preventing Recurrent Urinary Tract Infections - Hygiene - Shower rather than bathe in the tub because bacteria in the bathwater may enter the urethra. - Clean the perineum and urethral meatus from front to back after each bowel movement. This will help reduce concentrations of pathogens at the urethral opening and, in women, the vaginal opening. Fluid Intake - Drink liberal amounts of fluids daily to flush out bacteria. It may be helpful to include at least one glass of cranberry juice per day. - Avoid coffee, tea, colas, alcohol, and other fluids that are urinary tract irritants. Voiding Habits - Void every 2-3 hours during the day, and completely empty the bladder. This prevents overdistention of the bladder and compromised blood supply to the bladder wall. Both predispose the patient to urinary tract infection. Precautions expressly for women include voiding immediately after sexual intercourse. Interventions - Take medication exactly as prescribed. Special timing of administration may be required. - Keep in mind that if bacteria continue to appear in the urine, long-term antimicrobial therapy may be required to prevent colonization of the periurethral area and recurrence of infection. - For recurrent infection, consider acidification of the urine through ascorbic acid (vitamin C), 1000 mg daily, or daily consumption of cranberry juice. - To decrease recurrences, consider Lactobacillus probiotics use in oral or vaginal form. - If prescribed, test urine for presence of bacteria following manufacturer's and health care provider's instructions. - Notify the primary provider if fever occurs or if signs and symptoms persist. - Consult the primary provider regularly for follow-up. EVALUATION

46.2 Use the nursing process as a framework for care of patients with peptic ulcer

ASSESSMENT - Assess pain and methods used to relieve pain - Dietary intake and 72 hour diet diary - Lifestyle and habits such as cigarette and alcohol use - Medications; include use of NSAIDs - Sign and symptoms of anemia or bleeding - Abdominal assessment INTERVENTIONS - RELIEVING PAIN Pain relief can be achieved with prescribed medications. The patient should avoid aspirin and other NSAIDs as well as alcohol. In addition, meals should be eaten at regularly paced intervals in a relaxed setting. Medications prescribed to treat the peptic ulcer should provide relief of ulcer-associated pain. - REDUCING ANXIETY The nurse assesses the patient's level of anxiety. Explaining diagnostic tests and administering medications as scheduled help reduce anxiety. - MAINTAINING OPTIMAL NUTRITIONAL STATUS The nurse assesses the patient for malnutrition and weight loss. After recovery from an acute phase of peptic ulcer disease, the patient is advised about the importance of adhering to the medication regimen and dietary restrictions. EDUCATION Medication education Dietary restrictions Lifestyle changes Expected patient outcomes may include: - Reports freedom from pain between meals and at night - Reports feeling less anxiety - Maintains weight - Demonstrates knowledge of self-care activitiesAvoids irritating foods and beverages (alcohol) and medications (NSAIDs) - Takes medications as prescribed - No evidence of complications (e.g., hemorrhage, perforation or penetration, gastric outlet obstruction) At the completion of education, the patient and/or caregiver will be able to: - State the impact of peptic ulcer disease on physiologic functioning, ADLs, IADLs, roles, relationships, and spirituality. - Explain the importance of and necessity for adherence with prescribed medication regimen. - Demonstrate methods of keeping track of the medication regimen and storage of the prescribed medications, and use reminders such as beepers and/or pillboxes. - State the name, dose, side effects, frequency, and schedule for all medications. - Identify foods and other substances to avoid (e.g., food and drinks with extreme temperatures, coffee and other caffeinated beverages, alcohol, foods that were not tolerated in the past). - Identify side effects and complications that should be reported to primary provider: ---- Hemorrhage—cool skin, confusion, increased heart rate, labored breathing, blood in stool (either bright red or tarry black) ---- Penetration and perforation—severe abdominal pain, rigid and tender abdomen, vomiting, elevated temperature, increased heart rate ---- Gastric outlet obstruction—nausea and vomiting, distended abdomen, abdominal pain - State how to reach primary provider with questions or complications. - State time and date of follow-up appointments and testing. - Identify the need for health promotion (e.g., cessation of use of tobacco products, stress management), disease prevention and screening activities. Management of Potential Complications #1 Management of hemorrhage - Assess for evidence of bleeding, hematemesis or melena, and symptoms of shock/impending shock and anemia - Treatment includes IV fluids, NG, and saline or water lavage; oxygen, treatment of potential shock including monitoring of VS and UO; may require endoscopic coagulation or surgical intervention Pyloric obstruction - Symptoms include nausea and vomiting, constipation, epigastric fullness, anorexia, and (later) weight loss - Insert NG tube to decompress the stomach, provide IV fluids and electrolytes. Balloon dilation or surgery may be required Management of perforation or penetration - Signs include severe upper abdominal pain that may be referred to the shoulder, vomiting and collapse, tender board-like abdomen, and symptoms of shock or impending shock - Patient requires immediate surgery

47.5 Use the nursing process as a framework for care of the patient with inflammatory bowel disease/intestinal obstruction.

ASSESSMENT - Health history to identify onset, duration and characteristics of pain, diarrhea, urgency, tenesmus, nausea, anorexia, weight loss, bleeding, and family history - Discuss dietary patterns, alcohol, caffeine, and nicotine use - Assess bowel elimination patterns and stool - Abdominal assessment COMPLICATIONS - Electrolyte imbalance - Cardiac dysrhythmias - GI bleeding with fluid loss - Perforation of the bowel INTERVENTIONS Maintaining Normal Elimination Pattern - Identify relationship between diarrhea and food, activities, or emotional stressors - Provide ready access to bathroom or commode - Encourage bed rest to reduce peristalsis - Administer medications as prescribed Record frequency, consistency, character, and amounts of stools Assessment and treatment of pain or discomfort, anticholinergic medications before meals, analgesics, positioning, diversional activities, and prevention of fatigue Fluid deficit, I&O, daily weight, assessment of symptoms of dehydration or fluid loss, encourage oral intake, measures to decrease diarrhea Optimal nutrition; elemental feedings that are high in protein and low residue or PN may be needed Reduce anxiety, use a calm manner, allow patient to express feelings, listening, patient education PATIENT EDUCATION - Understanding of disease process - Nutrition and diet - Medications - Information sources: National Foundation for Ileitis and Colitis - Ileostomy care if applicable a bland, low-residue, high-protein, high-calorie, and high-vitamin diet relieves symptoms and decreases diarrhea. It is important to explain the rationale for the use of corticosteroids and anti-inflammatory, antibacterial, and antidiarrheal medications. The nurse emphasizes the importance of taking medications as prescribed and not abruptly discontinuing them (especially corticosteroids) to avoid development of serious medical problems Major goals may include - Attainment of normal bowel elimination patterns - Relief of abdominal pain and cramping - Prevention of fluid deficit - Maintenance of optimal nutrition and weight - Avoidance of fatigue - Reduction of anxiety - Promotion of effective coping - Absence of skin breakdown - Increased knowledge of disease process - Therapeutic regimen - Avoidance of complications

47.1 & 47.3 Describe the pathophysiology, clinical manifestations, and nursing management of patients with irritable bowel syndrome and intestinal obstruction.

Chronic functional disorder characterized by recurrent abdominal pain associated with disordered bowel movements, which may include diarrhea, constipation, or both 15% of adults in the United States report symptoms of IBS; More common in women than men Triggers: chronic stress, sleep deprivation, surgery, infections, diverticulitis, and some foods Inflammatory bowel disease (IBD) is a group of chronic disorders: Crohn's disease (i.e., regional enteritis) and ulcerative colitis that result in inflammation or ulceration (or both) of the bowel. - Both disorders have striking similarities but also several differences. RISK FACTORS - Family history predisposes people to IBD, particularly if a first-degree relative has the disease - Other risk factors: being Caucasian, of Ashkenazi Jewish background, living in a northern climate, and living in an urban area. - Men are at a slightly higher risk for ulcerative colitis; whereas, women are at greater risk for Crohn's disease - People between the ages of 20 and 29 are at greatest risk for Crohn's disease; whereas, people between the ages of 15 and 30 are at greatest risk and those older than 60 years of age are at slightly greater risk for ulcerative colitis. - Current smokers are at risk for Crohn's disease, but those who are ex-smokers or nonsmokers are at risk for ulcerative colitis Despite extensive research, the cause of IBD is still unknown. Researchers theorize that environmental triggers (e.g., exposure to air pollutants), food, tobacco, and viral illnesses in people genetically predisposed to developing an IBD can trigger the cell-mediated immune response that results in the inflammatory changes that characterize IBDs. OBSTRUCTION - Intestinal obstruction exists when blockage prevents the normal flow of intestinal contents through the intestinal tract - Mechanical obstruction: Intraluminal obstruction or mural obstruction from pressure on the intestinal wall - Functional or paralytic obstruction: --- The intestinal musculature cannot propel the contents along the bowel --- The blockage also can be temporary and the result of the manipulation of the bowel during surgery The obstruction can be partial or complete. Severity depends on the region of bowel affected, the degree to which the lumen is occluded, and especially the degree to which the vascular supply to the bowel wall is disturbed. Most bowel obstructions occur in the small intestine. The most common causes are carcinoma, diverticulitis, inflammatory bowel disorders, and fecal impaction Clinical Manifestations The initial symptom is usually crampy pain that is wavelike and colicky due to persistent peristalsis both above and below the blockage. The patient may pass blood and mucus but no fecal matter and no flatus. Vomiting occurs. If the obstruction is complete, the peristaltic waves initially become extremely vigorous and eventually assume a reverse direction, with the intestinal contents propelled toward the mouth instead of toward the rectum. The signs of dehydration become evident: intense thirst, drowsiness, generalized malaise, aching, and a parched tongue and mucous membranes. The patient may continue to have flatus and stool early in the process due to distal peristalsis. The abdomen becomes distended. The lower the obstruction in the GI tract, the more marked the abdominal distention; this may cause reflux vomiting. Vomiting results in loss of hydrogen ions and potassium from the stomach, leading to reduction of chloride and potassium in the blood and to metabolic alkalosis. Dehydration and acidosis develop from loss of water and sodium. With acute fluid losses, hypovolemic shock may occur; septic shock may also occur Cramping pain May pass blood and mucous No fecal matter/no flatus Vomiting Distended abdomen Metabolic alkalosis DIAGNOSTICS - Abdominal x-ray/CT Scan (scan findings include abnormal quantities of gas, fluid, or both in the intestines and sometimes collapsed distal bowel.) - Labs- electrolytes, CBC Dehydration, loss of plasma volume, infection MANAGEMENT OF OBSTRUCTION - Maintaining the function of the nasogastric tube - Assessing and measuring the nasogastric output - Assessing for fluid and electrolyte imbalance - Monitoring nutritional status, and Assessing for manifestations consistent with resolution (e.g., return of normal bowel sounds, decreased abdominal distention, subjective improvement in abdominal pain and tenderness, passage of flatus or stool) Medical Management Decompression of the bowel through an NG tube is necessary for all patients with small bowel obstruction; this may be tried for up to 3 days for patients with partial obstructions; resting the bowel in this manner can result in resolution of the obstruction (Nobie, 2015). When the bowel is completely obstructed, the possibility of strangulation and tissue necrosis (i.e., tissue death) warrants surgical intervention. Before surgery, IV fluids are necessary to replace the depleted water, sodium, chloride, and potassium. Surgical Management The surgical treatment of intestinal obstruction depends on the cause of the obstruction. For the most common causes of obstruction, such as hernia and adhesions, the surgical procedure involves repairing the hernia or dividing the adhesion to which the intestine is attached. In some instances, the portion of affected bowel may be removed and an anastomosis performed. The complexity of the surgical procedure depends on the duration of the intestinal obstruction and the condition of the intestine. OBSTRUCTION SAFETY ALERT - ELECTROLYTE IMBALANCE - Maintaining fluid and electrolyte balance is a priority area to monitor in the patient with a small bowel obstruction. The presence of the NG tube in conjunction with the patient's nothing-by-mouth (NPO) status place the patient at significant risk of fluid imbalance. Thus, measures to promote fluid balance are critically important.

46.1 & 46.3 Describe the etiology, clinical manifestations, pharmacologic, dietary, surgical treatment and management of peptic ulcer

Erosion of a mucous membrane forms an excavation in the stomach, pylorus, duodenum, or esophagus The most common site for peptic ulcer formation is the duodenum Peptic ulcers are more likely to occur in the duodenum than in the stomach. As a rule they occur alone, but they may occur in multiples. Associated with infection of H. pylori Risk factors include excessive secretion of stomach acid, dietary factors, chronic use of NSAIDs, alcohol, smoking, and familial tendency In the past, stress and anxiety were thought to be causes of peptic ulcers, but research has documented that most peptic ulcers result from infection with the gram-negative bacteria H. pylori, which may be acquired through ingestion of food and water. Person-to-person transmission of the bacteria also occurs through close contact and exposure to emesis. The use of NSAIDs such as ibuprofen and aspirin is also a major risk factor for peptic ulcers. Furthermore, infection with H. pylori and concomitant use of NSAIDs are synergistic risks. It is believed that smoking and alcohol consumption may be risks, although the evidence is inconclusive. There is no evidence that the ingestion of milk, caffeinated beverages, and spicy foods are associated with the development of peptic ulcers. Familial tendency also may be a significant predisposing factor. People with blood type O are more susceptible to the development of peptic ulcers than are those with blood type A, B, or AB. There also is an association between peptic ulcer disease and chronic obstructive pulmonary disease, cirrhosis of the liver, and chronic kidney disease. Peptic ulcer disease is also associated with Zollinger-Ellison syndrome (ZES). ZES is a rare condition in which benign or malignant tumors form in the pancreas and duodenum that secrete excessive amounts of the hormone gastrin. The excessive amount of gastrin results in extreme gastric hyperacidity and severe peptic ulcer disease. While the exact cause of ZES is unknown, 25% of cases are linked to an inherited, genetic condition called multiple endocrine neoplasia, type 1 (MEN 1) Manifestations - include a dull gnawing pain or burning in the midepigastrium; heartburn and vomiting may occur Many patients with peptic ulcers have no signs or symptoms. These silent peptic ulcers most commonly occur in older adults and those taking aspirin and other NSAIDs There are few clinical manifestations that differentiate gastric ulcers from duodenal ulcers; however, classically, the pain associated with gastric ulcers most commonly occurs immediately after eating, whereas the pain associated with duodenal ulcers most commonly occurs 2 to 3 hours after meals. Other nonspecific symptoms of either gastric ulcers or duodenal ulcers may include pyrosis vomiting, constipation or diarrhea, and bleeding. These symptoms are often accompanied by sour eructation (burping), which is common when the patient's stomach is empty. The patient with bleeding peptic ulcers may present with evidence of GI bleeding, such as hematemesis (vomiting blood) or the passage of melena (black, tarry stools) Treatment includes medications, lifestyle changes, and occasionally surgery Once the diagnosis is established, the patient is informed that the condition can be managed. Recurrence may develop; however, peptic ulcers treated with antibiotics to eradicate H. pylori have a lower recurrence rate than those not treated with antibiotics. The goals are to eradicate H. pylori as indicated and to manage gastric acidity. Methods used include medications, lifestyle changes, and surgical intervention. Pharmacologic Therapy Currently, the most commonly used therapy for peptic ulcers is a combination of antibiotics, proton pump inhibitors, and sometimes bismuth salts that suppress or eradicate H. pylori. Recommended combination drug therapy is typically prescribed for 10 to 14 days and may include triple therapy with two antibiotics (e.g., metronidazole [Flagyl] or amoxicillin [Amoxil] and clarithromycin [Biaxin]) plus a proton pump inhibitor (e.g., lansoprazole [Prevacid], omeprazole [Prilosec], or rabeprazole [AcipHex]), or quadruple therapy with two antibiotics (metronidazole and tetracycline) plus a proton pump inhibitor and bismuth salts (Pepto-Bismol) - H2 blockers and proton pump inhibitors that reduce gastric acid secretion are used to treat ulcers not associated with H. pylori infection LIFESTYLE CHANGES - Smoking Cessation Smoking decreases the secretion of bicarbonate from the pancreas into the duodenum, resulting in increased acidity of the duodenum. Continued smoking is also associated with delayed healing of peptic ulcers - Dietary Modification The intent of dietary modification for patients with peptic ulcers is to avoid oversecretion of acid and hypermotility in the GI tract. These can be minimized by avoiding extremes of temperature in food and beverages and overstimulation from the consumption of alcohol, coffee (including decaffeinated coffee, which also stimulates acid secretion), and other caffeinated beverages. In addition, an effort is made to neutralize acid by eating three regular meals a day. Small, frequent feedings are not necessary as long as an antacid or an H2 blocker is taken. Diet compatibility becomes an individual matter: The patient eats foods that are tolerated and avoids those that produce pain. Surgical Management - surgery is usually recommended for patients with intractable ulcers (those failing to heal after 12 to 16 weeks of medical treatment), life-threatening hemorrhage, perforation, or obstruction and for those with ZES that is unresponsive to medications Surgical procedures include vagotomy, with or without pyloroplasty (transecting nerves that stimulate acid secretion and opening the pylorus), and antrectomy, which is removal of the pyloric (antrum) portion of the stomach with anastomosis (surgical connection) to either the duodenum (gastroduodenostomy or Billroth I) or jejunum (gastrojejunostomy or Billroth II)

45.5 & 45.6 Apply the nursing process as a framework for care of patients with GERD and the clinical manifestations and management

Gastroesophageal reflux disease (GERD) is a fairly common disorder marked by backflow of gastric or duodenal contents into the esophagus that causes troublesome symptoms and/or mucosal injury to the esophagus. Incidence seems to increase: - With aging patients With irritable bowel syndrome and obstructive airway disorders (asthma, COPD, cystic fibrosis) - Barrett esophagus peptic ulcer disease and angina GERD is associated with: - Tobacco use - Coffee drinking - Alcohol consumption - Gastric infection with Helicobacter pylori Clinical Manifestations Symptoms may include - pyrosis (heartburn, specifically more commonly described as a burning sensation in the esophagus), - dyspepsia (indigestion) - regurgitation - dysphagia or odynophagia, hypersalivation, and esophagitis. The symptoms may mimic those of a heart attack. GERD can result in dental erosion, ulcerations in the pharynx and esophagus, laryngeal damage, esophageal strictures, adenocarcinoma, and pulmonary complications ASSESSMENT - Pt. history - Endoscopy or barium swallow : To evaluate damage to esophageal mucosa - Esophageal pH monitoring : Ambulatory 12- to 36-hour esophageal pH monitoring is used to evaluate the degree of acid reflux. MANAGEMENT OF GERD - Low-fat diet - Avoid caffeine, tobacco, beer, milk, foods containing peppermint or spearmint, and carbonated beverages - Avoid eating or drinking 2 hours before bedtime - Elevate the head of the bed by at least 30 degrees - maintain normal body weight; avoid tight-fitting clotheS Medications commonly used to manage GERD 1) Antacids/Acid neutralizing agents - Calcium carbonate (Tums) - Aluminum hydroxide, magnesium, hydroxide, and simethicone (Maalox) Neutralize acid (Therapeutic and Pharmacologic class—Antacid) 2) Histamine-2 (H2) receptor antagonists - Famotidine (Pepcid) - Ranitidine (Zantac) - Cimetidine (Tagamet) Decrease gastric acid production (Therapeutic class—Antiulcer drugs Pharmacologic class—H2-receptor antagonists) 3) Prokinetic agents - Metoclopramide (Reglan) Accelerate gastric emptying (Therapeutic class—GI stimulants Pharmacologic class—Dopamine antagonist) 4) Proton pump inhibitors (PPIs) - Pantoprazole (Protonix) - Omeprazole (Prilosec) - Esomeprazole (Nexium) - Lansoprazole (Prevacid) - Rabeprazole (AcipHex) - Dexlansoprazole (Dexilant) Decrease gastric acid production (Therapeutic class—Antiulcer drugs Pharmacologic class—Proton pump inhibitors) 5) Reflux inhibitors - Bethanechol chloride (Urecholine) Stimulates parasympathetic (Therapeutic and Pharmacologic class—Cholinergic) 6) Surface Agents/Alginate-based barriers - Sucralfate Preserve mucosal barrier (Therapeutic class—Antiulcer drugs Pharmacologic class--GI protectants) - Give on an empty stomach hour before or 2 hours after meals - Separate from doses of antacid by 30 minutes

49.3 & 49.4 Describe medical, surgical, and nursing management jaundice, portal hypertension, ascites, esophageal varices, nutritional deficiencies, and hepatic encephalopathy and coma to pathophysiologic alterations of the liver.

Jaundice The bilirubin concentration in the blood may be increased in the presence of liver disease, if the flow of bile is impeded (e.g., by gallstones in the bile ducts), or if there is excessive destruction of red blood cells. With bile duct obstruction, bilirubin does not enter the intestine; as a consequence, urobilinogen is absent from the urine and decreased in the stool When the bilirubin concentration in the blood is abnormally elevated, all of the body tissues, including the sclerae and the skin, become tinged yellow or greenish-yellow, a condition known as jaundice. Jaundice becomes clinically evident when the serum bilirubin level exceeds 2.0 mg/dL (34 mmol/L) - Increased serum bilirubin levels and jaundice may result from impairment of hepatic uptake, conjugation of bilirubin, or excretion of bilirubin into the biliary system. There are several types of jaundice: hemolytic, hepatocellular, and obstructive jaundice, and jaundice due to hereditary hyperbilirubinemia. Hepatocellular and obstructive jaundice are the two types commonly associated with liver disease. - Hepatocellular jaundice is caused by the inability of damaged liver cells to clear normal amounts of bilirubin from the blood. - Patients with hepatocellular jaundice may be mildly or severely ill, with lack of appetite, nausea, malaise, fatigue, weakness, and possible weight loss. In some cases of hepatocellular disease, jaundice may not be obvious. The serum bilirubin concentration and the urine urobilinogen level may be elevated. In addition, AST and ALT levels may be increased, indicating cellular necrosis. The patient may report headache, chills, and fever if the cause is infectious. Depending on the cause and extent of the liver cell damage, hepatocellular jaundice may be completely reversible. Obstructive Jaundice Obstructive jaundice resulting from extrahepatic obstruction may be caused by occlusion of the bile duct from a gallstone, an inflammatory process, a tumor, or pressure from an enlarged organ (e.g., liver, gallbladder). The obstruction may also involve the small bile ducts within the liver (i.e., intrahepatic obstruction); this may be caused, for example, by pressure on these channels from inflammatory swelling of the liver or by an inflammatory exudate within the ducts themselves. Portal Hypertension Portal hypertension is the increased pressure throughout the portal venous system that results from obstruction of blood flow into and through the damaged liver. Commonly associated with hepatic cirrhosis, it can also occur with noncirrhotic liver disease. Although splenomegaly (enlarged spleen) with possible hypersplenism is a common manifestation of portal hypertension, the two major consequences of portal hypertension are ascites and varices. Ascites Clinical Manifestations - Increased abdominal girth and rapid weight gain are common presenting symptoms of ascites. - patient may be short of breath and uncomfortable from the enlarged abdomen, and striae and distended veins may be visible over the abdominal wall. - Umbilical hernias also occur frequently in those patients with cirrhosis. - Fluid and electrolyte imbalances are common. Assessment and Diagnostic Findings The presence and extent of ascites are assessed by percussion of the abdomen. When fluid has accumulated in the peritoneal cavity, the flanks bulge when the patient assumes a supine position. Medical Management The medical management of the patient with ascites includes dietary modifications, pharmacologic therapy, bed rest, paracentesis, the use of shunts, and other therapies. Nutritional Therapy The goal of treatment for the patient with ascites is a negative sodium balance to reduce fluid retention. Table salt, salty foods, salted butter and margarine, and all canned and frozen foods that are not specifically prepared for low-sodium (2-g sodium) diets should be avoided - Most salt substitutes contain potassium and should be avoided if the patient has impaired renal function. The patient should make liberal use of powdered, low-sodium milk and milk products. If fluid accumulation is not controlled with this regimen, the daily sodium allowance may be reduced further to 500 mg, and diuretic agents may be given. Pharmacologic Therapy The use of diuretic agents along with sodium restriction is successful in 90% of patients with ascites - Spironolactone (Aldactone), an aldosterone-blocking agent, is most often the first-line therapy in patients with ascites from cirrhosis. When used with other diuretic agents, spironolactone helps prevent potassium loss. - Oral diuretic agents such as furosemide (Lasix) may be added but should be used cautiously, because long-term use may induce severe sodium depletion (hyponatremia). - Ammonium chloride and acetazolamide (Diamox) are contraindicated because of the possibility of precipitating hepatic encephalopathy and coma. - Daily weight loss should not exceed 1 kg (2.2 lb) in patients with ascites and peripheral edema or 0.5 to 0.75 kg (1.1 to 1.65 lb) in patients without edema Bed Rest In patients with ascites, an upright posture is associated with activation of the renin-angiotensin-aldosterone system and sympathetic nervous system. - This causes reduced renal glomerular filtration and sodium excretion and a decreased response to loop diuretics. Therefore, bed rest may be a useful therapy, especially for patients whose condition is refractory to diuretic agents. Paracentesis Paracentesis is the removal of fluid (ascites) from the peritoneal cavity through a puncture or a small surgical incision through the abdominal wall under sterile conditions - Paracentesis was once considered a routine form of treatment for ascites. However, it is now performed primarily for diagnostic examination of ascitic fluid; in treatment for massive ascites that is resistant to nutritional and diuretic therapy and is causing severe problems to the patient; and as a prelude to diagnostic imaging studies, peritoneal dialysis, or surgery. A sample of the ascitic fluid may be sent to the laboratory for cell count, albumin and total protein levels, culture, and other tests. Transjugular Intrahepatic Portosystemic Shunt TIPS is a method of treating ascites in which a cannula is threaded into the portal vein by the transjugular route - To reduce portal hypertension, an expandable stent is inserted to serve as an intrahepatic shunt between the portal circulation and the hepatic vein. This is extremely effective in decreasing sodium retention, improving the renal response to diuretic therapy, and preventing recurrence of fluid accumulation Nursing Management of ascites If a patient with ascites from liver dysfunction is hospitalized, nursing measures include assessment and documentation of intake and output (I&O), abdominal girth, and daily weight to assess fluid status. - monitor respiratory status because large volumes of ascites can compress the thoracic cavity and inhibit adequate lung expansion. - monitor serum ammonia, creatinine, and electrolyte levels to assess electrolyte balance, response to therapy, and indications of hepatic encephalopathy. Educating Patients About Self-Care - avoid all alcohol intake, adhere to a low-sodium diet, take medications as prescribed, and check with the primary provider before taking any new medications. AFTER EDUCATING, PT WILL: - Make appropriate dietary choices consistent with dietary prescription and recommendations. Explain the use of salt substitutes must be approved by primary provider. - State the importance of weighing self-daily and keeping a daily record of weight. - Maintain record of daily weight, and identify daily weight-loss goals. - List weight changes (loss or gain) that should be reported to the primary provider. - Identify rationale for fluid restrictions (if needed) monitoring and keeping a daily record intake and output. - Maintain a record of daily intake and output.Identify changes in output that should be reported to primary provider (e.g., decreasing urine output). - Identify need to stop all alcohol intake as critical to well-being. - Identify early signs and symptoms of complications (encephalopathy, spontaneous bacterial peritonitis, dehydration, electrolyte abnormalities, azotemia). Esophageal Varices - Esophageal varices are present in 30% of patients with compensated cirrhosis and 60% of patients with decompensated cirrhosis at the time of diagnosis CAUSE - Esophageal varices are dilated, tortuous veins that are usually found in the submucosa of the lower esophagus but may develop higher in the esophagus or extend into the stomach. This condition is almost always caused by portal hypertension, which results from obstruction of the portal venous circulation within the damaged liver. Varices are varicosities that develop from elevated pressure in the veins that drain into the portal system. They are prone to rupture and often are the source of massive hemorrhages from the upper GI tract and the rectum. In addition, abnormalities in blood clotting, often seen in patients with severe liver disease, increase the likelihood of bleeding with significant blood loss. Clinical Manifestations The patient with bleeding esophageal varices may present with hematemesis, melena, or general deterioration in mental or physical status and often has a history of alcohol abuse. Signs and symptoms of shock (cool clammy skin, hypotension, tachycardia) may be present Medical Management Bleeding from esophageal varices is an emergency that can quickly lead to hemorrhagic shock. The patient is critically ill, requiring aggressive medical care and expert nursing care, and is usually transferred to the intensive care unit (ICU) for close monitoring and management. - Because patients with bleeding esophageal varices have intravascular volume depletion and are subject to electrolyte imbalance, IV fluids, electrolytes, and volume expanders are provided to restore fluid volume and replace electrolytes. Transfusion of blood components also may be required. - Caution must be taken with volume resuscitation so that overhydration does not occur, because this would raise portal pressure and increase bleeding. An indwelling urinary catheter is usually inserted to permit frequent monitoring of urine output. Pharmacologic Therapy - Octreotide (Sandostatin), a synthetic analog of the hormone somatostatin, is effective in decreasing bleeding from esophageal varices, and lacks the vasoconstrictive effects of vasopressin. Because of this safety and efficacy profile, octreotide is considered the preferred treatment regimen for immediate control of variceal bleeding. Nursing Management - includes monitoring the patient's physical condition and evaluating emotional responses and cognitive status. - The nurse monitors and records vital signs and assesses the patient's nutritional and neurologic status. This assessment assists in identifying hepatic encephalopathy - If complete rest of the esophagus is indicated because of bleeding, parenteral nutrition is initiated. - Gastric suction usually is initiated to keep the stomach as empty as possible and to prevent straining and vomiting. - The patient often complains of severe thirst, which may be relieved by frequent oral hygiene and moist sponges to the lips. - The nurse closely monitors the blood pressure. - Vitamin K therapy and multiple blood transfusions often are indicated because of blood loss. - A quiet environment and calm reassurance may help to relieve the patient's anxiety and reduce agitation. - Bleeding anywhere in the body is anxiety provoking, resulting in a crisis for the patient and family. If the patient has been a heavy user of alcohol, delirium secondary to alcohol withdrawal can complicate the situation. Hepatic Encephalopathy and Coma Hepatic encephalopathy, or portosystemic encephalopathy, is a life-threatening complication of liver disease that occurs with profound liver failure. Patients with this condition may have no overt signs of the illness but have abnormalities on neuropsychologic testing The onset is often insidious and subtle, and initially the disease is termed subclinical or minimal hepatic encephalopathy. Clinical Manifestations - The earliest symptoms of hepatic encephalopathy include mental status changes and motor disturbances. - The patient appears confused and unkempt and has alterations in mood and sleep patterns. - The patient tends to sleep during the day and has restlessness and insomnia at night. - As hepatic encephalopathy progresses, the patient may become difficult to awaken and completely disoriented with respect to time and place. - With further progression, the patient lapses into frank coma and may have seizures. It is vital for the nurse to understand the four stages of hepatic encephalopathy and common signs and symptoms. Stages of Hepatic Encephalopathy 1) Normal level of consciousness with periods of lethargy and euphoria; reversal of day-night sleep patterns - Impaired writing and ability to draw line figures. Normal EEG. 2) Increased drowsiness; disorientation; inappropriate behavior; mood swings; agitation - Asterixis; fetor hepaticus. Abnormal EEG with generalized slowing. 3) Stuporous; difficult to rouse; sleeps most of time; marked confusion; incoherent speech - Asterixis; increased deep tendon reflexes; rigidity of extremities. EEG markedly abnormal. 4) Comatose; may not respond to painful stimuli - Absence of asterixis; absence of deep tendon reflexes; flaccidity of extremities. EEG markedly abnormal. ** Fetor hepaticus - a sweet, slightly fecal odor to the breath that is presumed to be of intestinal origin, may be noticed. The odor has also been described as similar to that of freshly mowed grass, acetone, or old wine. Fetor hepaticus is prevalent with extensive collateral portal circulation in chronic liver disease. Medical Management - initiating ammonia-lowering therapy, minimizing potential medical complications of cirrhosis and depressed consciousness, and reversing the underlying liver disease, if possible. - Correction of the possible reasons for the deterioration such as bleeding, electrolyte abnormalities, sedation, or azotemia is essential - Lactulose (Cephulac) is given to reduce serum ammonia levels. It acts by trapping and expelling the ammonia in the feces - Two or three soft stools per day are desirable; this indicates that lactulose is performing as intended. Quality and Safety Nursing Alert The patient receiving lactulose is monitored closely for the development of watery diarrhea stools, because they indicate a medication overdose. Serum ammonia levels are closely monitored as well. Possible side effects of lactulose include intestinal bloating and cramps, which usually disappear within a week. - The patient is closely monitored for hypokalemia and dehydration. Other laxatives are not prescribed during lactulose administration because their effects disturb dosage regulation. Lactulose may be given by nasogastric tube or enema for patients who are comatose or for those in whom oral administration is contraindicated or not possible Other management strategies include IV administration of glucose to minimize protein breakdown, administration of vitamins to correct deficiencies, and correction of electrolyte imbalances (especially potassium). Antibiotics may also be added to the treatment regimen. Additional principles of management of hepatic encephalopathy include the following: - Neurologic status is assessed frequently. - Mental status is monitored by keeping a daily record of handwriting and arithmetic performance. - I&O and body weight are recorded each day. - Vital signs are measured and recorded every 4 hours. - Potential sites of infection (peritoneum, lungs) are assessed frequently, and abnormal findings are reported promptly. - Serum ammonia level is monitored daily. - Dietary protein intake should not be restricted in hepatic encephalopathy as recommended in the past. Protein intake should be maintained at 1.2 to 1.5 g/kg per day --- The danger of protein malnutrition far outweighs the risk of worsening hepatic encephalopathy caused by increased protein intake - Enteral feeding is provided for patients whose encephalopathic state persists. - Reduction in the absorption of ammonia from the GI tract is accomplished by the use of gastric suction, enemas, or oral antibiotics. - Electrolyte status is monitored and corrected if abnormal. - Sedatives, tranquilizers, and analgesic medications are discontinued. - Benzodiazepine antagonists such as flumazenil (Romazicon) may be administered IV to improve encephalopathy, whether or not the patient has previously taken benzodiazepines. This action may have short-term efficacy because patients with hepatic encephalopathy have an increased concentration of benzodiazepine receptors NURSING MANAGEMENT - The nurse is responsible for maintaining a safe environment to prevent injury, bleeding, and infection. - The nurse administers the prescribed treatments and monitors the patient for the numerous potential complications. - The potential for respiratory compromise is great given the patient's depressed neurologic status. - The nurse encourages deep breathing and position changes to prevent the development of atelectasis, pneumonia, and other respiratory complications. - Despite aggressive pulmonary care, patients may develop respiratory compromise. They may require intubation and mechanical ventilation to protect the airway, and they are frequently admitted to the ICU. Other Manifestations of Hepatic Dysfunction - Edema and Bleeding - Many patients with liver dysfunction develop generalized edema caused by hypoalbuminemia due to decreased hepatic production of albumin. The production of blood clotting factors by the liver is also reduced, leading to an increased incidence of bruising, epistaxis, bleeding from wounds, and, as described previously, GI bleeding. Vitamin Deficiency Decreased production of several clotting factors may be partially due to deficient absorption of vitamin K from the GI tract. This probably is caused by the inability of liver cells to use vitamin K to make prothrombin. - Absorption of the other fat-soluble vitamins (vitamins A, D, and E) as well as dietary fats may also be impaired because of decreased secretion of bile salts into the intestine. Metabolic Abnormalities - Abnormalities of glucose metabolism also occur; the blood glucose level may be abnormally high shortly after a meal (similar to that when diabetes is present), but hypoglycemia may occur during fasting because of decreased hepatic glycogen reserves and decreased gluconeogenesis. - Many endocrine abnormalities also occur with liver dysfunction because the liver cannot properly metabolize hormones, including androgens and sex hormones. - Failure of the damaged liver to inactivate estrogens normally can cause gynecomastia, amenorrhea, testicular atrophy, loss of pubic hair in the male, menstrual irregularities in the female, and other disturbances of sexual function and sex characteristics. Pruritus and Other Skin Changes - Patients with liver dysfunction resulting from biliary obstruction commonly develop severe pruritus due to retention of bile salts. Patients may develop vascular (or arterial) spider angiomas on the skin usually above the waistline. These are numerous small vessels resembling a spider's legs. They are most often associated with cirrhosis, especially in alcoholic liver disease. - Patients may also develop reddened palms ("liver palms" or palmar erythema).

49.2 Explain liver function tests and the clinical manifestations of liver dysfunction in relation to pathophysiologic alterations of the liver

Liver Function Tests - More than 70% of the parenchyma of the liver may be damaged before liver function test results become abnormal. Function is generally measured in terms of serum enzyme activity (i.e., serum aminotransferases, alkaline phosphatase, lactic dehydrogenase) and serum concentrations of proteins (albumin and globulins), bilirubin, ammonia, clotting factors, and lipids - Several of these tests may be helpful for assessing patients with liver disease. However, the nature and extent of hepatic dysfunction cannot be determined by these tests alone, because other disorders can affect test results. Serum aminotransferases are sensitive indicators of injury to the liver cells and are useful in detecting acute liver disease such as hepatitis. - Alanine aminotransferase (ALT), aspartate aminotransferase (AST), and gamma-glutamyl transferase (GGT) (also called gamma-glutamyl transpeptidase [GGTP]) are the most frequently used tests of liver damage ALT levels increase primarily in liver disorders and may be used to monitor the course of hepatitis or cirrhosis or the effects of treatments that may be toxic to the liver. AST is present in tissues that have high metabolic activity; therefore, the level may be increased if there is damage to or death of tissues of organs such as the heart, liver, skeletal muscle, and kidney. Although not specific to liver disease, levels of AST may be increased in cirrhosis, hepatitis, and liver cancer. Increased GGT levels are associated with cholestasis but can also be due to alcoholic liver disease. Although the kidney has the highest level of the enzyme, the liver is considered the source of normal serum activity. The test determines liver cell dysfunction and is a sensitive indicator of cholestasis. Its main value in liver disease is confirming the hepatic origin of an elevated alkaline phosphatase level. Liver Biopsy Liver biopsy is the removal of a small amount of liver tissue, usually through needle aspiration. It permits examination of liver cells. The most common indication is to evaluate diffuse disorders of the parenchyma and to diagnose space-occupying lesions. Liver biopsy is especially useful when clinical findings and laboratory tests are not diagnostic. Among the most common and significant manifestations of liver disease are - jaundice - portal hypertension (elevated pressure in your portal venous system. The portal vein is a major vein that leads to the liver. The most common cause of portal hypertension is cirrhosis (scarring) of the liver) - ascites (Abdominal swelling caused by accumulation of fluid, most often related to liver disease) and varices (enlarged or swollen veins develop when normal blood flow to the liver is blocked by a clot or scar tissue in the liver) - nutritional deficiencies (resulting from the inability of damaged liver cells to metabolize certain vitamins) - hepatic encephalopathy - coma other manifestations from text: - Abdominal bloating, and constipation - Changes to skin color or yellow hue to sclera - Enlarged liver, spleen, or abdomen - Episodes of nausea and vomiting - Hemorrhoids, esophageal varices, or gallstones - Intolerance to fatty foods or alcohol - Pale-colored stools - Presence and frequency of indigestion or reflux - Unexplained weight loss

16.10 Support imminently dying patients and their families

Nursing care measures aimed at patient comfort, such as pain medications (given rectally or sublingually), turning, mouth care, eye care, positioning to facilitate draining of secretions, and measures to protect the skin from urine or feces (if the patient is incontinent), should be continued. The nurse should consult with the interprofessional team about discontinuing measures that no longer contribute to patient comfort, such as drawing blood, administering tube feedings, suctioning (in most cases), and invasive monitoring. The nurse should prepare the family for the normal, expected changes that accompany the period immediately preceding death. Although the exact time of death cannot be predicted, it is often possible to identify when the patient is very close to death. Signs of Approaching Death The person shows less interest in eating and drinking. For many patients, refusal of food is an indication that they are ready to die. Fluid intake may be limited to that which will keep their mouths from feeling too dry. - What you can do: Offer, but do not force, fluids and medication. Sometimes pain or other symptoms that have required medication in the past may no longer be present. For most patients, pain medications are still needed, and they can be provided by concentrated oral solutions placed under the tongue or by rectal suppository. Urinary output may decrease in amount and frequency. - What you can do: No response is needed unless the patient expresses a desire to urinate and cannot. Call the hospice nurse for advice if you are not sure. As the body weakens, the patient will sleep more and begin to detach from the environment. He or she may refuse your attempts to provide comfort. - What you can do: Allow your loved one to sleep. You may wish to sit with him or her, play soft music, or hold hands. Your loved one's withdrawal is normal and is not a rejection of your love. Mental confusion may become apparent. This occurs because less oxygen is available to supply the brain. The patient may report strange dreams or visions. - What you can do: As he or she awakens from sleep, remind him or her of the day and time, where he or she is, and who is present. This is best done in a casual, conversational way. Vision and hearing may become somewhat impaired, and speech may be difficult to understand. - What you can do: Speak clearly but no more loudly than necessary. Keep the room as light as the patient wishes, even at night. Carry on all conversations as if they can be heard, because hearing may be the last of the senses to cease functioning. Many patients are able to talk until minutes before death and are reassured by the exchange of a few words with a loved one. Secretions may collect in the back of the throat and rattle or gurgle as the patient breathes through the mouth. He or she may try to cough, and their mouth may become dry and encrusted with secretions. - What you can do: If the patient is trying to cough up secretions and is experiencing choking or vomiting, call the hospice nurse for assistance. Secretions may drain from the mouth if you place the patient on their side and provide support with pillows. Cleansing the mouth with moistened mouth swabs will help relieve the dryness that occurs with mouth breathing. Offer water in small amounts to keep the mouth moist. A straw with one finger placed over the end can be used to transfer sips of water to the patient's mouth. Breathing may become irregular with periods of no breathing (apnea). The patient may be working very hard to breathe and may make a moaning sound with each breath. As the time of death nears, the breathing remains irregular and may become more shallow and mechanical. - What you can do: Raising the head of the bed may help the patient to breathe more easily. The moaning sound does not mean that the patient is in pain or other distress; it is the sound of air passing over very relaxed vocal cords. As the oxygen supply to the brain decreases, the patient may become restless. It is not unusual to pull at the bed linens, to have visual hallucinations, or even to try to get out of bed at this point. - What you can do: Reassure the patient in a calm voice that you are there. Prevent him or her from falling by trying to get out of bed. Soft music or a back rub may be soothing. The patient may feel hot one moment and cold the next as the body loses its ability to control temperature. As circulation slows, the arms and legs may become cool and bluish. The underside of the body may darken. It may be difficult to feel a pulse at the wrist. - What you can do: Provide and remove blankets as needed. Avoid using electrical blankets, which may cause burns because the patient cannot tell you if he or she is too warm. Sponge the patient's head with a cool cloth if this provides comfort. Loss of bladder and bowel control may occur around the time of death. - What you can do: Protect the mattress with waterproof padding, and change the padding as needed to keep the patient comfortable. As people approach death, many times they report seeing gardens, libraries, or family or friends who have died. They may ask you to pack their bags and find tickets or a passport. Sometimes they may become insistent and attempt to do these chores themselves. They may try getting out of bed (even if they have been confined to bed for a long time) so that they can "leave." - What you can do: Reassure the patient that it is all right; he or she can "go" without getting out of bed. Stay close, share stories, and be present. Death is generally preceded by a period of gradual diminishment of bodily functions, increased intervals between respirations, a weakened and irregular pulse, diminished blood pressure, and skin color changes or mottling. Family members should be encouraged to be with the patient, to speak and reassure the patient of their presence, to stroke or touch the patient, or to lie alongside the patient (even in the hospital or long-term care facility) if the family members are comfortable with this degree of closeness and can do so without causing discomfort to the patient.

50.4 & 50.5 Describe acute and chronic pancreatitis, including clinical manifestations, medical/nursing management.

Pancreatitis (inflammation of the pancreas) is a serious disorder. Acute pancreatitis can be a medical emergency associated with a high risk of life-threatening complications and mortality, whereas chronic pancreatitis often goes undetected because classic clinical and diagnostic findings are not always present in the early stages of the disease Acute: pancreatic duct becomes obstructed, and enzymes back up, causing autodigestion and inflammation of the pancreas. Chronic: progressive inflammatory disorder with destruction of the pancreas; cells are replaced by fibrous tissue; pressure within the pancreas increases, obstructing the pancreatic and common bile ducts. Acute pancreatitis does not usually lead to chronic pancreatitis unless complications develop. However, chronic pancreatitis can be characterized by acute episodes. ACUTE PANCREATITIS PATHO Self-digestion of the pancreas by its own proteolytic enzymes, principally trypsin, causes acute pancreatitis. - These patients usually have had undiagnosed chronic pancreatitis before their first episode of acute pancreatitis. - Gallstones enter the common bile duct and lodge at the ampulla of Vater, obstructing the flow of pancreatic juice or causing a reflux of bile from the common bile duct into the pancreatic duct, thus activating the powerful enzymes within the pancreas. Normally, these remain in an inactive form until the pancreatic secretions reach the lumen of the duodenum. - Activation of the enzymes can lead to vasodilation, increased vascular permeability, necrosis, erosion, and hemorrhage - Other less common causes of pancreatitis include bacterial or viral infection, with pancreatitis occasionally developing as a complication of mumps viral infection. CLINICAL MANIFESTATIONS - Severe abdominal pain is the major symptom of pancreatitis that causes the patient to seek medical care. - Abdominal pain and tenderness and back pain result from irritation and edema of the inflamed pancreas. Increased tension on the pancreatic capsule and obstruction of the pancreatic ducts also contribute to the pain. - Typically, the pain occurs in the midepigastrium. - Pain is frequently acute in onset, occurring 24 to 48 hours after a very heavy meal or alcohol ingestion, and it may be diffuse and difficult to localize. - It is generally more severe after meals and is unrelieved by antacids. - Pain may be accompanied by abdominal distention; a poorly defined, palpable abdominal mass; decreased peristalsis; and vomiting that fails to relieve the pain or nausea. - The patient appears acutely ill. Abdominal guarding is present. A rigid or boardlike abdomen may develop and is generally an ominous sign, usually indicating peritonitis - Ecchymosis (bruising) in the flank or around the umbilicus may indicate severe pancreatitis. - Nausea and vomiting are common in acute pancreatitis. The emesis is usually gastric in origin but may also be bile stained. - Fever, jaundice, mental confusion, and agitation may also occur. - Hypotension is typical and reflects hypovolemia and shock caused by the loss of large amounts of protein-rich fluid into the tissues and peritoneal cavity. - patient may develop tachycardia; cyanosis; and cold, clammy skin. - Acute kidney injury is common. - Respiratory distress and hypoxia are common, and the patient may develop diffuse pulmonary infiltrates, dyspnea, tachypnea, and abnormal blood gas values. - Myocardial depression, hypocalcemia, hyperglycemia, and disseminated intravascular coagulation may also occur with acute pancreatitis. LABS AND DIAGNOSTICS - Diagnosis: Based on hx of abdominal pain, physical findings, diagnostic findings Diagnostics: CT,MRI, Xray Labs: Serum amylase and lipase elevate within 24 hours of symptoms Increased WBC, hypoglycemia, increased bilirubin, monitor hgb/hct MEDICAL MANAGEMENT - Management of acute pancreatitis is directed toward relieving symptoms and preventing or treating complications. - All oral intake is withheld to inhibit stimulation of the pancreas and its secretion of enzymes. - Ongoing research has shown positive outcomes with the use of enteral feedings. - The current recommendation is that, whenever possible, the enteral route should be used to meet nutritional needs in patients with pancreatitis. - Parenteral nutrition has a role in the nutritional support of patients with severe acute pancreatitis, particularly in those who are unable to tolerate enteral nutrition - Nasogastric suction may be used to relieve nausea and vomiting and to decrease painful abdominal distention and paralytic ileus MEDICATIONS Histamine-2 (H2) antagonists such as cimetidine (Tagamet) and ranitidine (Zantac) may be prescribed to decrease pancreatic activity by inhibiting secretion of gastric acid. Proton pump inhibitors such as pantoprazole (Protonix) may be used for patients who do not tolerate H2 antagonists or for whom this therapy is ineffective Pain Management Adequate administration of analgesia is essential during the course of acute pancreatitis to provide sufficient pain relief and to minimize restlessness, which may stimulate pancreatic secretion further. Pain relief may require parenteral opioids such as morphine, fentanyl (Sublimaze), or hydromorphone (Dilaudid) Intensive Care Correction of fluid and blood loss and low albumin levels is necessary to maintain fluid volume and prevent acute kidney injury. The patient is usually acutely ill and is monitored in the intensive care unit, where hemodynamic monitoring and arterial blood gas monitoring are initiated. Antibiotic agents may be prescribed if infection is present. Prophylactic antibiotics are not recommended for patients with acute pancreatitis Respiratory Care Aggressive respiratory care is indicated because of the high risk of elevation of the diaphragm, pulmonary infiltrates and effusion, and atelectasis. Hypoxemia occurs in a significant number of patients with acute pancreatitis, even with normal x-ray findings. Respiratory care may range from close monitoring of arterial blood gases to the use of humidified oxygen to intubation and mechanical ventilation Biliary Drainage Placement of biliary drains (for external drainage) and stents (indwelling tubes) in the pancreatic duct through endoscopy has been performed to reestablish drainage of the pancreas. This has resulted in decreased pain. Surgical Intervention Although the acutely ill patient is at high risk for surgical complications, surgery may be performed to assist in the diagnosis of pancreatitis (diagnostic laparotomy); to establish pancreatic drainage; or to resect or débride an infected, necrotic pancreas. Postacute Management Oral feedings that are low in fat and protein are initiated gradually. Caffeine and alcohol are eliminated from the diet. If the episode of pancreatitis occurred during treatment with thiazide diuretics, corticosteroids, or oral contraceptives, these medications are discontinued. Follow-up may include ultrasound, x-ray studies, or ERCP to determine whether the pancreatitis is resolving and to assess for abscesses and pseudocysts. ERCP may also be used to identify the cause of acute pancreatitis if it is in question and for endoscopic sphincterotomy and removal of gallstones from the common bile duct. NURSING MANAGEMENT/INTERVENTIONS - NPO (enteral route is ideal, but may need TPN) - NG - Pain Management - Hemodynamic monitoring - Respiratory - Education Relieving Pain and Discomfort - Because the pathologic process responsible for pain is autodigestion of the pancreas, the objectives of therapy are to relieve pain and decrease secretion of pancreatic enzymes. The pain of acute pancreatitis is often very severe, necessitating the liberal use of analgesic agents. The current recommendation for pain management in this population is parenteral opioids, including morphine, hydromorphone, or fentanyl via patient-controlled analgesia or bolus - Nonpharmacologic interventions such as proper positioning, music, distraction, and imagery may be effective in reducing pain when used along with medications. - Parenteral fluids and electrolytes are prescribed to restore and maintain fluid balance. Nasogastric suction may be used to relieve nausea and vomiting or to treat abdominal distention and paralytic ileus. The nurse provides frequent oral hygiene and care to decrease discomfort from the nasogastric tube and relieve dryness of the mouth. Improving Breathing Pattern - The nurse maintains the patient in a semi-Fowler position to decrease pressure on the diaphragm by a distended abdomen and to increase respiratory expansion. Frequent changes of position are necessary to prevent atelectasis and pooling of respiratory secretions. Pulmonary assessment, including monitoring of pulse oximetry or arterial blood gases, is essential to detect changes in respiratory status so that early treatment can be initiated. The nurse instructs the patient in techniques of coughing and deep breathing and in the use of incentive spirometry to improve respiratory function and assists the patient to perform these activities every hour. Improving Nutritional Status The nurse assesses the patient's nutritional status and notes factors that alter the patient's nutritional requirements (e.g., temperature elevation, surgery, drainage). - Laboratory test results and daily weights are useful to monitor the nutritional status. - Enteral or parenteral nutrition may be prescribed. In addition to administering enteral or parenteral nutrition, the nurse monitors serum glucose levels every 4 to 6 hours. As the acute symptoms subside, oral feedings are gradually reintroduced. Between acute attacks, the patient receives a diet that is high in protein and low in fat - The patient should avoid heavy meals and alcoholic beverages. Maintaining Skin Integrity - The patient is at risk for skin breakdown because of poor nutritional status, enforced bed rest, and restlessness, which may result in pressure ulcers and breaks in tissue integrity. In addition, the patient who has undergone surgery may have multiple drains or an open surgical incision and is at risk for skin breakdown and infection. The nurse carefully assesses the wound, drainage sites, and skin for signs of infection, inflammation, and breakdown. The nurse carries out wound care as prescribed and takes precautions to protect intact skin from contact with drainage. - patient must be turned every 2 hours Monitoring and Managing Potential Complications Fluid and electrolyte disturbances are common complications because of nausea, vomiting, movement of fluid from the vascular compartment to the peritoneal cavity, diaphoresis, fever, and the use of gastric suction. The nurse assesses the patient's fluid and electrolyte status by noting skin turgor and moistness of mucous membranes. The nurse weighs the patient daily and carefully measures fluid intake and output, including urine output, nasogastric secretions, and diarrhea. In addition, it is important to assess for other factors that may affect fluid and electrolyte status, including increased body temperature and wound drainage. The nurse assesses the patient for ascites and measures abdominal girth daily if ascites is suspected. Fluids are administered IV and may be accompanied by infusion of blood or blood products to maintain the blood volume and to prevent or treat hypovolemic shock. Emergency medications must be readily available because of the risk of circulatory collapse and shock. The nurse promptly reports decreased blood pressure and reduced urine output, which indicate hypovolemia and shock or acute kidney injury. Low serum calcium and magnesium levels may occur and require prompt treatment. Pancreatic necrosis is a major cause of morbidity and mortality in patients with acute pancreatitis because of resulting hemorrhage, septic shock, and MODS. Shock and MODS may occur with acute pancreatitis. Hypovolemic shock may occur as a result of hypovolemia and sequestering of fluid in the peritoneal cavity. Hemorrhagic shock may occur with hemorrhagic pancreatitis. Septic shock may occur with bacterial infection of the pancreas. Cardiac dysfunction may occur as a result of fluid and electrolyte disturbances, acid-base imbalances, and release of toxic substances into the circulation. The nurse closely monitors the patient for early signs of neurologic, cardiovascular, renal, and respiratory dysfunction. The nurse must be prepared to respond quickly to rapid changes in the patient's status, treatments, and therapies. Educating Patients About Self-Care After an episode of acute pancreatitis, the patient is often still weak and debilitated for weeks or months. A prolonged period may be needed to regain strength and return to the previous level of activity. The nurse educates the patient about the factors implicated in the onset of acute pancreatitis and about the need to avoid high-fat foods, heavy meals, and alcohol. CHRONIC PANCREATITIS Chronic pancreatitis is an inflammatory disorder characterized by progressive destruction of the pancreas. As cells are replaced by fibrous tissue with repeated attacks of pancreatitis, pressure within the pancreas increases. The result is obstruction of the pancreatic and common bile ducts and the duodenum. In addition, there is atrophy of the epithelium of the ducts, inflammation, and destruction of the secreting cells of the pancreas. Alcohol consumption in Western societies and malnutrition worldwide are the major causes of chronic pancreatitis. Smoking is another factor in the development of chronic pancreatitis. Because they are often associated, it is difficult to separate the effects of the alcohol abuse and smoking CLINICAL MANIFESTATIONS - recurring attacks of severe upper abdominal and back pain, accompanied by vomiting. - Attacks are often so painful that opioids, even in large doses, do not provide relief. The risk of opioid dependence is increased in pancreatitis because of the chronic nature and severity of the pain. - As the disease progresses, recurring attacks of pain are more severe, more frequent, and of longer duration. Some patients experience continuous severe pain, and others have dull, nagging constant pain. Periods of well-being sometimes follow the episodes of pain - In some patients, chronic pancreatitis is painless. The natural history of abdominal pain (character, timing, severity) is variable, and many studies have documented a decrease in pain ("burnout") over time in a majority of patients - Weight loss is a major problem in chronic pancreatitis. More than 80% of patients experience significant weight loss, which is usually caused by decreased dietary intake secondary to anorexia or fear that eating will precipitate another attack - Malabsorption occurs late in the disease, when as little as 10% of pancreatic function remains. As a result, digestion, especially of proteins and fats, is impaired. The stools become frequent, frothy, and foul smelling because of impaired fat digestion, which results in stools with a high fat content referred to as steatorrhea. As the disease progresses, calcification of the gland may occur, and calcium stones may form within the ducts. Assessment and Diagnostic Findings ERCP is the most useful study in the diagnosis of chronic pancreatitis. It provides details about the anatomy of the pancreas and the pancreatic and biliary ducts. It is also helpful in obtaining tissue for analysis and differentiating pancreatitis from other conditions, such as carcinoma - Various imaging procedures, including MRI, CT scans, and ultrasound, are used in the diagnostic evaluation of patients with suspected pancreatic disorders. A CT scan or ultrasound study is also helpful to detect pancreatic cysts - A glucose tolerance test evaluates pancreatic islet cell function and provides necessary information for making decisions about surgical resection of the pancreas. An abnormal glucose tolerance test may indicate the presence of diabetes associated with pancreatitis. Acute exacerbations of chronic pancreatitis may result in increased serum amylase levels. Steatorrhea is best confirmed by laboratory analysis of fecal fat content MEDICAL MANAGEMENT OF CHRONIC PANCREATITIS The management of chronic pancreatitis depends on its probable cause in each patient. Treatment is directed toward preventing and managing acute attacks, relieving pain and discomfort, and managing exocrine and endocrine insufficiency of pancreatitis

16.9 Implement nursing measures to manage physiologic responses to terminal illness.

Patients approaching the end of life experience many of the same symptoms, regardless of their underlying disease processes. Symptoms in terminal illness may be caused by the disease, either directly (e.g., dyspnea owing to chronic obstructive lung disease) or indirectly (e.g., nausea and vomiting related to pressure in the gastric area), by the treatment for the disease, or by a coexisting disorder that is unrelated to the disease. At the end of life, hospice programs typically provide "emergency kits" containing ready-to-administer doses of various medications that are useful to treat symptoms in advanced illness. For example, a kit might contain small doses of oral morphine liquid for pain or shortness of breath, a benzodiazepine for restlessness, and an acetaminophen suppository for fever. Family members can be instructed to administer a prescribed dose from the emergency kit, often avoiding prolonged suffering for the patient as well as rehospitalization for symptom management. Pain In the final stages of illnesses such as cancer, heart disease, COPD, and renal disease, pain and other symptoms are common. Pain results from the diseases as well as the modalities used to treat them. - Pain at the end of life is preventable or treatable in most cases: it is every nurse's role to ensure that pain is assessed, prevented where possible, and managed. Patients who are receiving an established regimen of analgesics should continue to receive those medications as they approach the end of life. Inability to communicate pain should not be equated with the absence of pain - IV pain administration - for those that cannot swallow, sublingual morphine is available - As long as the patient continues to receive opioids, a regimen to combat constipation must be implemented. If the patient cannot swallow laxatives or stool softeners, rectal suppositories or enemas may be necessary. -Because the analgesics given orally or rectally are short acting and typically scheduled as frequently as every 3 to 4 hours around the clock, there is always a strong possibility that a patient approaching the end of life will die in close proximity to the time of analgesic administration. If the patient is at home, family members administering analgesics should be prepared for this possibility. They need reassurance that they did not "cause" the death of the patient by administering a dose of analgesic medication. Dyspnea Dyspnea, an uncomfortable awareness of breathing, is one of the most prevalent symptoms at the end of life and can be challenging to manage Nursing Assessment for dyspnea As with assessment of pain, reports of dyspnea by patients must be believed. As is true for physical pain, the meaning of dyspnea to an individual patient may increase their suffering. For example, the patient may interpret increasing dyspnea as a sign that death is approaching. For some patients, sensations of breathlessness may invoke frightening images of drowning or suffocation, and the resulting cycle of fear and anxiety may increase the sensation of breathlessness. Therefore, the nurse should conduct a careful assessment of the psychosocial and spiritual components of the dyspnea. Physical assessment parameters include symptom intensity, distress, and interference with activities; auscultation of lung sounds; assessment of fluid balance, including measurement of dependent edema (circumference of lower extremities) and abdominal girth; temperature; skin color; sputum quantity and character; and cough. Nursing Management Nursing management of dyspnea at the end of life is directed toward administering medical treatment for the underlying pathology, monitoring the patient's response to treatment, helping the patient and the family manage anxiety (which exacerbates dyspnea), altering the perception of the symptom, and conserving energy. Pharmacologic intervention is aimed at modifying lung physiology and improving performance as well as altering the perception of the symptom. Bronchodilators and corticosteroids are used to treat underlying obstructive pathology, thereby improving overall lung function. Low doses of opioids effectively relieve dyspnea, although the mechanism of relief is not entirely clear. Although dyspnea in terminal illness is typically not associated with diminished blood oxygen saturation, low-flow oxygen often provides psychological comfort to both patients and families, particularly in the home setting. Palliative Nursing Interventions for Dyspnea Decrease Anxiety - Administer prescribed anxiolytic medications as indicated for anxiety or panic associated with dyspnea. - Assist with relaxation techniques, guided imagery. - Provide patient with a means to call for assistance (call bell/light within reach in a hospital or long-term care facility; handheld bell or other device for home). Treat Underlying Pathology - Administer prescribed bronchodilators and corticosteroids (obstructive pathology). - Administer blood products, erythropoietin as prescribed (typically not beneficial in advanced disease). - Administer prescribed diuretics and monitor fluid balance. Alter Perception of Breathlessness - Administer prescribed oxygen therapy via nasal cannula, if tolerated; masks may not be well tolerated. - Administer prescribed low-dose opioids via oral route (morphine sulfate is used most commonly). - Provide air movement in the patient's environment with a portable fan. Reduce Respiratory Demand - Educate patient and family to implement energy conservation measures. - Place needed equipment, supplies, and nourishment within reach. - For home or hospice care, offer bedside commode, electrical bed (with head that elevates). Nutrition and Hydration at the End of Life - Anorexia and cachexia are common in the seriously ill. The profound changes in the patient's appearance and a lack of interest in the socially important rituals of mealtime are particularly disturbing to families. - The anorexia-cachexia syndrome is characterized by disturbances in carbohydrate, protein, and fat metabolism; endocrine dysfunction; and anemia. The syndrome results in severe asthenia (loss of energy). Anorexia and cachexia differ from starvation (simple food deprivation) in several important ways. Appetite is lost early in the process, the body becomes catabolic in a dysfunctional way, and supplementation by gastric feeding (tube feeding) or parenteral nutrition in advanced disease does not replenish lean body mass that has been lost. Anorexia Although causes of anorexia may be controlled for a period of time, progressive anorexia is an expected and natural part of the dying process. Anorexia may be related to or exacerbated by situational variables (e.g., the ability to have meals with the family vs. eating alone in the "sick room"), progression of the disease, treatment of the disease, or psychological distress. - Offer small portions of favorite foods. - Be aware that cool foods may be better tolerated than hot foods. - Offer cheese, eggs, peanut butter, mild fish, chicken, or turkey. Meat (especially beef) may taste bitter and unpleasant. - Add milk shakes, meal replacement drinks, or other liquid supplements. - Place nutritious foods at the bedside (fruit juices, milk shakes in insulated drink containers with straws). - Schedule meals when family members can be present to provide company and stimulation. - Offer ice chips made from frozen fruit juices. - Allow the patient to refuse foods and fluids.

Gerontologic Considerations for UTI

The incidence of bacteriuria in older adults differs from that in younger adults. Bacteriuria increases with age and disability, and women are affected more frequently than men. - UTI is the most common infection of older adults and increases in prevalence with age. - UTIs occur more frequently in women than in men at younger ages but the gap between the sexes narrows in later life, which is due to reduced sexual intercourse in women and a higher incidence of bladder outlet obstruction secondary to benign prostatic hyperplasia in men Factors That Contribute to Urinary Tract Infection in Older Adults - Cognitive impairment - Frequent use of antimicrobial agents - High incidence of multiple chronic medical conditions - Immunocompromise - Immobility and incomplete emptying of bladder - Obstructed flow of urine (e.g., urethral strictures, neoplasms, or a clogged indwelling catheter) Early symptoms of UTI in older adults include burning, urgency, and fever Some patients develop incontinence and delirium with the onset of a UTI. Antibiotics are prescribed when bacteriuria is present - Treatment regimens are generally the same as those for younger adults, although age-related changes in the intestinal absorption of medications and decreased kidney function and hepatic flow may necessitate alterations in the antimicrobial regimen. - Kidney function must be monitored, and medication dosages should be altered accordingly. - The nurse carefully monitors fluid intake and output. Increasing fluid intake is advisable, provided that the patient's cardiac status does not contraindicate this action CLINICAL MANIFESTATIONS OF THE OLDER ADULT - Sudden, acute change in mental status (confusion, delirium (Family reports change in patient) - Won't present with high fever, is low grade (maybe 99.5) - Dysuria not always present - Urine: odorous, cloudy -Increased WBC

16.8 Provide culturally and spiritually sensitive care to seriously ill patients and their families.

The nurse's role is to assess the values, preferences, and practices of every patient, regardless of ethnicity, socioeconomic status, or background. The nurse can share knowledge about a patient's and family's cultural beliefs and practices with the health care team and facilitate the adaptation of the care plan to accommodate these practices. For example, a nurse may find that a male patient prefers to have his eldest son make all of his care decisions. Institutional practices and laws governing informed consent are also rooted in the Western notion of autonomous decision making and informed consent. If a patient wishes to defer decisions to his son, the nurse can work with the team to negotiate informed consent, respecting the patient's right not to participate in decision making and honoring his family's cultural practice. Disclosure/truth telling: "Tell me how you/your family talk about very sensitive or serious matters." Decision-making style: "How are decisions made in your family? Who would you like to be involved in decisions about your treatment or care?" Symptom management: "How would you like us to help you to manage the physical effects of your illness?" Life-sustaining treatment expectations: "Have you thought about what type of medical treatment you or your loved one would want as the end of life is nearing? Do you have an advance directive (living will and/or durable power of attorney)?" - Nutrition/hydration at the end of life - Cardiopulmonary resuscitation - Ventilator - Dialysis - Antibiotics - Medications to treat infection Desired location of dying: "Do you have a preference about being at home or in some other location when you die?" Desired role for family members in providing care: "Who do you want to be involved in caring for you at the end of life?" Gender-specific prohibitions: "Are you uncomfortable having either males or females provide your care or your loved one's personal care?" Spiritual/religious practices and rituals: "Is there anything that we should know about your spiritual or religious beliefs about death? Are there any practices that you would like us to observe as death is nearing?" Care of the body after the death: "Is there anything that we should know about how a body/your body should be treated after death?" Expression of grief: "What types of losses have you and your family experienced? How do you and your family express grief?" Funeral and burial practices: "Are there any rituals or practices associated with funerals or burial that are especially important to you?" Mourning practices: "How have you and your family carried on after a loss in the past? Are particular behaviors or practices expected or required?"

55.6 Describe the pathophysiology, clinical manifestations, medical management, and nursing management for care of the patient with kidney stones

Urolithiasis and nephrolithiasis refer to stones (calculi) in the urinary tract and kidney, respectively. Urinary stones predominantly occur in the third to fifth decades of life and affect men twice as often as women Pathophysiology Stones are formed in the urinary tract when urinary concentrations of substances such as calcium oxalate, calcium phosphate, and uric acid increase. Referred to as supersaturation, this depends on the amount of the substance, ionic strength, and pH of the urine. Stones may be found anywhere from the kidney to the bladder and may vary in size from minute granular deposits, called sand or gravel, to bladder stones as large as an orange. Certain factors favor the formation of stones, including infection, urinary stasis, and periods of immobility, all of which slow kidney drainage and alter calcium metabolism 80% of all kidney stones are calcium based Causes of hypercalcemia (high serum calcium) and hypercalciuria (high urine calcium) may include the following: - Hyperparathyroidism - Renal tubular acidosis - Cancers (e.g., leukemia, multiple myeloma) - Dehydration - Granulomatous diseases (e.g., sarcoidosis, tuberculosis), which may cause increased vitamin D production by the granulomatous tissue - Excessive intake of vitamin D - Excessive intake of milk and alkali - Myeloproliferative diseases such as polycythemia vera, which produce an unusual proliferation of blood cells from the bone marrow Medications known to cause stones in some patients include antacids, acetazolamide (Diamox), vitamin D, laxatives, and high doses of aspirin - However, in many patients, no cause may be found. cause excruciating pain, can cause shock dehydration any stone may result in obstruction may affect gfr of kidneys infection and impaired kidney function radiography collect stones to lab and identify what stone is composed of and can modify pt education 1633 potential sites of stones (urine calculi) 1636 education after xray procedure can take 6 weeks for fragments to pass hematuria is expectd for 4-5 days following procedure what to monitor for and when to contact doctor 55-112 pt education erradicate stone, determine type of stone pain meds - opioids pains, prevent shock and syncope nsaids can be used which can also help to pass stone hot baths and moist heat increase fluid intake

49.5 Compare the various types of hepatitis and their causes, prevention, clinical manifestations, management, prognosis, and home health care needs.

Viral hepatitis is a systemic, viral infection in which necrosis and inflammation of liver cells produce a characteristic cluster of clinical, biochemical, and cellular changes. To date, five definitive types of viral hepatitis that cause liver disease have been identified: hepatitis A, B, C, D, and E. Hepatitis A and E are similar in mode of transmission (fecal-oral route), whereas hepatitis B, C, and D share many other characteristics. HEPATITIS A VIRUS The HAV accounts for 20% to 25% of cases of clinical hepatitis in the United States - transmitted primarily through the fecal-oral route, by the ingestion of food or liquids infected with the virus. - It is more prevalent in countries with overcrowding and poor sanitation. - The virus has been found in the stool of infected patients before the onset of symptoms and during the first few days of illness. TYPICAL TRANSMISSION - Typically, a child or a young adult acquires the infection at school through poor hygiene, hand-to-mouth contact, or other close contact. The virus is carried home, where haphazard sanitary habits spread it through the family. - An infected food handler can spread the disease, and people can contract it by consuming water or shellfish from sewage-contaminated waters. - Outbreaks have occurred in day care centers and institutions as a result of poor hygiene among people with developmental disabilities. - Hepatitis A can be transmitted during sexual activity; this is more likely with oral-anal contact or anal intercourse and with multiple sex partners - Hepatitis A is NOT transmitted by blood transfusions incubation period is estimated to be between 2 and 6 weeks, with a mean of approximately 4 weeks - illness may be prolonged, lasting 4 to 8 weeks. - It usually lasts longer and is more severe in those older than 40 years. - Most patients recover from hepatitis A; it rarely progresses to acute liver necrosis or fulminant hepatic failure resulting in cirrhosis of the liver or death. Clinical Manifestations - Many patients are anicteric (without jaundice) and symptomless. - When symptoms appear, they resemble those of a mild, flu-like upper respiratory tract infection, with low-grade fever. - Anorexia, an early symptom, is often severe. It is thought to result from release of a toxin by the damaged liver or from failure of the damaged liver cells to detoxify an abnormal product. - Later, jaundice and dark urine may become apparent. Indigestion is present in varying degrees, marked by vague epigastric distress, nausea, heartburn, and flatulence. - patient may also develop a strong aversion to the taste of cigarettes or the presence of cigarette smoke and other strong odors - These symptoms tend to clear as soon as the jaundice reaches its peak, perhaps 10 days after its initial appearance. - Symptoms may be mild in children; in adults, they may be more severe and the course of the disease prolonged. PREVENTION OF HAV - Scrupulous hand hygiene, safe water supplies, and proper control of sewage disposal - Effective (95% to 100% after two to three doses) and safe HAV vaccines include Havrix and Vaqta - It is recommended that the two-dose vaccine be given to adults 18 years of age or older, with the second dose given 6 to 12 months after the first. Protection against HAV develops within several weeks after the first dose of the vaccine. - Children and adolescents 1 to 18 years of age receive three doses; the second dose is given 1 month after the first, and the third dose is given 6 to 12 months later. - HAV routine immunization of young children has proved to be effective in reducing disease incidence and maintaining very low incidence levels among vaccine recipients and across all age groups in many settings - Vaccination is also recommended for those from high-risk groups, such as men who have sex with men, people who use IV or injection drugs, staff of day care centers, health care personnel and those who work with the virus in research or animal care settings - A combined HAV and HBV vaccine (Twinrix) is available for vaccination of people 18 years of age and older with indications for both HAV and HBV vaccination. Vaccination consists of three doses, given on the same schedule as that used for single-antigen HBV vaccine. - OTHER OPTION: Immune globulin may suppress overt symptoms of the disease; the resulting subclinical case of HAV would produce immunity to subsequent episodes of the virus. - Educate patients regarding safe practices for preparing and dispensing food. - Encourage conscientious individual hygiene. - Encourage proper community and home sanitation. - Facilitate mandatory reporting of viral hepatitis to local health departments. - Promote community health education programs. - Promote vaccination to interrupt community-wide outbreaks. - Recommend pre-exposure vaccination for all children 12-23 months of age. Continue existing immunization programs for children 1-18 years of age. - Recommend vaccination for travelers to developing countries, illegal drug users (injection and noninjection drug users), men who have sex with men, people with chronic liver disease, people who work with HAV-infected animals or work with HAV in research facilities and recipients (e.g., hemophiliacs) of pooled plasma products for clotting factor disorders. - Support effective health supervision of schools, dormitories, extended care facilities, barracks, and camps. Medical Management Bed rest during the acute stage and a nutritious diet are important aspects of treatment. During the period of anorexia, the patient should receive frequent small feedings, supplemented if necessary by IV fluids with glucose. Because the patient often has an aversion to food, gentle persistence, and creativity may be required to stimulate appetite. Optimal food and fluid levels are necessary to counteract weight loss and to speed recovery. Nursing Management Management usually occurs in the home unless symptoms are severe. - patient and family need specific guidelines about diet, rest, follow-up blood work, and the importance of avoiding alcohol, as well as sanitation and hygiene measures (particularly hand hygiene) to prevent spread of the disease to other family members. - Specific education for patients and families about reducing the risk of contracting HAV includes good personal hygiene, stressing careful hand hygiene (after bowel movements and before eating) and environmental sanitation (safe food and water supply, effective sewage disposal). HEPATITIS B VIRUS - Unlike HAV, the HBV is transmitted primarily through blood (percutaneous and permucosal routes). - HBV can be found in blood, saliva, semen, and vaginal secretions and can be transmitted through mucous membranes and breaks in the skin. - HBV is also transferred from carrier mothers to their infants, especially in areas with a high incidence (e.g., Southeast Asia). - The infection usually is not transmitted via the umbilical vein but from the mother at the time of birth and during close contact afterward. - HBV has a long incubation period. It replicates in the liver and remains in the serum for relatively long periods, allowing transmission of the virus. - Most people (more than 90%) who contract HBV infection develop antibodies and recover spontaneously in 6 months. Clinical Manifestations of HBV Clinically, HBV closely resembles HAV, but the incubation period is much longer (1 to 6 months). - Signs and symptoms of HBV may be insidious and variable. - Fever and respiratory symptoms are rare; some patients have arthralgias and rashes. - The patient may have loss of appetite, dyspepsia, abdominal pain, generalized aching, malaise, and weakness. - Jaundice may or may not be evident. If jaundice occurs, light-colored stools and dark urine accompany it. - The liver may be tender and enlarged to 12 to 14 cm vertically. The spleen is enlarged and palpable in a few patients; the posterior cervical lymph nodes may also be enlarged. Subclinical episodes also occur frequently. PREVENTION - Preventing Transmission Continued screening of blood donors for the presence of hepatitis B antigen (HBAg) further decreases the risk of transmission by blood transfusion. The use of disposable syringes, needles, and lancets and the introduction of needleless IV administration systems have reduced the risk of spreading this infection from one patient to another or to health care personnel during the collection of blood samples or the administration of parenteral therapy. In the clinical laboratory and the hemodialysis unit, work areas are disinfected daily. Gloves are worn when handling all blood and body fluids, as well as HBAg-positive specimens, or when there is potential exposure to blood (e.g., blood drawing) or to patients' secretions. Eating is prohibited in the laboratory and in other areas exposed to secretions, blood, or blood products. - Active Immunization: HBV Active immunization is recommended for people who are at high risk for HBV (e.g., health care personnel, patients undergoing hemodialysis). In addition, people with HCV and other chronic liver diseases should receive the vaccine. A yeast-recombinant hepatitis B vaccine (Recombivax HB) is used to provide active immunity and has shown rates of protection greater than 90% in healthy people - Passive Immunity: Hepatitis B Immune Globulin Hepatitis B immune globulin (HBIG) provides passive immunity to HBV and is indicated for people exposed to HBV who have never had hepatitis B and have never received hepatitis B vaccine. Hepatitis B - Advise avoidance of high-risk behaviors. - Avoid multidose vials in patient care settings. - Monitor cleaning, disinfection, and sterilization of reusable devices in patient care settings. - Recommend vaccination for international travelers to regions with high or intermediate levels of endemic hepatitis B virus infection and for persons with chronic liver disease or with human immune deficiency virus infection. - Recommend vaccination for persons at risk for infection by sexual exposure, by percutaneous or mucosal exposure to blood. - Recommend vaccination of all infants in the United States regardless of the mother's hepatitis B. - Use barrier precautions in situations of contact with blood or body fluids. - Use needleless IV and injection systems in health care. - Use standard precautions in clinical care. Medical Management - Goals are to minimize infectivity and liver inflammation and decrease symptoms. - alpha-interferon is the single modality of therapy that offers the most promise - Two antiviral agents, entecavir (ETV) and tenofovir (TDF), which are oral nucleoside analogs, have been approved for use in chronic hepatitis B in the United States. - Bed rest may be recommended until the symptoms of hepatitis have subsided. Activities are restricted until the hepatic enlargement and levels of serum bilirubin and liver enzymes have decreased. Gradually, increased activity is then allowed. - Adequate nutrition should be maintained. Proteins are not restricted. Protein intake should be 1.2 to 1.5 g/kg/day. NURSING MANAGEMENT - Convalescence may be prolonged, with complete symptomatic recovery sometimes requiring 3 to 4 months or longer - During this stage, gradual resumption of physical activity is encouraged after the jaundice has resolved. - The nurse identifies psychosocial issues and concerns, particularly the effects of separation from family and friends if the patient is hospitalized during the acute and infective stages. Even if not hospitalized, the patient will be unable to work and must avoid sexual contact. Planning is required to minimize social isolation. Planning that includes the family helps to reduce their fears and anxieties about the spread of the disease. HEPATITIS C VIRUS Blood transfusions and sexual contact once accounted for most cases of HCV in the United States, but other parenteral means, such as sharing of contaminated needles by those who use IV or injection drugs and unintentional needlesticks and other injuries in health care workers now account for a significant number of cases. AT RISK POPULATIONS - those who use IV or injection drugs - people who are sexually active with multiple partners - patients receiving frequent transfusions - those who require large volumes of blood - health care personnel The incubation period is variable and may range from 15 to 160 days. The clinical course of acute HCV is similar to that of HBV; symptoms are usually mild or absent. There is no benefit from rest, diet, or vitamin supplements. Simeprevir (Olysio) plus sofosbuvir (Sovaldi), ledipasvir-sofosbuvir (Harvoni) and ombitasvir-paritaprevir-ritonavir packaged with dasabuvir (Viekira Pak) have fewer side effects, shorter treatment durations and higher cure rates than the previously recommended antiviral agents RISK FACTORS - Children born to women infected with hepatitis C virus - Health care and public safety workers after needlestick injuries or mucosal exposure to blood - Multiple contacts with a hepatitis C virus-infected person - Multiple sex partners, history of sexually transmitted infection, unprotected sex - Past/current illicit IV/injection drug use - Recipient of blood products or organ transplant before 1992 or clotting factor concentrates before 1987 EDUCATION - Advise avoidance of high-risk behaviors such as IV drug use. - Avoid multidose vials in patient care settings. - Monitor cleaning, disinfection, and sterilization of reusable devices in patient care settings. - Use barrier precautions in situations of contact with blood or body fluids. - Use needleless IV and injection systems in health care. - Use standard precautions in clinical care. HEPATITIS D VIRUS - Hepatitis D virus (delta agent) infection occurs in some cases of hepatitis B. Because the virus requires HBsAg for its replication, only people with hepatitis B are at risk for hepatitis D. Hepatitis D is common among those who use IV or injection drugs, patients undergoing hemodialysis, and recipients of multiple blood transfusions. Sexual contact with those who have hepatitis B is considered to be an important mode of transmission of hepatitis B and D. The incubation period varies between 30 and 150 days The symptoms of hepatitis D are similar to those of hepatitis B, except that patients are more likely to develop fulminant hepatic failure and to progress to chronic active hepatitis and cirrhosis. Treatment is similar to that of other forms of hepatitis. Currently, interferon alfa is the only licensed drug available in the treatment for HDV infection. The rate of recurrence is high, and the efficacy of interferon is related to the dose and duration of treatment. High-dose, long-duration therapy for at least a year is recommended HEPATITIS E VIRUS - It is believed that HEV is transmitted by the fecal-oral route, principally through contaminated water in areas with poor sanitation. The incubation period is variable, estimated to range between 15 and 65 days. - In general, hepatitis E resembles hepatitis A. It has a self-limited course with an abrupt onset. - Jaundice is almost always present. Chronic forms do not develop. Avoiding contact with the virus through good hygiene, including handwashing, is the major method of prevention of hepatitis E. The effectiveness of immune globulin in protecting against HEV is uncertain.

55.1 Explain the factors contributing to upper and lower urinary tract infections (UTIs).

normal urinary tract is sterile above the urethra Lower UTIs include bacterial cystitis (inflammation of the urinary bladder), bacterial prostatitis (inflammation of the prostate gland), and bacterial urethritis (inflammation of the urethra). Acute or chronic nonbacterial causes of inflammation in any of these areas can be misdiagnosed as bacterial infections. Upper UTIs are much less common and include acute or chronic pyelonephritis (inflammation of the renal pelvis), interstitial nephritis (inflammation of the kidney), and kidney abscesses. Upper and lower UTIs are further classified as uncomplicated or complicated, depending on whether the UTI is recurrent and the duration of the infection. Most uncomplicated UTIs are community acquired Complicated UTIs usually occur in people with urologic abnormalities or recent catheterization and are often acquired during hospitalization. Classifying Urinary Tract Infections Urinary tract infections (UTIs) are classified by location: the lower urinary tract (which includes the bladder and structures below the bladder) or the upper urinary tract (which includes the kidneys and ureters). They can also be classified as uncomplicated or complicated UTIs. Lower UTIs - Cystitis, prostatitis, urethritis Upper UTIs - Acute pyelonephritis, chronic pyelonephritis, renal abscess, interstitial nephritis, perirenal abscess Uncomplicated Lower or Upper UTIs - Community-acquired infection; common in young women and not usually recurrent Complicated Lower or Upper UTIs - Often acquired in the hospital and related to catheterization; occur in patients with urologic abnormalities, pregnancy, immunosuppression, diabetes, and obstructions and are often recurrent LOWER UTI How it happens For infection to occur, bacteria must gain access to the bladder, attach to and colonize the epithelium of the urinary tract to avoid being washed out with voiding, evade host defense mechanisms, and initiate inflammation. Many UTIs result from fecal organisms ascending from the perineum to the urethra and the bladder and then adhering to the mucosal surfaces. RISK FACTORS OF UTI Contributing conditions such as: - Female gender - Diabetes - Pregnancy - Neurologic disorders - Gout - Altered states caused by incomplete emptying of the bladder and urinary stasis - Decreased natural host defenses or immunosuppression - Inability or failure to empty the bladder completely - Inflammation or abrasion of the urethral mucosa - Instrumentation of the urinary tract (e.g., catheterization, cystoscopic procedures) Obstructed urinary flow caused by: - Congenital abnormalities - Urethral strictures - Contracture of the bladder neck - Bladder tumors - Calculi (stones) in the ureters or kidneys - Compression of the ureters -Sexual intercourse and history of UTI-urinary tract obstruction, kidney surgery, catheterization, GU malformation, diabetes and pregnancy - Bacterial invasion of the urinary tract - Urethrovesical reflux : With coughing and straining, bladder pressure rises, which may force urine from the bladder into the urethra. When bladder pressure returns to normal, the urine flows back to the bladder, which introduces bacteria from the urethra to the bladder. - Ureterovesical reflux: With failure of the ureterovesical valve, urine moves up the ureters during voiding and flows into the bladder when voiding stops. This prevents complete emptying of the bladder. It also leads to urinary stasis and contamination of the ureters with bacteria-laden urine. - Uropathogenic bacteria: Bacteriuria is the term used to describe the presence of bacteria in the urine. The organisms most frequently responsible for UTIs are those normally found in the lower gastrointestinal (GI) tract, usually Escherichia coli - Shorter urethra in women