Management of Patients With Gastric and Duodenal Disorders

Chapter 37 Management of Patients With Gastric and Duodenal Disorders LEARNING OBJECTIVES On completion of this chapter, the learner will be able to: 1. Compare the etiology, clinical manifestations, and management of acute gastritis, chronic gastritis, and peptic ulcer. 2. Use the nursing process as a framework for care of patients with gastritis. 3. Use the nursing process as a framework for care of patients with peptic ulcer. 4. Describe the dietary, pharmacologic, and surgical treatment of peptic ulcer. 5. Describe the nursing management of patients who undergo surgical procedures to treat obesity. 6. Use the nursing process as a framework for care of patients with gastric cancer. 7. Use the nursing process as a framework for care of patients undergoing gastric surgery. 8. Identify the complications of gastric surgery and their prevention and management. 9. Describe the home health care needs of the patient who has had gastric surgery. 1010

Chapter 37 Management of Patients With Gastric and Duodenal Disorders 1011 An individual s nutritional status depends not only on the type and amount of intake but also on the functioning of the gastric and intestinal portions of the gastrointestinal (GI) system. This chapter describes disorders of the stomach and duodenum and their treatment. Gastritis Gastritis (inflammation of the gastric or stomach mucosa) is a common GI problem. Gastritis may be acute, lasting several hours to a few days, or chronic, resulting from repeated exposure to irritating agents or recurring episodes of acute gastritis. Acute gastritis is often caused by dietary indiscretion the person eats food that is contaminated with disease-causing microorganisms or that is irritating or too highly seasoned. Other causes of acute gastritis include overuse of aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs), excessive alcohol intake, bile reflux, and radiation therapy. A more severe form of acute gastritis is caused by the ingestion of strong acid or alkali, which may cause the mucosa to become gangrenous or to perforate. Scarring can occur, resulting in pyloric obstruction. Gastritis also may be the first sign of an acute systemic infection. Chronic gastritis and prolonged inflammation of the stomach may be caused by either benign or malignant ulcers of the stomach or by the bacteria Helicobacter pylori. Chronic gastritis is sometimes associated with autoimmune diseases such as pernicious anemia; dietary factors such as caffeine; the use of medications, especially NSAIDs; alcohol; smoking; or reflux of intestinal contents into the stomach. Pathophysiology In gastritis, the gastric mucous membrane becomes edematous and hyperemic (congested with fluid and blood) and undergoes superficial erosion (Fig. 37-1). It secretes a scanty amount of gastric juice, containing very little acid but much mucus. Superficial ulceration may occur and can lead to hemorrhage. Clinical Manifestations The patient with acute gastritis may have abdominal discomfort, headache, lassitude, nausea, anorexia, vomiting, and hiccupping. Some patients, however, have no symptoms. The patient with chronic gastritis may complain of anorexia, heartburn after eating, belching, a sour taste in the mouth, or nausea and vomiting. Patients with chronic gastritis from vitamin deficiency usually have evidence of malabsorption of vitamin B 12 caused by antibodies against intrinsic factor. Assessment and Diagnostic Findings Gastritis is sometimes associated with achlorhydria or hypochlorhydria (absence or low levels of hydrochloric acid [HCl]) or with hyperchlorhydria (high levels of HCl). Diagnosis can be determined by endoscopy, upper GI radiographic studies, and histologic examination of a tissue specimen obtained by biopsy. In addition to biopsy, other diagnostic measures for detecting H. pylori include serologic testing for antibodies against the H. pylori antigen, a 1-minute ultrarapid urease test, and a breath test. Medical Management The gastric mucosa is capable of repairing itself after a bout of gastritis. As a rule, the patient recovers in about 1 day, although the appetite may be diminished for an additional 2 or 3 days. Acute gastritis is also managed by instructing the patient to refrain from alcohol and food until symptoms subside. After the patient can take nourishment by mouth, a nonirritating diet is recommended. If the symptoms persist, fluids may need to be administered parenterally. If bleeding is present, management is similar to the procedures used for upper GI tract hemorrhage (discussed later in this chapter). If gastritis is caused by ingestion of strong acids or alkalis, treatment consists of diluting and neutralizing the offending agent. To neutralize acids, common antacids (eg, aluminum hydroxide) are used; to neutralize an alkali, diluted lemon juice or diluted vinegar is used. If corrosion is extensive or severe, emetics and lavage are avoided because of the danger of perforation and damage to the esophagus. Therapy is supportive and may include nasogastric (NG) intubation, analgesic agents and sedatives, antacids, and intravenous (IV) fluids. Fiberoptic endoscopy may be necessary. In extreme cases, emergency surgery may be required to remove gangrenous or perforated tissue. Gastrojejunostomy or gastric resection may be necessary to treat pyloric obstruction, a narrowing of the pyloric orifice. Chronic gastritis is managed by modifying the patient s diet, promoting rest, reducing stress, and initiating pharmacotherapy. H. pylori may be treated with antibiotics (eg, tetracycline or amoxicillin, combined with clarithromycin) and a proton pump inhibitor (eg, lansoprazole [Prevacid]), and possibly bismuth salts (Pepto-Bismol) (Table 37-1). Research is being conducted to develop a vaccine against H. pylori (Alsahli et al., 2001). NURSING PROCESS: THE PATIENT WITH GASTRITIS Assessment When obtaining the history, the nurse asks about the patient s presenting signs and symptoms. Does the patient have heartburn, indigestion, nausea, or vomiting? Do the symptoms occur Glossary antrectomy: removal of the pyloric (antrum) portion of the stomach with anastomosis (surgical connection) to the duodenum (gastroduodenostomy or Billroth I) or anastomosis to the jejunum (gastrojejunostomy or Billroth II) dumping syndrome: physiologic response to rapid emptying of gastric contents into the jejunum, manifested by nausea, weakness, sweating, palpitations, syncope, and possibly diarrhea; occurs in patients who have had partial gastrectomy and gastrojejunostomy duodenum: first portion of the small intestine, between the stomach and the jejunum gastric: refers to the stomach gastritis: inflammation of the stomach hematemesis: vomiting of blood melena: tarry or black stools; indicative of blood in stools morbid obesity: 100 pounds or more over ideal body weight pyloroplasty: surgical procedure to increase the opening of the pyloric orifice pylorus: opening between the stomach and the duodenum pyrosis: heartburn

1012 Unit 7 DIGESTIVE AND GASTROINTESTINAL FUNCTION Damaged mucosa Cells secrete hydrochloric (HCl) acid or pepsinogen and intrinsic factor Mucosa (provides a barrier to protect stomach from HCL acid) Submucosa Muscularis Serosa FIGURE 37-1 Endoscopic view of erosive gastritis (left ). Damage from irritants (right) results in increased intracellular ph, impaired enzyme function, disrupted cellular structures, ischemia, vascular stasis, and tissue death. From Porth, C. (2002). Pathophysiology: Concepts of altered health states (6th ed.). Philadelphia: Lippincott Williams & Wilkins. at any specific time of the day, before or after meals, after ingesting spicy or irritating foods, or after the ingestion of certain drugs or alcohol? Has there been recent weight gain or loss? Are the symptoms related to anxiety, stress, allergies, eating or drinking too much, or eating too quickly? How are the symptoms relieved? Is there a history of previous gastric disease or surgery? A diet history plus a 72-hour dietary recall (a list of everything the patient ate and drank in the last 72 hours) may be helpful. A thorough history is important because it helps the nurse to identify whether known dietary excesses or other indiscretions are associated with the current symptoms, whether others in the patient s environment have similar symptoms, whether the patient is vomiting blood, and whether any known caustic element has been ingested. The nurse also identifies the duration of the current symptoms, any methods used by the patient to treat these symptoms, and whether the methods are effective. Signs to note during the physical examination include abdominal tenderness, dehydration, and evidence of any systemic disorder that might be responsible for the symptoms of gastritis. Nursing Diagnoses Based on the assessment data, the patient s major nursing diagnoses may include the following: Anxiety related to treatment Imbalanced nutrition, less than body requirements, related to inadequate intake of nutrients Risk for imbalanced fluid volume related to insufficient fluid intake and excessive fluid loss subsequent to vomiting Deficient knowledge about dietary management and disease process Acute pain related to irritated stomach mucosa Planning and Goals The major goals for the patient may include reduced anxiety, avoidance of irritating foods, adequate intake of nutrients, maintenance of fluid balance, increased awareness of dietary management, and relief of pain. Nursing Interventions REDUCING ANXIETY If the patient has ingested acids or alkalis, emergency measures may be needed. The nurse offers supportive therapy to the patient and family during treatment and after the ingested acid or alkali has been neutralized or diluted. In some cases, the nurse may need to prepare the patient for additional diagnostic studies (endoscopy) or surgery. The patient usually feels anxious about the pain and the treatment modalities. The nurse uses a calm approach to assess the patient and to answer all questions as completely as possible. It is important to explain all procedures and treatments according to the patient s level of understanding. PROMOTING OPTIMAL NUTRITION For acute gastritis, the nurse provides physical and emotional support and helps the patient manage the symptoms, which may include nausea, vomiting, heartburn, and fatigue. The patient should take no foods or fluids by mouth possibly for days until the acute symptoms subside, thus allowing the gastric mucosa to heal. If IV therapy is necessary, the nurse monitors it regularly, along with serum electrolyte values. After the symptoms subside, the nurse can offer the patient ice chips followed by clear liquids. Introducing solid food as soon as possible will provide oral nutrition, decrease the need for IV therapy, and minimize irritation to the gastric mucosa. As food is introduced, the nurse evaluates and reports any symptoms that suggest a repeat episode of gastritis.

Chapter 37 Management of Patients With Gastric and Duodenal Disorders 1013 Table 37-1 Pharmacologic Therapy for Peptic Ulcer Disease and Gastritis PHARMACOLOGIC AGENT MAJOR ACTION NURSING CONSIDERATIONS Antibiotics and Bismuth Salts Tetracycline (plus metronidazole, proton pump inhibitor, and bismuth salts) Amoxicillin (plus clarithromycin and proton pump inhibitor such as omeprazole [Prilosec]) Metronidazole (Flagyl); use with clarithromycin and proton pump inhibitor Clarithromycin (Biaxin); use with proton pump inhibitor and amoxicillin Bismuth subsalicylate (Pepto-Bismol); use with antibiotics Histamine 2 (H 2 ) Receptor Antagonists Cimetidine (Tagamet) Ranitidine (Zantac) Famotidine (Pepcid) Nizantidine (Axid) Proton (Gastric Acid) Pump Inhibitor Omeprazole (Prilosec) Lansoprazole (Prevacid) Rabeprazole (Aciphex) Exerts bacteriostatic effects to eradicate Helicobacter pylori bacteria in the gastric mucosa A bactericidal antibiotic that assists with eradicating H. pylori bacteria in the gastric mucosa An amebocide that assists with eradicating H. pylori bacteria in the gastric mucosa Exerts bactericidal effects to eradicate H. pylori bacteria in the gastric mucosa Suppresses H. pylori bacteria in the gastric mucosa and assists with healing of mucosal lesions Inhibits acid secretion by blocking the action of histamine on the histamine receptors of the parietal cells in the stomach Inhibits acid secretion by blocking the action of the histamine on the histamine receptors of the parietal cells in the stomach Inhibits acid secretion by blocking the action of histamine on the histamine receptors on the parietal cells in the stomach Inhibits acid secretion by blocking the action of histamine on the histamine receptors on the parietal cells in the stomach Decreases gastric acid secretion by slowing the hydrogen-potassium adenosine triphosphatase (H+, K+-ATPase) pump on the surface of the parietal cells Decreases gastric acid secretion by slowing the H+, K+-ATPase pump on the surface of the parietal cells. Decreases gastric acid secretion by slowing the H+, K+-ATPase pump on the surface of the parietal cells May cause photosensitivity reaction; warn patient to use sunscreen. Use with caution in patients with renal or hepatic impairment. Milk or dairy products may reduce medication effectiveness. May cause diarrhea. Do not use in patients allergic to penicillin. Administer with meals to decrease GI distress. Administer with other antibiotics and proton pump inhibitors. May cause GI upset. Given concurrently with antibiotics to cure H. pylori infection. Should be taken on an empty stomach. Least expensive of the H 2 receptor antagonists. May cause confusion, agitation, or coma in the elderly or those with renal or hepatic insufficiency. Long-term use may cause gynecomastia, impotence, and diarrhea. Prolonged drug half-life in patients with renal and hepatic insufficiency. Causes fewer side effects than cimetidine. Rarely causes constipation, diarrhea, dizziness, and depression. Best choice for critically ill patient because it is known to have least risk of interaction with other medications. (It is unclear whether other H 2 receptor antagonists are as safe as famotidine.) Does not alter medication metabolism in the liver. Prolonged half-life in patients with renal insufficiency. Short-term relief for gastroesophageal reflux. Dilute before IV injection. Rarely causes constipation or diarrhea. Used for duodenal ulcers. Prolonged half-life in patients with renal insufficiency. Rarely causes sweating, increased liver enzymes, nausea, urticaria. Long-term use may cause gastric tumors and bacterial invasion. May cause diarrhea, additional pain, and nausea. A delayed-release capsule that is to be swallowed whole and taken before meals. A delayed-release tablet; swallow whole. (continued)

1014 Unit 7 DIGESTIVE AND GASTROINTESTINAL FUNCTION Table 37-1 Pharmacologic Therapy for Peptic Ulcer Disease and Gastritis (Continued) PHARMACOLOGIC AGENT MAJOR ACTION NURSING CONSIDERATIONS Cytoprotective Medications Misoprostol (Cytotec) Sucralfate (Carafate) A synthetic prostaglandin; protects the gastric mucosa from ulcerogenic agents; also increases mucus production and bicarbonate levels In the presence of gastric acid, sucralfate creates a viscous substance that forms a protective layer at the site of the ulcer and prevents digestion by pepsin Used as a preventive medication (to prevent ulceration in patients using NSAIDs). Administer with food. May cause diarrhea and cramping (including uterine cramping). May cause constipation or nausea. Approved for duodenal not gastric ulcers. The nurse discourages the intake of caffeinated beverages, because caffeine is a central nervous system stimulant that increases gastric activity and pepsin secretion. It also is important to discourage alcohol use. Discouraging cigarette smoking is important because nicotine reduces the secretion of pancreatic bicarbonate and thus inhibits the neutralization of gastric acid in the duodenum (Eastwood, 1997). When appropriate, the nurse refers the patient for alcohol counseling and smoking cessation programs. PROMOTING FLUID BALANCE Daily fluid intake and output are monitored to detect early signs of dehydration (minimal urine output of 30 ml/hour, minimal intake of 1.5 L/day). If food and fluids are withheld, IV fluids (3 L/day) usually are prescribed and a record of fluid intake plus caloric value (1 L of 5% dextrose in water = 170 calories of carbohydrate) needs to be maintained. Electrolyte values (sodium, potassium, chloride) are assessed every 24 hours to detect imbalance. The nurse must always be alert for any indicators of hemorrhagic gastritis, which include hematemesis (vomiting of blood), tachycardia, and hypotension. If these occur, the physician is notified and the patient s vital signs are monitored as the patient s condition warrants. Guidelines for managing upper GI tract bleeding are discussed later in this chapter. RELIEVING PAIN Measures to help relieve pain include instructing the patient to avoid foods and beverages that may be irritating to the gastric mucosa (described earlier) and instructing the patient about using medications to relieve chronic gastritis. To follow up, the nurse assesses the patient s level of pain and the extent of comfort attained from the use of medications and avoidance of irritating substances. PROMOTING HOME AND COMMUNITY-BASED CARE Teaching Patients Self-Care The nurse evaluates the patient s knowledge about gastritis and develops an individualized teaching plan that includes information about stress management, diet, and medications (Chart 37-1). Dietary instructions take into account the patient s daily caloric needs, food preferences, and pattern of eating. The nurse and patient review foods and other substances to be avoided (eg, spicy, irritating, or highly seasoned foods; caffeine; nicotine; alcohol). Consultation with a dietitian may be recommended. Providing information about prescribed antibiotics, bismuth salts, medications to decrease gastric secretion, and medications to protect mucosal cells from gastric secretions can help the patient recover and prevent recurrence. Patients with pernicious anemia need information about long-term vitamin B 12 injections; the nurse may instruct a family member about administering these injections or make arrangements for the patient to receive the injections from a health care provider. Finally, the nurse emphasizes the importance of keeping follow-up appointments with health care providers. Evaluation EXPECTED PATIENT OUTCOMES Expected patient outcomes may include the following: 1. Exhibits less anxiety 2. Avoids eating irritating foods or drinking caffeinated beverages or alcohol 3. Maintains fluid balance a. Has intake of at least 1.5 L daily b. Drinks six to eight glasses of water daily Chart 37-1 Home Care Checklist The Patient With Gastritis At the completion of the home care instruction, the patient or caregiver will be able to: Patient Caregiver Identify foods and other substances that may cause gastritis. Describe medication regimen to follow. State need for vitamin B 12 injections if patient has pernicious anemia.

Chapter 37 Management of Patients With Gastric and Duodenal Disorders 1015 c. Has a urinary output of about 1 L daily d. Displays adequate skin turgor 4. Adheres to medical regimen a. Selects nonirritating foods and beverages b. Takes medications as prescribed 5. Maintains appropriate weight 6. Reports less pain Gastric and Duodenal Ulcers A peptic ulcer is an excavation (hollowed-out area) that forms in the mucosal wall of the stomach, in the pylorus (opening between stomach and duodenum), in the duodenum (first part of small intestine), or in the esophagus. A peptic ulcer is frequently referred to as a gastric, duodenal, or esophageal ulcer, depending on its location, or as peptic ulcer disease. Erosion of a circumscribed area of mucous membrane is the cause (Fig. 37-2). This erosion may extend as deeply as the muscle layers or through the muscle to the peritoneum. Peptic ulcers are more likely to be in the duodenum than in the stomach. As a rule they occur alone, but they may occur in multiples. Chronic gastric ulcers tend to occur in the lesser curvature of the stomach, near the pylorus. Table 37-2 compares the features of gastric and duodenal ulcers. Peptic ulcer disease occurs with the greatest frequency in people between the ages of 40 and 60 years. It is relatively uncommon in women of childbearing age, but it has been observed in children and even in infants. After menopause, the incidence of peptic ulcers in women is almost equal to that in men. Peptic ulcers in the body of the stomach can occur without excessive acid secretion. Table 37-2 Comparing Duodenal and Gastric Ulcers DUODENAL ULCER GASTRIC ULCER Incidence Age 30 60 Male: female 2 3:1 80% of peptic ulcers are duodenal Signs, Symptoms, and Clinical Findings Hypersecretion of stomach acid (HCl) May have weight gain Pain occurs 2 3 hours after a meal; often awakened between 1 2 AM; ingestion of food relieves pain Vomiting uncommon Hemorrhage less likely than with gastric ulcer, but if present melena more common than hematemesis More likely to perforate than gastric ulcers Malignancy Possibility Rare Risk Factors H. pylori, alcohol, smoking, cirrhosis, stress Usually 50 and over Male: female 1:1 15% of peptic ulcers are gastric Normal hyposecretion of stomach acid (HCl) Weight loss may occur Pain occurs 1 2 to 1 hour after a meal; rarely occurs at night; may be relieved by vomiting; ingestion of food does not help, sometimes increases pain Vomiting common Hemorrhage more likely to occur than with duodenal ulcer; hematemesis more common than melena Occasionally H. pylori, gastritis, alcohol, smoking, use of NSAIDs, stress FIGURE 37-2 Deep peptic ulcer. From Porth, C. (2002). Pathophysiology: Concepts of altered health states (6th ed). Philadelphia: Lippincott Williams & Wilkins. In the past, stress and anxiety were thought to be causes of ulcers. Research has identified that peptic ulcers result from infection with the gram-negative bacteria H. pylori (Tytgat, 2000). However, ulcers do seem to develop more commonly in people who are tense; whether this is a contributing factor to the condition is uncertain. In addition, excessive secretion of HCl in the stomach may contribute to the formation of gastric ulcers, and stress may be associated with its increased secretion. The ingestion of milk and caffeinated beverages, smoking, and alcohol also may increase HCl secretion. Familial tendency may be a significant predisposing factor. A further genetic link is noted in the finding that people with blood type O are more susceptible to peptic ulcers than are those with blood type A, B, or AB. There also is an association between duodenal ulcers and chronic pulmonary disease or chronic renal disease. Other predisposing factors associated with peptic ulcer include chronic use of NSAIDs, alcohol ingestion, and excessive smoking. Rarely, ulcers are caused by excessive amounts of the hormone gastrin, produced by tumors. This Zollinger-Ellison syndrome (ZES) consists of severe peptic ulcers, extreme gastric hyperacidity, and gastrin-secreting benign or malignant tumors of the pancreas. Stress ulcers, which are clinically different from peptic ulcers, are ulcerations in the mucosa that can occur in the gastroduodenal area. Stress ulcers may occur in patients who are exposed to stressful conditions. Esophageal ulcers occur as a result of the backward flow of HCl from the stomach into the esophagus (gastroesophageal reflux disease [GERD]).

1016 Unit 7 DIGESTIVE AND GASTROINTESTINAL FUNCTION Pathophysiology Peptic ulcers occur mainly in the gastroduodenal mucosa because this tissue cannot withstand the digestive action of gastric acid (HCl) and pepsin. The erosion is caused by the increased concentration or activity of acid-pepsin, or by decreased resistance of the mucosa. A damaged mucosa cannot secrete enough mucus to act as a barrier against HCl. The use of NSAIDs inhibits the secretion of mucus that protects the mucosa. Patients with duodenal ulcer disease secrete more acid than normal, whereas patients with gastric ulcer tend to secrete normal or decreased levels of acid. ZES is suspected when a patient has several peptic ulcers or an ulcer that is resistant to standard medical therapy. It is identified by the following findings: hypersecretion of gastric juice, duodenal ulcers, and gastrinomas (islet cell tumors) in the pancreas. Ninety percent of tumors are found in the gastric triangle, which encompasses the cystic and common bile ducts, the second and third portions of the duodenum, and the neck and body of the pancreas. Approximately one third of gastrinomas are malignant. Diarrhea and steatorrhea (unabsorbed fat in the stool) may be evident. The patient may have coexisting parathyroid adenomas or hyperplasia and may therefore exhibit signs of hypercalcemia. The most common complaint is epigastric pain. H. pylori is not a risk factor for ZES. Stress ulcer is the term given to the acute mucosal ulceration of the duodenal or gastric area that occurs after physiologically stressful events, such as burns, shock, severe sepsis, and multiple organ traumas. These ulcers are most common in ventilator-dependent patients after trauma or surgery. Fiberoptic endoscopy within 24 hours after injury reveals shallow erosions of the stomach wall; by 72 hours, multiple gastric erosions are observed. As the stressful condition continues, the ulcers spread. When the patient recovers, the lesions are reversed. This pattern is typical of stress ulceration. Differences of opinion exist as to the actual cause of mucosal ulceration in stress ulcers. Usually, it is preceded by shock; this leads to decreased gastric mucosal blood flow and to reflux of duodenal contents into the stomach. In addition, large quantities of pepsin are released. The combination of ischemia, acid, and pepsin creates an ideal climate for ulceration. Stress ulcers should be distinguished from Cushing s ulcers and Curling s ulcers, two other types of gastric ulcers. Cushing s ulcers are common in patients with trauma to the brain. They may occur in the esophagus, stomach, or duodenum and are usually deeper and more penetrating than stress ulcers. Curling s ulcer is frequently observed about 72 hours after extensive burns and involves the antrum of the stomach or the duodenum. Clinical Manifestations Symptoms of an ulcer may last for a few days, weeks, or months and may disappear only to reappear, often without an identifiable cause. Many people have symptomless ulcers, and in 20% to 30% perforation or hemorrhage may occur without any preceding manifestations. As a rule, the patient with an ulcer complains of dull, gnawing pain or a burning sensation in the midepigastrium or in the back. It is believed that the pain occurs when the increased acid content of the stomach and duodenum erodes the lesion and stimulates the exposed nerve endings. Another theory suggests that contact of the lesion with acid stimulates a local reflex mechanism that initiates contraction of the adjacent smooth muscle. Pain is usually relieved by eating, because food neutralizes the acid, or by taking alkali; however, once the stomach has emptied or the alkali s effect has decreased, the pain returns. Sharply localized tenderness can be elicited by applying gentle pressure to the epigastrium at or slightly to the right of the midline. Other symptoms include pyrosis (heartburn), vomiting, constipation or diarrhea, and bleeding. Pyrosis is a burning sensation in the esophagus and stomach that moves up to the mouth. Heartburn is often accompanied by sour eructation, or burping, which is common when the patient s stomach is empty. Although vomiting is rare in uncomplicated duodenal ulcer, it may be a symptom of a peptic ulcer complication. It results from obstruction of the pyloric orifice, caused by either muscular spasm of the pylorus or mechanical obstruction from scarring or acute swelling of the inflamed mucous membrane adjacent to the ulcer. Vomiting may or may not be preceded by nausea; usually it follows a bout of severe pain and bloating, which is relieved by ejection of the gastric contents. Emesis often contains undigested food eaten many hours earlier. Constipation or diarrhea can occur, probably as a result of diet and medications. Fifteen percent of patients with gastric ulcers experience bleeding. Patients may present with GI bleeding as evidenced by the passage of tarry stools. A small portion of patients who bleed from an acute ulcer have had no previous digestive complaints, but they develop symptoms thereafter (Yamada, 1999). Assessment and Diagnostic Findings A physical examination may reveal pain, epigastric tenderness, or abdominal distention. A barium study of the upper GI tract may show an ulcer; however, endoscopy is the preferred diagnostic procedure because it allows direct visualization of inflammatory changes, ulcers, and lesions. Through endoscopy, a biopsy of the gastric mucosa and of any suspicious lesions can be obtained. Endoscopy may reveal lesions that are not evident on x-ray studies because of their size or location. Stools may be tested periodically until they are negative for occult blood. Gastric secretory studies are of value in diagnosing achlorhydria and ZES. H. pylori infection may be determined by biopsy and histology with culture. There is also a breath test that detects H. pylori, as well as a serologic test for antibodies to the H. pylori antigen. Pain that is relieved by ingesting food or antacids and absence of pain on arising are also highly suggestive of an ulcer. Medical Management Once the diagnosis is established, the patient is informed that the problem can be controlled. 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 and to manage gastric acidity. Methods used include medications, lifestyle changes, and surgical intervention. PHARMACOLOGIC THERAPY Currently, the most commonly used therapy in the treatment of ulcers is a combination of antibiotics, proton pump inhibitors, and bismuth salts that suppresses or eradicates H. pylori; histamine 2 (H 2 ) receptor antagonists and proton pump inhibitors are used to treat NSAID-induced and other ulcers not associated with H. pylori ulcers. Table 37-1 provides details about pharmacologic treatment.

Chapter 37 Management of Patients With Gastric and Duodenal Disorders 1017 The patient is advised to adhere to the medication regimen to ensure complete healing of the ulcer. Because most patients become symptom-free within a week, it becomes a nursing responsibility to stress the importance of following the prescribed regimen so that the healing process can continue uninterrupted and the return of chronic ulcer symptoms can be prevented. Rest, sedatives, and tranquilizers may add to the patient s comfort and are prescribed as needed. Maintenance dosages of H 2 receptor antagonists are usually recommended for 1 year. For patients with ZES, hypersecretion of acid may be controlled with high doses of H 2 receptor antagonists. These patients may require twice the normal dose, and dosages usually need to be increased with prolonged use. Octreotide (Sandostatin), a medication that suppresses gastrin levels, also may be prescribed. Patients at risk for stress ulcers may be treated prophylactically with IV H 2 receptor antagonists and cytoprotective agents (e.g., misoprostol, sucralfate) because of the risk for upper GI tract hemorrhage. Frequent gastric aspiration is performed to allow monitoring of gastric secretion ph. STRESS REDUCTION AND REST Reducing environmental stress requires physical and psychological modifications on the patient s part as well as the aid and cooperation of family members and significant others. The patient may need help in identifying situations that are stressful or exhausting. A rushed lifestyle and an irregular schedule may aggravate symptoms and interfere with regular meals taken in relaxed settings and with the regular administration of medications. The patient may benefit from regular rest periods during the day, at least during the acute phase of the disease. Biofeedback, hypnosis, or behavior modification may be helpful. SMOKING CESSATION Studies have shown that smoking decreases the secretion of bicarbonate from the pancreas into the duodenum, resulting in increased acidity of the duodenum. Research indicates that continuing to smoke cigarettes may significantly inhibit ulcer repair. Therefore, the patient is strongly encouraged to stop smoking. Smoking cessation support groups and other smoking cessation approaches are helpful for many patients (Eastwood, 1997). 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 and overstimulation from consumption of meat extracts, alcohol, coffee (including decaffeinated coffee, which also stimulates acid secretion) and other caffeinated beverages, and diets rich in milk and cream (which stimulate acid secretion). 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 a histamine blocker is taken. Diet compatibility becomes an individual matter: the patient eats foods that can be tolerated and avoids those that produce pain. SURGICAL MANAGEMENT The introduction of antibiotics to eradicate H. pylori and of H 2 receptor antagonists as treatment for ulcers has greatly reduced the need for surgical interventions. However, surgery is usually recommended for patients with intractable ulcers (those that fail to heal after 12 to 16 weeks of medical treatment), life-threatening hemorrhage, perforation, or obstruction, and for those with ZES not responding to medications (Yamada, 1999). Surgical procedures include vagotomy, with or without pyloroplasty, and the Billroth I and Billroth II procedures (Table 37-3; see also the section on gastric surgery later in this chapter). Patients who need ulcer surgery may have had a long illness. They may be discouraged and have had interruptions in their work role and pressures in their family life. FOLLOW-UP CARE Recurrence within 1 year may be prevented with the prophylactic use of H 2 receptor antagonists given at a reduced dose. Not all patients require maintenance therapy; it may be prescribed only for those with two or three recurrences per year, those who have had a complication such as bleeding or outlet obstruction, or those who are candidates for gastric surgery but are at too high a risk for surgery. The likelihood of recurrence is reduced if the patient avoids smoking, coffee (including decaffeinated coffee) and other caffeinated beverages, alcohol, and ulcerogenic medications (eg, NSAIDs). NURSING PROCESS: THE PATIENT WITH ULCER DISEASE Assessment The nurse asks the patient to describe the pain and the methods used to relieve it (e.g., food, antacids). The patient usually describes peptic ulcer pain as burning or gnawing; it occurs about 2 hours after a meal and frequently awakens the patient between midnight and 3 AM. Taking antacids, eating, or vomiting often relieves the pain. If the patient reports a recent history of vomiting, the nurse determines how often emesis has occurred and notes important characteristics of the vomitus: Is it bright red, does it resemble coffee grounds, or is there undigested food from previous meals? Has the patient noted any bloody or tarry stools? The nurse also asks the patient to list his or her usual food intake for a 72-hour period and to describe food habits (e.g., speed of eating, regularity of meals, preference for spicy foods, use of seasonings, use of caffeinated beverages and decaffeinated coffee). Lifestyle and habits are a concern as well. Does the patient use irritating substances? For example, does he or she smoke cigarettes? If yes, how many? Does the patient ingest alcohol? If yes, how much and how often? Are NSAIDs used? The nurse inquires about the patient s level of anxiety and his or her perception of current stressors. How does the patient express anger or cope with stressful situations? Is the patient experiencing occupational stress or problems within the family? Is there a family history of ulcer disease? The nurse assesses vital signs and reports tachycardia and hypotension, which may indicate anemia from GI bleeding. The stool is tested for occult blood, and a physical examination, including palpation of the abdomen for localized tenderness, is performed as well. Diagnosis NURSING DIAGNOSES Based on the assessment data, the patient s nursing diagnoses may include the following: Acute pain related to the effect of gastric acid secretion on damaged tissue Anxiety related to coping with an acute disease Imbalanced nutrition related to changes in diet Deficient knowledge about prevention of symptoms and management of the condition

1018 Unit 7 DIGESTIVE AND GASTROINTESTINAL FUNCTION Table 37-3 Surgical Procedures for Peptic Ulcer Disease OPERATION DESCRIPTION COMMENTS Vagotomy Vagotomy Severing of the vagus nerve. Decreases gastric acid by diminishing cholinergic stimulation to the parietal cells, making them less responsive to gastrin. May be done via open surgical approach, laparoscopy, or thoracoscopy May be performed to reduce gastric acid secretion. A drainage type of procedure (see pyloroplasty) is usually performed to assist with gastric emptying (because there is total denervation of the stomach). Some patients experience problems with feeling of fullness, dumping syndrome, diarrhea, and gastritis. Truncal vagotomy Selective vagotomy Proximal (parietal cell) gastric vagotomy without drainage Pyloroplasty Pylorus note longitudinal incision Severs the right and left vagus nerves as they enter the stomach at the distal part of the esophagus. Severs vagal innervation to the stomach but maintains innervation to the rest of the abdominal organs. Denervates acid-secreting parietal cells but preserves vagal innervation to the gastric antrum and pylorus. A surgical procedure in which a longitudinal incision is made into the pylorus and transversely sutured closed to enlarge the outlet and relax the muscle This type of vagotomy is most commonly used to decrease acid secretions and reduce gastric and intestinal motility. Recurrence rate of ulcer is 10% 15%. No dumping syndrome. No need for drainage procedure. Recurrence rate of ulcer is 10% 15%. Usually accompanies truncal and selective vagotomies, which produce delayed gastric emptying due to decreased innervation. Transverse suture Antrectomy Billroth I (Gastroduodenostomy) Antrectomy Body Fundus Removal of the lower portion of the antrum of the stomach (which contains the cells that secrete gastrin) as well as a small portion of the duodenum and pylorus. The remaining segment is anastomosed to the duodenum (Billroth I) or to the jejunum (Billroth II) May be performed in conjunction with a truncal vagotomy. The patient may have problems with feeling of fullness, dumping syndrome, and diarrhea. Recurrence rate of ulcer is < 1%. Duodenum Duodenal anastomosis Billroth I (continued)

Chapter 37 Management of Patients With Gastric and Duodenal Disorders 1019 Table 37-3 Surgical Procedures for Peptic Ulcer Disease (Continued) OPERATION DESCRIPTION COMMENTS Billroth II (Gastrojejunostomy) Fundus Antrectomy Body Jejunal anastomosis Jejunal loop Billroth II Subtotal gastrectomy with Billroth I or II anastomosis Removal of distal third of stomach; anastomosis with duodenum or jejunum. Removes gastrin-producing cells in the antrum and part of the parietal cells. Dumping syndrome, anemia, malabsorption, weight loss. Recurrence rate of ulcer is 10% 15%. COLLABORATIVE PROBLEMS/ POTENTIAL COMPLICATIONS Potential complications may include the following: Hemorrhage Perforation Penetration Pyloric obstruction (gastric outlet obstruction) Planning and Goals The goals for the patient may include relief of pain, reduced anxiety, maintenance of nutritional requirements, knowledge about the management and prevention of ulcer recurrence, and absence of complications. Nursing Interventions RELIEVING PAIN Pain relief can be achieved with prescribed medications. The patient should avoid aspirin, foods and beverages that contain caffeine, and decaffeinated coffee, and meals should be eaten at regularly paced intervals in a relaxed setting. Some patients benefit from learning relaxation techniques to help manage stress and pain and to enhance smoking cessation efforts. REDUCING ANXIETY The nurse assesses the patient s level of anxiety. Patients with peptic ulcers are usually anxious, but their anxiety is not always obvious. Appropriate information is provided at the patient s level of understanding, all questions are answered, and the patient is encouraged to express fears openly. Explaining diagnostic tests and administering medications on schedule also help to reduce anxiety. The nurse interacts with the patient in a relaxed manner, helps identify stressors, and explains various coping techniques and relaxation methods, such as biofeedback, hypnosis, or behavior modification. The patient s family is also encouraged to participate in care and to provide emotional support. 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 complying with the medication regimen and dietary restrictions. MONITORING AND MANAGING POTENTIAL COMPLICATIONS Hemorrhage Gastritis and hemorrhage from peptic ulcer are the two most common causes of upper GI tract bleeding (which may also occur with esophageal varices, as discussed in Chapter 39). Hemorrhage, the most common complication, occurs in about 15% of patients with peptic ulcers (Yamada, 1999). The site of bleeding is usually the distal portion of the duodenum. Bleeding may be manifested by hematemesis or melena (tarry stools). The vomited blood can be bright red, or it can have a coffee grounds appearance (which is dark) from the oxidation of hemoglobin to methemoglobin. When the hemorrhage is large (2000 to 3000 ml), most of the blood is vomited. Because large quantities of blood may be lost quickly, immediate correction of blood loss may be required to prevent hemorrhagic shock. When the hemorrhage is small, much or all of the blood is passed in the stools, which will appear tarry black because of the digested hemoglobin. Management depends on the amount of blood lost and the rate of bleeding. The nurse assesses the patient for faintness or dizziness and nausea, which may precede or accompany bleeding. It is important to monitor vital signs frequently and to evaluate the patient for tachycardia, hypotension, and tachypnea. Other nursing interventions include monitoring the hemoglobin and hematocrit,

1020 Unit 7 DIGESTIVE AND GASTROINTESTINAL FUNCTION testing the stool for gross or occult blood, and recording hourly urinary output to detect anuria or oliguria (absence or decreased urine production). Many times the bleeding from a peptic ulcer stops spontaneously; however, the incidence of recurrent bleeding is high. Because bleeding can be fatal, the cause and severity of the hemorrhage must be identified quickly and the blood loss treated to prevent hemorrhagic shock. Management of upper GI tract bleeding consists of quickly determining the amount of blood lost and the rate of bleeding, rapidly replacing the blood that has been lost, stopping the bleeding, stabilizing the patient, and diagnosing and treating the cause. Related nursing and collaborative interventions include the following: Inserting a peripheral IV line for the infusion of saline or lactated Ringer s solution and blood products. The nurse may need to assist with the placement of a pulmonary artery catheter for hemodynamic monitoring. Blood component therapy is initiated if there are signs of shock (eg, tachycardia, sweating, coldness of the extremities). Monitoring the hemoglobin and hematocrit to assist in evaluating blood loss Inserting an NG tube to distinguish fresh blood from coffee grounds material, to aid in the removal of clots and acid, to prevent nausea and vomiting, and to provide a means of monitoring further bleeding Administering a room-temperature lavage of saline solution or water. This is controversial; some authorities recommend using ice lavage (Yamada, 1999). Inserting an indwelling urinary catheter and monitoring urinary output Monitoring vital signs and oxygen saturation and administering oxygen therapy Placing the patient in the recumbent position with the legs elevated to prevent hypotension; or, to prevent aspiration from vomiting, placing the patient on the left side Treating hemorrhagic shock (described in Chapter 15) If bleeding cannot be managed by the measures described, other treatment modalities may be used. Transendoscopic coagulation by laser, heat probe, medication, a sclerosing agent, or a combination of these therapies can halt bleeding and make surgical intervention unnecessary. There is much debate regarding how soon endoscopy should be performed. Some believe that endoscopy should be performed in the first 24 hours after hemorrhage has been stabilized. Others believe that endoscopy may be performed during acute bleeding, as long as the esophageal or gastric area can be visualized (blood may decrease visibility) (Yamada, 1999). For those who are unable to undergo surgery, selective embolization may be used. This procedure involves forcing emboli of autologous blood clots with or without Gelfoam (absorbable gelatin sponge) through a catheter in the artery to a point above the bleeding lesion. A radiologist performs this procedure. Rebleeding may occur and often warrants surgical intervention. The nurse monitors the patient carefully so that bleeding can be detected quickly. Signs of bleeding include tachycardia, tachypnea, hypotension, mental confusion, thirst, and oliguria. If bleeding recurs within 48 hours after medical therapy has begun, or if more than 6 to 10 units of blood are required within 24 hours to maintain blood volume, the patient is likely to require surgery. Some physicians recommend surgical intervention if a patient hemorrhages three times. Other criteria for surgery are the patient s age (massive hemorrhaging is three times more likely to be fatal in those older than 60 years of age); a history of chronic duodenal ulcer; and a coincidental gastric ulcer (Yamada, 1999). The area of the ulcer is removed or the bleeding vessels are ligated. Many patients also undergo procedures (eg, vagotomy and pyloroplasty, gastrectomy) aimed at controlling the underlying cause of the ulcers (see Table 37-3). Perforation and Penetration Perforation is the erosion of the ulcer through the gastric serosa into the peritoneal cavity without warning. It is an abdominal catastrophe and requires immediate surgery. Penetration is erosion of the ulcer through the gastric serosa into adjacent structures such as the pancreas, biliary tract, or gastrohepatic omentum. Symptoms of penetration include back and epigastric pain not relieved by medications that were effective in the past. Like perforation, penetration usually requires surgical intervention. Signs and symptoms of perforation include the following: Sudden, severe upper abdominal pain (persisting and increasing in intensity); pain may be referred to the shoulders, especially the right shoulder, because of irritation of the phrenic nerve in the diaphragm. Vomiting and collapse (fainting) Extremely tender and rigid (boardlike) abdomen Hypotension and tachycardia, indicating shock Because chemical peritonitis develops within a few hours after perforation and is followed by bacterial peritonitis, the perforation must be closed as quickly as possible. In a few patients, it may be deemed safe and advisable to perform surgery for the ulcer disease in addition to suturing the perforation. Postoperatively, the stomach contents are drained by means of an NG tube. The nurse monitors fluid and electrolyte balance and assesses the patient for peritonitis or localized infection (increased temperature, abdominal pain, paralytic ileus, increased or absent bowel sounds, abdominal distention). Antibiotic therapy is administered parenterally as prescribed. Pyloric Obstruction Pyloric obstruction, also called gastric outlet obstruction (GOO), occurs when the area distal to the pyloric sphincter becomes scarred and stenosed from spasm or edema or from scar tissue that forms when an ulcer alternately heals and breaks down. The patient has nausea and vomiting, constipation, epigastric fullness, anorexia, and, later, weight loss. In treating the patient with pyloric obstruction, the first consideration is to insert an NG tube to decompress the stomach. Confirmation that obstruction is the cause of the discomfort is accomplished by assessing the amount of fluid aspirated from the NG tube. A residual of more than 400 ml strongly suggests obstruction. Usually an upper GI study or endoscopy is performed to confirm gastric outlet obstruction. Decompression of the stomach and management of extracellular fluid volume and electrolyte balances may improve the patient s condition and avert the need for surgical intervention. A balloon dilatation of the pylorus via endoscopy may be beneficial. If the obstruction is unrelieved by medical management, surgery (in the form of a vagotomy and antrectomy or gastrojejunostomy and vagotomy) may be required. PROMOTING HOME AND COMMUNITY-BASED CARE Teaching Patients Self-Care To manage ulcer disease successfully, the patient is instructed about the factors that will help or aggravate the condition (Chart 37-2). The nurse reviews information about medications to be taken at