Practice nursing care for Clients with Stomach Disorders
Objectives
After studying this chapter, you should be able to:
· Compare etiologies and assessment findings of acute and chronic gastritis.
· Describe the key components of collaborative management for clients with gastritis.
· Compare and contrast assessment findings associated with gastric and duodenal ulcers.
· Identify the most common medical complications that can result from peptic ulcer disease (PUD).
· Analyze assessment data to determine commoursing diagnoses associated with PUD.
· Develop a teaching plan related to drug therapy for clients experiencing PUD.
· Prioritize interventions for clients with upper gastrointestinal bleeding.
· Plan preoperative and postoperative care for the client undergoing gastric surgery.
· Develop a community-based plan of care for clients who have undergone gastric surgery.
· Evaluate outcomes for clients with PUD.
· Explain Zollinger-Ellison syndrome and its associated clinical manifestations.
· Analyze risk factors for gastric carcinoma, including cultural considerations.
· Plan postoperative care for clients who have undergone surgery for gastric cancer.
· Discuss the psychologic and emotional concerns of clients with gastric cancer.
Although only a few diseases affect the stomach, they can be very serious and in some cases life threatening. The most common disorders include gastritis, peptic ulcer disease, Zollinger-Ellison syndrome, and gastric carcinoma (cancer).
GASTRITIS
OVERVIEW
Gastritis is defined as inflammation of the gastric mucosa (stomach lining). It can be diffuse or localized and can be classified according to cause, cellular changes, or distribution of the lesions. Gastritis can be designated as erosive (acute gastritis, stress ulcers) or nonerosive (chronic gastritis). Although the mucosal changes accompanying acute gastritis typically resolve after several months, this is not true for chronic gastritis.
Pathophysiology
Prostaglandins provide a protective mucosal barrier that prevents the stomach from digesting itself by a process called acid autodigestion. If there is a break in the protective barrier, mucosal injury occurs. The resulting injury is compounded byhistamine release and vagal nerve stimulation. Hydrochloric acid can then diffuse back into the mucosa and injure small vessels. This back-diffusion results in edema, hemorrhage, and erosion of the stomach’s lining. The pathologic changes of gastritis include vascular congestion, edema, acute inflammatory cell infiltration, and degenerative changes in the superficial epithelium of the stomach lining.
The early pathologic manifestation of gastritis is a thickened, reddened mucous membrane with prominent rugae, or folds. As the disease progresses, the walls and lining of the stomach thin and atrophy. With progressive gastric atrophy from chronic mucosal injury, the function of the parietal (acid-secreting) cells decreases and the source of intrinsic factor is lost. The intrinsic factor is critical for absorption of vitamin B,2. When body stores of vitamin B,2 are eventually depleted, pernicious anemia results. Theamount and concentration of acid in stomach secretions gradually decrease until the secretions consist of only mucus and water.
Chronic gastritis is associated with an increased risk of gastric cancer as the persistent inflammation extends deep into the mucosa, causing destruction of the gastric glands and cellular changes. Hemorrhage may occur after an episode of acute gastritis or with ulceration caused by chronic gastritis.
ACUTE GASTRITIS Inflammation of the gastric mucosa or submucosa after exposure to local irritants can result in acute gastritis. Various degrees of mucosal necrosis and inflammatory reaction occur in acute disease. The diagnosis cannot be based solely on clinical symptoms without an endoscopic examination. Complete regeneration and healing usually occur within a few days. If the stomach muscle is not involved, complete recovery usually occurs with no residual evidence of gastric inflammatory reaction.
CHRONIC GASTRITIS
Chronic gastritis appears as a patchy, diffuse (spread out) inflammation of the mucosal lining of the stomach. Chronic gastritis usually heals without scarring, but it can progress to hemorrhage and the formation of an ulcer.
Chronic gastritis may be categorized as type A, type B, or atrophic. Type A (nonerosive) chronic gastritis refers to an inflammation of the glands, as well as the fundus and body of the stomach. Type B chronic gastritis usually affects the glands of the antrum but may involve the entire stomach. In atrophic chronic gastritis, diffuse inflammation and destruction of deeply located glands accompany the condition. Chronic atrophic gastritis affects all layers of the stomach, thus decreasing the number of cells. The muscle becomes thickened, and inflammation is present. Chronic atrophic gastritis is characterized by total loss of fundal glands, minimal inflammation, thinning of the gastric mucosa, and intestinal metaplasia (abnormal tissue development).
Etiology
■ ACUTE GASTRITIS
The onset of infection with Helicobacter pylori can result in acute gastritis. H. pylori is a gram-negative, spiral-shaped organism that penetrates the mucosal gel layer of the gastric epithelium. Although it is uncommon, other forms of bacterial gastritis from organisms such as staphylococci, streptococci, Escherichia coli, or salmonella can cause life-threatening consequences such as sepsis and extensive tissue necrosis (Friedman & Peterson, 1998). Other infectious causes of acute gastritis can be found in clients with immunosuppres-sive disorders. In clients with acquired immunodeficiency syndrome (AIDS), for example, gastric erosions can be found with herpes simplex viral infection and disseminated cy-tomegalovirus (CMV) infection.
Nonsteroidal anti-inflammatory drug (NSAID) use poses a risk for the development of acute gastritis. Gastritis occurs in 5% to 25% of NSAID users, but the exact mechanism of the role of NSAIDs in the development of gastritis is not well understood. Other drugs, including alcohol, cytotoxic agents, caffeine, and corticosteroids, have also been implicated; however, scientific evidence is lacking. Acute gastritis is also caused by local irritation from radiation therapy and accidental or intentional ingestion of corrosive substances, including acids or alkalis (such as lye and drain cleaners [Mister Plumber, Drano]). In the client who is allowed nothing by mouth (NPO), gastritis may result from lack of stimulation of normal secretions. Acute stress-induced gastritis, characterized by multiple shallow erosions of the proximal stomach, may be present in 80% to 100% of critically ill clients.
CHRONIC GASTRITIS
Type A gastritis has been associated with the presence of antibodies to parietal cells and intrinsic factor; therefore an autoimmune pathogenesis for this type of gastritis has been proposed. Parietal cell antibodies have been found in 90% of clients with pernicious anemia and in more than one half of individuals with type A gastritis. A genetic link to this disease, with an autosomal dominant pattern of inheritance, has been noted in the relatives of clients with pernicious anemia (Centanni et al., 1999).
The most common form of the disease is type B gastritis, caused by H. pylori infection. There is a direct correlation between the number of organisms and the degree of cellular abnormality present. Although serum antibodies have been isolated in some clients, it is believed that these antibodies are not representative of an autoimmune process but are the result of prolonged inflammation. Fifty percent of clients who have gastric ulcers have associated chronic gastritis.
Chronic local irritation and toxic effects caused by alcohol ingestion, radiation therapy, and smoking have been implicated in the development of chronic gastritis. Surgical procedures that involve the pyloric sphincter, such as the Billroth II procedure, can lead to gastritis by causing reflux of alkaline secretions into the stomach. Other systemic disorders such as Crohn’s disease, graft-versus-host disease, and uremia can also precipitate the development of chronic gastritis.
CHRONIC ATROPHIC GASTRITIS. Atrophic gastritis is a type of chronic gastritis that is seen most often in older adults. It can occur after exposure to toxic substances in the workplace (e.g., benzene, lead, and nickel) or H. pylori infection, or it can be related to autoimmune factors.
Although atrophic gastritis is often present in people with gastric cancer, it is not always considered a precancerous lesion. Gastric carcinoma develops in fewer than 10% of clients who have atrophic gastritis. Chart 56-1 lists guidelines for preventing gastritis.
Incidence/Prevalence
Approximately 2.7 million people in the
CLIENT EDUCATION GUIDE Gastritis Prevention
• Avoid drinking excessive amounts of alcoholic beverages.
• Use caution in taking large doses of aspirin, nonsteroidal
anti-inflammatory drugs (such as ibuprofen), and corti
costeroids. Prolonged use of small doses of cortico
steroids may also cause gastritis.
s Avoid excessive intake of caffeine-containing beverages.
• Avoid eating contaminated foods or drinking contami
nated water.
• Stop smoking.
• Protect yourself against exposure to toxic substances in
the workplace, such as lead and nickel.
• Seek medical treatment if you are experiencing symp
toms of esophageal reflux.
COLLABORATIVE MANAGEMENT
Assessment
PHYSICAL ASSESSMENT/CLINICAL MANIFESTATIONS
Physical assessment findings may include abdominal tenderness and bloating, hematemesis (vomiting blood), or melena (traces of blood in the stool). In stress-induced gastritis, symptoms of intravascular volume depletion and shock may be present.
ACUTE GASTRITIS. Symptoms of acute gastritis can range from mild to severe. Epigastric discomfort, anorexia, cramping, nausea, and vomiting may be present. In some cases, gastric hemorrhage is the presenting symptom (Chart 56-2). The symptoms last only a few hours or days and vary with the cause. Aspirin-related gastritis may result in dyspepsia (heartburn). Gastritis from alcohol abuse may cause vomiting and hematemesis. Gastritis or food poisoning caused by endotoxins, such as staphylococcal endotoxin, has an abrupt onset; severe nausea and vomiting often occur within 5 hours of ingestion of the contaminated food.
CHRONIC GASTRITIS. Chronic gastritis causes few symptoms. Clients may complain of nausea, vomiting, or upper abdominal discomfort. Periodic epigastric pain may simulate ulcer-like distress, which is relieved on ingestion of food. Some clients may have anorexia, and pain may be exacerbated by eating fatty or spicy foods.
DIAGNOSTIC ASSESSMENT
Esophagogastroduodenoscopy (EGD) via an endoscope with biopsy is the gold standard for diagnosing gastritis, as well asdetecting the presence of H. pylori. The health care provider uses biopsy to establish a definitive diagnosis of the type of gastritis. If lesions are patchy and diffuse, biopsy of several suspicious areas may be necessary to avoid misdiagnosis. A cytologic examination of the biopsy specimen is performed to confirm or rule out gastric cancer.
Gastritis
Acute Gastritis
Rapid onset of epigastric pain or discomfort Nausea and vomiting Hematemesis (vomiting blood) Gastric hemorrhageDyspepsia (heartburn) Anorexia
Chronic Gastritis
Vague complaint of epigastric pain that is relieved by food
Anorexia
KEY FEATURES of nausea or vomiting
Intolerance of fatty and spicy foods
Pernicious anemia
Interventions
Clients with gastritis are not often seen in the acute care setting unless they have an exacerbation of acute or chronic gastritis that results in fluid and electrolyte imbalance or bleeding. Management is directed toward supportive care for relieving the symptoms and removing the cause of discomfort.
Acute gastritis is treated symptomatically and supportively because the healing process is spontaneous, usually occurring within a few days. When the cause is removed, pain and discomfort usually subside. If hemorrhage is severe, a blood transfusion may be necessary. Fluid replacement is indicated in clients with severe fluid loss. Surgery, such as partial gastrec-tomy, pyloroplasty, and/or vagotomy, may be indicated for clients with major bleeding or ulceration. Treatment of chronic gastritis varies with the cause. General treatment goals include the eradication of causative agents, treatment of any underlying disease (e.g., uremia, Crohn’s disease), and avoidance of toxic substances (e.g., alcohol, tobacco, nonsteroidal anti-inflammatory drugs [NSAIDs]).
NONSURGICAL MANAGEMENT. The identification and elimination of the causative factors, such as eradication of H. pyloriinfection, is the primary treatment modality. Drugs and diet therapy are also used in the treatment of gastritis.
DRUG THERAPY. In the acute phase, the nurse directs actions toward relief of pain and discomfort. The health care provider may order medications that block and buffer gastric acid secretions to relieve pain.
H2-receptor antagonists are commonly used to block gastric secretions. These agents include ranitidine (Zantac), famo-tidine (Pepcid), and nizatidine (Axid). Sucralfate (Carafate, Sulcrate4^), a mucosal barrier fortifier, may also be prescribed. Antacids used as buffering agents include aluminum hydroxide combined with magnesium hydroxide (Maalox) and aluminum hydroxide combined with simethicone and magnesium hydroxide (Mylanta) (Chart 56-3). The nurse monitors for symptom relief and side effects of these medications and notifies the health care provider of any untoward effects or worsening of gastric distress.
Clients with chronic gastritis may require vitamin B,2 for prevention or treatment of pernicious anemia. If//, pylori is found inbiopsy specimens, the health care provider may treat the infection and reverse or prevent impairment of mucosal defenses. A common drug regimen for H. pylori infection is bismuth subsalicy-lates (Pepto-Bismol), metronidazole (Flagyl, NovonidazoK‘), and tetracycline or ampicillin (Amcill, Ampicin40.
The nurse, health care provider, or pharmacist instructs clients about the medications associated with gastric irritation. Thesemedications include chemotherapeutic agents, corticosteroids, erythromycin (E-Mycin, Erythromid‘*1), and NSAIDs, such asaspirin, indomethacin (Indocin, Novomethacin1^) and ibuprofen (Motrin, Advil, Amersol^, Novo-Profen4*1).
The health care provider may change the dose, frequency, or type of medication if symptoms of gastric irritation appear or persist. The nurse instructs clients to avoid stomach-irritating over-the-counter (OTC) medications, such as aspirin and ibuprofen.
DIET THERAPY. The nurse or dietitian instructs the client with gastric disease to limit intake of any foods and spices
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that cause distress. Tea, coffee, cola, chocolate, mustard, paprika, cloves, pepper, and hot spices may increase discomfort.Alcohol and tobacco should also be avoided.
After the client has an acute episode of gastritis, the nurse helps him or her to identify foods that aggravate discomfort. New foods should be introduced one at a time. Avoidance of substances that cause symptoms is important. Most clients seem to progress better with a soft, bland diet and smaller, more frequent meals.
STRESS REDUCTION. The nurse may assist the client with various techniques that reduce stress and discomfort, such as progressive relaxation, cutaneous stimulation, guided imagery, and distraction. (See Chapter 4 for a discussion of these therapies.)
SURGICAL MANAGEMENT. Partial gastrectomy, py-loroplasty, vagotomy, or even total gastrectomy may be indicated for clients who have major bleeding caused by severe erosive gastritis. Such surgery is necessary only if more conservative measures have not controlled the bleeding. Surgical interventions are discussed under Surgical Management (Peptic Ulcer Disease), p. 1228.
PEPTIC ULCER DISEASE
OVERVIEW
A peptic ulcer is a mucosal lesion of the stomach or duodenum. The term peptic ulcer is used to describe both gastric and duodenal ulcers. Peptic ulcer disease (PUD) results
when gastric mucosal defenses become impaired and no longer protect the epithelium from the effects of acid and pepsin (Figure 56-1).
Pathophysiology
GASTRIC ULCERS
Acid, pepsin, and Helicobacter pylori infection play an important role in the development of gastric ulcers. The gastric mucosal barrier overlies the epithelium. The secretion of mucus and bicarbonate provides a first line of defense in maintaining a near-normal pH on the gastric epithelium and protects the mucosal barrier against acid. Gastromucosal prostaglandins increase the barrier’s resistance to ulceration. The integrity of the barrier is enhanced by the rich blood supply of the mucosa of the stomach and duodenum.
When a break in the mucosal barrier occurs, hydrochloric acid injures the epithelium. Gastric ulcers may then result from back-diffusion of acid or dysfunction of the pyloric sphincter (see Figure 56-1). Without normal functioning and competence of the pyloric sphincter, bile refluxes into the stomach. This reflux of bile acids may break the integrity of the mucosal barrier and produce hydrogen ion back-diffusion, which leads to mucosal inflammation. Toxic agents and bile then destroy the lipid plasma membrane of the gastric mucosa.
Gastric emptying is often delayed in clients with gastric ulceration; this causes regurgitation of duodenal contents, which compounds the gastric mucosal injury. A decreased blood flow to the gastric mucosa may also alter the defense barrier and thereby allow ulceration to occur. Characteristically, gastric ulcers are deep and penetrating, and they usually occur on the lesser curvature of the stomach, near the pylorus (Figure 56-2).
DUODENAL ULCERS
Ninety-five percent of duodenal ulcers occur in the first portion of the duodenum. Duodenal ulcers present as deep, sharply demarcated lesions that penetrate through the mucosa and submucosa into the muscularis propria (muscle layer). The floor of the ulcer consists of a necrotic area residing on granulation tissue and surrounded by areas of fibrosis.
The characteristic feature of a duodenal ulcer is high gastric acid secretion, although a wide range of secretory levels is found. In clients with duodenal ulcers, pH levels are low in the duodenum for long periods. Protein-rich meals, calcium, and vagal excitation stimulate acid secretion. Combined with hypersecretion, a rapid emptying of food from the stomach reduces the buffering effect of food and delivers a large acid bolus to the duodenum (see Figure 56-1). Inhibitory secretory mechanisms and pancreatic secretion may be insufficient to control the acid load.
Figure # The most common sites for peptic ulcers. Figure • The pathophysiology of peptic ulcer.
Up to 95% to 100% of clients with duodenal ulcer disease have confirmed H. pylori infection (Friedman & Peterson, 1998). H. pylori produces substances that damage the gastric mucosa. Urease produced by H. pylori catalyzes the hydrolysis of urea to ammonia. Hydrogen ions are then released in response to the presence of ammonia and contribute further to gastric mucosal damage.
STRESS ULCERS
Stress ulcers are acute gastric mucosal lesions occurring after an acute medical crisis or trauma. Stress ulcers have been associated with head injury, burns, respiratory failure, shock, and sepsis. Bleeding caused by gastric erosion is the principal manifestation of acute stress ulcers.
Multifocal lesions associated with stress ulcers occur in the proximal portion of the stomach and duodenum. These lesions begin as focal areas of ischemia and evolve into erosions and ulcerations that may progress to massive hemorrhage. Little is known of the exact etiology of stress ulcers; however, in the presence of elevated levels of hydrochloric acid, isch-emic areas can progress to erosive gastritis and subsequent ulcerations.
COMPLICATIONS OF ULCERS
The most common complications of PUD are hemorrhage, perforation, pyloric obstruction, and intractable disease.
HEMORRHAGE. Hemorrhage occurs in approximately 15% to 25% of clients with PUD and is the most serious complication (Figure 56-3). It tends to occur more often in clients with gastric ulcers and in older adults. Of those with an initial bleed, 40% experience a recurrence of bleeding if underlying infection with H. pylori remains untreated or if therapy does not include an H2 antagonist. With massive bleeding, the client
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vomits bright red or coffee-ground blood (hematemesis). He-matemesis usually indicates bleeding at or above the duodeno-jejunal junction (upper gastrointestinal [GI] bleeding).
Minimal bleeding, from ulcers is manifested by occult blood in a tarry stool (melena). Melena may occur in clients with gastric ulcers but is more common in those with duodenal ulcers. Gastric acid digestion of blood typically results in a granular dark vomitus (coffee-ground appearance); the digestion of blood within the duodenum and small intestine may result in a black stool.
PERFORATION. Perforation into the peritoneal cavity occurs in approximately 2% to 3% of clients with duodenal ulceration. Simultaneous hemorrhage accompanies perforation in 10% of clients and carries a 6% to 7% mortality rate (Blackington, 1999). In clients with perforation, the gastro-duodenal contents (acid peptic juice, bile, and pancreatic juice) empty through the anterior wall of the stomach or duodenum into the peritoneal cavity. Sudden, sharp pain begins in the mid-epigastric region and spreads over the entire abdomen. The amount of pain correlates with the amount and type of GI contents spilled. The characteristic pain causes theclient to be apprehensive. The abdomen is tender, rigid, and boardlike, and the client assumes the knee-chest position in an attempt to decrease the tension on the abdominal muscles. The client may become desperately ill within hours. Chemical peritonitis soon occurs; bacterial septicemia and hypovo-lemic shock follow. Peristalsis diminishes, and paralytic ileus develops. Peptic ulcer perforation is considered a surgical emergency.
PYLORIC OBSTRUCTION. Pyloric obstruction occurs in 2% to 4% of clients and is manifested by vomiting caused by stasis and gastric dilation. Obstruction occurs at the pylorus (the gastric outlet) and is caused by scarring, edema, inflammation, or a combination of these factors.
Symptoms of gastric outlet obstruction include abdominal bloating, nausea, and vomiting. When vomiting persists, the client may experience hypochloremic (metabolic) alkalosis from loss of large quantities of acid gastric juice (hydrogen and chloride ions) in the vomitus. Hypokalemia may also result from the vomiting or metabolic alkalosis. The health care provider typically hospitalizes the client so he or she may receive intravenous (IV) fluid and electrolyte replacement.
INTRACTABLE DISEASE. One third of all clients with ulcers have a single episode with no recurrence. Intractability may develop from complications of ulcers, excessive stressors in the client’s life, or an inability to adhere to long-term therapy. The client no longer responds to conservative management, or recurrences of symptoms interfere with activities of daily living (ADLs). In general, the client continues to have recurrent pain and discomfort despite treatment. Clients who fail to respond to traditional treatments or who have a relapse following discontinuation of therapy should be referred to a gastroenterologist.
Etiology
Peptic ulcer development is primarily associated with non-steroidal anti-inflammatory drug (NSAID) use and bacterial infection withH. pylori. NSAIDs (such as aspirin or ibupro-fen) break down the mucosal barrier and disrupt the mucosal protection mediated systemically by cyclooxygenase (COX) inhibition. In addition, NSAIDs cause the depletion of endogenous prostaglandins, resulting in local gastric mucosal injury. The risk of developing PUD is 5 to 20 times higher in individuals who use NSAIDs than in the general population (Graham et al., 1999c). GI complications from NSAID use can occur at any time, even after long-term uncomplicated use. NSAID-related ulcers are difficult to treat, even with long-term therapy, since these ulcers have a high rate of recurrence.
Certain drugs may contribute to gastroduodenal ulceration by altering gastric secretion, producing localized damage to mucosa and interfering with the healing process. Theophyl–line (Theo-Dur) and caffeine stimulate hydrochloric acid production. Caffeine may contribute to vascular stasis and mucosal anoxia. The use of corticosteroids is also associated with an increased incidence of peptic ulceration.
H. pylori infection is transmitted from person to person, but exactly how this transmission takes place remains unknown. In one study, H. pylori was successfully cultivated from vomitus and occasionally from stool and saliva, indicating that the organism may be transmissible during GI tract illness, particularly if the person is vomiting (see the Evidence-Based Practice for Nursing box on p. 1222).
Incidence/Prevalence
In the
The purpose of this study was to determine how humans shed the organism Helicobacter pylori into the environment. A controlled clinical experiment involving healthy volunteers recruited through advertisement was conducted from February through December 1998. All subjects meeting eligibility criteria underwent serum immunoglobulin G (IgG) and
The H. py/ori-infected subjects were given a cathartic (sodium phosphate) and an emetic (ipecac). One uninfected control subject also underwent the emesis portion of the experiment. Stool samples were collected during the 8 hours following cathartic administration. Following an overnight fast, subjects were administered 5 mL of ipecac followed by 480 mL of water. A saliva sample was obtained before and following emesis. Air samples were tested throughout the emesis period by using agar plates with a Fluoropore filter covering half of the plate’s diameter. A new plate was replaced every 30 minutes. Ten subjects had a second air sampler placed 1.2 m away to determine the radius of bacterial aerosolization. The 10 uninfected subjects provided normal stool and saliva samples.
All vomitus samples from infected subjects grew H. pylori, often in high quantities. Air samples taken during vomiting episodes grew H. pylori in 37.5% of infected subjects. Saliva tested before and after vomiting grew small quantities of H. pylori. Only 22 (21.8%) of 101 stools from infected subjects grew the organism, and no stools or other samples from uninfected subjects contained H. pylori.
Critique. Although the sample in this case control study is relatively small, this study provides intriguing evidence of the presence and possible routes of transmission of H. pylori.
Implications for Nursing. Since H. pylori can be cultured from both vomitus and stools of healthy H. py/ori-infected individuals, there may be implications for modifications iursing practice and client education. Since much of the culture grew from vomitus, episodes of emesis could be a mechanism for the spread of H. pylori into the environment by means of gastric-oral transmission. Organisms are also dispersed into the air during periods of emesis. H. pylori was also cultured from saliva of infected individuals, inferring an oral-oral transmission. Since transmission of H. pylori has been demonstrated to occur under conditions that induce vomiting, further research is needed to determine the extent of nursing interventions necessary during episodes of gastrointestinal illness to prevent spread of the organism. Furthermore, as more is learned about H. pylori transmission, client education initiatives to prevent spread within households may also be necessary.
CONSIDERATIONS FOR OLDER ADULTS
Both duodenal and gastric ulcers occur more often following the sixth decade of life. Older adults tend to use over-the-counter (OTC) remedies, often delaying appropriate treatment for symptoms of PUD. In addition, they often suffer from one or more chronic illnesses that require the use of medications that can precipitate or worsen PUD. There is also evidence that older adults may be at increased risk for complications and death following acute peptic ulcer bleeding.
CULTURAL CONSIDERATIONS
‘Rates of H. pylori infection are reportedly higher in African Americans and Hispanics. H. pylori infection is also more common in developing countries and among those living in overcrowded living conditions with poor sanitation and water supplies (Blackington, 1999).
COLLABORATIVE MANAGEMENT
Assessment
■ HISTORY
The nurse collects data related to the causes and risk factors for peptic ulcer disease (PUD). The client is questioned about dietary factors that can influence the development of PUD, such as alcohol intake and tobacco use. The nurse notes if certain foods, such as tomatoes, or caffeinated beverages precipitate or worsen symptoms. Information regarding actual or perceived daily stressors is also elicited.
A history of current or past medical conditions focuses on gastrointestinal (GI) tract problems, particularly any history of diagnosis or treatment for H. pylori infection. A complete evaluation of all prescription and OTC medications is obtained. The nurse specifically inquires if the client is taking cortico–steroids, aspirin, or other nonsteroidal anti-inflammatory drugs (NSAIDs). The nurse also asks whether the client has ever undergone radiation treatments.
A history of GI upset, pain and its relationship to eating and sleep patterns, and actions taken to relieve pain is also important. The nurse inquires about any changes in the character of the pain, since this may signal the development of complications. For example, if pain that was once intermittent and relieved by food and antacids becomes constant and radiates to the back or upper quadrant, this may indicate impending ulcer perforation. It is important to note that many individuals with active duodenal or gastric ulcers report having no ulcer symptoms.
PHYSICAL ASSESSMENT/CLINICAL MANIFESTATIONS
Physical assessment findings may reveal epigastric tenderness, usually located at the midline between the umbilicus and the xiphoid process. If perforation into the peritoneal cavity is present, the client will exhibit a rigid, boardlike abdomen accompanied by rebound tenderness. Initially, auscultation of the abdomen may reveal hyperactive bowel sounds, but these may diminish with progression of the disorder.
Dyspepsia (indigestion), which is defined as discomfort centered around the epigastrium or upper abdomen, is the most commonly reported symptom associated with PUD. This pain or discomfort is described as sharp, burning, or gnawing. Some clients may perceive discomfort as a sensation of abdominal pressure or of fullness or hunger. Pain is less often the initial complaint in the older client. In this age-group, melena is often the presenting sign.
Gastric ulcer pain often occurs in the upper epigastrium with localization to the left of the midline and may be accentuated by food. Duodenal ulcer pain is usually located to the right of the epigastrium (Table 56-1). The pain associated with a duodenal ulcer occurs 90 minutes to 3 hours after eating and often awakens the client at night. Pain may also be exacerbated by certain foods (such as tomatoes, hot spices, fried foods, onions, alcohol, or caffeine drinks) and certain medications (such as aspirin, NSAIDs, or corticosteroids).
Vomiting may be a symptom accompanying ulcer disease, most commonly in conjunction with pyloric sphincter dysfunction. It results from gastric stasis associated with pyloric obstruction. Appetite is generally maintained in clients with a peptic ulcer unless pyloric obstruction is present.
To assess for fluid volume deficit, which can occur secondary to bleeding, the nurse takes orthostatic vital signs of all clients suspected of PUD. Orthostatic changes are characterized by a decrease of more than
CRITICAL THINKING CHALLENGE
A client with a long-standing history of rheumatoid arthritis comes to the clinic where you work with complaints of vague, episodic epigastric abdominal discomfort over the last month.
• During the initial interview, what pertinent questions should
you ask regarding this client’s symptoms?
• How might the treatment for arthritis relate to the client’s
symptoms?
• What might you expect to find when assessing this client?
PSYCHOSOCIAL ASSESSMENT
The nurse assesses the impact of ulcer disease on the client’s lifestyle, occupation, family, and social and leisure activities.Questions about lifestyle, occupation, and leisure can yield important information. The nurse evaluates the impact that lifestyle changes will have on the client. This assessment determines the client’s ability to comply with the prescribed treatment regimen and to obtain the needed social support to alter his or her lifestyle.
■ LABORATORY ASSESSMENT
Hemoglobin and hematocrit values may be low, indicating bleeding. The stool specimen may be positive for occult blood if bleeding is present.
RADIOGRAPHIC ASSESSMENT
A barium examination of the GI tract can be used to establish a duodenal ulcer. A duodenal ulcer appears as a discrete crater in the duodenal bulb. This is often the initial test for a client who does not have severe symptoms. If perforation is suspected, the health care provider usually first orders a flat-plate film of the abdomen to identify the presence of free air.
K OTHER DIAGNOSTIC ASSESSMENT
The major diagnostic test for PUD is esophagogastroduo-denoscopy (EGD), which is the most accurate means of establishing a diagnosis. Visualization of the ulcer crater by EGD allows the health care provider to take specimens for H. pylori testing and for biopsy and cytologic studies for ruling out gastric cancer (see the Legal/Ethical Issues in Health Care box on p. 1224). EGD may be repeated at 4- to 6-week intervals while the health care provider evaluates the progress of healing in response to therapy.
Urea breath testing has been employed to detect H. pylori when endoscopy is not clinically indicated. To perform this test, the client must be on NPO status after midnight on the night before the test. The client drinks a carbon-enriched urea solution. The presence of H. pylori will cause the bacteria to break down the solution and release carbon dioxide, which the client inhales in a collection container for analysis. The carbon dioxide excreted in the breath is then measured and compared with a baseline measurement to determine the presence of H. pylori. In addition to its noninvasive nature, this test assesses the entire stomach and may prove especially helpful after the client has been treated to determine if treatment was successful (Blackington, 1999).
A second noninvasive test for H. pylori involves IgG serologic testing. Infection with H. pylori causes immunoglobulin antibodies to form. Although antibody assays have a high sensitivity and specificity (>95%) for detecting H. pylori, antibody assays cannot be used to document eradication of the organism, since antibody levels can remain elevated despite successful treatment.
Legal ETHICAL ISSUES
QUALITY OF CARE FOR MEDICARE CLIENTS WITH PEPTIC ULCER DISEASE
Economic constraints on the health care system have resulted in efforts to provide cost-effective, high-quality care. In an effort to improve the quality of care delivered to Medicare beneficiaries with peptic ulcer disease (PUD), a chart review of 2644 Medicare beneficiaries was conducted to measure compliance with National Institute of Health (NIH) guidelines for the detection and treatment of Helicobacter pylori in PUD.
In this particular study, only 57% of hospitalized Medicare recipients with PUD were tested for H. pylori. In addition, only 74% of clients with known H. pylori infection were treated with appropriate antimicrobial therapy. Medical record review also noted that 74% of clients were screened for nonsteroidal anti-inflammatory drug (NSAID) use. Only 24% had documented counseling regarding the risks associated with NSAID use, and only 2% had documented education of the ulcer-associated risks of NSAID use.
Although limited documented education may be in part to blame for the poor quality of care regarding H. py/ori-related ulcers, NIH clinical practice guidelines for the diagnosis and treatment of peptic ulcer disease are clearly underutilized. Quality improvement initiatives are needed to improve the care delivered to Medicare beneficiaries with PUD. H. pylori screening and treatment guidelines need to be enforced to ensure that appropriate treatment is received, especially by older adults.
A complete medication history needs to be obtained before diagnostic testing is done for H. pylori. False-negative results could be obtained if the client has received antibiotic treatment, used a bismuth preparation (Pepto-Bismol), or used a proton-pump inhibitor within the 4-week period before testing for H. pylori. Other medications, such as misoprostol, su-cralfate, or an H2 blocker administered within the week before the test may also yield a false-negative result. Use of over-the-counter medications (OTC), such as Pepcid AC, Tagamet, and Zantac, can also affect test results.
Analysis
COMMON NURSING DIAGNOSES AND COLLABORATIVE PROBLEMS
The following are priority nursing diagnoses for clients with peptic ulcer disease (PUD):
1. Acute Pain or Chronic Pain related to gastric and/or
duodenal mucosal injury
2. Risk for Deficient Fluid Volume related to hemorrhage
or vomiting
ADDITIONAL NURSING DIAGNOSES AND COLLABORATIVE PROBLEMS
In addition to the commoursing diagnoses, clients with PUD may have one or more of the following:
• Ineffective Therapeutic Regimen Management related to long-term treatment and lifestyle changes
• Ineffective Coping related to intractable progressive
disease
• Imbalanced Nutrition: Less Than Body Requirements
related to anorexia, nausea, or diet constraints
• Disturbed Sleep Pattern related to discomfort
• Risk for Falls related to orthostatic hypotension
• A collaborative problem that could occur is Potential for
Metabolic Alkalosis.
Planning and Implementation
■ ACUTE PAIN; CHRONIC PAIN
PLANNING: EXPECTED OUTCOMES. PUD causes significant discomfort that impacts many aspects of daily living. The client with PUD is expected to experience reduction or alleviation of pain as indicated by self-report.
INTERVENTIONS. Interventions to manage pain related to PUD are accomplished with specific ulcer therapy and dietary modifications. One of the primary purposes for employing drug therapy in the management of PUD is to reduce or eliminate pain. Analgesics are not the mainstay of pain relief for PUD. Instead, the ulcer drug regimen itself promotes relief of pain by eradicatingH. pylori infection and promoting healing of gastric mucosa.
The nurse performs a comprehensive pain assessment that includes the following aspects of pain:
• Location
• Characteristics
• Onset/duration
• Frequency
• Quality
• Severity
• Precipitating and alleviating factors
Any changes in the characteristics or location of peptic ulcer pain are carefully assessed, since such changes often accompany the development of complications. The nurse teaches the client to eliminate factors (such as spicy foods) that can precipitate or increase pain from ulcer disease.
Measures to promote adequate rest and sleep may be necessary, since ulcer pain can cause the client to awaken. The nurse assists the client in achieving compliance with the medication regimen, since adherence to the drug regimen will promote relief of pain and discomfort. The client’s satisfaction with the level of pain relief achieved is monitored.
DRUG THERAPY. The primary goals of drug therapy in the treatment of PUD are (1) to provide pain relief, (2) to eradicate H. pylori infection, (3) to heal ulcerations, and (4) to prevent recurrence (see Chart 56-3). Several different regimens can be used to achieve these goals. In selecting a therapeutic drug regimen, the health care provider must consider the efficacy of the treatment, the anticipated side effects, the ability of the client to comply with the regimen, and the cost of the treatment (Astarita, 1999).
Although numerous drugs have been evaluated for the treatment of H. pylori infection, no single agent has been used successfully against the organism. Current practice involves using a combination of agents to achieve treatment goals. The most successful regimen used is a triple therapy consisting of a bismuth compound, metronidazole, and either amoxicillin or tetracycline. Triple therapy is supple mented by the addition of an H2-receptor antagonist to facilitate ulcer healing and prevent recurrence (see the Cost of Care box above). Although this regimen is the most effective and least expensive, adherence to the regimen is difficult for most clients. A client must consume medications four times daily, and adverse effects occur in 20% to 30% of individuals, especially older adults (Chart 56-4). Recently, some strains of H. pylori have begun to demonstrate metronida-zole resistance, raising concerns about long-term treatment with this regimen.
COST OF CARE
PEPTIC ULCER DISEASE
Cost of Care
• The cost of selected 2-week regimens for the treatment of
Helicobacter pylori-associated peptic ulcer disease (PUD)
ranges from $75 to $215, depending on the extent and
combination of drugs used.
• Treatment of H. py/on-associated PUD decreases the need
for hospitalization secondary to bleeding episodes. This re
duces the economic burden to the health care system.
• The direct and indirect costs of diagnosis and treatment ac
count for $5 billion to $6 billion annually.
• Treatment of H. py/ori-related PUD provides substantial
savings in terms of direct costs (e.g., medications, office
visits) and indirect costs (lost workdays due to the illness).
Implications for Nursing
The treatment of H. py/ori-associated PUD reduces recurrence from 80% to less than 10% in 1 year. However, in clinical practice, appropriate antimicrobial therapy is underutilized. Nurses need to understand the pathogenesis of PUD in order to advocate for appropriate treatment for their clients. In addition, nurses need to educate their clients concerning the role of H. pyloriinfection in ulcer disease in order to assist them in effective management of this disorder.
NURSING FOCUS on the OLDER ADULT
Giving Ulcer Medications Safely
Assess the client’s complete drug regimen. Older adults are more susceptible to adverse side effects from multiple drugs.
Monitor the client carefully for signs of adverse effects. Keep dosage schedules simple when a client is at home. Assess the client’s understanding of instructions related to medications. Provide a written list and instructions for each medication.
HYPOSECRETORY DRUGS. Hyposecretory drugs produce a reduction in gastric acid secretions. These drugs include antisecretory agents, H2-receptor antagonists, and prostaglandin analogs.
ANTISECRETORY AGENTS. Omeprazole (Prilosec), lan-soprazole (Prevacid), and the newest proton pump inhibitor,rabeprazole (Aciphex) suppress the H+,K+–ATPase enzyme system of gastric acid production. These medications are available as sustained-release tablets; therefore they must not be crushed before administration.
H2-RECEPTOR ANTAGONISTS. Drugs that block histamine-stimulated gastric secretions are effective in the management of ulcer disease. These medications may be used for indigestion and heartburn, and lower-dose forms are available in over-the-counter (OTC) products. H2-receptor antagonists block the action of the H2 receptors of the parietal cells, thus inhibiting gastric acid secretion. The most common drugs are ranitidine (Zantac), famotidine (Pepcid), and nizati–dine (Axid). These drugs are typically administered in a single dose at bedtime and are used for 4 to 6 weeks in combination with triple therapy.
PROSTAGLANDIN ANALOGS. Prostaglandins are naturally abundant in the gastrointestinal (GI) tract and have been shown to be effective in clinical trials in the treatment of duodenal ulcers. Prostaglandin analogs reduce gastric acid secretion and enhance gastric mucosal resistance to tissue injury. Misoprostol (Cytotec), the most commonly used drug in this category, prevents NSAID-induced ulcers. Some NSAIDs are being manufactured in combination with misoprostol. A significant adverse effect of this drug is uterine contraction; therefore its use is contraindicated in pregnant women.
ANTACIDS. Antacids buffer gastric acid and prevent the formation of pepsin. Antacids have demonstrated effectiveness in accelerating the healing of duodenal ulcers. Liquid suspensions are the most therapeutic form, but tablets may be more convenient and enhance compliance. The most widely used preparations are mixtures of aluminum hydroxide and magnesium hydroxide, since this combination overcomes the unpleasant GI side effects of either of these preparations when used alone. Mylanta and Maalox are examples of this type of combination antacid formulation. The aluminum and magnesium hydroxide combination products neutralize well at small doses. Aluminum and magnesium-based products must also be administered cautiously to those with renal impairment, since these substances cannot be eliminated adequately by the kidneys and are consequently retained in excessive amounts in the body.
The nurse instructs the client that to achieve a therapeutic effect, sufficient antacid must be ingested to neutralize the hourly production of acid. For optimal effect, antacids are given about 2 hours after meals to reduce the hydrogen ion load in the duodenum. Antacids may be effective from 30 minutes to 3 hours after ingestion. Antacids taken with an empty stomach are quickly evacuated; thus the neutralizing effect is reduced. Calcium carbonate (Turns) is a potent antacid, but it triggers gastrin release, causing a rebound acid secretion. Therefore its use in acid inhibition is not recommended.
Antacids can interact with certain drugs, such as phenytoin (Dilantin), tetracycline, and ketoconazole, and interfere with their effectiveness. The nurse determines what other drugs the client is using before recommending a specific antacid. Medications are administered 1 to 2 hours before or after the antacid. The nurse informs the client that flavored antacids, especially wintergreen, should be avoided. The flavoring increases the emptying time of the stomach; thus the desired effect of the antacid is negated.
The nurse teaches the client with past or present heart failure to avoid antacids containing a high sodium content, such as aluminum hydroxide, magnesium hydroxide, sodium bicarbonate, and simethicone combination products (Gelusil and Mylanta). Magaldrate (Riopan) has the lowest sodium concentration.
MUCOSAL BARRIER FORTIFIERS. Sucralfate (Carafate) is sulfonated disaccharide that forms complexes with proteins at the base of a peptic ulcer. This protective coat prevents further digestive action of both acid and pepsin. Sucralfate does not inhibit acid secretion. Rather, it binds bile acids and pepsins, reducing injury from these substances. Sucralfate may be used in conjunction with H2-receptor antagonists and antacids but should not be administered within 1 hour of the antacid. Sucralfate is given on an empty stomach 1 hour before each meal and at bedtime. The main side effect of this drug is constipation.
DIET THERAPY. The value of diet in the management of ulcer disease is highly controversial. There is no evidence that dietary restriction reduces gastric acid secretion or promotes tissue healing, although a bland diet may assist in relieving symptoms. Food itself acts as an antacid by neutralizing gastric acid for 30 to 60 minutes. An increased rate of gastric acid secretion, called rebound, may follow. If diet therapy is used, it may be directed toward neutralizing acid and reducing hy-permotility, which may alleviate symptoms.
The nurse instructs the client to avoid substances that increase gastric acid secretion. This includes caffeine-containing beverages (coffee, tea, and cola). Both caffeinated and decaffeinated coffees should be avoided, since coffee contains pep-tides that stimulate gastrin release.
In collaboration, the nurse and dietitian teach the client to exclude any foods that cause discomfort. A bland, nonirritat-ing diet is recommended during the acute symptomatic phase. Bedtime snacks are avoided because they may stimulate gastric acid secretion. Eating six smaller daily meals may help, but this regimen is no longer a regular part of therapy. There is no evidence to support the theory that eating six daily meals promotes healing of the ulcer, and this practice actually stimulates gastric acid secretion. Clients should avoid alcohol and tobacco because of their stimulatory effects on gastric acid secretion.
RISK FOR DEFICIENT FLUID VOLUME
PLANNING: EXPECTED OUTCOMES. Fluid volume loss secondary to the development of complications is a risk associated with PUD. Blood loss due to hemorrhage can carry significant morbidity and mortality. Fluid volume loss secondary to vomiting can lead to dehydration and electrolyte imbalances. The client with peptic ulcer disease (PUD) is expected to benefit from prevention or early detection of disease complications.
INTERVENTIONS. Monitoring and early recognition of complications are critical to the successful management of PUD. Interventions aimed at managing complications associated with PUD include prevention and/or management of bleeding, perforation, and gastric outlet obstruction. In some cases, surgical treatment of complications becomes necessary.
HYPOVOLEMIA MANAGEMENT. The purpose of managing hypovolemia is to expand intravascular fluid in a client who is volume depleted. The nurse or assistive nursing personnel monitors vital signs and observes for fluid loss from bleeding or vomiting. The nurse carefully monitors the client’s fluid status, including intake and output. Fluid replacement in older adults should be closely monitored to prevent fluid overload. An infusion pump is used to ensure accurate delivery of the desired volume. Serum electrolytes are also monitored, since depletions from vomiting or nasogastric suctioning must be replaced. The nurse should ensure that two large-bore peripheral IV catheters are inserted so that both fluids and blood lost to vomiting or hemorrhage can be replaced. Volume replacement with isotonic crystalloid solutions (0.9 normal saline solution, or lactated Ringer’s solution) should be started immediately, since adequate fluid volume replacement is essential. The health care provider may order blood products, such as packed red blood cells, to expand volume and correct abnormalities in the complete blood count (CBC). For clients with active bleeding, fresh frozen plasma may be given if the prothrombin time is 1.5 times higher than the midrange control value. To prevent injury from falls secondary to orthostatic hypotension, the client is assisted with ambulation.
BLEEDING REDUCTION: GASTROINTESTINAL. The purpose of interventions to reduce bleeding is to limit theamount of blood loss from the upper and lower gastrointestinal (GI) tract resulting from complications related to PUD. The nurse monitors the client for signs and symptoms indicating GI bleeding. All excretions are observed for the presence of frank or occult bleeding. With GI bleeding, the presence of frank blood or coffee-ground vomitus may be observed. Stools can contain frank blood or appear black and tarry. Occult blood loss may be detected by stool examination and may be accompanied by progressive iron deficiency anemia.
The nurse monitors the client’s hematocrit, hemoglobin, and coagulation studies for changes from the baseline measurements. The nurse or assistive nursing personnel monitors vital signs. With mild bleeding (less than 500 mL), slight feelings of weakness and mild perspiration may be present. When blood loss exceeds 1 L/24 hr, signs and symptoms of shock may be manifested, such as hypotension, chills, palpitations, diaphoresis, and a weak, thready pulse. (See Chapter 38 for the treatment of shock.)
The nurse immediately notifies the health care provider of major bleeding. Transfusion therapy may be required to replace blood loss. (See Chapter 40 for nursing interventions for clients undergoing blood transfusion.) The health care provider may order H2blockers to avoid extremes in gastric pH levels. If appropriate and as ordered, the nurse inserts a nasogastric (NG) tube, monitors secretions, and performs nasogastric lavage to decompress the stomach and alleviate bleeding. In addition, the client and family are instructed to avoid the use of anti-inflammatory medications that can precipitate or worsen GI bleeding.
NONSURGICAL MANAGEMENT. Because prevention or early detection of complications is critical in obtaining a satisfactory outcome, the nurse monitors the client carefully and immediately reports changes to the health care provider. The type of nonsurgical intervention selected will depend on the type and severity of the complication. The goals of therapeutic interventions for bleeding secondary to PUD are as follows:
· Cessation of the acute bleeding episode
· Prevention of rebleeding
INTERVENTION ACTIVITIES/or The Client with Stomach Disorders
Hypovolemia Management: The expansion of intravascular fluid volume in a client who is volume depleted
• Monitor vital signs, as appropriate.
• Monitor fluid status, including intake and output, as
appropriate.
• Monitor for fluid loss (e.g., bleeding, vomiting, diarrhea,
perspiration, and tachypnea).
• Arrange availability of blood products for transfusion, if
necessary.
• Administer blood products (e.g., platelets and fresh
frozen plasma), as appropriate.
• Monitor for blood reaction, if appropriate.
Bleeding Reduction: Gastrointestinal: The limitation of the amount of blood loss from the upper and lower gastrointestinal tract and related complications
• Monitor for signs and symptoms of persistent bleeding
(e.g., check all secretions for frank or occult blood).
• Hematest all excretions and observe for blood loss in
emesis, sputum, feces, urine, nasogastric drainage, and
wound drainage, as appropriate.
• Document color, amount, and character of stools.
• Monitor coagulation studies and complete blood count
(CBC) with WBC differential.
• Insert nasogastric tube to suction and monitor secre
tions, if appropriate
• Perform nasogastric lavage, as appropriate.
• Avoid extremes in gastric pH level by administration of
appropriate medication (e.g., antacids or histamine-2
blocking agent).
• Instruct the client and/or family on the need for blood re
placement, as appropriate.
• Instruct the client and/or family to avoid the use of anti-
inflammatory medications (e.g., aspirin and ibuprofen).
A combination of several different therapeutic interventions, including endoscopic therapy, acid suppression, NG tube placement, and saline lavage, can be used to control acute bleeding and prevent rebleeding. Therapeutic trials have been conducted to determine the optimal treatment for bleeding due to peptic ulcers. Endoscopic therapy and suppression of gastric acid are the primary therapies used to control active bleeding caused by PUD. H2-receptor antagonists, proton pump inhibitors, and antacids are the primary medications used to treat this bleeding.
ENDOSCOPIC THERAPY. Endoscopic therapy via an esophagogastroduodenoscopy (EGD) can assist in achieving homeostasis during an acute bleeding episode. The three primary methods of endoscopic therapy are (1) thermal contact using a heater probe or multi-electrocoagulation, (2) injection of the bleeding site with diluted epinephrine or a sclerosing agent (alcohol), and (3) laser therapy. All three methods are effective in achieving blood clot formation. Thermal contact and injection are most commonly used. Laser therapy is costly and therefore is used less often. Endoscopic therapy is most beneficial for clients with active bleeding; however, persistent or re-bleeding despite endoscopic therapy continues to be problematic. No consensus has been reached on the appropriate management of re-bleeding.
ACID SUPPRESSION. Aggressive acid suppression is used to prevent re-bleeding. When acute bleeding is stopped and clot formation has taken place within the ulcer crater, the clot remains in contact with gastric contents. Acid-suppressive agents are used to stabilize the clot by raising the pH level of gastric contents. Several drugs are used to achieve acid suppression in clients with a bleeding episode. H2-receptor antagonists prevent acid from being produced by parietal cells. Proton pump inhibitors prevent the transport of acid across the parietal cell membrane, whereas antacids buffer acid produced in the stomach.
NASOGASTRIC TUBE PLACEMENT. Upper GI bleeding may require the health care provider or nurse to insert a nasogastric (NG) tube to:
Ascertain the presence or absence of blood in the stomach
Assess the rate of bleeding
Prevent gastric dilation
Administer saline lavage
Nasogastric aspiration is an important part of diagnostic and prognostic evaluation of the client. The presence of red blood in emesis, nasogastric aspirate, or stools is correlated with a poor outcome (Terdiman, 1998).
Once the NG tube is placed, confirmation of proper positioning of the tube is determined by x-ray examination. The nurse irrigates the NG tube to maintain its patency and prevent obstruction with clotted blood.
SALINE LAVAGE. Saline lavage requires the insertion of a large-bore NG tube with instillation of saline in volumes of 50 to 200 mL. The saline and blood are repeatedly withdrawn until returns are clear or light pink and without clots. For protection against exposure to blood, practitioners may use the following procedure with a closed system for irrigation and suction. A Y-connector is attached to the NG tube, and an IV bag of normal saline is attached to tubing at one end of the Y-connector. The opposite connector is attached to tubing connected to wall suction. After the stomach is initially drained by suctioning, the tubing attached to the wall suction is clamped off, and up to 200 mL of normal saline is allowed to drain into the client through the NG tube. After the saline is instilled, the tube connecting the saline to the NG tube is clamped off, and the clamp to suction is released. The nurse instructs the client to lie on the left side during this procedure to limit the flow of saline out of the stomach and prevent aspiration.
NONSURGICAL MANAGEMENT OF PERFORATION.
To prevent peritonitis from GI contents that have entered the peritoneum, perforation is managed by the immediate replacement of fluid, blood, and electrolytes and the administration of antibiotics. The nurse maintains nasogastric suction to drain gastric secretions and thus prevent further peritoneal spillage. The client remains on NPO status, and the nurse carefully monitors intake and output. The nurse or assistive nursing personnel checks vital signs at least hourly and monitors the client for clinical manifestations of septic shock, such as fever, pain, tachycardia, lethargy, or anxiety.
NONSURGICAL MANAGEMENT OF PYLORIC OBSTRUCTION. Pyloric obstruction is caused by edema, spasm, or scar tissue. Symptoms of obstruction related to difficulty in emptying the stomach include feelings of fullness, distention, or nausea after eating, as well as vomiting of copious amounts of undigested food.
Treatment of obstruction is directed toward restoration of fluid and electrolyte balance and decompression of the dilated stomach. Obstruction related to edema and spasm generally responds to medical therapy. First, the stomach must be decompressed with nasogastric suction; next, interventions are directed at correcting metabolic alkalosis and dehydration. The NG tube is clamped after about 72 hours, and the client is checked for retention of gastric contents. If the amount retained is not more than 350 mL in 30 minutes, the health care provider may allow oral fluids. In some cases, surgical intervention may be required.
CRITICAL THINKING CHALLENGE
Your client has been diagnosed with a nonsteroidal anti-inflammatory drug (NSAID)-induced duodenal ulcer, and the presence ofH. pylori infection has been confirmed.
• What complications of peptic ulcer disease (PUD) is this
client most at risk for?
• What dietary instructions should you give to this client?
• What should you teach this client about the medical treat
ment for PUD?
SURGICAL MANAGEMENT. New guidelines for the treatment of PUD that include H. pylori eradication and the development of nonsurgical means of controlling bleeding have led to a decline in the need for surgical intervention. In PUD, surgical intervention is used to:
• Reduce the acid-secreting ability of the stomach
• Treat clients who do not respond to medical therapy
• Treat a surgical emergency that develops as a complica
tion of PUD
PREOPERATIVE CARE. Before surgery, an NG tube is inserted and connected to suction to remove secretions and empty the stomach. This allows surgery to take place without contamination of the peritoneal cavity by gastric secretions. Chart 56-6 describes the procedure for inserting the NG tube and nursing care associated with NG tube maintenance. The NG tube remains in place postoperatively to prevent the accumulation of secretions, which may lead to vomiting or gastrointestinal (GI) distention and pressure on the suture line.
Other preoperative nursing measures for the client undergoing gastric surgery are the same as those for any client undergoing abdominal surgery and general anesthesia (see Chapter 17).
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OPERATIVE PROCEDURES. There is no definitive single procedure for PUD. The most commonly performed surgical procedures are gastroenterostomy, vagotomy and pyloroplasty.
Gastroenterostomy. A simple gastroenterostomy permits neutralization of gastric acid by regurgitation of alkaline duodenal contents into the stomach. The surgeon creates a passage between the body of the stomach and the small bowel, often the jejunum (Figure 56-4). The benefit may be offset by interference with acid inhibition of gastrin release, which results in a net increase in acid secretion.
If the gastroenterostomy drains the stomach, it reduces motor activity in the pyloroduodenal area. Drainage of the gastric contents diverts acid from the ulcerated area and facilitates healing. However, the secretory capacity of the parietal cell mass of the stomach has not been reduced, and the gastrin mechanism continues to function. For this reason, a vagotomy is usually combined with gastroenterostomy for reduction of the vagal influences.
Vagotomy. Three types of vagotomy have been used in the treatment of duodenal ulcers: truncal vagotomy, selective vagotomy, and proximal gastric vagotomy (Figure 56-5). Vagotomy eliminates the acid-secreting stimulus to gastric cells and decreases the responsiveness of parietal cells. In a truncal vagotomy, the vagal trunks are transected and the antrum is removed. The remaining stomach is anastomosed to the proximal duodenum (Billroth I) or to a loop of jejunum (Billroth II) (Figures 56-6 and 56-7).
With selective vagotomy, only the branches of the vagus nerve that supply the stomach are transected; the remaining abdominal viscera still has intact vagal innervation. Selective vagotomy results in a more complete response, reduced ulcer recurrence, and fewer postoperative complications.
Proximal gastric vagotomy interrupts the nerve supply to only the acid-secreting portion of the stomach; it spares the branches of the vagus nerve that innervate the antrum, making pyloroplasty unnecessary.
Pyloroplasty. The surgeon often performs pyloroplasty in conjunction with a vagotomy to widen the exit of the pylorus. This facilitates emptying of stomach contents. The most common procedure is the Heineke-Mikulicz pyloroplasty (Figure 56-8). In this procedure the surgeon enlarges the py-loric stricture by incising the pylorus longitudinally and sutures the incision transversely.
POSTOPERATIVE CARE. The postoperative care is similar for all of the surgical procedures (see the Client Care Plan on p. 1231). The nurse provides the usual postoperative care for clients who have had general anesthesia (see Chapter 19).
In addition, the nurse monitors the client for the development of postoperative complications.
Nasogastric Tube Management. The nurse monitors the nasogastric (NG) tube for patency and carefully secures the tube to prevent dislodgment; this is critical for preventing the retention of gastric secretions. The nurse monitors the client to make sure that no more than a scant amount of blood drains from the tube and that abdominal distention does not develop. If these problems occur, the nurse reports them immediately to the surgeon. Irrigation or repositioning of the NG tube is not done after gastric surgery unless specifically ordered by the surgeon.
Monitoring for Postoperative Complications. The nurse observes the client carefully for possible complications and reports them immediately to the health care provider. In the immediate postoperative period, many complications may occur. Table 56-2 summarizes surgical procedures and potential complications.
A disruption in the patency of the NG tube can result in acute gastric dilation postoperatively; this is manifested by epigastric pain and a feeling of fullness, hiccups, tachycardia, and hypotension. Irrigation or replacement of the NG tube by order of the surgeon can relieve these symptoms.
Dumping syndrome is a term that refers to a constellation of vasomotor symptoms after eating, especially following a Billroth II procedure. This syndrome is believed to occur as a result of the rapid emptying of gastric contents into the small intestine, which shifts fluid into the gut, causing abdominal distension. The nurse observes for early manifestations of this syndrome, which typically occurs within 30 minutes of eating. Symptoms include vertigo, tachycardia, syncope, sweating, pallor, palpitations, and the desire to lie down.
Late dumping syndrome, which occurs 90 minutes to 3 hours after eating, is caused by a release of an excessive amount of insulin. The insulin release follows a rapid rise in the blood glucose level that results from the rapid entry of high-carbohydrate food into the jejunum. The nurse observes for intestinal manifestations, including dizziness, lighthead-edness, palpitations, diaphoresis, and confusion.
Dumping syndrome is managed by dietary measures that include decreasing the amount of food taken at one time and eliminating liquids ingested with meals. In collaboration with the dietitian, the nurse instructs the client to consume a high-protein, high-fat, low-carbohydrate diet (Table 56-3). Pectin administered in the form of a dry powder may prevent the syndrome. A somatostatin analog, octreotide, may be ordered in severe cases.
Alkaline reflux gastropathy, also known as bile reflux gas-tropathy, is a complication of gastric surgery in which the pylorus is bypassed or removed (e.g., pyloroplasty, gastric resection with gastroduodenostomy [Billroth I procedure], and gastrojejunostomy [Billroth II procedure]). Endoscopic examination reveals regurgitated bile in the stomach and mu-cosal hyperemia. Symptoms include early satiety, abdominal discomfort, and vomiting.
Delayed gastric emptying is often present after gastric surgery and usually resolves within 1 week. Edema at the anastomosis or adhesions obstructing the distal loop may be mechanical causes. Metabolic causes (such as hypokalemia, hypoproteinemia, or hyponatremia) should be considered. The edema is resolved with nasogastric suction, maintenance of fluid and electrolyte balance, and proper nutrition.
Afferent loop syndrome may occur when the duodenal loop is partially obstructed after a Billroth II resection. Pancreatic and biliary secretions fill the intestinal loop, which becomes distended. Painful contractions attempt to propel these secretions from the loop. The nurse monitors for clients reporting abdominal bloating and pain 20 to 60 minutes after eating, often followed by nausea and vomiting. Treatment consists of surgical correction of the incomplete loop obstruction.
Recurrent ulceration occurs in approximately 5% of clients who have undergone gastric surgery for PUD. Recurrent ulcers can be due to incomplete vagotomy or persistent H. pylori infection. Recurrence is most common following vagotomy with antrectomy, and ulcerations tend to occur at the site of anastomosis (stomal or marginal ulcer) or immediately distal in the small intestine. Abdominal pain, usually located in the epigastrium, is the most commonly reported symptom of recurrent peptic ulcer. The health care provider may order H2-receptor antagonists and proton pump inhibitors to assist with the healing process. The eradication of H. pylori in the case of recurrent stomal ulcerations is controversial.
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NUTRITIONAL MANAGEMENT. Several problems related to nutrition develop as a result of partial removal of the stomach, including deficiencies of vitamin B12, folic acid, and iron; impaired calcium metabolism; and reduced absorption of calcium and vitamin D. These problems are caused by a shortage of intrinsic factor. The shortage results from the resection and from inadequate absorption because of rapid entry of food into the bowel. In the absence of intrinsic factor, clinical manifestations of pernicious anemia occur. The nurse should assess for the development of atrophic glossitis secondary to vitamin B12 deficiency. In atrophic glossitis, the tongue takes on a shiny and “beefy” appearance. The client may also have signs of anemia secondary to folic acid andiron deficiency. The nurse monitors the complete blood count (CBC) for signs of megaloblastic anemia and leukopenia. These manifestations are corrected by the administration of vitamin B12. The health care provider may also prescribe folic acid or iron preparations.
Community-Based Care
Clients may be discharged from the hospital as long as there is no evidence of ongoing bleeding, orthostatic changes, or car-diopulmonary distress or compromise. Clients discharged following treatment for peptic ulcer disease (PUD) and/or complications secondary to the disease must face several challenges in order to manage the disease successfully. Long-term adherence to medication regimens requires the client to take many oral medications on a daily basis. Permanent lifestyle alterations in dietary habits must also be made. Clients must be knowledgeable about complications related to PUD and know when to report symptoms to the health care provider.
HOME CARE MANAGEMENT
Clients are discharged to the home, subacute unit, or skilled nursing facility to continue recuperation. Clients who have undergone surgery or have had complications, such as hemorrhage, may require visits from a home care nurse to assess clinical progress.
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HEALTH TEACHING
The primary focus of home care preparation is client teaching regarding risk factors for the recurrence of PUD; clients are alsotaught to recognize and report the development of complications related to the disease process or surgical intervention.
The nurse instructs the client and family or significant others about factors related to the development of an ulcer. A risk assessment assists in identifying gastric irritants and lifestyle stres-sors that may be contributory to ulcer formation. Strategies forlifestyle changes are developed together with the client. The nurse teaches about symptoms that should be brought to the attention of the health care provider after discharge from the hospital, such as abdominal pain; nausea and vomiting; black, tarry stools; and weakness or dizziness. To demonstrate understanding, the client describes the symptoms back to the nurse.
The nurse also teaches the client about diets to be used for avoiding postprandial distention or dumping syndrome. Forpostsurgical clients, especially those who have undergone partial stomach removal, a smaller meal may be required. In collaboration with the dietitian, the nurse instructs the client to:
• Eat small, frequent meals
• Avoid drinking liquids with meals
• Abstain from foods that contribute to discomfort
• Eliminate caffeine and alcohol consumption
• Begin a smoking cessation program
• Receive B12 injections, as appropriate
The client is also taught to avoid any over-the-counter (OTC) product containing aspirin or ibuprofen. The nurse emphasizes the importance of adhering to the treatment regimen. Long-term medication compliance is critical for eradicating H. pylori infection and achieving healing of the ulcer. The importance of keeping all follow-up appointments is also emphasized, since early detection of recurrence or the development of complications is desirable.
The nurse helps the client to identify situations that cause stress, describe feelings during stressful situations, and develop a plan for coping with stressors (Chart 56-7). The nurse encourages the client to learn and use relaxation techniques, such as exercise, biofeedback, humor, and imagery (see Chapter 4). Psychotherapy may be indicated to help some clients cope with excessive anxiety or stress. Ulcer disease is difficult to eradicate, so it is essential for the client and family to understand how modifying living, working, and eating habits minimizes the risk of ulcer recurrence.
HEALTH CARE RESOURCES
Following discharge, home care nursing visits may be indicated if clients and family members or significant others require instruction or assistance with follow-up care, such as dressing changes, monitoring of potential complications, and continued nutritional problems.
Evaluation: Outcomes
The nurse evaluates the care of the client with peptic ulcer disease (PUD) on the basis of the identified nursing diagnoses and collaborative problems. The expected outcomes are that the client:
• Maintains hemodynamic stability, free of disease or sur
gical complications
• States that pain is reduced or alleviated by prescribed
interventions
• Identifies potential causes and risks of disease recurrence
• Avoids the intake of irritating foods and beverages
• Avoids smoking
• Avoids over-the-counter medications containing aspirin
or ibuprofen
• Identifies early symptoms of recurrence or complications
• Identifies and copes successfully with stressful situations
• Adheres to long-term medication regimen and appropri
ate follow-up with the health care provider
FOCUSED ASSESSMENT of Ambulatory Care with Ulcer Disease
Assess gastrointestinal and cardiovascular status, including:
• Vital signs, including orthostatic vital signs
• Skin color
• Presence of abdominal pain (location, severity, charac
ter, duration, precipitating factors, and relief measures)
• Character, color, and consistency of stools
• Changes in bowel elimination pattern
• Hemoglobin and hematocrit
• Bowel sounds; palpate for areas of tenderness
Assess nutritional status, including:
• Dietary patterns and habits
• Intake of caffeine and alcohol
• Relationship of food to symptoms
Assess medication history.
• Use of steroids
• Use of nonsteroidal anti-inflammatory drugs (NSAIDs)
• Use of over-the-counter medications
Assess client’s coping style
• Recent stressors
• Past coping style
Assess client’s understanding of illness and ability to comply with therapeutic regimen.
• Symptoms to report to health care provider
• Expected and side effects of medications
• Food and drug interactions
• Need for smoking cessation
ZOLLINGER-ELLISON SYNDROME
OVERVIEW
Zollinger-Ellison syndrome (ZES) is manifested by upper gastrointestinal (GI) tract ulceration, increased gastric acid secretion, and the presence of a non-beta cell islet tumor of the pancreas, called a gastrinoma. Affected individuals may have more than one gastrinoma. Approximately two thirds of gastri-nomas are malignant. Recent developments indicate that a benign but aggressive form of the disease may exist (Yu et al., 1999). Although most gastrinomas grow slowly, a small portion of them develop rapidly and metastasize widely. Metastasis occurs mainly in the liver and regional lymph nodes. Gastrinoma remains a relatively uncommon disease, with an incidence of 1 to 3 new cases per year per million people.
In 20% to 60% of clients with ZES, the gastrinoma results from an autosomal dominant disorder called multiple endocrine neoplasia type 1 (MEN-1) syndrome. Gastrinomas contain multiple hormones, but adrenocorticotropic hormone (ACTH) is most commonly found. As a result, Cushing’s syndrome with increased ACTH levels is reported in approximately 8% of clients with ZES.
In the early course of the disease, symptoms resemble those of peptic ulcer disease (PUD). However, these symptoms tend to progress, and they respond poorly to traditional ulcer therapy. Diarrhea may be a manifestation of this disorder, occurring in 40% of clients. The diarrhea may be associated with large amounts of hydrochloric acid secreted into the proximal duodenum. Steatorrhea(an excessive amount of fat in the feces) results from the inactivation of pancreatic lipase secondary to the large concentrations of acid and decreased amounts of bile acids.
COLLABORATIVE MANAGEMENT
Assessment
Radiographic and endoscopic findings for ZES are similar to those for PUD. However, infection with Helicobacter pylori is usually absent. The diagnosis is usually made by radioim-munoassay studies that reveal increased serum gastrin levels in conjunction with the clinical features of the disease.
Interventions
The aim of therapy is to suppress acid secretion in order to control the client’s symptoms. The H+,K+–ATPase inhibitors, such as lansoprazole and omeprazole (given as 60 mg/day in a single dose) are the drugs of choice to reduce gastric acid secretion and heal ulcers in clients with ZES. However, long-term treatment with these drugs can lead to significant decreases in vitamin B12 levels (Termanini et al., 1998). High doses of H2-receptor antagonists, such as ranitidine (Zantac), are also effective in reducing gastric acid and providing symptom relief.
If medical therapy fails, the health care provider may choose to perform a vagotomy and pyloroplasty to supplement pharmacologic means of controlling hypersecretion. A total gastrectomy is the surgical approach of choice for this disorder if vagotomy, pyloroplasty, and medical therapy are inadequate. (See the earlier discussion of these surgeries under Surgical Management [Peptic Ulcer Disease], p. 1228.)
The consequences of the malignant properties of the tumor are now being more widely recognized, and complete surgical resection of the tumor appears to be the optimal treatment. Clients with aggressive disease can also be treated with chemotherapeutic agents such as 5-fluorouracil and doxoru-bicin to reduce the tumor and control symptoms.
GASTRIC CARCINOMA
OVERVIEW
Gastric carcinoma refers to malignant neoplasms in the stomach. Adenocarcinomas account for 85% to 95% of all gastric cancers (Mayer, 1998, O’Connor, 1999). The remaining 15% are due to non-Hodgkin’s lymphoma and leiomyosarcomas. In the
Pathophysiology
Gastric adenocarcinoma can be characterized as intestinal or diffuse. Intestinal adenocarcinomas result from atrophic gastritis or intestinal metaplasia, both of which are considered precancerous conditions. The diffuse form of the disease is found primarily in areas where gastric cancer is endemic. Early, superficial gastric cancers produce no notable symptoms. On microscopic examination, the cells resemble intestinal metaplasia (abnormal tissue development).
Gastric cancers spread by direct extension through the gastric wall and into regional lymphatics. The intramural lymphatics readily allow horizontal spread within the gastric wall. Extramural lymphatics carry tumor deposits to lymph nodes in more than 50% of operable cases. Direct invasion of and adherence to adjacent organs (e.g., the liver, pancreas, and transverse colon) may also result. Hematogenous spread via the portal vein to the liver and via the systemic circulation to the lungs and bones is the most common mode of metastasis. Peritoneal seeding of cancer cells from the involved gastric serosa to the omentum, peritoneum, ovary, and pelvic cul-de-sac can also occur.
In people with advanced gastric cancer, there is invasion of the muscularis (stomach muscle) or beyond. These lesions are not amenable to curative resection. Most clients in the
Etiology
Recent evidence has provided a strong link between infection with H. pylori and the subsequent development of gastric cancer. Metabolic products produced by the organism transform the gastric mucosa while producing a state of chronic inflammation. Such chronic inflammatory states can induce cancer by increasing cell proliferation and free radical formation.
Clients with pernicious anemia, gastric polyps, chronic atrophic gastritis, and achlorhydria (absence of secretion of hydrochloric acid) are two to three times more likely to develop gastric cancer.
Gastric cancer seems to be positively correlated with the ingestion of pickled foods, salted fish, salted meat, and nitrates from processed foods, as well as a high consumption of salt. The ingestion of these foods over a long period of time can lead to atrophic gastritis, a precancerous condition.
The role of cigarette smoking and alcohol consumption in the development of gastric carcinoma is controversial, although some studies support the conclusion that smokers are 1.5 to 3 times more likely to develop gastric cancer as compared with nonsmokers (O’Connor, 1999).
Genetic factors may play a role in the development of gastric cancer; an increased incidence of the disease has been noted among direct relatives of clients with gastric cancer. First-degree relatives of individuals with gastric cancer are two to three times more likely to develop the disease themselves. In addition, individuals with type A blood appear to have a slight risk of gastric cancer.
Gastric surgery, especially a Billroth II procedure, seems to increase the risk for gastric cancer because of the eventual development of atrophic gastritis, which results in changes to the mucosa. Clients with Barrett’s esophagus have an increased risk of adenocarcinoma of the gastric cardia.
Incidence/Prevalence
Although the incidence of gastric cancer is decreasing in the
CULTURAL CONSIDERATIONS
COLLABORATIVE MANAGEMENT
Assessment
HISTORY
The nurse questions the client regarding the known risk factors for the development of gastric cancer. The nurse elicits information regarding preferred foods, especially pickled, salted, or smoked foods. Information regarding tobacco use and alcohol ingestion is also gathered. The nurse inquires if the client has ever been diagnosed or treated for H. pylori infection, gastritis, or pernicious anemia. The nurse notes if the client has a history of gastric surgery or polyps. The nurse also inquires if any of the client’s immediate relatives have been diagnosed with gastric cancer. If known, the nurse makes a notation of the client’s blood type.
PHYSICAL ASSESSMENT/CLINICAL MANIFESTATIONS
Although clients with early gastric cancer may be asymptomatic, indigestion (heartburn) and abdominal discomfort are the mostcommon symptoms (Chart 56-8). These symptoms are often ignored, however, or a change in diet or use of antacids relieves them. As the tumor grows, these symptoms become more severe and do not respond to diet changes or antacids. Epigastric, back, or retrosternal pain is also an early symptom that may go unrecognized. Two thirds of clients will complain of epigastric pain following eating. This pain is described as a vague feeling of fullness or discomfort (Hawkins, 1999).
In advanced gastric carcinoma, progressive weight loss, nausea, and vomiting can occur. Vomiting represents pronounced dilation, thickening of the stomach wall, or pyloric obstruction. Obstructive symptoms appear earlier with tumors located near the pylorus than with fundic lesions. Clients with advanced disease may have weakness, fatigue, and anemia.
Physical assessment findings in advanced disease may be absent, or a palpable epigastric mass may suggest hepatomegaly from metastatic disease. Hard, enlarged lymph nodes in the left supraclavicular chain, left axilla, or umbilicus may be the result of metastasis from gastric cancer. Masses on the right suggest metastasis in the perigastric lymph nodes or liver. Signs of distant metastasis include the following:
• Virchow’s (sentinel or signal) nodes (enlarged supra-
clavicular lymph nodes, especially on the left)
• Blumer’s shelf, resulting from peritoneal seeding that
produces a firm mass palpable on rectal or vaginal ex
amination
• “Sister Mary Joseph nodes” (subcutaneous periumbilical
deposits)
• Krukenberg’s tumor (metastatic ovariaodules)
LABORATORY ASSESSMENT
In clients with advanced disease, anemia is evidenced by low hematocrit and hemoglobin values. Clients may have macro-cytic or microcytic anemia associated with decreased iron or vitamin B12 absorption.
KEY FEATURES of
Early Versus Advanced Gastric Cancer
EarSy Gastric Cancer
• Indigestion
• Abdominal discomfort initially relieved with antacids
• Feeling of fullness
• Epigastric, back, or retrosternat pain
(NOTE: Many clients with early gastric cancer have no clinical manifestations.)
Advanced Gastric Cancer
• Nausea and vomiting
• Obstructive symptoms
• Iron deficiency anemia
• Palpable epigastric mass
• Enlarged lymph nodes
• Weakness and fatigue
• Progressive weight loss
• Signs of distant metastasis
Virchow’s nodes
Blumer’s shelf
“Sister Mary Joseph nodes” Krukenberg’s tumor
The stool may be positive for occult blood.
Hypoalbuminemia and abnormal results of liver tests (such as bilirubin and alkaline phosphatase) occur with advanced disease and with hepatic metastasis. The level of carcinoem-bryonic antigen (CEA) is elevated in advanced cancer of the stomach.
RADIOGRAPHIC ASSESSMENT
A double-contrast upper gastrointestinal (GI) series is usually the first diagnostic test. The use of a double-contrast medium assists in the detection of small lesions. A polypoid mass, ulcer crater, or thickened fibrotic gastric wall may suggest gastric cancer.
A computed tomography (CT) scan is used to evaluate gastric malignancies. CT scans of the chest, abdomen, and pelvis are used in determining the extent of the disease.
OTHER DIAGNOSTIC ASSESSMENT
The health care provider uses esophagogastroduodenoscopy (EGD) for definitive diagnosis of gastric cancer. The lesion can be visualized directly, and biopsies of all visible lesions can be obtained to determine the presence of cancer cells. During the endoscopy, an endoscopic ultrasound (EUS) of the gastric mucosa can also be performed. This technology allows the health care provider to evaluate the depth of the tumor and the presence of lymph node involvement that permits more accurate staging of the disease.
Interventions
Management of gastric cancer includes drug therapy, radiation, and/or surgery.
NONSURGICAL MANAGEMENT. The treatment of gastric cancer is highly dependent on the stage of the disease. Surgical resection of the tumor is usually combined with chemotherapy and/or radiation. Radiation and chemotherapy commonly prolong survival of clients with advanced gastric disease.
DRUG THERAPY. The role of chemotherapy in gastric cancer remains uncertain. No specific chemotherapeutic protocol has had a positive effect on survival. Chemotherapy with single agents such as fluorouracil (5-FU), doxorubicin, mitomycin-C, cisplatin, and etoposide have been used, but the use of a combination of agents appears to have superior results. Bone marrow suppression, nausea, and vomiting are common side effects. Chapter 25 discusses chemotherapy in detail.
RADIATION THERAPY. Although gastric cancers are somewhat sensitive to the effects of radiation, the use of this treatment is limited, since the disease is often widely disseminated to other abdominal organs on diagnosis. Organs such as the liver and kidneys, as well as the spinal cord, have limits as to the amount of radiation they can endure. Postoperative radiation has not significantly increased survival. Intra-operative radiotherapy (IORT) is available at only a few institutions in the
The most common side effects experienced by clients undergoing radiation include impaired skin integrity, fatigue, and anorexia. Nausea, vomiting, and diarrhea may occur approximately 1 week after treatment is initiated and diminish a month or more after treatment ends. (See Chapter 25 for more information on radiation therapy.) The most common potential problems of IORT are hemorrhage and fistula development.
SURGICAL MANAGEMENT. Surgical resection is the preferred method for treating gastric cancer. The primary surgical procedures for the treatment of gastric cancer are total gastrectomy and subtotal gastrectomy. In early stages, surgery plus adjuvant chemotherapy or radiation may be curative. Most clients with advanced disease are candidates for palliative surgical treatment. Metastasis in the supraclavicular lymph nodes (Virchow’s nodes), inguinal lymph nodes, liver, umbilicus, or perirectal wall indicates that the opportunity for cure by resection has been lost. Palliative resection may significantly improve the quality of life for a client suffering from obstruction, hemorrhage, or pain.
PREOPERATIVE CARE. The health care provider gives the client and family an explanation of the disease and the available treatment options (potentially curative or palliative). The nurse reinforces and clarifies the information given. Pre-operative care is similar to that provided for the client undergoing general anesthesia and abdominal surgery (see Chapter 17).
OPERATIVE PROCEDURES. When the tumor is located in the mid or distal (lower) portions of the stomach, a subtotalgastrectomy is typically performed. The surgeon uses a Bill-roth I or Billroth II procedure (discussed earlier under Operative Procedures [Peptic Ulcer Disease], p. 1229). The omen-tum, spleen, and relevant nodes are also removed.
For the client with a resectable growth in the upper third of the stomach, a total gastrectomy is performed (Figure 56-9). In this procedure the surgeon removes the entire stomach along with en bloc removal of the lymph nodes and omentum. The surgeon sutures the esophagus to the duodenum or jejunum to re-establish continuity of the GI tract. More radical surgery involving removal of the spleen and distal pancreas is controversial. The overall mortality rate for clients undergoing total gastrectomy surgery is 10% to 15% (Hawkins, 1999). For clients with advanced disease, total gastrectomy is performed only when gastric bleeding or obstruction is present.
Clients with tumors at the gastric outlet who are not candidates for subtotal or total gastrectomy may undergo gas-troenterostomy for palliation. The surgeon creates a passage between the body of the stomach and the small bowel, often the duodenum (see Figure 56-4).
POSTOPERATIVE CARE. Clients require the standard postoperative care that is given to those who have had general anesthesia (see Chapter 19). Complications after gastric surgery may include the following: Pneumonia
« Anastomotic leak
• Hemorrhage
• Reflux aspiration
Sepsis
• Reflux (acute) gastritis (discussed earlier under Acute
Gastritis, p. 1216)
• Paralytic ileus
Bowel obstruction
* Wound infection
Dumping syndrome (discussed earlier under Monitoring for Postoperative Complications [Peptic Ulcer Disease], p. 1230).
The nurse monitors the client for the development of postoperative complications. The nurse auscultates the lungs for adventitious sounds and monitors for the return of bowel sounds. Monitoring vital signs is performed as appropriate to detect signs of infection or bleeding. Aggressive pulmonary exercises and early ambulation can help prevent respiratory complications and deep vein thrombosis. The nurse also inspects the operative site every 8 hours for the presence of redness, swelling, or drainage, which indicates wound infection. The nurse also ensures proper positioning of the client to prevent aspiration from reflux.
Since weight loss is problematic for clients with gastric cancer, nutrition therapy is a vital aspect of preoperative and postoperative management. Preoperatively, compression by the tumor can impede adequate nutritional intake. To correct malnutrition before surgery, the health care provider may prescribe supplements to the diet and/or total parenteral nutrition (TPN). Vitamin, mineral, iron, and protein supplements are essential for correction of nutritional deficits.
Postoperatively, the client’s inability to ingest normal-size meals, along with poor nutrient absorption due to decreased stomach size, can prevent the client from taking in adequate nutrition. Therefore the surgeon may place an enteral feeding tube during surgery for continued nutritional support. When feasible, oral intake should begin with fluids and progress to solids as tolerated. For clients who have undergone gastric surgery, regurgitation may result from overeating or from eating too quickly.
After oral feedings are restarted, the nurse observes the client for signs and symptoms of dumping syndrome and teaches the manifestations and management of this syndrome. The client is advised to eat six small meals per day and to consume a diet high in protein and fat but low in carbohydrate-rich foods (see Table 56-3). Liquids should not be taken with meals. Milk and dairy products are usually eliminated because many clients are lactose-intolerant and have symptoms after the ingestion of milk-containing products.
In collaboration with the dietitian, the nurse guides the client and family in providing the most nutrients and calories. Counseling about methods of preparation and types of foods that increase caloric and protein intake is essential. The nurse maintains intake, output, and calorie counts on a daily basis and records weights at least weekly. Anemia, as well as vitamin B12 and folate deficiency, can result following gastrec-tomy. Oral folate and iron replacement and vitamin B12 injections can help correct these deficiencies.
Community-Based Care
Clients who have undergone total gastrectomy and those who are debilitated with advanced gastric cancer are discharged to home with maximal assistance or to a subacute unit or skilled nursing facility. Clients who have undergone subtotal gastrectomy and are not debilitated may be discharged to home with partial assistance for activities of daily living (ADLs). Recurrence of the cancer is common, and clients will need regular follow-up examinations and radiographic assessments. A case manager may be assigned to ensure continuity of care and thorough follow-up with diagnostic testing.
HOME CARE MANAGEMENT
Gastric cancer is considered a life-threatening illness; therefore the client and family members require physical and emotional care from the health care team. The side effects of gastric cancer treatment can be debilitating, and clients need to learn symptom management strategies. Hospice programs can help both the client and the family to cope with these physical and emotional needs.
Clients may fear returning home because of their inability to care for themselves adequately. Enlisting family and health care resources for the client may ease some of this anxiety. The family needs adequate information and support systems to make the transition to home care easier for the client. If the prognosis is poor, the client and family need continued professional support to cope with death and dying. (See Chapter 9 for a discussion of end-of-life care.)
HEALTH TEACHING
The nurse instructs the client and family members about any continuing postoperative needs, adjuvant treatment, and nutrition therapy. If clients are discharged to home with surgical dressings, the nurse teaches the client and family to perform dressing changes. The nurse identifies the signs and symptoms of incisional infection (e.g., fever, redness, and drainage) that are to be reported.
Clients who will be receiving radiation therapy or chemotherapy require instructions related to the side effects of these
treatments. Nausea and vomiting are common side effects of chemotherapy, and instruction in the use of prescribed anti-emetics may be needed. (See Chapter 25 for education for clients receiving chemotherapy or radiation therapy.)
The nurse, in conjunction with the dietitian, educates the client and family concerning the type and quantity of foods that will provide optimal nutritional value. Interventions to minimize dumping syndrome are also emphasized (see Table 56-3).
HEALTH CARE RESOURCES
A home care referral provides ongoing assessment, assistance, and encouragement to the client and family or significant others at home. A home care nurse can help with physical care procedures and can also provide valuable psychologic support. Additional referrals to a dietitian, professional counselor, or clergy may be necessary. Referral to a hospice agency can be of great assistance. Hospice care may be delivered in the home or in an institutional setting. Appropriate support groups (such as I Can Cope, provided by the American Cancer Society) can be a major resource.