Interventions for Clients with Esophageal Problems
Objectives
After studying this chapter, you should be able to:
1. Explain the pathophysiology of gastroesophageal reflux disease (GERD).
2. Assess the client who is experiencing GERD.
3. Plan the nursing care for clients with GERD.
4. Develop a postoperative teaching plan for the client having a hiatal hernia repair.
5. Identify the differences in the incidence of esophageal cancer among cultural groups.
6. Describe the risk factors for esophageal cancer.
7. Analyze assessment data to determine commoursing diagnoses for the client with esophageal cancer.
8. Discuss the priorities for postoperative care of the client undergoing surgery for esophageal cancer.
9. Plan community-based care for clients diagnosed with esophageal cance.
Etsophageal disorders affect approximately 546,000 people in the
GASTROESOPHAGEAL REFLUX DISEASE
OVERVIEW
Esophageal reflux is defined as the backward flow of gastrointestinal contents into the esophagus. Reflux produces its characteristic symptoms by exposing the esophageal mucosa to the irritating effects of gastric and/or duodenal contents, resulting in inflammatory changes of the esophageal mucosa. A person with acute symptoms of inflammation is often described as having reflux esophagitis, a hallmark of gastroesophageal reflux disease (GERD). Reflux esophagitis is graded according the extent and severity of the lesions.
Pathophysiology
The following physiologic factors are implicated in the development of GERD (Tucker & Schumann, 1999):
· An incompetent lower esophageal sphincter
· Irritation from the refluxate
· Abnormal esophageal clearance
· Delayed gastric emptying
The reflux of gastric contents into the esophagus is normally prevented by the presence of two high-pressure areas that remain relatively contracted in the resting phase. A 3-cm (1.2-inch) segment at the proximal end of the esophagus is called the upper esophageal sphincter (UES). Another 2- to 4-cm (0.8- to 1.6-inch) portion just proximal to the gastroesophageal junction is called the lower esophageal sphincter (LES). The function of the LES is supported by its anatomic placement in the abdomen, where the surrounding pressure is significantly higher than in the low-pressure thorax. Sphincter function is also supported by the acute angle (angle of His) that is formed as the esophagus enters the stomach. Esophageal reflux can occur when gastric volume or intra-abdominal pressure is elevated, when the sphincter tone of the LES is decreased, or when the LES undergoes inappropriate relaxation.
COST OF CARE
ESOPHAGEAL PROBLEMS
Cost of Care
· Ambulatory care for clients with Barrett’s esophagus costs
approximately $103 per month, or $1241 per year.
· Clients with low-grade dysplasia (tissue changes) are three
times as likely to have more than 3 endoscopies per year as
compared to clients who do not have dysplasia.
· Endoscopies and clinic visits account for 31% and 5.9%,
respectively, of the monthly medical costs.
· The medication costs per month for clients with Barrett’s
esophagus is $65.
· Proton-pump inhibitors account for 64.6% of the total med
ication cost.
· Medications account for more than 50% of the total cost of
care.
implications for Nursing
Prolonged gastrointestinal reflux leading to Barrett’s esophagus or disease results in a relatively high cost of care in terms of the need for health care services. Clients require ongoing monitoring by endoscopy for dysplastic changes in the mu-cosa, long-term medication adherence to control reflux, and primary care provider visits. Nurses can play an integral role in the prevention of gastrointestinal reflux by educating their clients about the risk factors for developing reflux, strategies for managing reflux, and the necessity of making lifestyle adjustments that prevent esophageal damage.
An individual experiencing reflux may be asymptomatic and relatively unaware that reflux is occurring. However, the esophagus has only a limited resistance to the damaging effects of the acidic gastrointestinal (GI) contents. The pH of acid secreted by the stomach ranges from 1.5 to 2.0, whereas the pH of the distal esophagus is normally neutral (6.0 to 7.0). Repeated exposure of the esophageal mucosa to highly acid gastric secretions is associated with the development of erosive esophagitis.
Refluxed material is returned to the stomach by a combination of gravity, saliva, and peristalsis. The effectiveness of the clearance mechanism is very important. An inflamed esophagus cannot eliminate the refluxed material as quickly or efficiently as a healthy one, and therefore the duration of exposure increases with each reflux episode.
Hyperemia (increased blood flow) and erosion occur in the esophagus in response to the chronic inflammation. Gastric acid and pepsin are responsible for the tissue injury. Minor capillary bleeding often accompanies the erosion, but frank hemorrhage is rare. During the process of healing, the body may substitute a columnar epithelium (Barrett’s epithelium) for the normal squamous cell epithelium of the lower esophagus. Although this new tissue is more resistant to acid and therefore supports esophageal healing, it is considered pre-malignant and is associated with an increased risk of cancer in 10% to 15% of clients with prolonged GERD (Sharma, 1999). The fibrosis and scarring that accompanies the healing process can produce esophageal stricture, resulting in a narrowing of the esophageal lumen. The stricture leads to progressive difficulty in swallowing. Uncontrolled esophageal reflux also creates a risk for other serious complications such as esophageal ulceration, hemorrhage, and aspiration pneumonia. GERD has been implicated as one of the causes of adult-onset asthma, laryngitis, and dental deterioration.
TABLE55-1 FACTORS CONTRIBUTING TO DECREASED
LOWER ESOPHAGEAL SPHINCTER PRESSURE
Fatty foods
Caffeinated beverages, such as coffee, tea, and cola
Chocolate
Nicotine in cigarette smoke
Calcium channel blockers
Nitrates
Peppermint, spearmint
Alcohol
Anticholinergic drugs
High levels of estrogen and progesterone
Nasogastric tube placement
Etiology
Current evidence suggests that GERD is a result of impaired LES function, which permits the reflux of gastric contents into the esophagus and the subsequent exposure of the esophageal mucosa to gastric contents from impaired esophageal clearance (Claussen, 1999). Currently, the role that hiatal hernia (see p. 1198) plays in the development of GERD is controversial, because each of these disorders often present independently of one another. Nighttime reflux tends to result in prolonged exposure of the esophagus to acid because recumbency tends to impair peristalsis and gravity clearance mechanisms.
Gastric distention caused by the ingestion of large meals or by conditions associated with delayed gastric emptying predispose the client to reflux. A number of individual factors, including certain foods and medications, have been identified as influencing the tone and contractility of the LES (Table 55-1). Clients who have a nasogastric tube often experience compromised esophageal sphincter function. The tube keeps the cardiac sphincter open and allows acidic contents from the stomach to enter the esophagus. Other factors that increase intra-abdominal and intragastric pressure (e.g., wearing tight belts, obesity, bending over, and ascites) overcome the gastroesophageal pressure gradient maintained by the LES and allow reflux to occur.
Incidence/Prevalence
The incidence of GERD is approximately 2% to 3% per year and affects 25% to 35% of the population. Ten percent of the population reports experiencing symptoms of reflux daily, and 44% report experiencing symptoms once a month (Scott & Gelhot, 1999). Gastroesophageal reflux disease (GERD) can occur at any age but is more common in people over 45 years of age. The incidence of GERD may be underestimated because many people with mild disease relate the symptoms to episodes of stress or dietary indiscretion.
CULTURAL CONSIDERATIONS
? The prevalence of GERD is higher in females than in males and is found more often in Caucasians than in other ethnic groups. Severe esophagitis is more common in males than in females and is more prevalent in Caucasians than in African Americans.
COLLABORATIVE MANAGEMENT Assessment
■ HISTORY
The nurse assesses the client for a history of heartburn or atypical chest pain associated with the reflux of gastrointestinal contents. The client is assessed for dysphagia (difficulty swallowing) or odynophagia (painful swallowing), either of which can indicate the development of a stricture. The nurse further investigates whether the client has a history of newly diagnosed asthma, morning hoarseness, or pneumonia, which are suggestive of severe reflux reaching the pharynx or mouth and/or pulmonary aspiration.
■ PHYSICAL ASSESSMENT/CLINICAL
MANIFESTATIONS
The clinical manifestations of reflux may vary substantially in severity (Chart 55-1).
DYSPEPSIA. A diagnosis of GERD is made principally by a history of dyspepsia (also called pyrosis or heartburn), which is the characteristic symptom. Clients often describe this pain as a substernal or retrosternal burning sensation that tends to move up and down the chest in a wavelike fashion. If severe, the pain may radiate to the neck or jaw or may be referred to the back. The pain typically worsens when the client bends over, strains, or is in a recumbent position.
With severe GERD, the pain occurs after each meal and persists for 20 minutes to 2 hours. Clients usually experience prompt relief by ingesting fluids or antacids or by maintaining an upright posture. Some clients experience atypical chest pain, which mimics angina and needs to be carefully differentiated from cardiac disease.
REGURGITATION. Regurgitation, which is associated with neither belching nor nausea, is another common symptom. The client reports the occurrence of warm fluid traveling up the throat. If the fluid reaches the level of the pharynx, the client notes a sour or bitter taste in the mouth. This effortless regurgitation can even occur when the client is in an upright position. The danger of aspiration is increased if regurgitation occurs when the client is in a recumbent position.
If the client experiences regurgitation, the nurse carefully auscultates the chest for crackles, which is an indication of associated aspiration. The nurse assesses for coughing, hoarseness, or wheezing at night, which may be related to recumbent regurgitation. Assessment for bronchitis may be necessary in clients experiencing long-term regurgitation.
KEY FEATURES of Gastroesophageal Reflux Disease
Dyspepsia (heartburn or pyrosis)
Regurgitation (may lead to aspiration or bronchitis)
Coughing, hoarseness, or wheezing at night
Water brash
Dysphagia
Odynophagia (painful swallowing)
Chest pain
Belching
Flatulence
HYPERSALIVATION. A reflex salivary hypersecretion known as water brash occurs in response to reflux. Water brash must be carefully distinguished from regurgitation. The client reports a sensation of fluid in the throat, but unlike with regurgitation, there is no bitter or sour taste.
DYSPHAGIA AND ODYNOPHAGIA. Chronic GERD can involve dysphagia (difficulty in swallowing). Dysphagia may be the presenting symptom in 33% of clients with GERD. This symptom is usually fairly mild; it is not progressive and occurs with the first swallow of each meal. Dysphagia does not interfere with oral nutrition and does not produce weight loss. Careful assessment is required if a client reports progressive or persistent dysphagia, because this usually indicates the development of a stricture or cancer. The nurse assesses the following:
• The degree of dysphagia
• Whether dysphagia occurs with the ingestion of solids, liquids, or both
• Whether dysphagia is intermittent or occurs with each swallowing effort
Odynophagia (painful swallowing) is a possible symptom of GERD but is relatively rare in people with uncomplicated reflux disease. Severe and long-lasting chest pain may be present if spasms occurring in the esophagus cause the muscle to contract with excess force. The resulting pain can be agonizing and last for hours.
OTHER CLINICAL MANIFESTATIONS. Eructation (belching), flatulence (gas), or bloating after eating are other common complaints. Nausea and vomiting occur infrequently, and unplanned weight loss is rare.
RADIOGRAPHIC ASSESSMENT
No single test is considered to be a gold standard for diagnosing GERD. A barium swallow can be used to rule out complications associated with GERD or to evaluate dysphagia, but it is not sensitive enough to be diagnostic. The most accurate method of diagnosing gastroesophageal reflux disease (GERD) is 24-hour pH monitoring; this involves placing pH probes 2 inches (5 cm) above the lower esophageal sphincter (LES). A barium swallow with fluoroscopy then outlines the structure of the esophagus and its peristaltic patterns. Twenty-four hour ambulatory pH monitoring is widely used but is helpful only in evaluating acid reflux. Endoscopy is useful in diagnosing or evaluating reflux esophagitis or in monitoring complications such as Barrett’s esophagus. During endoscopy, tissue samples can be obtained for biopsy, and strictures can be dilated (see Chapter 53).
OTHER DIAGNOSTIC ASSESSMENT
The health care provider orders esophageal manometry, or motility testing, when the diagnosis is uncertain. Water-filled catheters are inserted via the client’s nose or mouth and are connected to transducers that record pressures from various sites in the esophagus as the catheters are withdrawn. Manometry quantifies the resting pressure of the LES and helps to evaluate sphincter competence, but when used alone it is not sensitive or specific enough to establish a diagnosis of GERD. In Bernstein’s test, an acidic solution is infused via a tube inserted into the distal esophagus. Clients with normal esophageal mucosa experience no symptoms when acid is infused, but clients with esophagitis experience immediate heartburn.
Scintigraphy involves preloading the stomach with a liquid radioisotope via the mouth or a tube. Scintillation counts are performed over the lower esophagus and are compared with counts obtained over the stomach. If a client is experiencing frequent reflux, the radioisotope will be refluxed back into the esophagus, which significantly elevates the scintillation counts over the lower esophageal region. Scintigraphy may be used in conjunction with pH monitoring.
Interventions
Interventions begin with thorough teaching that GERD is a chronic condition that warrants ongoing management. This knowledge base is essential for a client’s understanding of and adherence to the prescribed regimen of drugs, diet therapy, and lifestyle modifications.
NONSURGICAL MANAGEMENT. The goals of treatment for GERD are the relief of symptoms, treatment of esophagitis, and prevention of complications such as strictures or Barrett’s esophagus. Although GERD can be controlled by diet therapy, education, lifestyle changes, and drug therapy, it is important to note that, even after the esophagitis is healed, 40% to 80% of clients relapse in 6 months after their medication is discontinued.
DIET THERAPY. Diet therapy is used to relieve symptoms in clients with relatively mild GERD. In collaboration with the dietitian, the nurse explores the client’s basic meal patterns and food preferences. The nurse and dietitian work with both the client and the family to plan modifications that may decrease reflux symptoms. For adherence at home to be successful, it is essential that family members who do the shopping and cooking be included in this discussion.
In conjunction with the dietitian, the nurse counsels the client to limit or eliminate foods that decrease LES pressure. The client should also restrict spicy and acidic foods (e.g., orange juice, tomatoes) until esophageal healing can occur, because these foods irritate the inflamed tissue and cause heartburn (Goldsmith, 1998).
Because large meals increase the volume of and pressure in the stomach and delay gastric emptying, the nurse or dietitian instructs the client to eat four to six small meals each day rather than three large ones. Carbonated beverages should also be avoided because they increase pressure in the stomach. Clients are encouraged to avoid evening snacks and to eat no food for at least 3 hours before going to bed, because reflux episodes are most damaging at night. Clients may have the most difficulty adhering to the restriction of evening snacks. The nurse also advises the client to eat slowly and chew thoroughly to facilitate digestion and prevent eructation (belching). The client is encouraged to investigate which particular diet changes best reduce the frequency and severity of symptoms.
CLIENT EDUCATION. The nurse educates the client about the risk factors for the development of reflux, including contributing lifestyle factors. Lifestyle factors that can exacerbate the disease are reviewed, and the client is counseled on ways to eliminate them. The nurse also educates the client regarding the need for ongoing monitoring, particularly if the client has developed strictures, ulcerations, or Barrett’s esophagus.
LIFESTYLE CHANGES. The control of GERD involves some lifestyle adjustments on the part of the client. For example, he or she is instructed to elevate the head of the bed by 8 to 12 inches for sleep to prevent nighttime reflux. In addition, he or she is instructed to sleep in the left lateral decubi-tus position to minimize the effects of nighttime episodes of reflux (see the Evidence-Based Practice for Nursing box below). Nighttime reflux is extremely common, and infrequent swallowing in combination with a recumbent position significantly impairs esophageal clearance. Although wooden blocks have traditionally been recommended to elevate the head of the bed, foam wedges may also achieve satisfactory results. The client or the client’s spouse or partner may find elevation of the bed unacceptable at first. The nurse emphasizes the importance of this intervention and investigates all possible approaches for achieving compliance (Chart 55-2).
For clients with a history of smoking, the nurse explores the possibility and means of smoking cessation and makes the appropriate referrals. The nurse explains that smoking causes a prompt and significant drop in LES pressure and optimally should be stopped. The nurse also explores the client’s normal pattern and amount of alcoholic beverage use. The client is taught about the effects of alcohol on LES sphincter pressure. The nurse can assist the client in finding appropriate alcohol cessation programs if needed.
EVIDENCE-BASED PRACTICE
The purpose of this study was to investigate the influence of body position during sleep on recumbent reflux in 10 clients with gastroesophageal reflux disease. The 10 subjects (3 female, 7 male) were fed a standardized, high-fat dinner and bedtime snack. A single-channel pH probe was placed 5 cm above the lower esophageal sphincter (LES) in each client to measure the percentage of reflux episodes (pH <4) that occurred during four sleeping positions. A body position sensor taped to the client’s sternum recorded spontaneous changes in posture during sleep.
The right lateral position was associated with the greatest percentage of time the pH remained under 4 and longer esophageal acid clearance when compared to the left, supine, and prone positions. The supine position resulted in a greater overall number of gastroesophageal reflux episodes that occurred within 1 minute of assuming this position. This study determined that the preferred sleeping position for clients with gastroesophageal reflux is the left lateral position.
Critique. Although the sample size was small, this was the first study to examine the effects of sleeping positions on recumbent reflux in clients with gastroesophageal reflux.
Implications for Nursing. Previous research supports the theory that body position influences gastroesophageal reflux. Nurses can incorporate information concerning sleeping position into their teaching plan for clients faced with damaging nighttime reflux. In addition to elevating the head of the bed, clients can be instructed to lie in the left lateral position for sleep to reduce the number of reflux episodes and the length of time the esophageal mucosa is exposed to acidic contents.
CLIENT EDUCATION GUIDE
Lifestyle Modifications to Control Reflux
· Eat four to six small meals a day.
· Limit or eliminate fatty foods, coffee, tea, cola, and
chocolate.
· Reduce or eliminate from your diet any food or spice that
causes pain.
· Limit or eliminate alcohol and tobacco.
· Do not snack in the evening, and take no food for 2 to 3
hours before you go to bed.
· Eat slowly, and chew your food thoroughly to reduce
belching.
· Remain upright for 1 to 2 hours after meals, if possible. Elevate the head of your bed 8 to 12 inches using wooden blocks or a foam wedge. Never sleep flat in bed.
· If you are overweight, lose weight.
Do not wear constrictive clothing.
· Avoid heavy lifting, straining, and working in a bent-over position.
If the client is obese, the nurse collaborates with the dietitian to examine approaches to weight reduction. Decreasing intra-abdominal pressure often reduces reflux symptoms.
Other lifestyle factors cause increased abdominal pressure, and the nurse explores these with the client. Wearing constrictive clothing, lifting heavy objects or straining, and working in a bent-over or stooped position should be avoided. The nurse emphasizes that these general adaptations are an essential and effective component of disease management and can produce prompt results in uncomplicated cases.
DRUG THERAPY. Some medications can cause reflux. Therefore the nurse, in conjunction with the primary health care provider, explores the possibility of eliminating from the client’s regimen those medications implicated in reflux. Three principles guide drug therapy for gastroesophageal reflux: (1) to inhibit gastric acid secretion, (2) to accelerate gastric emptying, and (3) to protect the gastric mucosa (Chart 55-3).
Antacids. In uncomplicated cases of GERD, antacids are effective for occasional episodes of heartburn. Antacids act by elevating the pH level of the gastric contents, thereby deactivating pepsin. They are inadequate for the control of frequent symptoms because their duration of action is too short and their nighttime effectiveness is minimal.
Antacids containing aluminum hydroxide or magnesium hydroxide may be used. Maalox and Mylanta consist of a combination of these two agents, and clients often tolerate them better because they produce fewer side effects such as constipation and diarrhea. The nurse instructs the client to take the antacid 1 hour before and 2 to 3 hours after each meal. Some antacids are prepared as double-strength (DS) suspensions or tablets. The advantage of DS preparations is that the client can take a smaller amount of the drug. For example, 30 mL of regular Mylanta equals 15 mL of Mylanta-II (DS preparation).
Gaviscon, a combination of aluminum hydroxide and magnesium carbonate, is a commonly used and very effective medication for GERD. It forms a viscous foam that floats on top of the gastric contents and theoretically decreases the incidence of reflux. If reflux occurs, the foam enters the esophagus first and buffers the acid in the refluxed material. The nurse reminds the client to take this drug when food is in the stomach.
Histamine Receptor Antagonists. Histamine blockers, such as famotidine (Pepcid), ranitidine (Zantac), cimetidine (Tagamet), and nizatidine (Axid) are the main pharmacologic means of inhibiting gastric acid secretion. With histamine receptor antagonists available over the counter (OTC) and widely advertised for heartburn, many clients self-medicate before seeking professional assistance from their health care provider. When clients who have self-medicated with OTC preparations experience uncontrolled symptoms, the health care provider usually prescribes a higher dose of a histamine receptor antagonist.
Cimetidine (Tagamet) is not used as often as the longer-acting preparations. It has an inhibitory effect on the elimination of certain other medications, and therefore significant drug interactions can occur in clients taking warfarin, theo-phylline, phenytoin, nifedipine, or propranolol. Ranitidine and the other preparations are longer acting, and less frequent dosing is necessary. They also appear to produce fewer side effects and are safe for long-term administration. Although these drugs do not affect the occurrence of reflux directly, they do reduce gastric acid secretion, provide symptomatic improvement, and support healing of the inflamed esophageal tissue.
The proton pump inhibitors, such as omeprazole (Prilosec), lansoprazole (Prevacid), and rabeprazole (Aciphex), demonstrate effective, long-acting inhibition of gastric acid secretion. They are typically reserved for the treatment of severe GERD that is refractory to treatment with histamine blockers, and they play an important role in maintaining the remission of both GERD and Barrett’s esophagus. These potent drugs can reduce gastric acid secretion by about 90% over a 24-hour period and can be given in a single daily dose. If once-a-day dosing fails to control symptoms, twice-a-day dosing is appropriate (Sharma, 1999). For example, omeprazole (Prilosec) is usually prescribed as a 20-mg oral dose once a day for 4 to 8 weeks. Complete healing of esophagitis is seen in 80% to 97% of clients (Tucker & Schumann, 1999). Proton pump inhibitors promote rapid tissue healing, but recurrence is common when the drug is stopped.
Other Drugs. Prokinetic drugs are used to accelerate gastric emptying and improve lower esophageal sphincter (LES) pressure and esophageal peristalsis. The health care provider may add bethanechol (Urecholine) or metoclopramide (Reglan) to the drug regimen for clients who experience severe and ongoing symptoms of reflux.
Bethanechol is a cholinergic drug; it increases the secretion of gastric acid and usually requires the simultaneous administration of a histamine receptor antagonist and antacids. Bethanechol is usually prescribed in 25-mg doses four times a day. The nurse teaches the client to take bethanechol 30 to 60 minutes before meals and warns the client about the typical side effects, which include abdominal cramping, diarrhea, increased salivation, and urinary urgency.
The primary action of metoclopramide is to increase the rate of gastric emptying. It does not affect gastric acid secretion or directly heal esophageal tissue. Its use is also associated with a high incidence of neurologic and psychotropic side effects such as fatigue, anxiety, ataxia, and hallucinations. Long-term use is not recommended.
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SURGICAL MANAGEMENT. Antireflux surgery is usually indicated for otherwise healthy clients who have failed to respond to medical treatment or to demonstrate complications related to GERD or for whom the cost of long-term drug ther-
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apy is prohibitive. Various surgical procedures may be used. The three major surgical procedures are Nissen fundoplica-tion, the Hill repair, and the Belsey repair (Figure 55-1).
In each of these procedures, the surgeon wraps and sutures the gastric fundus around the esophagus, which anchors the LES area below the diaphragm and reinforces the high-pressure area. For a more complete description of the three major procedures, see Operative Procedures (Hiatal Hernia), p. 1202.
The Client Care Plan on pp. 1199 and 1200 outlines the nursing care of clients undergoing esophageal surgery. Clients who have surgery are encouraged to continue following the basic antireflux regimen of antacids and diet therapy, because the rate of recurrence is significant.
Placement of the synthetic Angelchik prosthesis is also used for clients with severe reflux. This surgical procedure is associated with fewer long-term problems with achalasia (failure of the lower esophageal muscles and sphincter to relax properly). The surgeon performs a laparotomy and ties a C-shaped silicone prosthesis filled with gel around the distal esophagus (Figure 55-2). The prosthesis anchors the LES in the abdomen and reinforces sphincter pressure. Dysphagia is the primary complication of this procedure.
OVERVIEW
The esophageal hiatus is the opening in the diaphragm through which the esophagus passes from the thorax to the abdomen. Hiatal hernias, also called diaphragmatic hernias, involve the protrusion of the stomach through the esophageal hiatus of the diaphragm into the thorax. Clients with hiatal hernias may be completely asymptomatic or may experience daily symptoms similar to those of clients with GERD.
Pathophysiology
The two major types of hiatal hernias are sliding hernias and paraesophageal (rolling) hernias.
SLIDING HERNIA
Sliding hernias are the most common type of hernia and account for 90% of the total number of hiatal hernias. The esophagogastric junction and a portion of the fundus of the stomach slide upward through the esophageal hiatus into the thorax (Figure 55-3). The hernia generally moves freely and slides into and out of the thorax during changes in position or intra-abdominal pressure. Although volvulus (twisting) and obstruction do occur rarely, the major concern in a client with a sliding hernia is the development of esophageal reflux and its complications. The development of reflux appears to be related to chronic exposure of the lower esophageal sphincter (LES) to the low pressure of the thorax, which significantly reduces the effectiveness of the LES. Symptoms associated with LES pressure are worsened by positions that favor reflux, such as bending or lying supine.
ROLLING HERNIA
With paraesophageal hernias, the gastroesophageal junction remains in its normal intra-abdominal location, but the fundus
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Stomach |
Figure 55-1 • Nissen fundoplication for gastroesophageal reflux disease or hiatal hernia repair.
(and possibly portions of the stomach’s greater curvature) roll through the esophageal hiatus and into the thorax beside the esophagus (see Figure 55-3). The herniated portion of the stomach may be small or quite large; in rare cases, the stomach completely inverts into the thorax. Reflux is rarely a concern because the LES remains anchored below the diaphragm, but the risks of volvulus, obstruction, and strangulation are high. The development of iron deficiency anemia is common, because slow bleeding secondary to venous obstruction causes the gastric mucosa to become engorged and ooze. Significant bleeding or hemorrhage is rare.
Figure 55-3
Etiology
Sliding hiatal hernias are believed to develop from muscle weakening in the esophageal hiatus, which loosens the esophageal supports and permits the lower portion of the esophagus to rise into the thorax. Congenital weaknesses, trauma, obesity, or surgery may also play a significant role. The development of the hernia is the result of the combined effects of weakened support structures and prolonged increases in abdominal pressure.
Muscle weakening does not appear to cause paraesoph-ageal hernias. Instead, it is theorized that the stomach is not properly anchored below the diaphragm, and the hernia results from an anatomic defect rather than a structural weakness. Paraesophageal hernias can also be caused by previous esophageal surgeries, including sliding hernia repair.
Incidence/Prevalence
Hiatal hernia is one of the more common disorders that affect the upper gastrointestinal tract, and it affects women more often than men. Hiatal hernias have been reported in up to 20% of adults (Crawford, 1999).
CONSIDERATIONS FOR OLDER ADULTS
Ebb The incidence of sliding hiatal hernias increases with age in both genders and reaches a prevalence of approximately 60% in the sixth decade of life. As many as 80% of clients with hiatal hernias are asymptomatic or experience only mild, transient symptoms associated with reflux.
COLLABORATIVE MANAGEMENT
Assessment
The nurse carefully assesses for heartburn, regurgitation, pain, dysphagia, and belching. An assessment of the client’s general physical appearance and nutritional status is also included. The nurse notes the location, onset, duration, quality, and aggravating and alleviating factors associated with the presence of pain. The primary symptoms of sliding hiatal hernias are associated with reflux. The nurse auscultates the thorax and lungs, as pulmonary symptoms similar to asthma may be triggered by episodes of aspiration, particularly at night. A detailed history is crucial in attempting to differentiate angina from noncardiac chest pain due to gastroesophageal reflux. Symptoms resulting from hiatal hernia typically worsen after a meal or when the client is in a recumbent position (Chart 55-4).
In clients with paraesophageal (rolling) hernias, the nurse assesses for symptoms related to the stretching or displacement of thoracic contents by the hernia. Clients may report a feeling of fullness after eating and may even experience breathlessness or a feeling of suffocation if the hernia interferes with breathing. Some clients experience chest pain associated with reflux that mimics angina.
The barium swallow study with fluoroscopy is the most specific diagnostic test for identifying hiatal hernia. Paraesophageal hernias are usually clearly visible, and sliding hernias can often be observed as the client is moved through a series of positions that increase intra-abdominal pressure.
Clients with sliding hernias usually experience symptoms of reflux. Therefore any or all of the diagnostic tests used for gastroesophageal reflux disease (GERD) may be used to fully evaluate the extent of reflux and the degree of esophageal damage (see Other Diagnostic Assessment [GERD], p. 1194).
Interventions
Clients with hiatal hernias may be managed either medically or surgically. The health care provider’s choice of management is based on the severity of the client’s symptoms and the risk of serious complications. Sliding hiatal hernias are most commonly treated medically. Large paraesophageal hernias can become strangulated or obstructed; therefore early surgical repair is encouraged.
NONSURGICAL MANAGEMENT. The interventions for clients with hiatal hernia closely follow those outlined for clients with GERD and include drug therapy, diet therapy, lifestyle modifications, and client education. The health care provider typically prescribes antacids and histamine receptor antagonists, such as ranitidine (Zantac), in an attempt to control reflux and its symptoms.
Diet therapy is also an integral part of the conservative management of hiatal hernia and follows the guidelines discussed earlier for GERD, p. 1195. The client is encouraged to avoid eating in the late evening and to avoid foods associated with reflux. In collaboration with the dietitian, the nurse works with the client to modify the diet to reduce body weight (if appropriate), because obesity increases intra-abdominal pressure and worsens both the hernia and the symptoms of reflux.
The nurse carefully explains the underlying condition to increase the client’s understanding of the disorder and increase adherence to the treatment regimen. Teaching about positioning, as described earlier for GERD (p. 1195) is also extremely important. It is essential that clients:
• Sleep at night with the head of the bed elevated 8 to 12
inches
• Remain upright for several hours after eating
• Avoid straining or excessive vigorous exercise
• Refrain from wearing clothing that is tight or constric-
tive around the abdomen
SURGICAL MANAGEMENT. The physician usually schedules surgery when the risk of complications is high or when damage from chronic reflux becomes severe.
PREOPERATIVE CARE. If the surgery is not urgent, the surgeon encourages clients who are overweight to lose weight before surgery. Clients are advised to quit or significantly reduce smoking. As part of preoperative teaching, the nurse reinforces the surgeon’s instructions and prepares the client for the postoperative course. Before developing the teaching plan, the nurse must know which surgical approach is planned. For the thoracic surgical approach, for example, the client is taught about chest tubes. The nurse also informs the client that a nasogastric tube will be inserted during surgery and will remain in place for several days. Oral intake is started gradually with clear liquids after peristalsis is re-established, or to stimulate peristalsis. The nurse also instructs the client about techniques for effective deep breathing and use of the incentive spirometer. These measures are essential to prevent postoperative respiratory complications. The high incision makes deep breathing extremely painful for the client. The nurse educates the client concerning the aspects of postoperative pain and assures the client that adequate postoperative analgesia will be administered.
OPERATIVE PROCEDURES. Although several hiatal hernia repair procedures are in use, each involves reinforcement of the lower esophageal sphincter (LES) through some degree of fundoplication. The surgeon wraps a portion of the stomach fundus around the distal esophagus to anchor it and reinforce the LES. The eventual recurrence for either type of hernia following surgical repair is 10% to 15% over 5 years (
The Nissen repair is the most commonly used procedure (see Figure 55-1) for hiatal hernia repair. An abdominal approach is usually chosen. The surgeon wraps the fundus a full 360 degrees around the lower esophagus. The sphincter reinforcement is tight and usually controls reflux effectively. Lap-aroscopic Nissen fundoplication (LNF) is a relatively new surgical technique that involves the creation of an antireflux valve or fundoplication laparoscopically through 5 ‘/2-inch incisions in the abdomen. The fundus is then wrapped 360 degrees around the LES to strengthen it (Vaca et al., 1998).
In the Hill repair, an abdominal approach is also used, but the fundoplication is wrapped 180 degrees around the esophagus. The angle of His is restructured to accentuate the angle at which the esophagus enters the stomach. The Belsey repair usually involves a 280-degree esophageal wrap and uses a thoracic approach.
Surgeons do not agree about which surgical repair is most appropriate or effective, because each procedure has unique advantages and disadvantages. For example, the laparoscopic Nissen fundoplication is associated with all the risks of a major surgery; pneumonia, myocardial infarction, wound infection, and bleeding (Vaca et al., 1998).
POSTOPERATIVE CARE. Postoperative care following hiatal hernia repair closely follows that required after any esophageal surgery (see the Client Care Plan on pp. 1199 and 1200). The nurse carefully assesses for complications of fundoplication surgery and reports their occurrence to the physician (Chart 55-5).
Respiratory Care. The primary focus of postoperative care is the prevention of respiratory complications. The nurse or assistive nursing personnel elevates the head of the client’s bed at least 30 degrees to lower the diaphragm and facilitate lung expansion. The client is assisted out of bed and is ambulated as soon as possible. The incision must be supported during coughing to reduce pain and to prevent excessive strain on the suture line, especially with obese clients.
BEST PRACTICE/or
Assessment of Postoperative Complications Related to
Fundoplication Procedures
|
COMPLICATION Temporary dysphagia Gas bloat syndrome Atelectasis, pneumonia Obstructed nasogastric tube |
ASSESSMENT FINDINGS
The client has difficulty swallowing when oral feeding begins.
The client has difficulty belching to relieve distention.
The client experiences dyspnea, chest pain, and/or fever.
The client experiences nausea, vomiting, and/or abdominal distention. The nasogastric tube does not drain.
Incentive spirometry and deep breathing are routinely used after surgery to maintain patency of the airways. Adequate analgesia is essential for client compliance and should be administered as needed. Clients with a smoking history or chronic airway limitation (chronic obstructive pulmonary disease, asthma) require more aggressive respiratory management by the respiratory therapist to prevent atelectasis and pneumonia. Clients with large hiatal hernias are at high risk for developing respiratory complications.
Nasogastric Tube Management. Postoperative management also involves the care of the nasogastric (NG) tube. Inserting a large-diameter NG tube during surgery prevents the fundoplication wrap from becoming too tight around the esophagus. The nasogastric drainage is initially dark brown with old blood but should become normal yellowish green within the first 8 hours after surgery. The nurse checks every 4 to 8 hours for proper placement of the tube in the stomach. The NG tube should be properly anchored so it cannot be displaced, because it cannot be safely reinserted without risking perforation of the incision.
Frequent assessment of the patency of the tube is essential to keep the stomach decompressed; this prevents retching or vomiting, which can strain or rupture the stomach sutures. Because the tube is irritating, the nurse or assistive nursing personnel provides frequent oral hygiene. The nurse also assesses the client’s hydration status regularly, including accurate measures of intake and output. Adequate fluid replacement helps to thin respiratory secretions.
Nutritional Care. The client may begin oral intake with clear fluids after peristalsis is re-established or in an effort to stimulate peristalsis. Some surgeons create a temporary gas-trostomy for feeding to allow for undisturbed healing of the repair. The client gradually progresses to a near-normal diet during the first 6 weeks. A few foods, such as caffeinated or carbonated beverages and alcohol, are either restricted or eliminated. The food storage area of the stomach is reduced by the surgery, and meals need to be both smaller and more frequent.
The nurse carefully supervises the first oral feedings, because temporary dysphagia is common. Persistent dysphagia usually indicates that the fundoplication is too tight, and dilation may be required.
Another common complication of fundoplication surgery is the gas bloat syndrome, in which clients are unable to voluntarily eructate (belch). The syndrome is usually temporary but may persist. The nurse teaches the client to avoid drinking carbonated beverages, eating gas-producing foods (especially high-fat foods), chewing gum, and drinking with a straw.
Many clients acquire the habit of aerophagia (air swallowing) from attempting to reverse or clear acid reflux. The nurse teaches these clients to consciously relax before and after meals, eat and drink slowly, and chew all food thoroughly.
Air in the stomach that cannot be removed by belching can be extremely uncomfortable. Frequent position changes and ambulation are effective interventions for eliminating air from the gastrointestinal tract.
P Community-Based Care
Clients undergoing one of the three major surgical repairs require activity restrictions during the 4- to 6-week postoperative recovery period. For laparoscopic surgery, activity is typically restricted for a shorter time, and the client can return to his or her usual lifestyle more quickly. For long-term management, the nurse teaches the client and family about appropriate diet modifications, but the use of stool softeners or bulk laxatives is recommended for the first postoperative weeks until healing is complete. The nurse instructs the client to avoid straining and prevent constipation.
The client is taught to inspect the healing incision daily and to notify the physician or health care provider if swelling, redness, tenderness, discharge, or fever occurs. The nurse advises the client to avoid contact with people with respiratory infections and to contact the physician if symptoms of a cold or influenza develop. Persistent coughing can cause the incision or the fundoplication to dehisce. The client is also advised to avoid smoking.
The nurse and dietitian educate the entire family or significant other about diet. Full support is essential for the client to successfully modify the size and timing of meals. Relatively few ongoing diet restrictions are needed, but overeating or eating the wrong types of foods can produce discomfort if the client cannot belch. The client avoids foods that produce discomfort, and the nurse encourages cautious experimentation with new foods. The nurse instructs the client to report the recurrence of reflux symptoms to the health care provider.
Although severe surgical complications are relatively rare, conditions such as gas bloat syndrome and dysphagia are common and may persist. The nurse helps the client prepare for these problems and for the potential that reflux rriay not be completely controlled or may occur again. Although surgery controls the condition, a cure is rare, and lifestyle modifications need to be ongoing.
ACHALASIA
OVERVIEW
Achalasia is an esophageal motility disorder in which the lower esophageal sphincter (LES) fails to relax properly with swallowing and in which the normal peristalsis of the esophagus is replaced with abnormal contractions. It is characterized by chronic and progressive dysphagia. Regurgitation of ingested food may also occur, especially at night, resulting in aspiration. If left untreated, progressive dysphagia can result in weight loss. Chest pain is experienced by one third of clients with the disorder.
Achalasia is thought to result from esophageal denervation (loss of nerve impulse passage). The exact cause of denervation is unknown. A genetic basis to the disorder has been proposed as suggested by occasional familial clustering and phe-notype (observable characteristics) association.
Over time, peristaltic failure plus spasm can produce a massively dilated esophagus, which further slows food passage. Achalasia is an uncommon disorder that usually manifests itself in young adulthood. Both genders appear to be equally affected. Approximately 5% to 10% of individuals with this disorder develop esophageal squamous cell carcinoma (Crawford, 1999). Complications of achalasia also include esophageal candidiasis, lower esophageal diverticula, airway obstruction, and aspiration pneumonia.
COLLABORATIVE MANAGEMENT B> Assessment
The nurse assesses for the primary symptoms of achalasia, such as dysphagia and regurgitation of solids, liquids, or both. The client is asked about the presence of chest pain associated with these symptoms.
Achalasia is often a chronic condition. The symptoms worsen over time, which poses an increased threat to health and functioning as the disorder progresses. The nurse questions the client about factors that aggravate the symptoms (e.g., body position or diet changes) as well as medications or home treatments that relieve the symptoms. The client is asked about a history of previous esophageal surgery or trauma, which compound the progressive dysphagia. Respiratory history and current respiratory-associated symptoms are particularly important with regard to their direct relationship to reflux, regurgitation, and aspiration.
To determine the effect of the esophageal symptoms, the nurse obtains a nutritional history, including dietary habits, food tolerances, and weight loss. The nurse also notes the presence of halitosis (foul mouth odor), which can be caused by the regurgitation of previously ingested food. The nurse auscultates the lungs for adventitious sounds secondary to pulmonary aspiration of retained saliva and food. The nurse or assistive nursing personnel weighs the client and compares this weight with the client’s usual weight.
A chest x-ray study reveals a distorted and dilated tubular esophagus, the absence of a gastric air bubble and, occasionally, a tubular mediastinal mass next to the aorta. A barium swallow reveals esophageal dilation with a persistent beaklike narrowing at the terminal esophagus—the hallmark of a non-relaxing LES. Esophageal manometry typically reveals an elevated resting LES pressure and incomplete sphincter relaxation when the client swallows. Endoscopy is used to evaluate the appearance of the esophageal mucosa, especially for changes associated with cancer or the presence of Candida.
Interventions
The symptoms associated with achalasia can be treated with a variety of approaches. A combination of dietary measures, pharmacologic agents, esophageal dilation and surgery are used.
DRUG AND DIET THERAPY. Mild cases of achalasia can be managed with calcium channel blockers or nitrates to reduce LES pressure. Drug therapy is given for symptom relief and is not recommended as an alternative to more definitive therapy.
The nurse advises the client to experiment with changes in diet because they can often ease the pressure and reflux associated with achalasia. The nurse discusses with the client any food habits he or she has noted that aggravate or relieve the symptoms. Semisoft foods are often better tolerated, as are warm foods and liquids. Eating four to six smaller meals rather than three large meals during the day facilitates the passage of food. The nurse collaborates with the dietitian for additional suggestions about diet changes and nutritional balance. Nocturnal reflux of foods and liquids from the dilated esophagus into the hypopharynx and oral cavity often can be prevented if the client sleeps with the head of the bed elevated or in a semisitting position. The nurse also advises the client to experiment with various changes in position while eating, because such changes can reduce pressure sensations during meals. Some clients benefit from arching the back while swallowing. The nurse cautions the client to avoid wearing restrictive clothing, which can increase esophageal pressure and regurgitation.
ESOPHAGEAL DILATION. More severe cases of achalasia require dilation of the LES. The traditional treatment involves the passage of progressively larger sizes of esophageal bougies (dilators). Balloon dilation of the esophagus (using polyurethane balloons on a catheter) is considered the most effective treatment for achalasia. The procedure is performed on an ambulatory care basis. Typically, pneumatic dilators are positioned across the esophageal junction with fluoroscopy and local anesthesia. The balloon, which is filled with air or water, is inflated to a predetermined level for 30 to 60 seconds (Figure 55-4). This method lowers the basal LES pressure by tearing the esophageal sphincter muscle fibers.
After the procedure, the nurse monitors the client for bleeding and signs of perforation, such as chest and shoulder pain, elevated temperature, subcutaneous emphysema (air under the skin), or hemoptysis (coughing up blood). The client is taught to expectorate ramer than swallow any secretions that may be produced. The client is also instructed to take nothing by mouth (NPO) for 1 hour and is instructed to limit dietary intake to liquids for 24 hours. The procedure may be repeated in 2 to 3 months if needed. Most clients report improvement in swallowing.
ESOPHAGOMYOTOMY. Surgical procedures for clients with achalasia are aimed at facilitating the passage of food. Esophagomyotomy, in which the LES is incised, has been used successfully for decades. Both thoracic and abdominal approaches can be used. An antireflux wrap (fundoplication) may or may not be part of the procedure. Esophagomyotomy is a more complex surgical treatment for achalasia. General anesthesia is required, and the client is hospitalized for several days. A thoracotomy approach permits exposure of the esophagus. The surgeon cuts muscle fibers around the LES to open the sphincter and thereby provide less obstruction to food passage. For long-term refractory achalasia, the surgeon may attempt excision of the affected portion of the esophagus, with or without replacement by a segment of colon or jejunum (partial esophagectomy).
Postoperative care for clients undergoing esophagomyotomy or esophagectomy includes managing chest tubes and drains, assessing healing of the thoracotomy or abdominal incision, pain control, and managing nasogastric feedings. (See Chapter 19 for general postoperative care and Chapter 30 for care of the client with a thoracotomy.)
ESOPHAGEAL TUMORS
OVERVIEW
Tumors occurring in the esophagus can be benign or malignant. Benign tumors, usually in the form of leiomyomas, are extremely uncommon and are usually asymptomatic. No specific treatment is required unless they produce symptoms, and then they are generally removed.
Worldwide, esophageal cancer is the third most common gastrointestinal (GI) cancer and the eighth most common cancer (Parkin, Pisani, & Ferlay, 1999). A relatively uncommon cancer in the
I Pathophysiology
Most malignant esophageal tumors arise from the epithelium. Fifteen percent of all esophageal cancers are located in the upper esophagus and are primarily squamous cell in origin. Thirty-five percent of tumors appear in the mid-thoracic region and can be either squamous cell or adenocarcinomas. The lower esophagus is the site of approximately 50% of all esophageal cancers, primarily adenocarcinomas. The local and regional lymphatic spread of the disease differs according to the site of the original tumor. It has been proposed that esophageal cancers result from mutations in suppressor genes and proto-oncogenes (see Chapter 24 for a more complete discussion).
Esophageal tumors exhibit rapid local growth because there is no serosal layer to limit their extension. Because the esophageal mucosa is richly supplied with lymphatics, there is early spread of tumors to lymph nodes. Esophageal tumors can protrude into the esophageal lumen and either take on a flattened and infiltrative form to cause thickening of the lumen or manifest as a necrotic ulceration that invades deeply into surrounding tissue. In rare cases the lesion may be confined to the epithelial layer (in situ). In the majority of cases, the tumor is relatively large and well established on diagnosis.
Etiology
In the
Long-term exposure to gastric contents, such as that caused by gastroesophageal reflux disease (GERD), also plays a role in esophageal cancer development. Exposure to acid and pepsin leads to the replacement of normal distal squamous mucosa with columnar epithelium as a response to tissue injury, causing Barrett’s disease or esophagus. This tissue undergoes dysplasia and, ultimately, malignant transformation.
In other parts of the world where esophageal cancer is common, the incidence of squamous cell carcinoma appears to be linked to high levels of nitrosamines (which are found in pickled and fermented foods) and foods high iitrate. Diets that are chronically deficient in fresh fruits and vegetables have been implicated in the development of squamous cell carcinoma.
Certain genetic factors may have a role in the development of esophageal cancer. Overexpression and/or mutations of the p53 tumor suppressor gene have been found in esophageal cancer. In addition, the presence of the p53 gene may be an indication of advanced disease. Tumor cells with a mutated p53 gene have demonstrated resistance to chemotherapy.
Incidence/Prevalence
In the
an estimated 316,000 new cases of esophageal cancer and 286,000 deaths worldwide (Parkin, Pisani, & Ferley, 1999). Although squamous cell cancer accounts for most cases, the rate of adenocarcinoma of the esophagus is also rapidly increasing. It is usually found at the gastroesophageal junction and the distal portion of the esophagus. The greatest incidence of adenocarcinoma can be found in Caucasian males of middle to upper socioeconomic status (Quinn & Reedy, 1999).
Esophageal cancer is extremely virulent and has a 5-year survival rate of less than 5%.
CULTURAL CONSIDERATIONS
Over the past several decades there have been statistically significant annual increases in the incidence of squamous cell cancer of the esophagus in the
The incidence of esophageal cancer is extremely high in areas of northwest
Slit?
COLLABORATIVE MANAGEMENT
Assessment
history
The nurse assesses the client’s racial and cultural background, age, sex, and any pertinent history of alcohol consumption, tobacco use, dietary habits, and other esophageal problems (e.g., dysphagia, stricture, or reflux). In collaboration with the dietitian, the nurse also collects a nutrition history, including the ingestion of pickled foods, changes in appetite, changes in taste, or a decline in weight. The degree of weight loss over time is also an important consideration.
Cancer of the esophagus is a silent tumor in its early stages, with few signs to identify on assessment. By the time the tumor causes symptoms, it usually has spread rather extensively.
PHYSICAL ASSESSMENT/CLINICAL MANIFESTATIONS
The primary clinical manifestations of esophageal cancer are dysphagia (most common) and weight loss (Brooks-Brunn, 2000). The nurse carefully assesses the degree and severity of dysphagia. Tumor-induced dysphagia is both persistent and progressive. It is initially associated with swallowing solids, particularly meat, and then progresses rapidly over a period of weeks or months to difficulty in swallowing soft foods and liquids. Late in the disease, even saliva can induce choking. Clients usually report a sensation that food is sticking in the throat or in the substernal area. Careful assessment of the dysphagia is an important part of the diagnosis because the dysphagia associated with other esophageal disorders is not usually continuous. Dysphagia does not usually appear until at least 60% of the esophageal diameter is narrowed by the tumor.
Odynophagia (painful swallowing) is present in most clients and is reported as a steady, dull, substernal pain that may radiate. The presence of severe or persistent pain often indicates tumor invasion of the mediastinal structures. The nurse also assesses for the occurrence of regurgitation, vomiting, foul breath, and chronic hiccups, which often accompany advanced disease. In most clients, pulmonary complications develop at some point, and the nurse assesses for the presence of chronic cough, increased secretions, and a history of recent infections.
Tumors in the upper esophagus may involve the larynx and thus cause hoarseness. Chart 55-6 summarizes the clinical manifestations of esophageal tumors.
PSYCHOSOCIAL ASSESSMENT
The symptoms and diagnosis of esophageal cancer can affect a client in profound ways. The disease produces significant daily symptoms, requires major modifications in basic eating patterns, and is terminal. The fear of choking can transform normal mealtimes into frightening experiences that the client may wish to avoid. The nurse carefully assesses the client’s response to the diagnosis and prognosis and explores his or her coping strengths and resources. The impact of the disease on the usual pattern of activities is also assessed. The nurse also assesses the availability of support systems and the potential financial impact of the disease and its treatment.
RADIOGRAPHIC ASSESSMENT
To arrive at a diagnosis of esophageal cancer, the physician first uses a barium swallow study with fluoroscopy. The tumor margins of large masses can often be outlined during this test. A definitive diagnosis of cancer necessitates histologic evidence by means of a tissue biopsy.
■ OTHER DIAGNOSTIC ASSESSMENT
The definitive diagnosis of esophageal cancer is made by esophagogastroduodenoscopy (EGD) with biopsies of the esophagus and tumor. The physician performs an endoscopic examination to inspect the esophagus and to obtain specimens for cytologic studies and staging. Multiple tissue samples may be required when the suspected tumor is in the distal esophagus, because clear tissue samples are difficult to obtain.
KEY FEATURES of Esophageal Tumors
Persistent and progressive dysphagia (most common
feature)
Feeling of food sticking in the throat
Odynophagia (painful swallowing)
Severe, persistent chest or abdominal pain or discomfort
Regurgitation
Chronic cough with increasing secretions
Hoarseness
Anorexia
Nausea and vomiting
Weight loss (often >20 pounds)
Changes in bowel habits (diarrhea, constipation, bleeding)
A complete staging workup is performed to determine the extent of the disease. A computed tomography (CT) scan assists in identifying metastatic disease that can be present in the chest or abdomen. Positron emission tomography (PET) is a newer technology that may identify metastatic disease with more accuracy than a CT scan. Metastasis can also be diagnosed by bone and brain scans or exploratory laparoscopy. An endoscopic ultrasound (EUS) is a staging technique that can help determine the size and depth of tumor invasion. (These tests are described elsewhere in this text.)
CRITICAL THINKING CHALLENGE
· You are gathering the initial history on a 65-year-old female Asian client admitted with dysphagia and a recent weight loss of 20 pounds over 3 months. The client states she used to smoke 2 packs of cigarettes per day for 30 years but quit 15 years ago. The client also admits to a 5-year history of gastrointestinal reflux, especially after eating in the late evening.
· What lifestyle and cultural factors place this client at risk for
esophageal cancer?
· What specific questions would you ask concerning her
swallowing difficulties?
· What additional clinical manifestations should you inquire
about?
Analysis
COMMON NURSING DIAGNOSES AND COLLABORATIVE PROBLEMS
The priority nursing diagnosis for clients with cancer of the esophagus is Imbalanced Nutrition: Less than Body Requirements related to impaired swallowing.
ADDITIONAL NURSING DIAGNOSES AND COLLABORATIVE PROBLEMS
In addition to the commoursing diagnosis, the client with esophageal cancer may develop any of the following due to the impact of the disease and/or treatment:
· Risk for Aspiration related to impaired swallowing sec
ondary to esophageal strictures
· Impaired Swallowing related to obstruction by the tumor
or the effects of radiotherapy
· Acute Pain or Chronic Pain related to the pressure of the tumor mass in the esophagus or mediastinum
· • Ineffective Coping and Compromised Family Coping re
lated to the effects of the disease and to the terminal
prognosis
· Anticipatory Grieving related to declining physical status and terminal prognosis
· • Spiritual Distress related to impending death
· The additional collaborative problem is Potential for Metastasis due to the close proximity of the esophagus to other body structures.
Planning and Implementation
■ IMBALANCED NUTRITION: LESS THAN BODY REQUIREMENTS
INTERVENTIONS. Interventions to maintain or improve the nutritional status of the client must focus on treatments to remove or shrink the obstructive tumor and on ameliorating the effects of treatment that can impact nutritional status.
Treatment options for cancer of the esophagus that can assist in both disease and nutrition management include the following:
· Nutritional support
Radiotherapy
· Photodynamic therapy
· Dilation of strictures
· Prosthesis insertion
· Chemotherapy Surgical removal of the tumor
Much has been done over the last decade to try to improve the outcome for clients diagnosed with esophageal cancer. The typical treatment plan uses a combination of the above approaches. The current trend includes chemotherapy with or without surgery in an effort to improve the odds of obtaining a cure. Clients with cancer of the esophagus can experience many problems, and relieving symptoms becomes an essential consideration.
NUTRITION THERAPY. The purpose of nutrition therapy is the administration of food and fluids to support the metabolic processes of a client who is malnourished or at high risk for becoming malnourished. A thorough nutritional assessment provides members of the health care team with baseline information concerning the client’s nutritional status. The dietitian determines the caloric needs of the client to meet nutritional requirements. The nurse or assistive nursing personnel weighs the client daily. Careful positioning is essential for a client who is experiencing frequent regurgitation or who has prosthetic tubes to keep the esophagus patent. The nurse teaches the client to remain upright for several hours after meals and to avoid lying completely flat. The head of the bed is always elevated 30 degrees or more to prevent reflux.
Semisoft foods and thickened liquids are preferred because they are easier to swallow. Caloric intake and the amount of fluids ingested are monitored daily to monitor progress toward nutritional goals. In addition, liquid nutritional supplements can be used between feedings to increase caloric intake. Ongoing efforts are made to preserve the ability to swallow, but feeding tubes may be needed temporarily when dysphagia is severe. In clients with complete obstruction or life-threatening fistula formation, it may be necessary to create a gastrostomy or jejunostomy. The nurse monitors laboratory and clinical indicators of nutritional status. The client may also benefit from diet teaching and planning.
SWALLOWING THERAPY. The nurse consults with the speech-language pathologist to assist with oral exercises to improve swallowing. A lollipop given to the client to suck on can enhance tongue strength. The client is instructed to reach for food particles on the lips or chin using the tongue. In preparation for swallowing, the nurse assists the client to position the head in forward flexion (chin tuck). The client is instructed to place food at the back of the mouth. The nurse
monitors for the sealing of lips and for tongue movements while eating and also checks for pocketing of food after swallowing. It is important the nurse monitor for signs of aspiration. Family members and/or caregivers are taught how to feed the client, monitor for aspiration, and institute appropriate measures should choking occur. Chart 55-7 provides a summary of NIC interventions.
NONSURGICAL MANAGEMENT. Treatment decisions are based on the location and size of the tumor, the presence of metastasis, the client’s concurrent health status, and the client’s ability to withstand radical surgery.
The focus of nonsurgical treatment is palliative care. The outcomes of palliative care are the relief of symptoms and improved duration of survival. A combination of chemotherapy, radiation, pain control, and nutritional support measures can be used. The physician selects nonsurgical management when a client is either unable or unwilling to undergo extensive surgery.
RADIATION THERAPY. Radiation therapy to manage esophageal cancer is only moderately effective and can be used alone or in combination with other modalities. Used alone, radiation has been effective in the palliation of advanced esophageal cancer, with improvement in symptoms in 50% to 76% of cases (Behrend, 1999). Radiation therapy is contraindicated for clients with tracheoesophageal fistula,
mediastinitis, mediastinal hemorrhage, or infiltration of the cancer to the trachea or bronchus (Gregoire & Fitzpatrick, 1998). Radiation reduces tumor size and offers clients consistent short-term relief. Although higher doses of radiation demonstrate better results, esophageal stricture or stenosis can result in 30% to 50% of clients requiring esophageal dilation. Normal esophageal tissue is very sensitive to the effects of radiation. The treatment is typically administered in twenty episodes over 4 weeks.
INTERVENTION ACTIVITIES/or
The Client with Esophageal Problems
Nutrition Therapy: Administration of food and fluids to support metabolic processes of a client who is malnourished or at high risk for becoming malnourished
• Determine—in collaboration with the dietitian, as appro
priate—number of calories and type of nutrients needed
to meet nutrition requirements.
• Assist the client to a sitting position before eating or
feeding.
• Encourage the client to select semisoft food, if lack of
saliva hinders swallowing.
• Select malts, shakes, and ice cream to supplement
nutrition
• Monitor food/fluid ingested and calculate daily caloric in
take, as appropriate
• Determine need for nasogastric tube feedings
Swallowing Therapy: Facilitating swallowing and preventing complications of impaired swallowing
• Collaborate with speech therapist to instruct client/family
about swallowing exercise regimen.
• Explain the rationale of the swallowing regimen to
client/family.
• Provide a lollipop for client to suck on to enhance tongue
strength, if appropriate.
• Assist client to position head in forward flexion in prepa
ration for swallowing (“chin tuck”).
• Assist client to place food at back of mouth and on unaf
fected side.
• Monitor for signs and symptoms of aspiration.
• Instruct family/caregiver how to position, feed, and moni
tor client.
• Instruct client/caregiver on emergency measures for
choking.
In the first weeks of treatment, radiation produces edema and epithelial desquamation, which often create acute esophagitis and odynophagia (painful swallowing). Profound anorexia, nausea, and vomiting may also result. Symptoms persist until treatment is completed. The nurse assesses the client frequently to determine the incidence and severity of symptoms. Systemic analgesics are often required to control discomfort, and the nurse administers topical lidocaine (Viscous Xylocaine) before each attempt at oral feeding.
The nurse works with the client to modify the diet to meet nutritional needs and maintain comfort. Small, frequent, soft or semiliquid meals are offered. Sweet, light foods are often tolerated best, and protein powder may be used to supplement the nutritional content of the diet. The nurse maintains accurate records of calorie counts, intake and output, and daily weights and also assesses skin turgor and mucous membranes regularly. In collaboration with the physician and dietitian, the nurse assesses the need for enteral nutrition if oral intake is insufficient.
For clients receiving radiation therapy, frequent gentle mouth care is important. Clients are at risk for monilial esophagitis, and the nurse is alert to any abrupt worsening of symptoms. Chapter 25 describes additional nursing interventions for the client undergoing radiation therapy.
PHOTODYNAMIC THERAPY. Photodynamic therapy (PDT) was originally used for the treatment of skin cancer. In 1995 it was approved for use as a palliative treatment for individuals with advanced esophageal cancer, who are not candidates for surgery. The client is injected with porfimer sodium (Sanofi Pharmaceuticals,
The side effects of Photofrin are rare but include nausea, fever, and constipation. After the procedure, the client is given written guidelines concerning photosensitivity measures. The client is instructed to avoid exposure to sunlight for 1 month. Sunglasses and protective clothing that covers all exposed body areas are essential. The client may experience chest pain secondary to tissue damage and will require pain relief with opioids for a short time. The client is instructed to follow a clear liquid diet for 3 to 5 days after the procedure and advance to full liquids as tolerated (Durkin, 1999).
ESOPHAGEAL DILATION. Esophageal dilation may be performed as necessary throughout the course of the disease to achieve temporary but immediate relief of dysphagia. Esophageal dilation can be performed on an ambulatory care basis. The physician uses dilators to tear soft tissue, widening the esophageal lumen. In most cases, malignant tumors may
be dilated safely, but perforation remains a significant risk. Bacteremia can also occur. To reduce the risk of endocarditis, the American Heart Association recommends prophylaxis with antibiotics (Behrend, 1999). The treatment is repeated as often as needed to preserve the client’s ability to swallow (see p. 1204).
PROSTHESIS INSERTION. The physician may insert a semirigid prosthesis to bypass disabling dysphagia and to prevent aspiration in clients who have advanced disease or tra-cheoesophageal (TE) or esophagobronchial (EB) fistulas. Prosthesis insertion can maintain an open esophagus and preserve the client’s ability to receive oral nourishment and thus palliate the symptoms related to obstruction. The procedure is not without risk, and acute complication rates have been reported to occur in 16% to 18% of clients (Raltz & Kozarek, 1999). The prosthesis can become dislodged, migrate, or perforate the esophagus as tumor bulk increases.
The nurse’s primary care emphasis is the prevention of aspiration. The prosthesis interrupts the function of the lower esophageal sphincter (LES) and permits the free reflux of gastric contents. The nurse supervises the client closely, offers small oral feedings, and ensures that the client does not lie flat in bed.
CHEMOTHERAPY. The use of chemotherapy in the treatment of esophageal cancer has been only moderately effective. The two chemotherapeutic agents used to treat squamous cell carcinoma are 5-fluorouracil (5-FU) and cisplatin. Currently, there is no standard treatment for adenocarcinoma of the esophagus. Chemotherapy can be given before surgery to decrease tumor size, thereby facilitating surgical resection (Quinn & Reedy, 1999). Chemotherapy appears to be more effective when given in combination with radiation. Cisplatin and 5-FU make the tumor cells more sensitive to the effects of radiation. Chemotherapy can be administered concurrently with radiotherapy before surgery. This treatment is thought to provide the client with the best chance of cure.
CRITICAL THINKING CHALLENGE
· Your client has been diagnosed with esophageal cancer and is undergoing preoperative radiation for tumor reduction before surgical resection.
· What possible complications related to this treatment
should the nurse assess for?
· What nursing interventions could be instituted to assist the
client in maintaining adequate nutritional intake?
· What should the nurse include in the teaching plan for this
client?
SURGICAL MANAGEMENT
Radical surgery represents the only definitive treatment for esophageal cancer and is the preferred treatment for clients with no evidence of advanced disease. The goals of surgical resection vary from palliation to cure. Esophagectomy is an extensive surgical procedure and is associated with significant morbidity and mortality. Mortality from the surgical procedure ranges from 10% to 20%. Complications from surgery (e.g., fistula formation, abscess, and respiratory complications) occur in 20% to 50% of individuals (Behrend, 1999; Mayer, 1998).
PREOPERATIVE CARE. Preoperative preparation for clients undergoing esophagectomy or esophagogastrostomy can be quite extensive. Clients are advised to stop smoking 2 to 4 weeks before surgery to enhance their pulmonary functioning. Client preparation for surgery may include 5 days to 2 to 3 weeks of nutritional support in an effort to improve their nutritional status and decrease postoperative morbidity. Ideally, this supplementation is given orally, but most clients usually require tube feeding or parenteral nutrition. The role of parenteral nutritional support in these clients remains controversial (Sikora et al., 1998). The nurse carefully monitors the client’s weight, intake and output, and fluid and electrolyte balance. A preoperative dental evaluation may be required to remove pre-existing dental caries. Meticulous oral care is performed four times daily to decrease the risk of postoperative infection.
Preoperative nursing care also focuses on teaching and on psychologic support. The nurse ensures that the client is knowledgeable about the surgery and its outcomes. The physician’s instructions are clarified and reinforced as needed. The nurse explains the following:
• The number and sites of all incisions and drains
• The placement of a jejunostomy tube for initial enteral
feedings
• The need for chest tubes if the pleural space is entered
• The purpose of the nasogastric tube
• The need for intravenous (IV) infusion
The client visits the critical care unit, if possible, and initiates contacts with unit staff.
The nurse instructs the client about routines for turning, coughing, deep breathing, and chest physiotherapy. The crucial nature of postoperative respiratory care is emphasized. The nurse addresses the probable need for ventilator support, because respiratory management is a major focus of postoperative care. If colon interposition is planned, the client also undergoes a complete bowel preparation with laxatives and enemas before surgery.
The client facing a serious illness and extensive surgery can be expected to display feelings of grief and anxiety. The nurse encourages the client to talk about personal feelings and fears and involves the family or significant others in all preoperative teaching and discussions. A primary nurse or case manager can be extremely helpful in providing continuity of care and support to the entire family.
OPERATIVE PROCEDURES. A subtotal or total esophagectomy is usually required because tumors are often quite large and involve distant lymph nodes. Several procedures have been used, but the preferred surgical procedure is an esophagogastrostomy. The diseased portion of the esophagus is removed, and the cervical portion is anastomosed (connected) to the stomach. The cervical portion of the stomach is then brought up into the thorax through the esophageal hiatus (Figure 55-5). A vagotomy is also usually performed with this type of resection, resulting in hypertonicity of the pylorus. A pyloromyotomy is created to prevent gastric motility disturbances. Lastly, a jejunostomy tube is placed for postoperative enteral feeding.
For a client with early stage tumors of the lower third of the esophagus, a transhiatal esophagectomy is the preferred surgical approach. The surgery is performed through an upper midline cervical incision. With this approach there is no entry into the pleural space, thereby minimizing respiratory complications.
For a client with tumors in the upper esophagus, radical neck dissection and laryngectomy may also be required because of the spread of disease to the larynx. The surgeon may perform a colon interposition when the tumor involves the stomach or the stomach is otherwise unsuitable for anastomosis. A section of right or left colon is removed and brought up into the thorax to substitute for the esophagus (see Figure 55-5).
These surgical procedures pose cardiovascular risks for the client. Intraoperative hypotension can result from pressure on the posterior heart. Decreased lymphatic pulmonary clearance can predispose the client to pulmonary edema when mediasti-nal lymph nodes and lymphatics are resected. The stress placed on the heart by extensive surgery can increase the risk of myocardial ischemia and dysrhythmias, especially if the client has underlying coronary disease.
The client with compromised nutritional status or prior radiation or chemotherapy is predisposed to an increased risk of infection. For clients who undergo more radical surgical procedures, there is a serious risk of leakage at the anastomosis site. This situation is especially true with colon interpositions because several anastomosis sites are vulnerable to the effects of tension, poor blood supply, and delayed healing. Medias-tinitis resulting from an anastomotic leak can lead to fatal sepsis.
POSTOPERATIVE CARE. The client requires meticulous postoperative care and is at risk for multiple serious complications. The Client Care Plan on pp. 1199 and 1200 outlines client interventions for esophageal surgery.
Respiratory Care. Respiratory care is the highest postoperative priority, and the client is usually intubated and mechanically ventilated for at least the first 24 hours. Postoperative pulmonary complications include atelectasis and pneumonia. The risk of postoperative pulmonary complications is increased in the client who has received preoperative radiation. Once the client is extubated, the nurse begins deep breathing, turning, and coughing routines. Chest physiotherapy is initiated as ordered, usually every 2 to 4 hours. The nurse assesses the client for decreased breath sounds and shortness of breath every 1 to 2 hours. Incisional support and adequate analgesia are essential for effective coughing and should be administered regularly if the client’s vital signs remain stable. The nurse keeps the client in a semi-Fowler’s or high Fowler’s position to support ventilation and prevent reflux. The physician prescribes prophylactic antibiotics and supplemental oxygen; blood gases are ordered regularly. The nurse ensures the patency of the water seal drainage system for chest tubes and monitors for changes in the volume or color of the drainage.
Cardiovascular Care. Hypotension can occur secondary to pressure placed on the posterior heart and may respond well to vigorous IV fluid administration. The nurse also monitors for signs and symptoms of fluid volume overload, particularly in clients who have undergone lymph node dissection. The nurse assesses for edema, crackles in the lungs, and increased jugular venous pressure. In the immediate postoperative phase, the client may be admitted to the intensive care unit. Critical care nurses assess hemodynamic parameters such as cardiac output, cardiac index, and systemic vascular resistance every 2 hours to monitor for myocardial ischemia.
I
Figure 55-5 • Surgical approaches to the treatment of esophageal cancer.
Atrial fibrillation is a dysrhythmia that results from irritation of the vagus nerve during surgery. Management of atrial fibrillation can include digitalization, beta blockers, or car-dioversion. (See Chapter 34 for more information on atrial fibrillation.)
Wound Management. Wound management is another significant postoperative concern because the client typically has multiple incisions and drains. The nurse provides inci-sional support during turning and coughing to prevent dehis-cence. Wound infection usually occurs 4 to 5 days after surgery. Postoperative leakage from the site of anastomosis is a dreaded complication that can appear 2 to 10 days after surgery. If an anastomic leak occurs, all oral intake is discontinued and is not resumed until the leak has healed. Nutrition may be given through the jejunostomy tube during the healing process. The nurse carefully assesses for fever, fluid accumulation, general signs of inflammation, and symptoms of early shock (e.g., tachycardia, tachypnea) and reports these findings to the health care provider immediately.
Nasogastric Tube Management. A nasogastric (NG) tube is placed intraoperatively to decompress the suture line. The nurse monitors the NG tube for patency and carefully secures the tube to prevent dislodgment, which can disrupt the sutures at the anastomosis. The nurse does not independently irrigate or reposition the NG tube in clients who have undergone esophageal surgery. The initial nasogastric drainage is bloody but should change to a greenish yellow color by the end of the first postoperative day. The continued presence of blood may indicate bleeding at the suture line. The nurse provides oral hygiene every 2 to 4 hours while the tube is in place (Chart 55-8).
BEST PRACTICE/or
Managing the Client with a Nasogastric Tube
After Esophageal Surgery
Check for tube placement every 4 to 8 hours. Ensure that the tube is patent (open) and draining; drainage should turn from bloody to yellowish green by the end of the first postoperative day. Secure the tube well to prevent dislodgment. Do not irrigate or reposition the tube without a physician’s order.
Provide meticulous oral and nasal hygiene every 2 to 4 hours.
Keep the head of the bed elevated to at least 30 degrees.
When the client is permitted to have a small amount of water, place the client in an upright position and observe for dysphagia (difficulty swallowing). Observe for leakage from the anastomosis site, as indicated by fever, fluid accumulation, and manifestations of early shock (tachycardia, tachypnea, altered mental status).
Nutritional Care. The nutritional management of the client who has undergone an esophageal surgery is an early postoperative concern. On the second postoperative day, initial feedings begin through the jejunostomy tube. The feedings are slowly increased over the next several days. Feeding by this method can be discontinued once the client is taking adequate oral nutrition. However, some clients may require jejunostomy feedings for approximately 1 month if small amounts of aspiration are detected.
Before beginning oral feedings, a cine-esophagram study is performed to detect the presence of anastomotic leaks, strictures, or signs of aspiration. If no leaks are detected, an esophageal diet is begun, starting with liquids. If liquids are well tolerated, the client’s diet is advanced to include semi-solid foods and then solid foods. The nurse supervises the client during all initial swallowing efforts and ensures that he or she is in an upright position. The food storage area of the stomach has been radically decreased, and gravity is the client’s only real defense against reflux. The nurse continues to assess for signs of leakage.
The client is instructed to consume 6 to 8 meals per day and to ingest fluids between, rather than with, meals to prevent diarrhea. Diarrhea can occur 20 minutes to 2 hours after eating and can be symptomatically managed with loperamide before meals. The diarrhea is thought to be the result of va-gotomy syndrome, which develops as a result of the interruption of vagal fibers to the abdominal viscera during surgery. This syndrome is diminished by pyloroplasty.
CRITICAL THINKING CHALLENGE
· Your client has completed a course of preoperative radiation therapy, and has undergone an esophagogastrostomy as part of her esophageal cancer treatment.
· What postoperative complications should you assess for
and why?
· What nursing interventions would be most appropriate for
preventing postoperative complications?
Community-Based Care
Clients with esophageal cancer have many challenges to face once they are discharged home. The combination treatment regimens cause long-lasting side effects, such as fatigue and weakness. These complex treatments also require the client to be knowledgeable about symptom management and to know when to report issues of concern to the health care provider. (See Chapter 25 for care of the client undergoing radiation therapy and chemotherapy.)
HOME CARE MANAGEMENT
The care given in the hospital is continued after discharge to the community. Ongoing respiratory care is a priority, and family members are instructed to assist with ambulation, splinting incisions, and use of the incentive spirometer. The nurse teaches the family to protect the client from infection and to contact the physician immediately if signs of respiratory infection develop. The client is encouraged to be as active as possible and to avoid excessive bedrest and its complications at all costs.
HEALTH TEACHING
Wound healing is also an ongoing concern. The nurse teaches the client and family to inspect the incisions daily for redness, tenderness, swelling, odor, and discharge. The client and family are instructed to report a temperature greater than 101° F (38.3° C).
The nurse prepares written instructions about the signs of anastomosis leakage and the importance of reporting them to the physician or other health care provider immediately. The client and family members are instructed to report the presence of fever and a swollen, painful neck incision, which indicates a cervical anastomotic leak (Gregoire & Fitzpatrick, 1998).
Nutritional support also remains a concern. The nurse encourages the client to continue increasing oral feedings as tolerated. The client is reminded to eat a high-calorie, high-protein diet that contains soft and easily swallowed foods. Meals should be small and frequent, and nutritionally empty foods are avoided. Eggnogs and milkshakes may be easily prepared and enriched to supplement meals. The client needs to learn what foods can be tolerated and needs to adjust his or her eating pattern to ingest food more slowly than before. Individuals who have undergone esophageal resection can lose up to 10% of their body weight. The client is taught to monitor his or her weight at home and to report a weight loss of 5 pounds or more. If sufficient oral intake is not possible, the family may need instruction about tube feedings or parenteral nutrition at home. (See the Legal/Ethical Issues in Health Care box above.)
WITHHOLDING FOOD AND FLUIDS
Providing nutrition and hydration by means of IV catheters or gastric intubation raises many issues. Societal norms surround the provision of food and fluids to individuals who are deemed vulnerable, and this act is viewed differently than complex medical interventions. In addition, there is concern that withholding food and fluids may cause discomfort or suffering. Although there is agreement that ethical principles should be used to guide decision making in the provision or withdrawal of food and fluids, there is evidence to suggest that there are few potential benefits to providing nutrition to those with terminal or protracted illnesses.
Although there are no easy answers to this dilemma, a guide to decision making is suggested. The first consideration should be the previous wishes and evidence of current sensation of the individual involved. Second, the benefits and burdens of nutrition and hydratioeed to be evaluated in terms of long- and short-term goals. Finally, the interests of all parties involved should be represented. Clinicians should focus on reaching a consensus by incorporating an existing knowledge of feeding and hydration with consideration based on the wishes of the individual. The views of all stakeholders, and the given benefits and burdens of each case should also weigh in the decision.
The nurse emphasizes the importance of keeping the client upright after meals and elevating the head of the bed on blocks. Families are counseled that dysphagia or odynophagia may recur because of stricture, reflux, or cancer recurrence. These symptoms should be promptly reported to the health care provider.
Despite radical surgery, the client with cancer of the esophagus still has a terminal illness and a relatively short life expectancy. Emphasis is placed on maximizing quality of life. Realistic planning is important as the client’s condition eventually worsens, and the client and family are assisted to plan for the future together. The nurse assists family members in exploring formal and informal sources of support. When
needed, the nurse helps the family or significant others arrange for hospice care.
HEALTH CARE RESOURCES
The nurse initiates referrals to community or home care organizations to assist the family in providing the needed home care. The client may need transportation to the radiation treatment center 5 times per week for up to 6 weeks. Oncology nursing care may be needed to monitor and evaluate the client who is receiving chemotherapy at home through venous access devices or portable infusion pumps. In addition, the nurse informs the family about the services available through the American Cancer Society. The nurse may also acquaint the family with area hospice services for future planning.
Evaluation: Outcomes
MM The nurse evaluates the care of the client with esophageal cancer on the basis of the identified nursing diagnoses and collaborative problems. The expected outcomes are that the client:
· Maintains hemodynamic stability free of cardiovascular
complications
· Maintains a patent airway free of respiratory complications
· Is free of infection
· » Is able to consume adequate nutrition and maintain a stable weight
· Is able to swallow comfortably
· States that pain is controlled through pharmacologic and
nonpharmacologic pain control measures
· Successfully adapts to the stresses surrounding the diag
nosis and treatment with meaningful support from fam
ily or significant others
DIVERTICULA
OVERVIEW
Diverticula are sacs resulting from the herniation of esophageal mucosa and submucosa into surrounding tissue. Clients complain of dysphagia, regurgitation, nocturnal cough, and halitosis (bad breath).
Diverticula may develop anywhere along the length of the esophagus. No environmental risk factors are known to be involved in the development of esophageal diverticula. The incomplete or late opening of the cricopharyngeal muscle during swallowing leads to high pressures in the hypopharynx and leads to Zenker’s diverticulum, the most common form. Zenker’s diverticulum occurs most often in older adults. Clients with esophageal diverticula can be at risk for esophageal perforation because the mucosa is without the protection of the normal esophageal muscle layer.
sists the client in exploring variations in the size and frequency of meals and in food texture and consistency. Semisoft foods and smaller meals are often best tolerated and may reduce or relieve the symptoms of pressure and reflux. Individual food tolerances and intolerances are explored with the client.
As with other forms of reflux, nocturnal problems associated with diverticula are best managed by sleeping with the head of the bed elevated and avoiding the recumbent position for at least 2 hours after eating. The client is also counseled to avoid vigorous exercise after meals. The nurse advises the client to avoid restrictive clothing and frequent stooping or bending.
Surgical management is aimed at excising the diverticula and reapproximating the mucosa. Most physicians use the cervical surgical approach above the clavicle. Postoperatively, the client takes nothing by mouth for several days to promote healing and receives IV fluids for hydration, tube feedings, and then oral fluid and food. The nurse provides pain relief measures and monitors for complications such as bleeding or perforation. A nasogastric (NG) tube is placed during surgery for decompression and is not irrigated or repositioned unless specifically ordered by the surgeon. This tube may be used later for feeding.
Community-based care includes teaching the client and family about the following:
* Tube feeding and resuming an oral diet
* Positioning guidelines to prevent reflux
* Warning signs of complications
Community resources are usually not needed for uncomplicated cases.
TRAUMA
OVERVIEW
Trauma to the esophagus can result from blunt injuries, chemical burns, surgery or endoscopy, or the stress of protracted severe vomiting (Table 55-2). Trauma may affect the esophagus directly, impairing swallowing and nutrition, or it may create problems and complications in related structures such as the lungs or mediastinum. The incidence of most forms of esophageal trauma is low in adults.
When excessive force is exerted on the esophageal mucosa, it may perforate or rupture, allowing the caustic acid secretions to enter the mediastinal cavity. These tears are associated with a high mortality rate related to shock, respiratory impairment, or sepsis.
Chemical injury is usually a result of the accidental or intentional ingestion of caustic substances. The oral cavity is also usually damaged, and the damage is rapid and severe. Acid burns tend to affect the superficial layers of the esophagus, whereas alkaline substances cause deeper penetrating injuries.
TABLE 55-2 CAUSES OF ESOPHAGEAL PERFORATION
Straining
Seizures
Trauma
Foreign objects
Instruments or tubes
Chemical injury
Complications of esophageal surgery
Ulcers
COLLABORATIVE MANAGEMENT
The diagnosis of esophageal diverticula is made by x-ray examination and barium swallow. Endoscopy must be performed with strict care in these clients, because perforation can occur.
Diet therapy and positioning are the major interventions for controlling symptoms related to diverticula. The dietitian asagement. When caustic burns involve the oral cavity, topical agents, such as 50/50 diphenhydramine hydrochloride (Ben-adryl) and kaolin with pectin (Ka-Pectolin) or topical lido-caine (Viscous Xylocaine), may be used for topical analgesia and local anti-inflammatory action.
If nonsurgical management is not effective in healing traumatized esophageal tissue, the client may need surgery to remove the damaged tissue. The client with severe injuries may require resection of part of the esophagus with a gastric pull-through and repositioning or replacement by a bowel segment. (See Surgical Management [Esophageal Tumors], pp. 1208 and 1209.)
2. Ihterventions 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 by
histamine 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. The amount 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 (see Chapter 55).
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 (see Chart 56-2).
DIAGNOSTIC ASSESSMENT
Esophagogastroduodenoscopy (EGD) via an endoscope with biopsy is the gold standard for diagnosing gastritis, as well as detecting 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.
KEY FEATURES of
Gastritis
Acute Gastritis
Rapid onset of epigastric pain or discomfort Nausea and vomiting Hematemesis (vomiting blood) Gastric hemorrhage Dyspepsia (heartburn) Anorexia
Chronic Gastritis
Vague complaint of epigastric pain that is relieved by food
Anorexia
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. pylori infection, 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 in biopsy 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. These medications include chemotherapeutic agents, corticosteroids, erythromycin (E-Mycin, Erythromid’*1), and NSAIDs, such as aspirin, 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
|
|
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).
i 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 56-2 # The most common sites for peptic ulcers. Figure 56-1 • 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 the client 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.
Figure 56-3 • Common causes of upper gastrointestinal bleeding.
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 with H. 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
EVIDENCE-BASED PRACTICE FOR NURSING
Fecal and oral shedding of Helicobacter pylori from healthy infected adults
Parsonnet, J., Shmuely, H. & Haggerty.T. (1999). Fecal and oral shedding of Helicobacter pylori from healthy adults. Journal of the American Medical Association, 282(23), 2240-2245.
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 13C breath testing for H. pylori infection. A total of 16 asymptomatic H. py/ori-infected adults and 10 uninfected adults participated in the study.
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 20 mm Hg in systolic blood pressure, a decrease of 10 mm Hg in diastolic blood pressure, and/or an increase in pulse when the client rises from a lying to an erect (sitting or, if possible, standing) position. The nurse also assesses for dizziness, especially when the client is upright, since this is another symptom of fluid volume deficit.
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 eradicating H. 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. pylori infection 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 the amount 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 H2 blockers 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 of H. 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 and iron 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 also taught 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 for lifestyle 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. For postsurgical 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 most common 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 subtotal gastrectomy 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.
