CHAPTER 55 Care of Patients with Stomach Disorders – Flashcards

Gastritis is the inflammation of gastric mucosa (stomach lining). Gastritis can be erosive (causing ulcers) or nonerosive. 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 worsened by histamine release and vagus nerve stimulation. Hydrochloric acid can then diffuse back into the mucosa and injure small vessels. This back-diffusion causes edema, hemorrhage, and erosion of the stomach's lining.

Inflammation of the gastric mucosa or submucosa after exposure to local irritants or other causes can result in acute gastritis. Early pathologic manifestation of gastritis is a thickened, reddened mucous membrane with prominent rugae, or folds. Chronic gastritis appears as a patchy, diffuse (spread out) inflammation of the mucosal lining of the stomach. 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. Intrinsic factor is critical for absorption of vitamin B12. When body stores of vitamin B12 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. Increased cancer risk. 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.

The onset of infection with Helicobacter pylori can result in acute gastritis. Less common, other forms of bacterial gastritis from organisms such as staphylococci, streptococci, Escherichia coli, or salmonella. Long-term NSAID use creates a high risk for acute gastritis. NSAIDs inhibit prostaglandin production in the mucosal barrier. Other risk factors include alcohol, coffee, caffeine, and corticosteroids. Acute gastritis is also caused by local irritation from radiation therapy and accidental or intentional ingestion of corrosives. Type A chronic gastritis has been associated with the presence of antibodies to parietal cells and intrinsic factor. Therefore an autoimmune cause for this type of gastritis is likely. The most common form of chronic gastritis is type B gastritis, caused by H. pylori infection. Chronic local irritation and toxic effects caused by alcohol ingestion, radiation therapy, and smoking have been linked to chronic 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, nickel) or H. pylori infection, or it can be related to autoimmune factors. Atrophic gastritis can lead to two types of cancer: gastric cancer and gastric mucosa-associated lymphoid tissue (MALT) lymphoma.

A balanced diet, regular exercise, and stress-reduction techniques can help prevent it (Chart 55-1). A balanced diet includes following the recommendations of the U.S. Department of Agriculture (USDA) and limiting intake of foods and spices that can cause gastric distress, such as caffeine, chocolate, mustard, pepper, and other strong or hot spices. Alcohol and tobacco should also be avoided. Regular exercise maintains peristalsis, which helps prevent gastric contents from irritating the gastric mucosa. Stress-reduction techniques can include aerobic exercise, meditation, reading, and/or yoga, depending on individual preferences. Excessive use of aspirin and other NSAIDs should also be avoided. If a family member has H. pylori infection or has had it in the past, patient testing should be considered.

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The patient may report epigastric discomfort or pain, anorexia, 1128cramping, nausea, and vomiting (Chart 55-2). Assess for abdominal tenderness and bloating, hematemesis (vomiting blood), or melena (dark, sticky feces, as evidence of blood in the stool). Aspirin/NSAID-related gastritis may result in dyspepsia (heartburn). 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. In some cases gastric hemorrhage is the presenting symptom, which is a life-threatening emergency. Chronic gastritis causes few symptoms unless ulceration occurs. Patients may report nausea, vomiting, or upper abdominal discomfort. Periodic epigastric pain may occur after a meal. Some patients have anorexia. Esophagogastroduodenoscopy (EGD) via an endoscope with biopsy is the gold standard for diagnosing gastritis. A cytologic examination of the biopsy specimen is performed to confirm or rule out gastric cancer. Tissue samples can also be taken to detect H. pylori infection using rapid urease testing. The results of these tests are more reliable if the patient has discontinued taking antacids for at least a week.

Acute gastritis is treated symptomatically and supportively. When the cause is removed, pain and discomfort usually subside. If bleeding is severe, a blood transfusion may be necessary. Fluid replacement is prescribed for patients with severe fluid loss. Surgery, such as partial gastrectomy, pyloroplasty, and/or vagotomy, may be needed for patients with major bleeding or ulceration. Treatment of chronic gastritis varies with the cause. The approach to management includes the elimination of causative agents, treatment of any underlying disease (e.g., uremia, Crohn's disease), avoidance of toxic substances (e.g., alcohol, tobacco), and health teaching. Drugs and nutritional therapy are also used. In the acute phase the health care provider prescribes drugs that block and buffer gastric acid secretions to relieve pain. H2-receptor antagonists, such as famotidine (Pepcid) and nizatidine (Axid), are typically used to block gastric secretions. Sucralfate (Carafate, Sulcrate ), 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). Antisecretory agents (proton pump inhibitors [PPIs]) such as omeprazole (Prilosec) or pantoprazole (Protonix) may be prescribed to suppress gastric acid secretion

Teach the patient to monitor for symptom relief and side effects of drugs to treat gastritis and to notify the health care provider of any adverse effects or worsening of gastric distress. The dose, frequency, or type of drug may need to be changed if symptoms of gastric irritation appear or persist. Remind patients not to take additional over-the-counter (OTC) drugs such as Pepcid AC or Axid AR if they are taking similar prescribed drugs.

Patients with chronic gastritis may require vitamin B12 for prevention or treatment of pernicious anemia. If H. pylori is found, the health care provider treats the infection. Avoid drugs and other irritants that are associated with gastritis episodes, if possible. These drugs include corticosteroids, erythromycin (E-Mycin, Erythromid ), ASA (aspirin), and NSAIDs such as naproxen (Naprosyn) and ibuprofen (Motrin, Advil, Amersol , Novo-Profen ). NSAIDs are also available as OTC drugs and should not be used. Teach patients to read all OTC drug labels because many preparations contain aspirin or other NSAID. Instruct the patient to limit intake of any foods and spices that cause distress, such as those that contain caffeine or high acid content (e.g., tomato products, citrus juices) or those that are heavily seasoned with strong or hot spices. Bell peppers and onions are also commonly irritating foods. Most patients seem to progress better with a bland, non-spicy diet and smaller, more frequent meals. Alcohol and tobacco should also be avoided. Teach the patient about various techniques that reduce stress and discomfort, such as progressive relaxation, cutaneous stimulation, guided imagery, and distraction.

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A peptic ulcer is a mucosal lesion of the stomach or duodenum. Peptic ulcer disease (PUD) results when mucosal defenses become impaired and no longer protect the epithelium from the effects of acid and pepsin.

Three types of ulcers may occur: gastric ulcers, duodenal ulcers, and stress ulcers (less common). Most gastric and duodenal ulcers are caused by H. pylori infection. Urease produced by H. pylori breaks down urea into ammonia, which neutralizes the acidity of the stomach. Urease can be detected through laboratory testing to confirm the H. pylori infection. Gastric ulcers usually develop in the antrum of the stomach near acid-secreting mucosa. When a break in the mucosal barrier occurs (such as that caused by H. pylori infection), hydrochloric acid injures the epithelium. Gastric ulcers may then result from back-diffusion of acid or dysfunction of the pyloric sphincter (Fig. 55-1). Without normal functioning of the pyloric sphincter, bile refluxes (backs up) into the stomach. This reflux of bile acids may break the integrity of the mucosal barrier, which leads to mucosal inflammation. Toxic agents and bile then destroy the membrane of the gastric mucosa. Gastric emptying is often delayed in patients with gastric ulceration. This causes regurgitation of duodenal contents, which worsens the gastric mucosal injury. Decreased blood flow to the gastric mucosa may also alter the defense barrier. Usually occur on the lesser curvature of the stomach, near the pylorus. Duodenal ulcers occur in the upper portion of the duodenum. They are 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 main feature of a duodenal ulcer is high gastric acid secretion. pH levels are low (excess acid) in the duodenum for long periods. Protein-rich meals, calcium, 1130and vagus nerve 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. Stress ulcers are acute gastric mucosal lesions occurring after an acute medical crisis or trauma, such as sepsis or a head injury. In the patient who is NPO for major surgery, gastritis may lead to stress ulcers, which are multiple shallow erosions of the stomach and occasionally the proximal duodenum. Patients who are critically ill, especially those with extensive burns (Curling's ulcer), sepsis (ischemic ulcer), or increased intracranial pressure (Cushing's ulcer), are also susceptible Bleeding caused by gastric erosion is the main manifestation of acute stress ulcers. Stress ulcers are associated with lengthened hospital stay and increased mortality rates. Therefore most patients who have major trauma or surgery receive IV drug therapy (e.g., PPI) to prevent stress ulcer development.

Common complications of PUD are hemorrhage, perforation, pyloric obstruction, and intractable disease. Hemorrhage is the most serious complication. It tends to occur more often in patients with gastric ulcers and in older adults. Many patients have a second episode of bleeding if underlying infection with H. pylori remains untreated or no H2 antagonist used. The patient vomits bright red or coffee-ground blood (hematemesis). Hematemesis usually indicates bleeding at or above the duodenojejunal junction (upper GI bleeding). Minimal bleeding from ulcers is manifested by occult blood in a dark, "tarry" stool (melena). The digestion of blood within the duodenum and small intestine may result in this black stool. Gastric acid digestion of blood typically results in a granular dark vomitus (coffee-ground appearance). Perforation occurs when the ulcer becomes so deep that the entire thickness of the stomach or duodenum is worn away. The stomach or duodenal contents can then leak into the peritoneal cavity. Sudden, sharp pain begins. The abdomen is tender, rigid, and boardlike (peritonitis). The patient often assumes a "fetal" position to decrease the tension on the abdominal muscles. He or she can become severely ill within hours. Bacterial septicemia and hypovolemic shock follow. Peristalsis diminishes, and paralytic ileus develops. Peptic ulcer perforation is a surgical emergency and can be life threatening! Pyloric (gastric outlet) obstruction (blockage) occurs in a small percentage of patients 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. Obstruction include abdominal bloating, nausea, and vomiting. When vomiting persists, the patient may have 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.

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Peptic ulcer disease is caused most often by bacterial infection with H. pylori and NSAIDs. NSAIDs (e.g., ibuprofen) break down the mucosal barrier and disrupt the mucosal protection mediated systemically by cyclooxygenase (COX) inhibition. COX-2 inhibitors (celecoxib [Celebrex]) are less likely to cause mucosal damage but place patients at high risk for cardiovascular event. NSAIDs cause decreased endogenous prostaglandins, resulting in local gastric mucosal injury. Corticosteroids (e.g., prednisone), theophylline (Theo-Dur), and caffeine stimulate hydrochloric acid production. Patients receiving radiation therapy may also develop GI ulcers. Other risk factors for PUD are the same as for gastritis (see Chart 55-1).

Collect data related to the causes and risk factors for peptic ulcer disease (PUD). Question the patient about factors that can influence the development of PUD, including alcohol intake and tobacco use. Note if certain foods such as tomatoes or caffeinated beverages precipitate or worsen symptoms. Information regarding actual or perceived daily stressors also. A history of current or past medical conditions focuses on GI problems, particularly any history of diagnosis or treatment for H. pylori infection. Review all prescription and OTC drugs the patient is taking. Specifically inquire whether the patient is taking corticosteroids, chemotherapy, or NSAIDs. Also ask whether he or she has ever undergone radiation treatments. Assess whether the patient has had any GI surgeries. A history of GI upset, pain and its relationship to eating and sleep patterns, and actions taken to relieve pain are also important. Inquire about any changes in the character of the pain.

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 patient typically has a rigid, boardlike abdomen accompanied by rebound tenderness and pain. Initially, auscultation of the abdomen may reveal hyperactive bowel sounds, but these may diminish. Dyspepsia (indigestion) is the most commonly reported symptom associated with PUD. It is typically described as sharp, burning, or gnawing pain. Some patients may perceive discomfort as a sensation of abdominal pressure or of fullness or hunger. Older adults often have more nausea and vomiting rather than abdominal discomfort. Gastric ulcer pain often occurs in the upper epigastrium with localization to the left of the midline and is aggravated by food. Duodenal ulcer pain is usually located to the right of or below the epigastrium. The pain associated with a duodenal ulcer occurs 90 minutes to 3 hours after eating and often awakens the patient at night. Made worse by certain foods (e.g., tomatoes, hot spices, fried foods, onions, alcohol, caffeine drinks) and certain drugs (e.g., NSAIDs, corticosteroids). Nausea and vomiting may be symptoms accompanying ulcer disease, most commonly with pyloric sphincter dysfunction. Appetite is generally maintained. Take orthostatic blood pressures and monitor for signs and symptoms of dehydration. Also assess for dizziness, especially when the patient is upright, because this is a symptom of fluid volume deficit. Older adults often experience dizziness when they get out of bed and are at risk for falls.

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Although the breath and stool tests are considered more accurate, serologic testing for H. pylori antibodies is the most common method to confirm H. pylori infection. The urea breath test involves swallowing a capsule, liquid, or pudding that contains urea with a special carbon atom. After a few minutes the patient exhales, and if the special carbon atom is found, the bacterium is present. The stool antigen test is performed on a stool sample provided by the patient and is tested for H. pylori antigens. Patients who have venous bleeding from a peptic ulcer may have decreased hemoglobin and hematocrit values. The stool may also be positive for occult (not seen) blood if bleeding is present.

If perforation is suspected, the health care provider may request a chest and abdomen x-ray series.

The major diagnostic test for PUD is esophagogastroduodenoscopy (EGD), which is the most accurate means of establishing a diagnosis. The rapid urease test can confirm a quick diagnosis because urease is produced by the bacteria in the gastric mucosa. GI bleeding may be tested using a nuclear medicine scan. No special preparation is required for this scan. The patient is injected with a contrast medium (usually Tc99m), and the GI system is scanned for the presence of bleeding after a waiting period.

1. Acute Pain or Chronic Pain related to gastric and/or duodenal ulceration (NANDA-I) 2. Upper GI bleeding related to perforation

The primary purposes of drug therapy in the treatment of PUD are to (1) provide pain relief, (2) eliminate H. pylori infection, (3) heal ulcerations, and (4) prevent recurrence. A common drug regimen for H. pylori infection is PPI-triple therapy, which includes a proton pump inhibitor (PPI) such as lansoprazole (Prevacid) plus two antibiotics such as metronidazole (Flagyl, Novonidazol ) and tetracycline (Ala-Tet, Panmycin, Nu-Tetra ) or clarithromycin (Biaxin, Biaxin XL) and amoxicillin (Amoxil, Amoxi ). (Pepto-Bismol)Bismuth therapy is often used in patients who are allergic to penicillin-based medications. Hyposecretory drugs reduce gastric acid secretions and are therefore used for both peptic ulcer disease (PUD) and gastritis management. The primary prescribed drugs include proton pump inhibitors and H2-receptor antagonists. Proton pump inhibitors (PPIs) is the drug class of choice for treating patients with acid-related disorders. Examples include omeprazole (Prilosec), lansoprazole (Prevacid), rabeprazole (Aciphex), pantoprazole (Protonix), and esomeprazole (Nexium). PPIs should not be discontinued abruptly to prevent rebound activation of the proton pump. Therefore, a step-down approach over several days is recommended.

H2-receptor antagonists are drugs that block histamine-stimulated gastric secretions. Two of the most common drugs are famotidine (Pepcid) and nizatidine (Axid) and are available as Pepcid OTC and Axid AR in OTC form. Antacids buffer gastric acid and prevent the formation of pepsin. They may help small duodenal ulcers heal but are usually not used alone as drug therapy. Calcium carbonate (Tums) is a potent antacid, but it triggers gastrin release, causing a rebound acid secretion. Therefore its use in acid inhibition is not recommended. Inform the patient 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. Teach the patient with past or present heart failure to avoid antacids with 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. Sucralfate (Carafate) is a mucosal barrier fortifier (protector) that forms complexes with proteins at the base of a peptic ulcer. This protective coat prevents further digestive action of both acid and pepsin. Bismuth subsalicylate (Pepto-Bismol) inhibits H. pylori from binding to the mucosal lining and stimulates mucosal protection and prostaglandin production. Teach patients they cannot take aspirin while on this drug because aspirin is a salicylic acid and could cause an overdose of salicylates. Patients should also be taught that this medication may cause the stools to be discolored black.

Many older adults have H. pylori infection that is undiagnosed because of vague symptoms associated with physiologic changes of aging and comorbidities that mask dyspepsia. Because the average age of gastric cancer diagnosis is 70 years, it is important to teach older adults about the symptoms of PUD and to consider H. pylori screening. Early detection and aggressive treatment can prevent PUD and gastric cancer.

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Teach the patient that to achieve a therapeutic effect, sufficient antacid must be ingested to neutralize the hourly production of acid. For optimal effect, take antacids 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. If taken on an empty stomach, they are quickly evacuated. Thus the neutralizing effect is reduced

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. An increased rate of gastric acid secretion, called rebound, may follow. Teach the patient to exclude any foods that cause discomfort. Bedtime snacks are avoided because they may stimulate gastric acid secretion. Patients should avoid alcohol and tobacco because of their stimulatory effects on gastric acid secretion.

Teach the patient with peptic ulcer disease to avoid substances that increase gastric acid secretion. This includes caffeine-containing beverages (coffee, tea, cola). Both caffeinated and decaffeinated coffees should be avoided, because coffee contains peptides that stimulate gastrin release.

Teach patients about complementary and alternative therapies that can reduce stress, including hypnosis and imagery. For example, the use of yoga and meditation techniques has demonstrated a beneficial effect on anxiety disorders. Many herbs, such as powders of slippery elm and marshmallow root, quercetin, and licorice, are used commonly by patients with gastritis and PUD. Other substances include zinc, vitamin C, essential fatty acids, acidophilus, vitamin A, and glutamine. Table 55-1 provides a list of therapies that have been used by many patients with gastric disorders.

Teach the patient who has peptic ulcer disease to seek immediate medical attention if experiencing any of these symptoms: • Sharp, sudden, persistent, and severe epigastric or abdominal pain • Bloody or black stools • Bloody vomit or vomit that looks like coffee grounds

The patient with upper GI bleeding (often called upper GI hemorrhage or UGH) is expected to have bleeding promptly and effectively controlled and vital signs within normal limits. Fluid volume loss secondary to vomiting can lead to dehydration and electrolyte imbalances. Interventions aimed at managing complications associated with PUD include prevention and/or management of bleeding, perforation, and gastric outlet obstruction. He or she needs supportive therapy to prevent hypovolemic shock and possible death. Carefully monitor the patient's fluid status, including intake and output. Fluid replacement in older adults should be closely monitored to prevent fluid overload. Serum electrolytes are also assessed because depletions from vomiting or nasogastric suctioning must be replaced. Volume replace with isotonic solutions (e.g., 0.9% normal saline solution, lactated Ringer's solution). The health care provider may prescribe blood products such as packed red blood cells to expand volume and correct a low hemoglobin and hematocrit. For patients with active bleeding, fresh frozen plasma may be given if the prothrombin time is 1.5 times higher than the midrange control value. Continue to monitor the patient's hematocrit, hemoglobin, and coagulation studies for changes from the baseline measurements. light feelings of weakness and mild perspiration may be present. When blood loss exceeds 1 L/24 hr, manifestations of shock may occur, such as hypotension, chills, palpitations, diaphoresis, and a weak, thready pulse. A combination of several different treatments, including nasogastric tube (NGT) placement and lavage, endoscopic therapy, interventional radiologic procedures, and acid suppression, can be used to control acute bleeding and prevent rebleeding. After the bleeding has stopped, H2-receptor antagonists, proton pump inhibitors, and antacids are the primary drugs used.

The first priority for care of the patient with upper GI bleeding is to maintain airway, breathing, and circulation (ABCs). Provide oxygen and other ventilatory support as needed. Start two large-bore IV lines for replacing fluids and blood. Monitor vital signs, hematocrit, and oxygen saturation.

Upper GI bleeding often requires the primary care provider or nurse to insert a large-bore nasogastric tube (NGT) to: • Determine the presence or absence of blood in the stomach • Assess the rate of bleeding • Prevent gastric dilation • Administer lavage Although not performed as commonly today, gastric lavage requires the insertion of a large-bore NGT with instillation of a room-temperature solution in volumes of 200 to 300 mL. There is no evidence that sterile saline or sterile water is better than tap water. Instruct the patient to lie on the left side during this procedure.

An esophagogastroduodenoscopy (EGD) can assist in achieving homeostasis during an acute hemorrhage by isolating the bleeding artery to embolize (clot) it. To stop bleeding in three different ways: (1) inject chemicals into the bleeding site; (2) treat the bleeding area with heat, electric current, or laser; or (3) close the affected blood vessels with a band or clip. A large catheter allows the patient to receive IV moderate sedation (e.g., midazolam 1137[Versed] and an opioid) and possibly a blood transfusion. Keep the patient NPO for 4 to 6 hours before the procedure. This prevents the risk for aspiration. A patient must sign a consent form before the EGD after the physician informs him or her.

After esophagogastroduodenoscopy (EGD), monitor vital signs, heart rhythm, and oxygen saturation frequently until they return to baseline. In addition, frequently assess the patient's ability to swallow saliva. The patient's gag reflex may initially be absent after an EGD because of anesthetizing (numbing) the throat with a spray before the procedure. After the procedure, do not allow the patient to have food or liquids until the gag reflex is intact!

Wth persistent, massive upper GI bleeding or those who are not surgical candidates, catheter-directed embolization may be performed. A femoral approach is most often used, but brachial access may be used. An arteriogram is performed to identify the arterial anatomy and find the exact location of the bleeding. The physician injects medication or other material into the blood vessels to stop the bleeding.

Aggressive acid suppression is used to prevent rebleeding. Several types of drugs are used. 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. Perforation is managed by immediately replacing fluid, blood, and electrolytes, administering antibiotics, and keeping the patient NPO. Maintain nasogastric suction to drain gastric secretions and thus prevent further peritoneal spillage. Carefully monitor intake and output and check vital signs at least hourly. Monitor the patient for clinical manifestations of septic shock, such as fever, pain, tachycardia, lethargy, or anxiety. 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 copious amounts of undigested food. Directed toward restoring fluid and electrolyte balance and decompressing the dilated stomach. The stomach must be decompressed with nasogastric suction. Next, interventions are directed at correcting metabolic alkalosis and dehydration. The NGT is clamped after about 72 hours. Check the patient for retention of gastric contents. If the amount retained is not more than 50 mL in 30 minutes, the health care provider may allow oral fluids.

In PUD, surgical intervention may be used to: • Treat patients who do not respond to medical therapy or other nonsurgical procedures • Treat a surgical emergency that develops as a complication of PUD, such as perforation Two general surgical approaches are available for PUD—minimally invasive surgery and conventional open surgery. Minimally invasive surgery (MIS) via laparoscopy (a type of endoscope) may be used to remove a chronic gastric ulcer or treat hemorrhage from perforation. May have partial stomach removal (subtotal gastrectomy), pyloroplasty (to open the pylorus), and/or a vagotomy (vagus nerve cutting) to control acid secretion. Acid-reduction surgery may not be necessary due to the increased use of PPIs and endoscopic procedures in the treatment of PUD.

Long-term adherence to drug therapy may require the patient to take several drugs each day. Permanent lifestyle alterations in nutrition habits must also be made. Most patients are discharged to the home to continue their recovery. Those who have had major surgery or have had complications, such as hemorrhage, may require one or two visits from a home care nurse.

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Patient and family teaching regarding risk factors for the recurrence of PUD. Teach them how to recognize new complications and what to do if they occur, especially abdominal pain; nausea and vomiting; black, tarry stools; and weakness or dizziness. Teach the patient and family about risk factors for recurring peptic ulcers. Help them plan ways to make needed lifestyle changes. Smaller meals may be required.

Teach the patient who has had surgery for PUD to avoid any OTC product containing aspirin or other NSAID. Emphasize the importance of following the treatment regimen for H. pylori infection and healing the ulcer. Emphasize the importance of keeping all follow-up appointments. Help the patient identify situations that cause stress, describe feelings during stressful situations, and develop a plan for coping with stressors.

Most cancers of the stomach are adenocarcinomas. Often there are no symptoms in the early stages and the disease is advanced when detected. Usually begins in the glands of the stomach mucosa. Atrophic gastritis and intestinal metaplasia (abnormal tissue development) are precancerous. Akaline environment that allows bacteria (especially H. pylori) to multiply. This infection causes mucosa-associated lymphoid tissue (MALT) lymphoma. Gastric cancers spread by direct extension through the gastric wall and into regional lymphatics. 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. Advanced gastric cancer, there is invasion of the muscularis (stomach muscle) or beyond. These lesions are not cured by surgical resection.

Infection with H. pylori is the largest risk factor for gastric cancer. Patients with pernicious anemia, gastric polyps, chronic atrophic gastritis, and achlorhydria (absence of secretion of hydrochloric acid) are 2 to 3 times more likely to develop gastric cancer. Positively correlated with eating pickled foods, nitrates from processed foods, and salt added to food. The ingestion of these foods over a long period can lead to atrophic gastritis, a precancerous condition. A low intake of fruits and vegetables is also a risk factor. Gastric surgery seems to increase the risk for gastric cancer because of the eventual development of atrophic gastritis. Patients with Barrett's esophagus from prolonged or severe gastroesophageal reflux disease (GERD) have an increased risk for cancer in the cardia (at the point where the stomach connects to the esophagus). Stomach cancer rates are about twice as high in males as in females.

Teach patients with gastritis and/or H. pylori infection to follow the treatment regimen to ensure that gastritis heals and H. pylori infection is eliminated. Stress the need for eating a well-balanced diet and limiting pickled foods, salted foods, and processed foods to help prevent gastric cancer.

Question the patient about known risk factors for the development of gastric cancer. Ask about preferred foods, especially pickled, salted, or smoked foods. Inquire whether the patient has ever been diagnosed with or treated for H. pylori infection, gastritis, or pernicious anemia. Note whether he or she has a history of gastric surgery or polyps. Also ask whether any of the patient's immediate relatives have gastric cancer. Indigestion (heartburn) and abdominal discomfort are the most common symptoms. As the tumor grows, these symptoms become more severe and do not respond to nutrition changes or antacids. Epigastric or back pain is also an early symptom that may go unrecognized. In advanced gastric cancer, 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. Patients 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 (liver enlargement) from metastasis. Hard, enlarged lymph nodes in the left supraclavicular chain, left axilla, or umbilicus result from metastasis. Masses on the right suggest metastasis in the perigastric lymph nodes or liver. In patients with advanced disease, anemia is evidenced by low hematocrit and hemoglobin values. Patients may have macrocytic or microcytic anemia associated with decreased iron or vitamin B12 absorption. The stool may be positive for occult blood. Hypoalbuminemia and abnormal results of liver tests (e.g., bilirubin and alkaline phosphatase) occur with advanced disease and with hepatic metastasis. The level of carcinoembryonic antigen (CEA) is elevated. The health care provider uses esophagogastroduodenoscopy (EGD) with biopsy for definitive diagnosis of gastric cancer.

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Radiation and chemotherapy commonly prolong survival of patients with advanced gastric disease. Combination chemotherapy with multiple cycles of drugs such as cisplatin (Platinol) and epirubicin (Elience) before and after surgery may be given. Bone marrow suppression, nausea, and vomiting are common adverse drug effects. Although gastric cancers are somewhat sensitive to the effects of radiation, the use of this treatment is limited because the disease is often widely spread. Radiation may be used for palliative management when surgery is not an option. The most common side effects of radiation include impaired skin integrity, fatigue, and anorexia. Nausea, vomiting, and diarrhea may occur about 1 week after treatment.

Surgical resection by removing the tumor is the preferred method for treating gastric cancer. The primary surgical procedures for the treatment of gastric cancer are total gastrectomy and subtotal (partial) gastrectomy. In early stages, laparoscopic surgery (minimally invasive surgery [MIS]) plus adjuvant chemotherapy or radiation may be curative. Most patients with advanced disease are candidates for palliative surgical treatment. Metastasis in the supraclavicular lymph nodes, inguinal lymph nodes, liver, umbilicus, or perirectal wall indicates that the opportunity for cure by resection has been lost.

A nasogastric tube (NGT) is often inserted and connected to suction to remove secretions and empty the stomach. The NGT remains in place for a few days postoperatively to prevent the accumulation of secretions, which may lead to vomiting or GI distention and pressure on the incision. Patients having laparoscopic surgery (minimally invasive surgery [MIS]) do not require an NGT. Nutrition therapy is a vital aspect of preoperative and postoperative management. Preoperatively, compression by the tumor can prevent adequate nutritional intake. To correct malnutrition before surgery, the health care provider may prescribe enteral supplements to the diet and/or total parenteral nutrition (TPN). Vitamin, mineral, iron, and protein supplements are essential to correct nutritional deficits.

The surgeon usually removes part or all of the stomach to take out the tumor. When the tumor is located in the mid-portion or distal (lower) portion of the stomach, a subtotal (partial) gastrectomy is typically performed. The omentum, spleen, and relevant nodes are also removed.

Provide the usual postoperative care for patients who have had general anesthesia to prevent atelectasis, paralytic ileus, wound infection, and peritonitis. Document and report any signs and symptoms of these complications immediately to the surgeon. Auscultate the lungs for adventitious sounds (crackles or reduced breath sounds), and monitor for the return of bowel sounds. Take vital signs as appropriate to detect signs of infection or bleeding. Aggressive pulmonary exercises and early ambulation can help prevent respiratory complications and deep vein thrombosis. Also inspect the operative site every 8 to 12 hours for the presence of redness, swelling, or drainage. Keep the head of the bed elevated to prevent aspiration from reflux. Decreased patency caused by a clogged NGT can result in acute gastric dilation after surgery. This problem is manifested by epigastric pain and a feeling of fullness, hiccups, tachycardia, and hypotension. Irrigation or replacement of the NGT by request of the surgeon. Dumping syndrome is a term that refers to a group of vasomotor symptoms that occur after eating. This syndrome is believed to occur as a result of the rapid emptying of food contents into the small intestine, which shifts fluid into the gut, causing abdominal distention. Observe for early manifestations of this syndrome, which typically occur within 30 minutes of eating. Symptoms include vertigo, tachycardia, syncope, sweating, pallor, palpitations, and the desire to lie down. Report these manifestations to the surgeon, and encourage the patient 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. Observe for manifestations, including dizziness, light-headedness, palpitations, diaphoresis, and confusion. Dumping syndrome is managed by nutrition changes that include decreasing the amount of food taken at one time and eliminating liquids ingested with meals Teach the patient to eat a high-protein, high-fat, low- to moderate-carbohydrate diet. Alkaline reflux gastropathy, also known as bile reflux gastropathy, is a complication of gastric surgery in which the pylorus is bypassed or removed. Endoscopic examination reveals regurgitated bile in the stomach and mucosal hyperemia. Symptoms include early satiety (satisfied quickly with little food), abdominal discomfort, and vomiting. Delayed gastric emptying is often present after gastric surgery and usually resolves within 1 week. Edema at the anastomosis (surgical connection areas) or adhesions (scar tissue) obstructing the distal loop may cause mechanical blockage. Metabolic causes (e.g., hypokalemia, hypoproteinemia, or hyponatremia) should be considered. The edema is resolved with nasogastric suction, maintenance of fluid and electrolyte balance, and proper nutrition. 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 reduction of intrinsic factor. In the absence of intrinsic factor, clinical manifestations of pernicious anemia may occur. Assess for the development of atrophic glossitis secondary to vitamin B12 deficiency. In atrophic glossitis, the tongue takes on a shiny, smooth, and "beefy" appearance. The patient may also have signs of anemia secondary to folic acid and iron deficiency. Monitor the complete blood count (CBC) for signs of megaloblastic anemia (low red blood cell [RBC] level) and leukopenia (low white blood cell [WBC] level).

PG 1140 IGGY

The debilitated with advanced gastric cancer are discharged to home with maximal assistance and support or to a transitional care unit or skilled nursing facility. Patients who have undergone subtotal gastrectomy and are not debilitated may be discharged to home with partial assistance for ADLs. Recurrence of cancer is common, and patients need regular follow-up examinations and imaging assessments.

Assess their ability to cope with the disease and the possible need for end-of-life care. Patients need to learn symptom management strategies. Hospice programs can help both the patient and the family cope with these physical and emotional needs. Patients may fear returning home because of their inability for self-management. Enlisting family and health care resources for the patient may ease some of this anxiety. Provide the family with adequate information about community support systems to make the transition to home care easier. If the prognosis is poor, they need continued professional support.

Educate the patient and family about any continuing needs, drug therapy, and nutrition therapy. If patients are discharged to home with surgical dressings, teach the patient and family how to change them. Review the manifestations of incisional infection (e.g., fever, redness, and drainage) that they should report. 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 antiemetics may be needed. Teach the patient and family about the type and quantity of foods that will provide optimal nutritional value. Interventions to minimize dumping syndrome and decrease gastric stimulants are also emphasized (see Table 55-3). Remind the patient to: • Eat small, frequent meals • Avoid drinking liquids with meals • Avoid foods that cause discomfort • Eliminate caffeine and alcohol consumption • Begin a smoking-cessation program, if needed • Receive B12 injections, as prescribed • Lie flat after eating for a short time

• Report of epigastric pain or indigestion before or after a meal • Report of inability to tolerate certain foods • Nausea and/or vomiting (with or without blood) • Melena or frank blood in stools

• Taking vital signs • Observing and documenting assessment findings • Interpreting laboratory values and other diagnostic findings: • Presence of H. pylori • Decreased hemoglobin and hematocrit

• Maintaining airway, breathing, and circulation (ABCs) • Placing the patient in a sitting position or on the left side to prevent aspiration if vomiting • Preparing to assist with gastric lavage if hematemesis is present

• When caring for patients with gastric health problems, collaborate with the pharmacist, dietitian, health care provider, and/or case manager.

• Refer the patient to the American Cancer Society if gastric cancer is the diagnosis. • Identify patients at risk for gastritis and PUD, especially older adults who take large amounts of NSAIDs and those with H. pylori. • Teach patients behaviors to prevent PUD, such as avoiding large consumption of caffeine, alcohol, coffee, aspirin, and other NSAIDs. Also teach them to avoid contaminated foods and water and to avoid smoking (Chart 55-1). • Teach patients the importance of adhering to H. pylori treatment to prevent the risk for gastric cancer.

• Allow patients with gastric cancer to express feelings of grief, fear, and anxiety. • For patients with advanced gastric cancer, identify the need for end-of-life care, including referral to hospice care.

• Recall that acute gastritis causes a rapid onset of epigastric pain and dyspepsia; chronic gastritis causes vague epigastric pain (usually relieved with food) and an intolerance to fatty and spicy foods (Chart 55-2). • Be aware that assessment findings vary depending on whether the patient has a gastric or duodenal ulcer: patients with gastric ulcers may be malnourished and have pain that is worsened by ingestion of food; patients with duodenal ulcers are usually well nourished, have pain that is relieved by ingestion of food, and usually awaken with pain during the night (Table 55-2). • For patients who have undergone a gastrectomy, collaborate with the dietitian and instruct the patient regarding diet changes to avoid abdominal distention and dumping syndrome. • Teach patients with abnormal symptoms (e.g., abdominal tenderness, abdominal pain that is relieved by food, or pain that becomes worse 3 hours after eating, dyspepsia, melena, and/or distention) to consult with their physician immediately for a prompt diagnosis and treatment. • Teach patients that hematemesis is a medical emergency and that they should go to the emergency department for prompt treatment. • Teach the proper administration of antacids (one or two after meals). Tell patients that antacids can interfere with the effectiveness of certain drugs, such as phenytoin (Dilantin). • Teach the proper administration of H2 antagonists. Explain that they should be given at bedtime (Chart 55-3). • Teach the proper administration of antisecretory agents, noting that most cannot be crushed because they are sustained-release or enteric-coated tablets. • Monitor patients with ulcers for any of the signs and symptoms of upper GI bleeding that are listed in Chart 55-4. Report any of these symptoms if noted to a physician immediately. • After an EGD, monitor the patient's vital signs, heart rhythm, and oxygen saturation frequently until they return to baseline. To prevent aspiration, assess the gag reflex and ensure that it is intact before giving the patient food or fluids. • Observe the patient for signs and symptoms of dumping syndrome after gastric surgery; teach the manifestations and management of this syndrome. Advise the patient to eat six small meals per day and to consume a diet high in protein and fat but low in carbohydrate-rich foods. Liquids should not be taken with meals.