Only $35.99/year

CHAPTER 55 Care of Patients with Stomach Disorders

Terms in this set (64)

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.
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.
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.
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.
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.
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).
• 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.