Peptic Ulcer Disease Nursing Care and Management

A peptic ulcer is acid winning the fight against mucosal defense: an excavation in the mucosal wall of the stomach, pylorus, duodenum, or esophagus that can erode through muscle all the way to the peritoneum. Most cases trace to H. pylori or NSAIDs. The teaching points matter, but the reason you watch these patients closely is the three complications that can kill: hemorrhage, perforation, and obstruction.

What is Peptic Ulcer Disease?

A peptic ulcer is named for its location, gastric, duodenal, or esophageal. The erosion of a circumscribed area may reach the muscle layers or run through muscle into the peritoneum.

Classification

Gastric ulcers tend to sit in the lesser curvature of the stomach near the pylorus. Duodenal ulcers are more common than gastric. Esophageal ulcers result from backward flow of HCl from the stomach into the esophagus.

Pathophysiology

Ulcers form mainly in the gastroduodenal mucosa, driven by increased concentration or activity of acid-pepsin or by reduced mucosal resistance. A damaged mucosa cannot secrete enough mucus to barrier against HCl. Patients with duodenal ulcers secrete more acid than normal, while those with gastric ulcers secrete normal or decreased acid. Damaged gastroduodenal mucosa also resists bacteria less, so H. pylori infection can take hold.

Statistics and Epidemiology

Peptic ulcer disease occurs in both sexes and at all ages, peaking between 40 and 60 years of age. It is relatively uncommon in women of childbearing age but is seen in children and even infants. After menopause, the incidence in women approaches that in men.

Causes

There are three major causes: H. pylori infection, chronic NSAID use, and pathologic hypersecretory disorders such as Zollinger-Ellison syndrome. H. pylori, a gram-negative bacterium acquired through food and water, damages the protective mucous coating of the stomach and duodenum. Salicylates and NSAIDs encourage ulcers by inhibiting prostaglandin secretion. Pancreatitis, hepatic disease, Crohn's disease, gastritis, and Zollinger-Ellison syndrome are also known causes. Excess HCl secretion contributes, and milk, caffeinated beverages, and alcohol raise HCl, speed gastric emptying, and promote mucosal breakdown. Gastric ulcers favor people with type A blood; duodenal ulcers favor type O.

Clinical Manifestations

Symptoms come and go over days, weeks, or months, often vanishing and returning with no clear cause. The classic complaint is dull, gnawing pain or burning in the midepigastrium or back that eases with eating. Pyrosis (heartburn) is a burning sensation in the stomach and esophagus that rises toward the mouth. Vomiting points to pyloric obstruction, from muscular spasm or mechanical scarring. Constipation or diarrhea may occur from diet and medications. About 15% of patients present with GI bleeding, shown by melena (tarry stools).

Complications

Hemorrhage is the most common complication, occurring in 10% to 20% of patients as hematemesis or melena. Perforation is erosion through the gastric serosa into the peritoneal cavity, often without warning; penetration is erosion through the serosa into adjacent structures. Pyloric obstruction develops when the area distal to the pyloric sphincter scars and stenoses from spasm, edema, or scar tissue laid down as an ulcer repeatedly heals and breaks down.

Assessment and Diagnostic Findings

Esophagogastroduodenoscopy confirms the ulcer and allows cytology and biopsy to rule out H. pylori or cancer. Physical exam may reveal pain, epigastric tenderness, or abdominal distention. A barium study of the upper GI tract may show an ulcer, though endoscopy is preferred because it directly visualizes inflammation, ulcers, and lesions. Stools are tested periodically until negative for occult blood. The carbon 13 (13C) urea breath test reflects H. pylori activity.

Medical Management

Once diagnosed, reassure the patient that the condition can be controlled. The mainstay is a combination of antibiotics, proton pump inhibitors, and bismuth salts to suppress or eradicate the infection. Reducing environmental stress takes physical and psychological changes by the patient plus support from family. Smoking cessation matters because smoking decreases pancreatic bicarbonate secretion into the duodenum, raising duodenal acidity. Diet should avoid temperature extremes and overstimulation from meat extracts, alcohol, coffee and other caffeinated beverages, and cream- and milk-rich diets.

Surgical Management

Antibiotics for H. pylori and H2 receptor antagonists have sharply cut the need for surgery. Pyloroplasty transects the nerves that stimulate acid secretion and opens the pylorus. Antrectomy removes the pyloric portion of the stomach with anastomosis to the duodenum or jejunum.

Nursing Management

Nursing Assessment

Assess the description of pain and what relieves it, the characteristics of any vomitus, and the patient's usual food intake and habits.

Nursing Diagnosis

Major diagnoses include acute pain related to gastric acid on damaged tissue, anxiety related to acute illness, imbalanced nutrition related to diet changes, and deficient knowledge about preventing symptoms and managing the condition.

Nursing Care Planning and Goals

The goals are relief of pain, reduced anxiety, maintained nutrition, knowledge of management and prevention of recurrence, and absence of complications.

Nursing Interventions

For pain and nutrition, give prescribed medications and have the patient avoid aspirin (an anticoagulant) and acid-enhancing foods and beverages (colas, tea, coffee, chocolate, and decaffeinated coffee). Encourage regularly spaced meals in a relaxed atmosphere, take regular weights, and reinforce dietary changes and relaxation techniques.

For anxiety, assess what the patient wants to know and the level of anxiety, and encourage open expression of fears without criticism. Explain diagnostic tests, give medications on schedule, interact calmly, help identify stressors, and teach coping and relaxation methods. Bring family into care and give emotional support.

Watch for complications. If hemorrhage is a concern, assess for faintness, dizziness, and nausea before or with bleeding; test stool for occult or gross blood; and monitor vital signs frequently for tachycardia, hypotension, and tachypnea. Insert an indwelling urinary catheter and track intake and output, establish an IV line for fluid and blood, and monitor hemoglobin and hematocrit. Insert and maintain a nasogastric tube, monitor drainage, and lavage as ordered. Monitor oxygen saturation and give oxygen. Position the patient recumbent with legs elevated to prevent hypotension, or on the left side to prevent aspiration, and treat hypovolemic shock as indicated. For penetration, report back and epigastric pain no longer relieved by previously effective medications. For perforation, report sudden abdominal pain, pain referred to the shoulders, vomiting and collapse, an extremely tender and rigid abdomen, hypotension and tachycardia, or other signs of shock.

For home self-care, help the patient understand the condition and what relieves or aggravates it. Teach prescribed medications by name, dosage, frequency, and side effects, and name the drugs to avoid such as aspirin. Identify foods that upset the gastric mucosa (coffee, tea, colas, alcohol). Encourage regular meals in a relaxed setting and no overeating. Explain that smoking interferes with healing and refer to cessation programs. Teach the warning signs to report: hemorrhage (cool skin, confusion, increased heart rate, labored breathing, blood in the stool), penetration and perforation (severe abdominal pain, rigid tender abdomen, vomiting, elevated temperature, increased heart rate), and pyloric obstruction (nausea, vomiting, distended abdomen, abdominal pain). To check for obstruction, insert and monitor a nasogastric tube; more than 400 mL residual suggests obstruction.

Evaluation

The patient reports relief of pain, reduced anxiety, maintained nutrition, knowledge of management and prevention of recurrence, and no complications.

Discharge and Home Care Guidelines

Teach self-care before discharge. Cover the factors that relieve and aggravate the condition. Review home medications by name, dosage, frequency, and side effects, stressing that the patient keep taking them even after symptoms ease. Instruct the patient to avoid medications and foods that worsen symptoms and any substances with acid-producing potential. Counsel eating meals at regular times in a relaxed setting and avoiding overeating.

Documentation Guidelines

Document the patient's description of and response to pain, acceptable level, and expectations of management, along with prior medication use. Record level of anxiety, the patient's expressed and displayed feelings and ability to recognize them, caloric intake, and any cultural, religious, or personal dietary preferences. Note learning style, identified needs, and learning blocks, the plan of care, the teaching plan, the response to interventions and teaching, progress toward outcomes, modifications to the plan, and long-term needs.