The most common form of peptic ulcer is the duodenal ulcer, which typically occurs in the proximal segment.
Peptic Ulcer Overview
The most common form of peptic ulcer is the duodenal ulcer, which typically occurs in the proximal segment. Gastric ulcers occur less often than duodenal ulcers in the absence of nonsteroidal anti-inflammatory drug (NSAID) use. Esophageal ulcers usually occur in the lower one-third of the esophagus and are often a result of gastroesophageal reflux disease. Other forms of peptic ulcers are caused by gastric ischemia, the stress from multiorgan-failure in patients in the intensive care unit, or Zollinger-Ellison syndrome and other rarer causes. Over time, the incidence of ulcer type has been decreasing asHelicobacter pyloriinfections are treated and as the use of NSAIDs increases.
Lesions represented by breaks smaller than 5 mm in the digestive mucosal lining that are found on endoscopy are considered erosions. Breaks larger than 5 mm, with a depth to the submucosa, are considered ulcerations.H. pyloriinfection is the most common cause of duodenal ulceration, while the use of NSAIDs or aspirin is the most common cause of gastric ulcers. Men have a higher risk than women of developing ulcers, and 70% of ulcers occur among the 25- to 64-year-old age group. Family history of ulcer disease, smoking cigarettes, gastrinoma, and some medications also increase risk (most notably corticosteroids in high doses or prolonged use of them, potassium chloride supplements, chemotherapy, and bisphosphonates). Familial occurrence of the infection suggests that genetic factors govern response to the infection. Approximately 500,000 new cases are diagnosed in the United States annually.1
The general preventive measure for NSAID-induced ulcers is to avoid these agents and salicylates and to instead use acetaminophen or tramadol. Cardiovascular risk should be assessed before using Cox-2 inhibitors. Proton pump inhibitor (PPI) use with lower doses of NSAIDs is advocated for those patients needing NSAID therapy. Eradication ofH. pyloribefore beginning NSAID therapy is recommended if the bacteria has been identified. Long-term PPI therapy is also suggested for patients with recurrent or complicated peptic ulcers.
The pathology develops as an imbalance among factors that maintain gastric mucosal integrity. Chronic inflammatory changes as a result ofH. pyloriand increased production of gastric hydrochloric acid, combined with refluxed pepsin and bile salts, overwhelm the gastric mucosal lining.
The diagnosis of peptic ulcer disease (PUD) is suspected when a patient reports epigastric burning or gnawing pain, often related to eating or having an empty stomach and during the night. The pain can be relieved by eating a meal or taking antacids or a PPI. More severe disease may present with anemia, hematemesis, and melena or hem occult positive stools. Vomiting, decreased appetite, and weight loss suggest obstruction. Pain patterns with back radiation suggest perforation.
Physical exam findings may encounter epigastric pain, but there may be no other tenderness. Patients can often point to the site of pain with a single finger. Hence, the physical exam is often nonspecific. Laboratory testing includes a complete blood count (CBC) and fecal occult blood testing. Testing forH. pyloriusing stool or the breath is a reasonable start for patients under the age of 55 who do not have alarming symptoms. Antibody testing is unreliable. Endoscopy is used for patients aged 55 and older with alarming features of upper gastrointestinal (GI) cancer, such as weight loss, vomiting, dysphagia, or severe dyspepsia. Serum gastrin levels are considered for patients with multiple recurrent ulcers and suspected Zollinger-Ellison syndrome. Barium contrast radiography is reserved for patients unsuitable for endoscopy.
First-line treatment consists of daily acid suppression with PPI therapy prior to breakfast for 8 weeks. However, removal of NSAIDs from medication regimens is necessary before this treatment begins. H2 agonists may be used if the patient does not respond to PPIs. Surgery is reserved for suspected perforated ulcers. With severe anemia, a transfusion is recommended of hemoglobin less than 7 g/dl.
After bleeding ulcers are healed, treatment of anH. pyloriinfection will begin if the bacteria has been identified. Multiple protocols for combination antibiotic therapy, which accommodate individual patient considerations, are found in the literature. Antibiotic resistance is noted in the literature, as well, with protocols for treating. Patients must be rechecked forH. pylori1 month after therapy is completed. Continued acid suppression therapy may not be needed in most patients.
For patients withoutH. pyloriinfection, removal of NSAIDs is imperative. Four weeks of PPI therapy should heal duodenal ulcers, while gastric ulcers require 8 weeks. H2 agonists or sucralfate may be used for those patients who do not respond to PPI therapy. For patients who require long-term NSAID therapy, the addition of misoprostol is indicated. Note that PPIs can cause decreases in bone density, hypomagnesemia, and increased risk of infection withClostridium difficile.
Complications of PUD may include upper GI hemorrhage, perforation, and penetration into nearby organs or gastric outlet obstruction. Gastric adenocarcinoma is increased in patients with anH. pyloriinfection.
Peptic Ulcer Case Study
John Bee is a 43-year-old man reporting a 4-year history of intermittent heartburn that he self-treats periodically with an OTC low-dose PPI for a few days. He points to the epigastric area, relating that he has a gnawing sensation here that has awakened him from sleep 4 of the last 7 nights and is worse now than in previous episodes. He is a nonsmoker with a family history positive for stomach ulcers, but denies malignancy in the family history. He rates the pain a 7 out of 10. He also reports frequent use of NSAIDs for headaches and muscular aches.
DISCUSSION QUESTION:What additional information would you want to know about John’s history and current illness?
ANSWER:Additional family history of GI cancers and treatment forH. pylorishould be solicited. Further review should be make of body systems information about stability of weight, nausea, vomiting, constipation or diarrhea, melena, hematemesis, anemia, early satiety, and other symptoms suggestive of GI malignancy. John denies any of the warning signs of malignancy.
John’s physical examination findings are of a normotensive, young man with a BMI of 25. He reports mild and reproducible pain in the epigastric area without masses, no hepatomegaly or splenomegaly, and normal bowel sounds.
DISCUSSION QUESTION:Should you consider diagnostic testing?
ANSWER:CBC and stool hem occult testing should be ordered to evaluate hemoglobin, and stool antigen testing for the presence ofH. pylori. In the absence of any red flag symptoms, endoscopy can still be delayed at this point.
DISCUSSION QUESTION:What is your working diagnosis?
ANSWER:PUD triggered by chronic NSAID use andH. pylorigastritis. In John’s case, theH. pyloristool antigen testing was positive, his CBC was normal, the stool hem occult was negative. Therapy goals include discontinuation of his NSAIDs, use of acetaminophen for pain, and evaluation for the source of his chronic pain.H. pyloritherapy with double or triple protocol, with the goal of eradication, is recommended in addition to acid suppression therapy for 8 weeks. At that time, endoscopy can be considered for evaluation of pathology and exclusion ofH. pylorivia biopsy.
If John is positive for active bleeding with or without anemia or if red flags are present, referral should be made for immediate endoscopy and PPI therapy, and surgery if indicated.
If John had tested negative forH. pylori, treatment of the underlying cause with PPI therapy for 6 to 8 weeks is indicated. Thereafter, use of an H2 antagonist or sucralfate is recommended as needed; if aspirin or NSAID therapy is resumed, misoprostol can be added. Ongoing acid suppression may be necessary with frequent reoccurrence or with large or refractory ulcers.
Marjorie Rachide, MSN, FNP, APRN, is a graduate of East Carolina University, Greenville, North Carolina, and is presently employed as clinic manager by Health Care Clinic at Walgreens in the Atlanta, Georgia, market area.