- Clinical science
Peptic ulcer disease (PUD) refers to the presence of one or more ulcerative lesions in the stomach or lining of the duodenum. Possible etiologies include infection with the bacterium Helicobacter pylori (most common), prolonged use of nonsteroidal anti-inflammatory medicines (possibly in combination with glucocorticoids), conditions associated with an overproduction of stomach acid (hypersecretory states), and stress. Epigastric pain is a typical symptom of PUD, however, some patients may remain asymptomatic until complications such as bleeding and perforation occur. Diagnosis occurs via direct visualization of the ulcer on esophagogastroduodenoscopy (EGD) and H. pylori detection (via biopsy or non-invasive testing). The first-line treatment for most peptic ulcers involves H. pylori eradication via triple therapy (a course of two different antibiotics in combination with a proton-pump inhibitor) and the withdrawal of offending agents. Antisecretory drugs (e.g., proton-pump inhibitors, or PPIs), which reduce stomach acid production, are continued for 4–8 weeks after eradication therapy and may be considered for maintenance therapy if symptoms recur. Surgical intervention may be necessary in rare cases, especially if complications such as perforation or massive bleeding occur. Stomach cancer is an important differential diagnosis and must be ruled out if risk factors are present.
- Incidence: > 6 million cases annually in the US
- Overall, the incidence of PUD is declining because of the high prevalence of PPI intake.
Epidemiological data refers to the US, unless otherwise specified.
- Chronic gastritis caused by H. pylori, a curved, flagellated gram-negative rod
- Chronic gastritis of other etiology (see )
- Long-term use of NSAIDs: risk increases 5-fold
- Long-term use of NSAIDs plus glucocorticoids: risk increases 10 to 15-fold!
- Smoking, alcohol consumption
- Age > 65 years
- Stress (see “Subtypes and variants” below)
- Rare: hyperparathyroidism, Zollinger-Ellison syndrome (gastrinoma)
- Gastric ulcer: lesser curvature and the gastric antrum
- Duodenal ulcer: duodenal bulb; ; patients with blood type O have a higher risk; hypertrophy of Brunner glands
- Erosive gastritis: acute mucosal inflammatory of the stomach that does not extend beyond the muscularis mucosa
An atypical location is suspicious for carcinoma!
Findings common to both
|Pain and eating|| |
|Nocturnal pain|| || |
Taking NSAIDs can often mask PUD symptoms until complications such as hemorrhage and perforation occur!
- Description: In this rare disease, minor mucosal trauma can lead to major bleeding. It is caused by an abnormal submucosal artery.
- Location: proximal stomach
- Clinical presentation: signs of acute upper GI bleeding
- Treatment: endoscopic hemostasis (injection therapy, hemoclips, etc.), excision of the susceptible mucosa
- Causes: polytrauma, major surgery, SIRS, kidney failure, etc.
- Curling ulcer: patients with severe burns → ↓ plasma volume → ↓ gastric blood flow → hypoxic tissue injury of stomach surface epithelium → weakening of the normal mucosal barrier
- Cushing ulcer: In patients with brain injury, increased vagal stimulation leads to an increased production of stomach acid via acetylcholine release.
- Nonulcer dyspepsia; : Symptoms including bloating, nausea, and belching persisting ≥ 3 months without organic cause (synonym: functional dyspepsia).
- ≤ 55 years of age without alarm features: for H. pylori
- > 55 years of age or presence of ≥ 1 alarm features: EGD with biopsies and rapid urease testing for H. pylori
- Negative for H. pylori infection and NSAID intake; trial therapy unsuccessful
Testing for Helicobacter pylori
- See “”
- Most accurate test
- Patients > 55 years of age or presence of ≥ 1 alarm features, which include:
- Biopsy samples from:
- If active bleeding, EGD can be performed for diagnosis and subsequent hemostasis treatment (electrocautery) in the same session.
General management of dyspepsia
- H. pylori positive → eradication therapy (with antibiotics and a PPI) and supportive treatment → continue PPIs for 4–8 weeks → follow-up
- H. pylori negative → medical acid suppression (with a PPI) and supportive treatment for 4–8 weeks → follow-up
- (with antibiotics)
- Acid suppression: PPIs (most effective), H2 blockers, antacids (mainly used for symptom relief)
- Mucosal protection: misoprostol , sucralfate (both substances are rarely used in PUD)
- Discontinue NSAIDs
- Restrict alcohol use/smoking/emotional stress
- Avoid eating before bedtime
- With the advent of potent acid suppression in the form of PPIs, surgical intervention is rarely needed.
- Refractory syndromes despite appropriate medical treatment
- If cancer is suspected
- Complications that cannot be treated endoscopically (see “Complications” below)
Partial gastrectomy (Billroth)
- Billroth I: distal gastrectomy with end-to-end or side-to-end gastroduodenostomy
- Billroth II: resection of the distal ⅔ of the stomach with a blind ending duodenal stump and end-to-side gastro-jejunostomy. The Billroth I and II methods without a Brown's anastomosis often lead to bile reflux into the stomach. This may result in type C gastritis in the region of the anastomosis. The chronic inflammation causes atrophic changes and increases the risk of cancer (anastomosis carcinoma).
- Truncal vagotomy: division of the anterior and posterior vagal trunk of the vagus nerve (CN X) at the lower esophagus
- Highly selective vagotomy (proximal gastric vagotomy): division of vagal fibers (CN X), supplying the proximal part of the stomach
Postvagotomy diarrhea and delayed gastric emptying
- Caused by intraoperative intestinal denervation
- Delayed gastric emptying in combination with early satiety, belching, loss of appetite, and acid reflux
- Intermittent diarrhea
- Management: supportive (e.g., fluid restriction, avoidance of dairy products, antidiarrheal/antimotility agents, and a therapeutic trial of cholestyramine)
- Bleeding (see )
Gastric/duodenal perforation (see )
- Second most common complication of PUD
- Duodenal ulcers of the anterior wall are more likely to perforate.
- Clinical presentation
- Management: : emergency surgery
- Subhepatic abscess (see below)
- Subhepatic abscess
Gastric outlet obstruction (GOO)
- Definition: mechanical obstruction of the pyloric channel or duodenum
- Postprandial, nonbilious vomiting
- Succussion splash
- Early satiety
- Progressive gastric dilation
- Weight loss
- Symptomatic: nasogastric suction, electrolyte and fluid replacement, and parental nutrition
- Definitive: surgery or endoscopic dilation
- Clinical presentation
- Conservative management: indicated in all patients, as most fistulas close spontaneously
- Surgical resection: in patients who are not responsive conservative management
- Malignant transformation
We list the most important complications. The selection is not exhaustive.
Endoscopic surveillance with biopsies
- Gastric ulcer: performed after 8–12 weeks of antisecretory treatment in patients with one or more of the following criteria:
- Duodenal ulcer: indicated if symptoms persist after an appropriate course of antisecretory treatment
- Bleeding peptic ulcer: endoscopic control on the following day
H. pylori eradication confirmation
- Smoking cessation and avoidance of other offending agents such as alcohol
- Reduce coffee consumption
- Avoid medications that are associated with the development of ulcers
- Rule out: Zollinger-Ellison syndrome, hyperparathyroidism
Stress ulcer prophylaxis
- PPIs or H2-blockers
- Indicated in severe organic disease/stress → shock, acidosis, brain trauma, severe burns, major surgery
- Disadvantage of prolonged PPI intake: potentially higher risk of pneumonia and gastroenteritis!