• Clinical science
  • Physician

Peptic ulcer disease (PUD)

Summary

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. 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.

Epidemiology

References:[1][2][3][4][5]

Epidemiological data refers to the US, unless otherwise specified.

Etiology

References:[2][6][7][8][9][10][11]

Classification

An atypical location is suspicious for carcinoma!

References:[12]

Pathophysiology

Gastric secretions

Disturbances

  • Helicobacter pylori gastritis: increased acid secretion, decreased protective factors/mucus production
  • NSAIDs inhibit COX-1 and COX-2 decrease in PGE2 (normally decreased gastric acid secretion and increased HCO3- and mucus secretion) → gastric mucosa erosions

Clinical features

Gastric ulcer

Duodenal ulcer

Findings common to both

  • Dyspepsia: postprandial heaviness, early satiety, and gnawing, aching or burning epigastric pain
  • Pain relief with antacids
  • Potential signs of internal bleeding (anemia, hematemesis, melena)
  • ∼ 70% of patients with PUD are asymptomatic
  • Stool sample positive for occult blood (see gastrointestinal bleeding)
Pain and eating
  • Pain increases shortly after eating → weight loss
  • Pain increases 2–5 hours after eating
  • Pain on an empty stomach (hunger pain) that is relieved with food intake weight gain
Nocturnal pain
  • 30–40% of patients
  • 50–80% of patients


Gastric ulcer is associated with pain after light (weight loss) Gorging. Duodenal ulcer is associated with relief after massive (weight gain) Desserts."

Taking NSAIDs can often mask PUD symptoms until complications such as hemorrhage and perforation occur!

References:[13][14][15][16]

Subtypes and variants

  • Dieulafoy's lesion
    • 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

Imagine a hot curling iron to remember that Curling ulcers occur in patients with severe burns.

Imagine a brain resting on a cushion to remember that patients with brain injury can develop Cushing ulcers.

References:[17][18][19]

Diagnostics

Diagnostic approach

Testing for Helicobacter pylori

Esophagogastroduodenoscopy (EGD)

  • Most accurate test
  • Patients > 60 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.

Alarm features of PUD include progressive dysphagia, odynophagia, persistent vomiting, jaundice, signs of GI bleeding, signs of malignancy, and a family history of upper GI malignancy!

To rule out gastric cancer, patients with stomach ulcers should undergo follow-up EGD and histology until the ulcer has healed completely!

References:[16][20][21][22][23][24][25]

Treatment

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

Medical treatment

Supportive treatment

  • Discontinue NSAIDs
  • Restrict alcohol use/smoking/emotional stress
  • Avoid eating before bedtime

Surgical treatment

  • With the advent of potent acid suppression in the form of PPIs, surgical intervention is rarely needed.
  • Indications
    • Refractory syndromes despite appropriate medical treatment
    • If cancer is suspected
    • Complications that cannot be treated endoscopically (see “Complications” below)
  • Partial gastrectomy (Billroth)
  • Vagotomy

References:[14][20][26][27]

Acute management checklist

  • Start a PPI (e.g., omeprazole ). [28][29]
  • Consider alternative therapies (see drugs for peptic ulcer disease).
  • H. pylori eradication therapy [30][23]
  • Lifestyle changes: Recommend avoidance of spicy foods and caffeine, remaining upright after eating, smoking cessation, and limiting/ceasing alcohol intake.
  • Discontinue NSAIDs, if possible.
  • Identify and treat complications
    • Suspected bleeding peptic ulcer: urgent GI consult for consideration of EGD (see upper gastrointestinal bleed)
    • Suspected perforation of peptic ulcer: urgent surgery consult for consideration of exploratory laparotomy

Complications

Posterior ulcers are more likely to bleed and anterior ulcers are more likely to perforate: Postal workers wear Blue collars and should not have an Antisocial Personality.

References:[27][31][32][33][34][35][36][37][38][39]

We list the most important complications. The selection is not exhaustive.

Prevention

Recurrence prophylaxis

Stress ulcer prophylaxis

References:[40]