3.2 Stomach & Duodenal Disease and Gastrointestinal Hemorrhage

1. Peptic Ulcer Disease & Helicobacter pylori

Peptic Ulcer Disease (PUD)

Peptic Ulcer Disease is characterized by mucosal defects in the stomach or duodenum extending through the muscularis mucosae.

• Etiologies:
  1. Helicobacter pylori infection: Responsible for 70–85% of duodenal ulcers and 50–60% of gastric ulcers.
  2. NSAIDs & Aspirin: Inhibit cyclooxygenase-1 (COX-1), depleting mucosal protective prostaglandins (PGE2, PGI2).
  3. Zollinger-Ellison Syndrome (ZES): Gastrin-secreting neuroendocrine tumor (gastrinoma) located in the duodenum or pancreas, causing profound gastric acid hypersecretion, severe refractory peptic ulcers (often post-bulbar or multiple), and secretory diarrhea (check fasting serum gastrin >1,000 pg/mL off PPI, secretin stimulation test).
  4. Stress Ulcers: In critically ill ICU patients with mechanical ventilation >48 hours or coagulopathy (INR >1.5, platelets <50,000/mcL).

Duodenal vs. Gastric Ulcers

Helicobacter pylori Infection: ACG 2024 Guidelines

Helicobacter pylori is a microaerophilic, spiral, gram-negative, urease-producing rod that colonizes gastric mucosa.

Diagnostic Testing Principles

• Active Infection Tests:
  1. Urea Breath Test ($^{13}\text{C}$ or $^{14}\text{C}$-UBT): High sensitivity and specificity (>95%).
  2. Stool Antigen Test (Monoclonal EIA): High sensitivity and specificity (>95%).
  3. Endoscopic Biopsy: Rapid Urease Test (CLOtest) or histopathology with Giemsa/Warthin-Starry stain.
• Crucial Diagnostic Washout Rules:
  • Must discontinue PPIs for at least 1 to 2 weeks prior to breath, stool, or biopsy testing.
  • Must discontinue antibiotics and bismuth compounds for at least 4 weeks prior to testing.
  • Failure to observe washouts causes false-negative test results due to temporary suppression of bacterial load.
• Serology (IgG antibodies): NOT recommended because it cannot distinguish active infection from past resolved infection and cannot be used to confirm eradication (antibodies persist for years).

ACG 2024 Eradication Regimens

[!IMPORTANT] Due to high worldwide and North American clarithromycin resistance rates (>15–20%), Clarithromycin-based triple therapy is NO LONGER recommended as empiric first-line therapy unless local resistance testing confirms susceptibility.

Confirmation of Eradication

• Eradication testing is mandatory for all treated patients.
• Perform Urea Breath Test, Stool Antigen Test, or Endoscopy Biopsy at least 4 weeks after completion of antibiotic therapy AND at least 1 to 2 weeks after stopping PPI therapy.

2. Acute Upper Gastrointestinal Bleeding (UGIB)

Clinical Triage & Risk Stratification

• Clinical Presentation: Hematemesis ("coffee-ground" emesis or bright red blood), melena (black, tarry stools; requires ~50–100 mL of blood in upper tract), or hematochezia (massive upper GI hemorrhage with rapid transit, hemodynamic instability).
• Glasgow-Blatchford Score (GBS): Triage tool based on admission BUN, hemoglobin, systolic blood pressure, heart rate, melena, syncope, hepatic disease, and heart failure (Scores 0–23).
  • GBS = 0–1: Extremely low risk (<1% intervention rate). Suitable for outpatient management without emergency endoscopy.
  • GBS $\ge 2$: High risk. Requires inpatient admission, active resuscitation, and early endoscopic evaluation.

Acute Resuscitation Protocol

1. Hemodynamic Stabilization & Access: Secure airway in patients with active hematemesis or altered mental status. Place two large-bore peripheral IV lines (16- or 18-gauge) or a large-bore central line.
2. Restrictive Transfusion Strategy (TRICC & Villanueva Guidelines):
   • Target Hemoglobin: 7.0 to 8.0 g/dL.
   • Transfusion threshold: Transfuse Packed Red Blood Cells (PRBCs) when $\text{Hb} < 7.0\text{ g/dL}$ (reduces rebleeding rates, fluid overload, and overall mortality compared to liberal transfusion threshold of $>9.0\text{ g/dL}$).
   • Exception: Patients with active acute coronary syndrome, severe symptomatic coronary artery disease, or ongoing hemodynamic instability (target $\text{Hb} \ge 8.0-9.0\text{ g/dL}$).
3. Pharmacotherapy:
   • Intravenous PPI: High-dose IV PPI (e.g., Pantoprazole 80 mg IV bolus followed by 8 mg/hour continuous IV infusion, or 40 mg IV BID) to maintain intragastric $\text{pH} > 6.0$, promoting platelet aggregation and clot stability.
   • Prokinetic Agent: Erythromycin 250 mg IV infused 30–60 minutes prior to endoscopy promotes gastric motility, clears blood and clots from the gastric fundus, and significantly improves endoscopic visualization.
4. Endoscopic Timing: Perform EGD within 24 hours of presentation following adequate hemodynamic resuscitation.

Peptic Ulcer Forrest Classification & Endoscopic Hemostasis

[!CAUTION] Epinephrine injection monotherapy is INSUFFICIENT because it achieves only transient local tamponade and vasoconstriction. It must ALWAYS be combined with a second mechanical (clips) or thermal modality to prevent early rebleeding.