PEPTIC ULCER DISEASE BERNARD M. Jaffe, MD Professor of Surgery Emeritus PEPTIC ULCER DISEASE • 8% Annual Incidence in the Population • 500,000 New Cases/Year • 4,000,000 Recurrences/Year • 130,000 Operations/Year • 9,000 Deaths/Year PEPTIC ULCER DISEASE • Elective Admissions Declining, for Complications Unchanging • Gastric Ulcer More Common in Elderly • Admissions for Bleeding GU Increasing • Decreasing Incidence in Males, Increasing in Females • ? Due to Changes in Smoking Patterns CAUSES OF PUD • • • • • H. Pylori Infection NSAID’s Acid Hypersecretion Zollinger- Ellison Syndrome Acid Plays a Role in All Four GASTRIC CELLS • • • • AcidGastrinPepsinogenHistamine- Fundus Antrum Diffuse Diffuse • Somatostatin- Parietal Cells G Cells Chief Cells EnterochromaffinLike Cells Diffuse D Cells H. Pylori INFECTION • 90% Duodenal, 75% Gastric Ulcers • Nearly 100% Have Antral Gastritis • Eradication Prevents Recurrence • Strong Association with MALT Lymphoma • Microaerophilic, Urease Producing • Can Live in Gastric Epithelium GASTROINTESTINAL INJURY • Production of Toxic Products • Ammonia, Cytokines, Mucinases, Phospholipases, Platelet Activating Factor • Induction in Local Mucosal Immune Responses • Increases Gastrin → Increasing Acid Secretion H. Pylori INFECTION • World-Wide Pandemic • Usually Acquired in Childhood • Inverse Relationship Between Infection Rates and Socio Economic Status • Transmission Mouth-to-Mouth • Higher Rate in Developing CountriesSanitation is a Real Issue NSAID’S • Second Most Common Cause of PUD • Increased Use in Women >50 Years Old • Risk of Ulcers/Bleeding Parallels Drug Use • 10% of Patients Taking NSAID’s Develop Acute Ulcer • 2-4% Develop GI Complications/Year ACID- INCREASED • Nocturnal Acid 70% • • • • Daytime Acid 50% Duodenal Acid Load Maximal Acid 65% 40% Gastrin Sensitivity Basal Gastrin 35% 35% Gastric Emptying 30% Parietal Cells 30% GASTRIC ULCERS • Type I- Lesser Curvature Near Incisura • 60% • Low Levels of Acid • Type II- Combination Type I Plus DU • 15% • Excess Acid Secretion GASTRIC ULCERS (2) • Type III- Pre-Pyloric • 20% • Behave Like DU’s • Excess Acid Secretion • Type IV- High on Lesser Curvature • <10% • Low Acid Secretion • <5% Greater Curvature GASTRIC ULCER • Rare Before Age 40, Common 55-65 Years • Caused By NSAID’s • Acid, Pepsin Abnormalities • Co-Existing DU • Delayed Gastric Emptying • Duodenal-Gastric Reflux • Gastritis • H. Pylori Infection DU PREDISPOSITION • • • • Chronic Alcohol Intake Smoking Long-Term Steroid Use Infection SYMPTOMS • • • • • • Mid-Epigastric Pain Relieved By Pain Spring > Fall Relapses with Stress Constant Pain- Deeper Penetration Back Pain- Penetration Into Pancreas COMPLICATIONS • • • • Perforation Bleeding Obstruction Chronicity PERFORATION • Sudden Abdominal Pain, Fever • Tachycardia, Ileus, Dehydration • Exquisite Abdominal Tenderness, Rebound, Rigidity • Free Air Under the Diaphragm, Can Verify by Gastrograffin Swallow • Surgical Emergency PERFORATION • Treat with Gramm Patch Omental Closure • Simultaneous Definitive Procedure IF • PUD with NO Symptoms • Failure to Respond to Medical Therapy • Best Definitive Procedure for PerforationParietal Cell Vagotomy • Non-Operative Therapy Reserved for Late Presentation with No Acute Abdomen BLEEDING • Most Common Cause of PUD Death • Bleeding Accounts for 25% of All Upper GI Bleeds • Can Present with Melena, Hematemesis, or Bright Red Rectal Bleeding • Gastroduodenal Artery Lies Posterior to Duodenal Bulb- “Visible Vessel” OBSTRUCTION • Chronic Scarring Can Occlude Pylorus • Acute Inflammation Also Causes Obstruction • Anorexia, Nausea, Vomiting • Hypochloremic, Hypokalemic Metabolic Alkalosis, Dehydration, Malnutrition • Stomach Becomes Massivel Dilated and Loses Muscular Tone GASTRIC ULCER • • • • • • Must Distinguish Benign From Malignant Causes Same Complications as DU 8-20% Need Operation for Complications Bleeding Occurs in 35-40% Perforation is Most Life-Threatening Obstruction Occurs in Types I and II ZOLLINGER-ELLISON SYNDROME • Triad- Gastric Acid Hypersecretion, Severe PUD, Non-β Islet Cell Tumors • Gastrinomas in Head of Pancreas, Duodenum • 50% Multiple, 65% Malignant, 25% Associated with MEN Syndrome • Abdominal Pain, Diarrhea, Steatorrhea • Elevated Basal, Stimulated Gastrin Levels • Treatment Focuses on Tumor Resection ELEVATED GASTRIN LEVELS • • • • • • Z-E Syndrome Antral G Cell Hyperplasia Retained Gastric Antrum Hypercalcemia Gastric Outlet Obstruction Anti-Secretory Drugs ELEVATED GASTRIN LEVELS • • • • • Previous Ulcer Operation Atrophic Gastritis Pernicious Anemia Chronic Renal Failure H. Pylori Infection PEPTIC ULCER DIAGNOSIS • EGD, Barium Swallow • H. Pylori Testing • Serology- ELISA 90% Sensitive • Urea Breath Test- Uses 14C Specificity, Sensitivity >95% • Rapid Urease- Endoscopic Biopsy, Tissue Placed in Urea, >90% Sensitive • Histology, Biopsy of Antrum- Best Test • Culture is Slow, Expensive MEDICAL MANAGEMENT • Avoid Smoking, Caffeine, Alcohol, NSAID’s • Antacids- Large Frequent Doses Needed • H2 Receptor Antagonists- 70-80% Healing in 4 Weeks, 80-90% in 8 Weeks • Proton Pump Inhibitors- Most Complete Acid Inhibition- Healing 85% in 4 Weeks, 90% in 8 Weeks • Sucralfate- Aluminum Salt of Sulfated Sucrose- Protective Coating OPERATIVE MANAGEMENT • Subtotal Gastrectomy- Highest Complication Rate • Vagotomy and Antrectomy- Most Efficacious • Vagotomy and Pyloroplasty- Major Indication is Bleeding Gastritis • Parietal Cell Vagotomy- Most Physiologic