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 Acid-FundusParietal Cells Gastrin- AntrumG Cells Pepsinogen-DiffuseChief Cells Histamine-DiffuseEnterochromaffin- Like Cells Somatostatin-DiffuseD 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 Countries- Sanitation 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 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 Perforation- Parietal 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 14 C 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 H 2 Receptor Antagonists % 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