PEPTIC ULCER DISEASE BERNARD M. Jaffe, MD Professor of Surgery

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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
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H. Pylori Infection
NSAID’s
Acid Hypersecretion
Zollinger- Ellison Syndrome
Acid Plays a Role in All Four
GASTRIC CELLS
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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%
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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
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60%
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Low Levels of Acid
• Type II- Combination Type I Plus DU
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15%
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Excess Acid Secretion
GASTRIC ULCERS (2)
• Type III- Pre-Pyloric
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20%
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Behave Like DU’s
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Excess Acid Secretion
• Type IV- High on Lesser Curvature
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<10%
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Low Acid Secretion
• <5% Greater Curvature
GASTRIC ULCER
• Rare Before Age 40, Common 55-65 Years
• Caused By NSAID’s
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Acid, Pepsin Abnormalities
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Co-Existing DU
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Delayed Gastric Emptying
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Duodenal-Gastric Reflux
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Gastritis
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H. Pylori Infection
DU PREDISPOSITION
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Chronic Alcohol Intake
Smoking
Long-Term Steroid Use
Infection
SYMPTOMS
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Mid-Epigastric Pain
Relieved By Pain
Spring > Fall
Relapses with Stress
Constant Pain- Deeper Penetration
Back Pain- Penetration Into Pancreas
COMPLICATIONS
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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
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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
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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
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Z-E Syndrome
Antral G Cell Hyperplasia
Retained Gastric Antrum
Hypercalcemia
Gastric Outlet Obstruction
Anti-Secretory Drugs
ELEVATED GASTRIN LEVELS
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Previous Ulcer Operation
Atrophic Gastritis
Pernicious Anemia
Chronic Renal Failure
H. Pylori Infection
PEPTIC ULCER DIAGNOSIS
• EGD, Barium Swallow
• H. Pylori Testing
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Serology- ELISA 90% Sensitive
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Urea Breath Test- Uses 14C
Specificity, Sensitivity >95%
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Rapid Urease- Endoscopic Biopsy, Tissue
Placed in Urea, >90% Sensitive
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Histology, Biopsy of Antrum- Best Test
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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
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