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PANCREATITIS Bernard M. Jaffe, MD Professor of Surgery, Emeritus
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INCIDENCE 300,000 New Cases/Year in US 10-20% Are Severe 3,000 Deaths/Year Contributing Factor in 4,000 More Deaths/Year $2 Billion/Year in Health Care Costs
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KNOWN CAUSES GallstonesDuct Occlusion AlcoholismDivisum HyperlipidemiaMedications TraumaHereditary Post-ERCPInfections Tumors (1-2%)Iatrogenic
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MEDICATIONS Steroids Thiazide Diuretics, Lasix Anti-Retrovirals Tetracycline Estrogens Azothioprine, 6-MP Dopaminergic Agents
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PATHOGENESIS Uncertain But Multiple Theories 1. Common Channel 2. Sphincter Incompetence 3. Ductal Occlusion- Most Likely Obstruction by Stone Papillary Stenosis
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COMMON CHANNEL Duct Blockage Below Confluence of Pancreatic and Bile Ducts BUT Duct Below is so Short That it Would Block Both Ducts Pancreatic Duct Hydrostatic Pressure Higher Than Biliary, SO Flow Would Go Pancreatic → Biliary Ducts
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SPHINCTER INCOMPETENCE Stone Blocks Sphincter → Incompetence Duodenal Fluid With Active Enzymes Refluxes Into Pancreas BUT Stone Passes Quickly, Minimal Incompetence Sphincterotomy Doesn’t Cause Pancreatitis
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DUCT OCCLUSION Ongoing Ductal Secretion Into Occluded Pancreatic Duct Increased Intraductal Pressure Ruptures Ducts Leakage of Pancreatic Fluid Into Parenchyma Activation of Local Tissue Proteases
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ALCOHOL Usually >10 Year History 100-150g of Alcohol/Day 10-15% Regular Alcohol Users Ethanol Causes Spasm of Sphincter of Oddi Metabolic Toxin to Acinar Cells Increases Ductal Permeability
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SYMPTOMS Severe Epigastric Pain Referred to Back Generally After a Meal Nausea Vomiting Dehydration, Weakness Fever
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PHYSICAL FINDINGS Epigastric Tenderness, Guarding Decreased Bowel Sounds Abdominal Distention Tachycardia, Tachypnea, Hypotension Elevated Temperature
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DIFFERENTIAL DIAGNOSIS Acute Cholecystitis Perforated Peptic Ulcer Gangrenous Small Bowel Obstruction Appendicitis Diverticulitis Leaking Abdominal Aortic Aneurism
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SERUM AMYLASE Elevation Immediate Peaks Several Hours Remains Elevated 5-6 Days Levels Can be Normal No Correlation With Disease Severity Urinary Levels More Sensitive Persist Longer
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SERUM LIPASE Specificity Higher 80-96% Fewer Other Causes of Elevation No Salivary Source of Lipase Lasts Longer Than Amylase Best Indicator of Disease
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ULTRASOUND Can Detect Gallstones Dilated Extrahepatic Ducts Pancreatic Edema, Swelling Peri-Pancreatic Fluid Collections 20% Unsatisfactory- Presence of Bowel Gas
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CT SCANNING Requires Intravenous Contrast Best Way to Assess Severity Identifies Necrosis- Absence of Microcirculation Air Bubbles- Infected Necrosis Pancreatic Abcess
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RANSON’S CRITERIA Estimates Severity of Pancreatitis Measured on Admission and 48 Hours Different for Gallstone and Non- Gallstone Disease <2 Signs-0 Mortality 3-5-10-20% >7->50% Not Useful Beyond 48 Hours
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NON-GALLSTONE Admission Age >55 WBC>16,000 Glucose >200mg/dL LDH >350 IU/L AST >250 IU/L 48 Hours Hematocrit Fall >10% BUN Increase >5mg/dL Calcium <8mEq/dL pO 2 <60mm/Hg Base Deficit >4 mEq/L Fluid Sequestered > 6L
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GALLSTONE Admission Age >70 WBC >18,000 Glucose >220mg/dL LDH >400 IU/L AST >250 IU/L 48 Hours Hematocrit Fall >16% BUN Increase >2 mg/dL Calcium <8 mEq/dL pO 2 <60mm/Hg Fluid Sequestered > 4L
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EXPLANATION Elevated Glucose- Pancreatic Destruction- Decreased Insulin Hematocrit Fall- Bleeding Into Retroperitoneum Blue Coloration Around Umbilicus- Cullen’s Sign Blue Flanks- Gray Turner Sign
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EXPLANATION Calcium Fall- Saponification- Precipitation of Salts Elevated BUN, Fluid Sequestration- Third Space, Dehydration Drop in pO 2 – Pleural Effusion, Respiratory Depression
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TREATMENT- MILD DISEASE Self-Limiting Illness Supportive Care, Resting Pancreas Resuscitation, Metabolic Control Demerol/NSAIDs for Pain, NOT Morphine No Need for NG Tube, Anti-Secretory Drugs No Antibiotics Oral Feedings When Amylase Normal
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GALLSTONE PANCREATITIS Determine if Stone Still in Common Duct Important Therapeutic Differential Measure Bilirubin, Alkaline Phosphatase Ultrasound to Look for Dilated Ducts Stone Still Present- Urgent ERCP Stone Passed- Avoid ERDP, Very Risky
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LOCAL COMPLICATIONS Phlegmon Necrosis Abcess Ascites Pseudocyst Involvement of Adjacent Organs Chronic Pancreatitis
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SYSTEMIC COMPLICATIONS Pulmonary- Pleural Effusion, Pneumonia, ARDS, Atelectasis Hematologic- DIC Gastrointestinal- Peptic Ulcer, Gastritis, Portal/Splenic Vein Thrombosis Renal- Oliguria, Renal Failure
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SYSTEMIC COMPLICATIONS Cardiovascular- Hypotension, Hypoxemia, Congestive Failure, Arrhythmias Metabolic- Hyperglycemia, Encephalopathy, Hypertriglyceridemia CNS- Psychosis, Delirium Fat Necrosis
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TREATMENT- SEVERE DISEASE Supportive But No Specific Therapy Aggressive Rehydration, Resuscitation Early Nutrition, Enteral or TPN Correct Metabolic Abnormalities Early Intubation/Ventilation FNA OF Necrotic Areas
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ANTIBIOTICS NOT For Routine Use Indications- Infected Necrosis Sepsis Abcess (Usually 2-6 Weeks) Associated Infections Imipenim is Most Effective Agent High Risk of Candida Superinfection
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CHOLECYSTECTOMY All Patients With Gallstone Pancreatitis During Same Hospitalization Once Pancreatitis is Resolved, Resolving Common Bile Duct Exploration for Choledocholithiasis Minimal Risk of Cholangitis
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PSEUDOCYST Fibrous Encapsulated Collection of Pancreatic Juice Results From Ruptured Duct/Ductule Treat When Wall is Thick, Usually 6 Weeks Ideally- Pseudocyst-Enteric Anastamosis Open Laparoscopic Endoscopic Percutaneous Drainage- High Recurrence
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