PANCREATITIS Bernard M. Jaffe, MD Professor of Surgery, Emeritus

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

KNOWN CAUSES GallstonesDuct Occlusion AlcoholismDivisum HyperlipidemiaMedications TraumaHereditary Post-ERCPInfections Tumors (1-2%)Iatrogenic

MEDICATIONS Steroids Thiazide Diuretics, Lasix Anti-Retrovirals Tetracycline Estrogens Azothioprine, 6-MP Dopaminergic Agents

PATHOGENESIS Uncertain But Multiple Theories 1. Common Channel 2. Sphincter Incompetence 3. Ductal Occlusion- Most Likely Obstruction by Stone Papillary Stenosis

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

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

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

ALCOHOL Usually >10 Year History g of Alcohol/Day 10-15% Regular Alcohol Users Ethanol Causes Spasm of Sphincter of Oddi Metabolic Toxin to Acinar Cells Increases Ductal Permeability

SYMPTOMS Severe Epigastric Pain Referred to Back Generally After a Meal Nausea Vomiting Dehydration, Weakness Fever

PHYSICAL FINDINGS Epigastric Tenderness, Guarding Decreased Bowel Sounds Abdominal Distention Tachycardia, Tachypnea, Hypotension Elevated Temperature

DIFFERENTIAL DIAGNOSIS Acute Cholecystitis Perforated Peptic Ulcer Gangrenous Small Bowel Obstruction Appendicitis Diverticulitis Leaking Abdominal Aortic Aneurism

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

SERUM LIPASE Specificity Higher 80-96% Fewer Other Causes of Elevation No Salivary Source of Lipase Lasts Longer Than Amylase Best Indicator of Disease

ULTRASOUND Can Detect Gallstones Dilated Extrahepatic Ducts Pancreatic Edema, Swelling Peri-Pancreatic Fluid Collections 20% Unsatisfactory- Presence of Bowel Gas

CT SCANNING Requires Intravenous Contrast Best Way to Assess Severity Identifies Necrosis- Absence of Microcirculation Air Bubbles- Infected Necrosis Pancreatic Abcess

RANSON’S CRITERIA Estimates Severity of Pancreatitis Measured on Admission and 48 Hours Different for Gallstone and Non- Gallstone Disease <2 Signs-0 Mortality % >7->50% Not Useful Beyond 48 Hours

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

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

EXPLANATION Elevated Glucose- Pancreatic Destruction- Decreased Insulin Hematocrit Fall- Bleeding Into Retroperitoneum Blue Coloration Around Umbilicus- Cullen’s Sign Blue Flanks- Gray Turner Sign

EXPLANATION Calcium Fall- Saponification- Precipitation of Salts Elevated BUN, Fluid Sequestration- Third Space, Dehydration Drop in pO 2 – Pleural Effusion, Respiratory Depression

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

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

LOCAL COMPLICATIONS Phlegmon Necrosis Abcess Ascites Pseudocyst Involvement of Adjacent Organs Chronic Pancreatitis

SYSTEMIC COMPLICATIONS Pulmonary- Pleural Effusion, Pneumonia, ARDS, Atelectasis Hematologic- DIC Gastrointestinal- Peptic Ulcer, Gastritis, Portal/Splenic Vein Thrombosis Renal- Oliguria, Renal Failure

SYSTEMIC COMPLICATIONS Cardiovascular- Hypotension, Hypoxemia, Congestive Failure, Arrhythmias Metabolic- Hyperglycemia, Encephalopathy, Hypertriglyceridemia CNS- Psychosis, Delirium Fat Necrosis

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

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

CHOLECYSTECTOMY All Patients With Gallstone Pancreatitis During Same Hospitalization Once Pancreatitis is Resolved, Resolving Common Bile Duct Exploration for Choledocholithiasis Minimal Risk of Cholangitis

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