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Wednesday, October 10, 2007

Nursing Reference: Acute and Chronic Pancreatitis

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Nursing Reference: Acute and Chronic Pancreatitis Slides Transcript
Slide 1: Acute & Chronic Pancreatitis Marcos Machado, M.D. Heedong Park, M.D. November 8, 2006

Slide 2: Anatomy

Slide 3: Physiology • Endocrine (20%) • Exocrine (80%) – Islets of Langerhans – Digestive enzymes (pro-enzymes) • Insulin (beta) • Trypsinogen • Glucagon (alpha) • Chymotrypsinogen • Somatostatin (delta) – Controlled by • Gastrin • CCK • Secretin

Slide 4: Pathophysiology – Acute Initiating event Injury to acinar cells impairs release of proenzymes (in zymogen granules) Premature activation of enzymes Autodigestion

Slide 5: Pathophysiology – Acute Normal Pancreatitis

Slide 6: AP: Causes – The Big Ones • Biliary Tract Disease (40%) • Alcohol (35%) – Usually Acute on Chronic • Idiopathic (10-30%) – Most (70%): likely occult microlithiasis • Post-ERCP (4%) • Trauma (1.5%) • Drugs (1.4%) • Azathioprine, sulfa, sulindac, valproic acid, tetracycline, methyldopa, estrogens, lasix, corticosteroids, octreotide • Poss: HCTZ, flagyl, nitrofurantoin, procainamide, cimetidine, other chemo drugs

Slide 7: AP: Other Causes – Each <1% • Infection » Viral (EBV, VZV, cocksackie), Bact (M. pneumo, Salmonella, Campy, TB), ascariasis • Hereditary » AD – mutation of trypsinogen gene, premature activation • Hypercalcemia • Developmental Abn Pancreas » Annular pancreas, pancreas divisum, SOD dysfunction) • Hypertriglyceridemia (>1000) • Tumor ( obstruction of ducts) • Toxin (scorpion, pesticide) • Post-Op

Slide 8: Pathophysiology – Chronic Progressive inflammatory changes Chronic irreversible inflammation Fibrosis with calcification Loss of pancreatic function

Slide 9: Causes - CP • Alcohol (60%) – Genetic predisposition? • Genetic Causes (CF, hered pancreatitis) • Ductal Obstruction – Trauma, pseudocysts, stones, tumors) • Systemic Dz – SLE, high TG • Autoimmune • Idiopathic

Slide 10: Symptoms – Acute & Chronic • Acute • Chronic – Dull, boring – mid upper abd pain – midepigastric, radiates chronic, intermittently to back severe, may rad to back – Usually sudden onset – Diarrhea, wt loss – Nausea/vomiting – Steatorrhea, diabetes

Slide 11: Signs – Acute & Chronic • Acute • Chronic – Fever (76%), tachy – ± epigastric tender mass (65%) or fullness (pseudocyst) – Abd tenderness, – Advanced: malnutrition, guarding (68%), decreased subcut fat hypoactive BS – ± jaundice – Severe: hemodynamic instability, hematemesis

Slide 12: DDx – Acute & Chronic • Acute • Chronic – Cancer (pancreatic, – Cancer (pancreatic, colon) ampullary) – Cholangitis – Cholangitis – Cholecystitis, – Cholecystitis Choledocholithiasis, – Crohn’s Dz Cholelithiasis – Chronic Gastritis – Colonic Obstruction – Bowel perforation – Ulcers – Mesenteric Ischemia – IBS – MI – MI – PUD

Slide 13: Labs – Acute & Chronic • Acute • Chronic – Amy/lip: 3x above Nl to – CBC, LFTs Chem Nl be diagnostic. Lipase – Amy/Lip: Nl to slightly high has longer T1/2 and is – Compression of duct: high more specific bili and ALP – Gallstone panc: ALP, – AI: high ESR, RF, ANA Tbili, AST, ALT – Adv: low serum trypsin, – Ca, cholesterol, TG steatorrhea – CBC – hemoconc-might – Poss: high Ca, high TG be severe

Slide 14: Labs – cont. • Other causes of elevated amylase – SBO – Mesenteric ischemia – Tubo-ovarian dz – Renal insuff – Parotitis

Slide 15: Imaging • When to obtain imaging – uncertain diagnosis – Severe disease

Slide 16: Imaging • Choice – U/S – most useful initial test, TOC in gallstone • Sensitivity 70-80% – CT abd – if severe acute pancreatitis • Good for assessing complications

Slide 17: Imaging • Choice – ERCP, MRCP – duct obstruction • MRCP is safer, noninvasive and faster than ERCP but less sensitive • ERCP only if 2° to choledocholithiasis

Slide 18: Imaging • Choice – Abd xray – limited role • Calcifications 30% of chronic panc • Free air–perforation

Slide 19: Medical Treatment • Acute Pancreatitis – NPO – IVF – Pain relief – Antibiotics • If infected pancreatic necrosis • Antibiotic prophylaxis in severe pancreatitis is controversial

Slide 20: Medical Treatment • Chronic Pancreatitis – Behavior modification • Cessation of EtOH and tobacco use will help pain relief in early stages, not in late – Pain control – Restoration of digestion and absorption • enzyme replacement – ± insulin

Slide 21: Complications • Pseudocyst • Abscess formation • Pancreatic necrosis

Slide 22: Surgical Treatment • Pseudocysts – Peripancreatic fluid collections for >4wks – Intervention if: • >7cm and rapidly expanding • Symptomatic (pain, bleeding, infection)

Slide 23: Surgical Treatment • Pseudocysts – Percutaneous aspiration • Very large fluid collections • Pancreatic abcess – Also responds to percut drainage

Slide 24: Surgical Treatment • Pseudocysts – Transpapillary drainage • If pancreatic duct communicates with pseudocyst, can place stent

Slide 25: Surgical Treatment • Pseudocysts – Transmural enterocystostomy • Endoscopic if distance between lumen and pseudocyst is <1cm

Slide 26: Surgical Treatment • Pseudocysts – Transmural enterocystostomy

Slide 27: Surgical Treatment • Infected pancreatic necrosis – Abx not enough – Surgical debridement and drainage

Slide 28: Surgical Treatment • Stones – If evidence of biliary obstruction (jaundice, bile duct dilation), may benefit from ERCP

Slide 29: Surgical Treatment • Pancreatic Duct distruption – ERCP can provide dx and tx • Transpapillary stent placement – For distal leaks (tail of pancreas) • Distal pancreatectomy

Slide 30: Surgical Treatment • Pancreatic Duct distruption – Proximal leaks (head of pancreas) • Whipple

Slide 31: Prognosis • Acute Pancreatitis – Overall mortality – 15%, severe dz – 30% – Ranson’s Criteria • Chronic Pancreatitis – Poor prognostic factors: young, smoker, cont to use EtOH, +liver cirrhosis – Overall mortality 30% @ 10yrs, 55% @ 20yrs – 4% risk of developing pancreatic CA @ 20yrs

Slide 32: Prognosis • Ranson’s Criteria – Admission • Scoring • >55yo, WBC>16, – 0-2 = minimal mortality BG>200, LDH>350, – 3-5 = 10-20% AST>250 – >5 = >50% mortality – @ 48 hrs • HCT drops 10%, BUN increases by 5, Ca < 8, • APACHE II scoring is pO2 <60, Base deficit>4, fluid best validated, but sequestration > 6L cumbersome







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