Acute & Chronic  Pancreatitis Marcos Machado, M.D. Heedong Park, M.D. November 8, 2006
Anatomy
Physiology Endocrine (20%) Islets of Langerhans Insulin (beta) Glucagon (alpha) Somatostatin (delta) Exocrine (80%) Digestive enzymes (pro-enzymes) Trypsinogen Chymotrypsinogen Controlled by Gastrin CCK Secretin
Pathophysiology – Acute  Initiating event Injury to acinar cells impairs release of proenzymes (in zymogen granules) Premature activation of enzymes Autodigestion
Pathophysiology – Acute  Normal Pancreatitis
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
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
Pathophysiology – Chronic  Progressive inflammatory changes Chronic irreversible inflammation Fibrosis with calcification Loss of pancreatic function
Causes - CP Alcohol (60%) Genetic predisposition? Genetic Causes (CF, hered pancreatitis) Ductal Obstruction Trauma, pseudocysts, stones, tumors) Systemic Dz – SLE, high TG Autoimmune Idiopathic
Symptoms – Acute & Chronic Acute Dull, boring midepigastric, radiates to back Usually sudden onset Nausea/vomiting Chronic mid upper abd pain – chronic, intermittently severe, may rad to back Diarrhea, wt loss Steatorrhea, diabetes
Signs – Acute & Chronic Acute Fever (76%), tachy (65%) Abd tenderness, guarding (68%), hypoactive BS ± jaundice Severe: hemodynamic instability, hematemesis Chronic ± epigastric tender mass or fullness (pseudocyst) Advanced: malnutrition, decreased subcut fat
DDx – Acute & Chronic Acute Cancer (pancreatic, colon) Cholangitis Cholecystitis, Choledocholithiasis, Cholelithiasis Colonic Obstruction Ulcers IBS MI Chronic Cancer (pancreatic, ampullary) Cholangitis Cholecystitis Crohn’s Dz Chronic Gastritis Bowel perforation Mesenteric Ischemia MI PUD
Labs – Acute & Chronic Acute Amy/lip: 3x above Nl to be diagnostic.  Lipase has longer T1/2 and is more specific Gallstone panc: ALP, Tbili, AST, ALT Ca, cholesterol, TG CBC – hemoconc-might be severe Chronic CBC, LFTs Chem Nl Amy/Lip: Nl to slightly high Compression of duct: high bili and ALP AI: high ESR, RF, ANA Adv: low serum trypsin, steatorrhea Poss: high Ca, high TG
Labs – cont. Other causes of elevated amylase SBO Mesenteric ischemia Tubo-ovarian dz Renal insuff Parotitis
Imaging When to obtain imaging uncertain diagnosis Severe disease
Imaging Choice U/S – most useful initial test, TOC in gallstone Sensitivity 70-80% CT abd – if severe acute pancreatitis Good for assessing complications
Imaging Choice ERCP, MRCP – duct obstruction MRCP is safer, noninvasive and faster than ERCP but less sensitive ERCP only if 2 °  to choledocholithiasis
Imaging Choice Abd xray – limited role Calcifications 30% of chronic panc Free air–perforation
Medical Treatment Acute Pancreatitis NPO IVF Pain relief Antibiotics If infected pancreatic necrosis Antibiotic prophylaxis in severe pancreatitis is controversial
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
Complications Pseudocyst Abscess formation Pancreatic necrosis
Surgical Treatment Pseudocysts Peripancreatic fluid collections for >4wks Intervention if: >7cm and rapidly expanding Symptomatic (pain, bleeding, infection)
Surgical Treatment Pseudocysts Percutaneous aspiration Very large fluid collections Pancreatic abcess Also responds to percut drainage
Surgical Treatment Pseudocysts Transpapillary drainage If pancreatic duct communicates with pseudocyst, can place  stent
Surgical Treatment Pseudocysts Transmural enterocystostomy  Endoscopic if distance between lumen and pseudocyst is <1cm
Surgical Treatment Pseudocysts Transmural enterocystostomy
Surgical Treatment Infected pancreatic necrosis Abx not enough Surgical debridement and drainage
Surgical Treatment Stones If evidence of biliary obstruction (jaundice, bile duct dilation), may benefit from ERCP
Surgical Treatment Pancreatic Duct distruption ERCP can provide dx and tx Transpapillary stent placement For distal leaks (tail of pancreas) Distal pancreatectomy
Surgical Treatment Pancreatic Duct distruption Proximal leaks (head of pancreas) Whipple
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
Prognosis Ranson’s Criteria Admission >55yo, WBC>16, BG>200, LDH>350, AST>250 @ 48 hrs HCT drops 10%, BUN increases by 5, Ca < 8, pO2 <60, Base deficit>4, fluid sequestration > 6L Scoring 0-2 = minimal mortality 3-5 = 10-20% >5 = >50% mortality APACHE II scoring is best validated, but cumbersome
References http://www. emedicine .com http://hopkins- gi.nts.jhu.edu/pages/latin/templates/index.cfm? pg=disease4&organ=4&disease=24&lang_id=1 http://www.uptodate.com

Acute and Chronic Pancreatitis

  • 1.
    Acute & Chronic Pancreatitis Marcos Machado, M.D. Heedong Park, M.D. November 8, 2006
  • 2.
  • 3.
    Physiology Endocrine (20%)Islets of Langerhans Insulin (beta) Glucagon (alpha) Somatostatin (delta) Exocrine (80%) Digestive enzymes (pro-enzymes) Trypsinogen Chymotrypsinogen Controlled by Gastrin CCK Secretin
  • 4.
    Pathophysiology – Acute Initiating event Injury to acinar cells impairs release of proenzymes (in zymogen granules) Premature activation of enzymes Autodigestion
  • 5.
    Pathophysiology – Acute Normal Pancreatitis
  • 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
  • 7.
    AP: OtherCauses – 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
  • 8.
    Pathophysiology – Chronic Progressive inflammatory changes Chronic irreversible inflammation Fibrosis with calcification Loss of pancreatic function
  • 9.
    Causes - CPAlcohol (60%) Genetic predisposition? Genetic Causes (CF, hered pancreatitis) Ductal Obstruction Trauma, pseudocysts, stones, tumors) Systemic Dz – SLE, high TG Autoimmune Idiopathic
  • 10.
    Symptoms – Acute& Chronic Acute Dull, boring midepigastric, radiates to back Usually sudden onset Nausea/vomiting Chronic mid upper abd pain – chronic, intermittently severe, may rad to back Diarrhea, wt loss Steatorrhea, diabetes
  • 11.
    Signs – Acute& Chronic Acute Fever (76%), tachy (65%) Abd tenderness, guarding (68%), hypoactive BS ± jaundice Severe: hemodynamic instability, hematemesis Chronic ± epigastric tender mass or fullness (pseudocyst) Advanced: malnutrition, decreased subcut fat
  • 12.
    DDx – Acute& Chronic Acute Cancer (pancreatic, colon) Cholangitis Cholecystitis, Choledocholithiasis, Cholelithiasis Colonic Obstruction Ulcers IBS MI Chronic Cancer (pancreatic, ampullary) Cholangitis Cholecystitis Crohn’s Dz Chronic Gastritis Bowel perforation Mesenteric Ischemia MI PUD
  • 13.
    Labs – Acute& Chronic Acute Amy/lip: 3x above Nl to be diagnostic. Lipase has longer T1/2 and is more specific Gallstone panc: ALP, Tbili, AST, ALT Ca, cholesterol, TG CBC – hemoconc-might be severe Chronic CBC, LFTs Chem Nl Amy/Lip: Nl to slightly high Compression of duct: high bili and ALP AI: high ESR, RF, ANA Adv: low serum trypsin, steatorrhea Poss: high Ca, high TG
  • 14.
    Labs – cont.Other causes of elevated amylase SBO Mesenteric ischemia Tubo-ovarian dz Renal insuff Parotitis
  • 15.
    Imaging When toobtain imaging uncertain diagnosis Severe disease
  • 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
  • 17.
    Imaging Choice ERCP,MRCP – duct obstruction MRCP is safer, noninvasive and faster than ERCP but less sensitive ERCP only if 2 ° to choledocholithiasis
  • 18.
    Imaging Choice Abdxray – limited role Calcifications 30% of chronic panc Free air–perforation
  • 19.
    Medical Treatment AcutePancreatitis NPO IVF Pain relief Antibiotics If infected pancreatic necrosis Antibiotic prophylaxis in severe pancreatitis is controversial
  • 20.
    Medical Treatment ChronicPancreatitis 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
  • 21.
    Complications Pseudocyst Abscessformation Pancreatic necrosis
  • 22.
    Surgical Treatment PseudocystsPeripancreatic fluid collections for >4wks Intervention if: >7cm and rapidly expanding Symptomatic (pain, bleeding, infection)
  • 23.
    Surgical Treatment PseudocystsPercutaneous aspiration Very large fluid collections Pancreatic abcess Also responds to percut drainage
  • 24.
    Surgical Treatment PseudocystsTranspapillary drainage If pancreatic duct communicates with pseudocyst, can place stent
  • 25.
    Surgical Treatment PseudocystsTransmural enterocystostomy Endoscopic if distance between lumen and pseudocyst is <1cm
  • 26.
    Surgical Treatment PseudocystsTransmural enterocystostomy
  • 27.
    Surgical Treatment Infectedpancreatic necrosis Abx not enough Surgical debridement and drainage
  • 28.
    Surgical Treatment StonesIf evidence of biliary obstruction (jaundice, bile duct dilation), may benefit from ERCP
  • 29.
    Surgical Treatment PancreaticDuct distruption ERCP can provide dx and tx Transpapillary stent placement For distal leaks (tail of pancreas) Distal pancreatectomy
  • 30.
    Surgical Treatment PancreaticDuct distruption Proximal leaks (head of pancreas) Whipple
  • 31.
    Prognosis Acute PancreatitisOverall 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
  • 32.
    Prognosis Ranson’s CriteriaAdmission >55yo, WBC>16, BG>200, LDH>350, AST>250 @ 48 hrs HCT drops 10%, BUN increases by 5, Ca < 8, pO2 <60, Base deficit>4, fluid sequestration > 6L Scoring 0-2 = minimal mortality 3-5 = 10-20% >5 = >50% mortality APACHE II scoring is best validated, but cumbersome
  • 33.
    References http://www. emedicine.com http://hopkins- gi.nts.jhu.edu/pages/latin/templates/index.cfm? pg=disease4&organ=4&disease=24&lang_id=1 http://www.uptodate.com