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Please, silence your pagers

Please, silence your pagers. Yaroslavl, Russia (EST. 1010). Pancreatitis New in Diagnosis and Treatment. Boris V. Vinogradsky, MD Department of Surgery Medical College of Ohio Toledo, Ohio March 03, 2001.

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  1. Please, silence your pagers

  2. Yaroslavl, Russia (EST. 1010)

  3. PancreatitisNew in Diagnosis and Treatment Boris V. Vinogradsky, MDDepartment of SurgeryMedical College of OhioToledo, Ohio March 03, 2001

  4. “Theodor Kocher called the pancreas “the mischief maker of the abdomen.” Some surgeons have stronger language to describe this organ, but decorum demands that such a language be excluded from such a syllabus.” J.Patrick O’Leary, MD

  5. Pancreatitis: Classification Acute Pancreatitis Interstitial edematous pancreatitis Sterile necrotizing pancreatitis Infected pancreatic necrosis/abscess Hemorrhagic pancreatitis Chronic Pancreatitis Uncomplicated recurrent pancreatitis Calcifying chronic pancreatitis Obstructive chronic pancreatitis

  6. Pancreatitis Pancreatitis is a complex disorder of the exocrine pancreas with unclear pathogenic mechanisms, which is characterized by acute acinar cell injury and both regional and systemic inflammatory responses. Overall mortality 6.0-20.5% Acute necrotizing pancreatitis 50+% No specific treatment

  7. Normal Pancreatic Physiology The pancreas secretes 500-800 ml/day of an alkaline, colorless, odorless, isosmotic fluid containing large quantity of bicarbonate and digestive enzymes Stimulated by secretin, duodenal pH of less than 4.0 Vagal stimulation through acetylcholine Inhibited by truncal vagotomy, atropine

  8. Normal Release of Pancreatic Enzymes Greenfield LJ. Surgery: Scientific Principles and Practice, 1997

  9. Normal Pancreatic Physiology Enzymes are NOT secreted at a fixed ratio, specific nutrients can cause a relative increase of one of the fractions CCK is the primary regulator of enzymes secretion Ca++ and diacylglycerol are second messengers Greenfield LJ. Surgery: Scientific Principles and Practice, 1997

  10. Normal Release of Pancreatic Enzymes Greenfield LJ. Surgery: Scientific Principles and Practice, 1997

  11. Pancreatic Enzymes Pancreatic enzymes: Amylase Active Proteolytic enzymes Inactive Lipases Inactive Inhibitors: Alpha1-antitrypsin Beta2-macroglobulin Pancreatic secretory trypsin inhibitor

  12. Normal Pancreatic Physiology Proteolytic proenzymes such as trypsinogen convert to active form under the influence of ENTEROKINASE, luminal HCl and spontaneously

  13. Causes of Acute Pancreatitis Most common: Ethanol abuse Cholelithiasis Less common: ERCP Trauma Hyperlipidemia (types I, IV and V) Pancreas divisum Least common: Familial Idiopathic Drugs Baron TH, Morgan DE. Acute Necrotizing Pancreatitis, NEJM, 1999

  14. Initial triggering event in development of acute pancreatitis is DUCTAL HYPERTENSION

  15. Ethanol use is the most common cause of acute pancreatitis in the United States

  16. Alcohol in Acute Pancreatitis Acetaldehyde formation Microtubular disruption Increase in acinar cell membrane permeability Elevated triglycerides level Formation of cytotoxic free fatty acids Increased HCl production stimulates secretin release and increases pancreatic ductal flow Elevation of pancreatic intraductular pressure

  17. Protein Stones Formation Greenfield LJ. Surgery: Scientific Principles and Practice, 1997

  18. Gallstones in Acute Pancreatitis Simple cholelithiasis 72% of patients Choledocholithiasis 20% Cholecystitis 8% Stool screening 85-94% patients for stones within 10 days of onset of disease (late Dr.Kelly from Akron, OH) Greenfield LJ. Surgery: Scientific Principles and Practice, 1997

  19. Common Channel Concept Greenfield LJ. Surgery: Scientific Principles and Practice, 1997

  20. Acute Pancreatitis Fundamental pathologic event is injury to acinar cell Process begins within minutes

  21. Acute Pancreatitis: Pathogenesis Autophagic cytoplasmic vacuoles (zymogen lakes) formation Elevated levels of TNF-alpha, IL-1, IL-6 Hypoxia Loss of normal cell polarity Basolateral disordered discharge Greenfield LJ. Surgery: Scientific Principles and Practice, 1997

  22. Acute Pancreatitis: Initiation Greenfield LJ. Surgery: Scientific Principles and Practice, 1997

  23. Acute Pancreatitis: Pathology Greenfield LJ. Surgery: Scientific Principles and Practice, 1997

  24. Acute Pancreatitis: Pathogenesis Microvascular endothelial cell injury in multiple target organs Greenfield LJ. Surgery: Scientific Principles and Practice, 1997

  25. Changes in Lung Alveoli Greenfield LJ. Surgery: Scientific Principles and Practice, 1997

  26. Shifting Gears

  27. Yaroslavl Medical School: Class of 1986

  28. Russia Yahoo!Maps - Europe, Russia, 2001

  29. Cardinal symptom of acute pancreatitis is epigastric abdominal PAIN

  30. Symptoms and Signs Abdominal pain 85-100% Nausea and vomiting 55-90% Anorexia 80% Tachicardia 65-80% Fever 12-80% Ileus 50-80% Abdominal tenderness/mass 90-99% All non-specific Baron TH, Morgan DE. Acute Necrotizing Pancreatitis, NEJM, 1999

  31. Other Signs Grey-Turner sign Cullen sign Fox sign All non-specific and present in less than 20% of patients

  32. Hyperamylasemia Salivary gland injury Burns Small bowel injury Cerebral trauma Multiple trauma Diabetic ketoacidosis Macroamylasemia Renal failure/transplantation Pregnancy Dissecting aortic aneurysm Larvin M, McMahon MJ. APACHE II score for assessment and monitoring of acute pancreatitis. Lancet 1989; 2; 738

  33. CT scanning is the BEST imaging study in evaluation of acute pancreatitis

  34. Acute Pancreatitis: CT Scanning Lillemoe KD, Yeo CJ Management of Complications of Pancreatitis, 1998

  35. Acute Fluid Collection Lillemoe KD, Yeo CJ Management of Complications of Pancreatitis, 1998

  36. Ultrasound of the Pancreas Staren ED. Ultrasound for the Surgeon, 1997

  37. Ranson’s Criteria On admission Age >55 years WBC >16,000 Glucose >200 LDH >350 AST >250 After 48 hours Drop in Hct >10% Increase in BUN >5 Ca <8.0 Arterial PaO2 <60 mm Hg Base deficit >4 Fluid deficit >6 L Total Ranson score of 3 or more indicates severe acute pancreatitis Banks PA, AJG, Vol..92, No.3, 1997

  38. APACHE-II A Total Acute Physiology Score Temperature (Rectal) MAP (mmHg) Heart rate Respiratory Rate Oxygenation (PaO2 - mmHg) Serum Na, K, Cre, Hct, WBC Glasgow Coma Score B Age points C Chronic health points Total APACHE II score of 8 or more indicates severe acute pancreatitis Banks PA, AJG, Vol..92, No.3, 1997

  39. Acute Pancreatitis: Complications Early SystemicLocal ARDS GI bleeding ARF Adjacent bowel necrosis/fistula Hypocalcemia formation Shock Hydronephrosis Coagulopathy Splenic rupture or hematoma Hyperglycemia Splenic vein thrombosis Infected necrosis/abscess Steinberg et al., Acute Pancreatitis, NEJM, 1994

  40. Acute Pancreatitis: Complications Late Pseudocyst (1-4%) Duct obstruction Endocrine insufficiency Diabetes Steinberg et al., Acute Pancreatitis, NEJM, 1994

  41. Acute Pancreatic Necrosis Acute necrotizing pancreatitis - process when one or more diffuse or focal areas of nonviable pancreatic parenchyma are present. The International Symposium on Acute Pancreatitis, 1992 Present in 20-30% of the 185,000 new cases of acute pancreatitis per year in the United States Pancreatic glandular necrosis usually associated with necrosis of peripancreatic fat Beger HG et al. Natural course of acute pancreatitis. World J Surgery 1997

  42. Acute Pancreatic Necrosis Acute necrotizing pancreatitis - affected portions do not show normal contrast enhancement Contrast-enhanced dynamic CT scanning - GOLD standard (accuracy 90% if more than 30% of the gland is affected) Patients with necrosis have 82% morbidity and 23% mortality Patients without 6% and 0% Beger HG et al. Natural course of acute pancreatitis. World J Surgery 1997

  43. Pancreatic Abscess Lillemoe KD, Yeo CJ Management of Complications of Pancreatitis, 1998

  44. Infected Pancreatic Necrosis Lillemoe KD, Yeo CJ Management of Complications of Pancreatitis, 1998

  45. Acute Pancreatic Necrosis Infected necrosis develops in 30-70% of patients with acute necrotizing pancreatitis and accounts for more than 80% of deaths from acute pancreatitis Deaths occur in two phases: Early - 1-2 weeks due to multisystem organ failure due to release of inflammatory mediators and cytokines Late - due to systemic infections Sterile necrosis mortality - 10% Rau B et al.. Surgical treatment of infected necrosis. World J Surgery 1997

  46. Sterile Pancreatic Necrosis* Lived (n=16) Died (n=10) Ranson’s Score 4.6 +/- 0.4 6.3 +/- 0.5 APACHE II, adm. 6.9 +/- 0.8 13.0 +/- 2.5 APACHE II, 48 hrs 8.9 +/- 1.1 16.5 +/- 3.0 No. of complications 2.2 +/- 0.2 3.6 +/- 0.3 Shock 12.5% 90.0% Renal failure 50.0% 90.0% BMI 25.2 +/- 0.9 28.9 +/- 1.0 * - Severe disease with systemic complications Karimgani I et al. Prognostic Factors in Sterile Pancreatic Necrosis Gastroenterology 1992; 103; 1636-40

  47. Pancreatic Necrosis: CTSI Acute pancreatitis: Groups A-E - 0-4 points Necrosis: <30% - 2, 30-50% - 4, >50% - 6 points Balthazar EJ et al. Imaging and Intervention in Acute Pancreatitis Radiology1994; 193;297-306

  48. General Treatment Issues Patients need to be placed in intensive care environment with constant monitoring Aggressive fluid resuscitation Nasogastric suction is appropriate in patients with ileus and vomiting for symptomatic relief Administration of Imipenem-Cilastatin is recommended. Start as soon as the diagnosis is made and continued for 2-4 weeks.

  49. Pancreatic Necrosis: Antibiotics Foitzik et al.Pathogenesis and prevention of early pancreatic infection, Ann Surg, 1995

  50. ERCP Kelly and Wagner randomly assigned patients with gallstone-induced pancreatitis to early (<48 hours) or late (>48 hours) surgery/ERCP - 12% and 48% mortality Neoptolemos (England) showed lower morbidity 24% vs. 64% in group with ERCP vs. conventional treatment ERCP within 24 hours of admission reduced the incidence of biliary sepsis, but it only benefited severely ill patients and while reducing morbidity, it did not change mortality. Neoptolemos JP et al.,Controlled Trial of Urgent ERCP, Lancet, 1988 Fan S-T et al.,Early Treatment of Acute Biliary Pancreatitis, NEJM, 1993

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