Acute-Pancreatitis copy 1.pptx

1. Acute Pancreatitis Name : Kyem Issac Opoku Group :649 Acute urgent pathology ( Acute Pancreatitis)

2. Normal Anatomy & Physiology • neutralize chyme • digestive enzymes • hormones

3. Exocrine Function pancreatic duct common bile duct ampulla pancreatic enzymes TAIL BODY HEAD UNCINATE

4. Enzyme Secretion pancreatic duct duodenum acinus microscopic view of pancreatic acini

5. Enzyme Secretion Hormonal CCK gastrin Neural acetylcholine VIP GRP Secretin (hormonal) H2O bicarbonate

6. Digestive Enzymes in the Pancreatic Acinar Cell PROTEOLYTIC LIPOLYTIC ENZYMES ENZYMES Lipase Trypsinogen Prophospholipase A2 Chymotrypsinogen Carboxylesterase lipase Proelastase Procarboxypeptidase A NUCLEASES Procarboxypeptidase B Deoxyribonuclease (DNAse) Ribonuclease (RNAse) AMYOLYTIC ENZYMES Amylase OTHERS Procolipase Trypsin inhibitor

7. Normal Enzyme Activation trypsinogen trypsin chymotrypsin elastase phospholipase carboxypeptidase enterokinase chymotrypsinogen proelastase prophospholipase procarboxypeptidase duodenal lumen

8. Exocrine Stimulation • The more proximal the nutrient infusion…the greater the pancreatic stimulation (dog studies) - stomach – maximal stimulation - duodenum – intermediate stimulation - jejunum – minimal / negligible stimulation • Elemental formulas tend to cause less stimulation than standard intact formulas - intact protein > oligopeptides > free amino acids • Intravenous nutrients (even lipids) do not appear to stimulate the pancreas

9. Protective Measures • COMPARTMENTALIZATION - digestive enzymes are contained within zymogen granules in acinar cells • REMOTE ACTIVATION - digestive enzymes are secreted as inactive proenzymes within the pancreas • PROTEASE INHIBITORS – trypsin inhibitor is secreted along with the proenzymes to suppress any premature enzyme activation • AUTO “SHUT-OFF” – trypsin destroys trypsin in high concentrations

10. Acute Pancreatitis Definition • Acute inflammatory process involving the pancreas • Usually painful and self-limited • Isolated event or a recurring illness • Pancreatic function and morphology return to normal after (or between) attacks

11. EtOH 35% Idiopathic 10% Other 10% Gallstones 45% Acute Pancreatitis Etiology

12. • Cholelithiasis • Ethanol abuse • Idiopathic • Medications • Hyperlipidemia • ERCP • Trauma • Pancreas divisum • Hereditary • Hypercalcemia • Viral infections - Mumps - Coxsackievirus • End-stage renal failure • Penetrating peptic ulcer Acute Pancreatitis Associated Conditions

13. Acute Pancreatitis Causative Drugs • AIDS therapy: didanosine, pentamidine • Anti-inflammatory: sulindac, salicylates • Antimicrobials: metronidazole, sulfonamides, tetracycline, nitrofurantoin • Diuretics: furosemide, thiazides • IBD: sulfasalazine, mesalamine • Immunosuppressives: azathioprine, 6-mercaptopurine • Neuropsychiatric: valproic acid • Other: calcium, estrogen, tamoxifen, ACE-I

14. Adjusted ORs for Pancreatitis 2.5 4.8 12.4 42.1 0 5 10 15 20 25 30 35 40 45 Pancreatitis, ORs Female Nl TBili SOD Difficult cannulation Freeman et al. Gastrointest Endosc. ‘97.

15. Pancreas divisum

16. Hereditary Pancreatitis • Autosomal dominant with 80% phenotypic penetrance • Recurrent acute pancreatitis, chronic pancreatitis, and 50-fold increased risk of pancreatic cancer • Mutation in cationic trypsinogen gene (R122H) • Other genetic defects - CFTR - SPINK1

17. failed protective mechanisms acinar cell injury premature enzyme activation Acute Pancreatitis Pathogenesis

18. autodigestion of pancreatic tissue release of enzymes into the circulation activation of white blood cells local complications local vascular insufficiency premature enzyme activation distant organ failure Acute Pancreatitis Pathogenesis

19. • STAGE 1: Pancreatic Injury - Edema - Inflammation • STAGE 2: Local Effects - Retroperitoneal edema - Ileus • STAGE 3: Systemic Complications - Hypotension/shock - Metabolic disturbances - Sepsis/organ failure SEVERITY Mild Severe Acute Pancreatitis Pathogenesis

20. • Abdominal pain - Epigastric - Radiates to the back - Worse in supine position • Nausea and vomiting • Fever Acute Pancreatitis Clinical Presentation

21. Acute Pancreatitis Differential Diagnosis • Choledocholithiasis • Perforated ulcer • Mesenteric ischemia • Intestinal obstruction • Ectopic pregnancy

22. • Symptoms - Abdominal pain • Laboratory - Elevated amylase or lipase • > 3x upper limits of normal • Radiology - Abnormal sonogram or CT Acute Pancreatitis Diagnosis

23. Causes of Increased Pancreatic Enzymes Amylase Lipase Pancreatitis ↑ ↑ Parotitis ↑ Normal Biliary stone ↑ ↑ Intestinal injury ↑ ↑ Tubo-ovarian disease ↑ Normal Renal failure ↑ ↑ Macroamylasemia ↑ Normal

24. Acute Pancreatitis Diagnosis • EtOH: history • Gallstones: abnormal LFTs & sonographic evidence of cholelithiasis • Hyperlipidemia: lipemic serum, Tri>1,000 • Hypercalcemia: elevated Ca • Trauma: history • Medications: history, temporal association

25. Acute Pancreatitis Clinical Manifestations PANCREATIC PERIPANCREATIC SYSTEMIC Mild: edema, inflammation, fat necrosis Severe: phlegmon, necrosis, hemorrhage, infection, abscess, fluid collections Retroperitoneum, perirenal spaces, mesocolon, omentum, and mediastinum Adjacent viscera: ileus, obstruction, perforation Cardiovascular: hypotension Pulmonary: pleural effusions, ARDS Renal: acute tubular necrosis Hematologic: disseminated intravascular coag. Metabolic: hypocalcemia, hyperglycemia

26. Acute Pancreatitis Time Course 0 12 24 36 48 60 72 84 96 hours from pain onset ER presentation cytokine release organ failure

27. Predictors of Severity • Why are they needed? - appropriate patient triage & therapy - compare results of studies of the impact of therapy • When are they needed? - optimally, within first 24 hours (damage control must begin early) • Which is best?

28. Severity Scoring Systems • Ranson and Glasgow Criteria (1974) - based on clinical & laboratory parameters - scored in first 24-48 hours of admission - poor positive predictors (better negative predictors) • APACHE Scoring System - can yield a score in first 24 hours - APACHE II suffers from poor positive predictive value - APACHE III is better at mortality prediction at > 24 hours • Computed Tomography Severity Index - much better diagnostic and predictive tool - optimally useful at 48-96 hours after symptom onset

29. Ranson Criteria Alcoholic Pancreatitis AT ADMISSION 1. Age > 55 years 2. WBC > 16,000 3. Glucose > 200 4. LDH > 350 IU/L 5. AST > 250 IU/L WITHIN 48 HOURS 1. HCT drop > 10 2. BUN > 5 3. Arterial PO2 < 60 mm Hg 4. Base deficit > 4 mEq/L 5. Serum Ca < 8 6. Fluid sequestration > 6L Number Mortality <2 1% 3-4 16% 5-6 40% 7-8 100%

30. Glasgow Criteria Non-alcoholic Pancreatitis 1. WBC > 15,000 2. Glucose > 180 3. BUN > 16 4. Arterial PO2 < 60 mm Hg 5. Ca < 8 6. Albumin < 3.2 7. LDH > 600 U/L 8. AST or ALT > 200 U/L

31. CT Severity Index appearance normal enlarged inflamed 1 fluid collection 2 or more collections grade A B C D E score 0 1 2 3 4 necrosis none < 33% 33-50% > 50% score 0 2 4 6 score morbidity mortality 1-2 4% 0% 7-10 92% 17% Balthazar et al. Radiology 1990.

32. Severe Acute Pancreatitis • Scoring systems -  3 Ranson criteria -  8 APACHE II points -  5 CT points • Organ failure - shock (SBP < 90 mmHg) - pulmonary edema / ARDS (PaO2 < 60 mmHg) - renal failure (Cr > 2.0 mg/dl) • Local complications - fluid collections  pseudocysts - necrosis (mortality 15% if sterile, 30-35% if infected) - abscess

33. Goals of Treatment • Limit systemic injury - support and resuscitation – effective - decrease pancreatic secretion – ineffective / harmful? - inhibit inflammatory mediators – ineffective - inhibit circulating trypsin – ineffective (too late) - removing gallstones – mostly ineffective • Prevent necrosis – how? • Prevent infection - antibiotics (imipenem and ciprofloxacin) – probably effective in necrotic pancreatitis - prevent colonic bacterial translocation - removing gallstones – variably effective

34. Treatment of Mild Pancreatitis • Pancreatic rest • Supportive care - fluid resuscitation – watch BP and urine output - pain control - NG tubes and H2 blockers or PPIs are usually not helpful • Refeeding (usually 3 to 7 days) - bowel sounds present - patient is hungry - nearly pain-free (off IV narcotics) - amylase & lipase not very useful here

35. Treatment of Severe Pancreatitis • Pancreatic rest & supportive care - fluid resuscitation* – may require 5-10 liters/day - careful pulmonary & renal monitoring – ICU - maintain hematocrit of 26-30% - pain control – PCA pump - correct electrolyte derangements (K+, Ca++, Mg++) • Rule-out necrosis - contrasted CT scan at 48-72 hours - prophylactic antibiotics if present - surgical debridement if infected • Nutritional support - may be NPO for weeks - TPN vs. enteral support (TEN)

36. Role of ERCP • Gallstone pancreatitis - Cholangitis - Obstructive jaundice • Recurrent acute pancreatitis - Structural abnormalities - Neoplasm - Bile sampling for microlithiasis • Sphincterotomy in patients not suitable for cholecystectomy

37. Nutrition in Acute Pancreatitis • Metabolic stress - catabolism & hypermetabolism seen in 2/3 of patients - similar to septic state (volume depletion may be a major early factor in the above derangements) • Altered substrate metabolism - increased cortisol & catecholamines - increased glucagon to insulin ratio - insulin resistance • Micronutrient alterations - calcium, magnesium, potassium, etc

38. Systemic Changes in Acute Pancreatitis • Hyperdynamic - Increased cardiac output - Decreased systemic vascular resistance - Increased oxygen consumption • Hypermetabolism - Increased resting energy expenditure • Catabolism - Increased proteolysis of skeletal muscle

39. Reduced Oral Intake in Acute Pancreatitis • Abdominal pain with food aversion • Nausea and vomiting • Gastric atony • Ileus • Partial duodenal obstruction

40. Factors Differentiating Mild from Severe Pancreatitis Parameter Mild Pancreatitis Severe Pancreatitis Admissions 80% 20% Pancreatic necrosis No Yes Oral diet within 5 days 80% 0% Morbidity 8% 38% Mortality 3% 27%

41. TPN in Acute Pancreatitis • delay until volume repleted & electrolytes corrected • check triglycerides first – goal <400 • lipids are OK to use (possible exception of sepsis) • monitor glucose levels carefully - can see insulin insufficiency and resistance - may need to limit calories at first - separate insulin drip may be needed

42. TPN in Acute Pancreatitis • Benefit or harm? - early uncontrolled studies suggested benefit - two retrospective studies (70’s & 80’s) showed no benefit with TPN in pancreatitis - 1987 – randomized study of early TPN vs. IVF alone showed more sepsis, longer stays, & no fewer complications with TPN • When to use TPN? - jejunal access is unavailable - ileus prevents enteral feeding - patients in whom TEN clearly exacerbates pancreatitis

43. Enteral Nutrition in Acute Pancreatitis • studies - late 80’s – patients who received jejunal feeding tubes at the time of surgery, did well with early post-op enteral support - 1991 – randomized study of early TPN vs. early TEN post-op showed no short-term difference - 1997 – early TPN vs. early TEN (Peptamen) via nasojejunal tube in 32 patients showed no difference except 4x less cost & less hyperglycemia - 1997 – similar study showed fewer complications and lower cost without change in length of stay - 1998 – similar study showed more sepsis and organ failure in the TPN group

44. McClave et al. 1997 Kalfarenztos et al. 1997 Windsor et al. 1998 No of patients 32 38 34 Etiology EtOH 19/32 - - Biliary 23/34 Severe pancreatitis 19% 100% 38% Enteral formula Semi-elemental Semi-elemental Polymeric Cost 5x less 3x less - - Outcome No difference Fewer comp Less SIRS Summary of Prospective RCTs Enteral vs Parenteral Nutrition for Acute Pancreatitis

45. Total Enteral Nutrition in Severe Pancreatitis • may start as early as possible - when emesis has resolved - ileus is not present • nasojejunal route preferred over nasoduodenal • likely decreases risk of infectious complications by reducing transmigration of colonic bacteria

46. Conclusions • Acute pancreatitis is a self-limited disease in which most cases are mild. • Gallstones and alcohol are the leading causes of acute pancreatitis. • In mild pancreatitis, nutritional support is usually not required • In severe pancreatitis, nutritional support will likely be required with the enteral route preferred over TPN because of both safety and cost.

Acute-Pancreatitis copy 1.pptx

Acute-Pancreatitis copy 1.pptx

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