ACUTE PANCREATITIS

1. GROUP D Mamba-Medinilla ACUTE PANCREATITIS

2. Etiologies of Acute Pancreatitis Common Causes Uncommon Causes Vascular causes CT disorders Cancer of the pancreas Hypercalcemia Periampullary diverticulum Pancreas divisum Hereditary pancreatitis Cystic Fibrosis Renal Failure • Gallstones • Alcohol Intake • Hypertriglyceridemia • ERCP especially after biliarymanometry • Blunt abdominal trauma • Postoperative operations • Drugs (sulfonamides, 6-MP) • Sphincter of Oddi dysfunction

3. Pathogenesis of Acute Pancreatitis • Autodigestion theory • Proteolytic enzymes activated in the pancreas rather than in the intestinal lumen Source: p. 2006-2007

4. Autodigestion theory Proenzymes Activating Factors Endotoxins Exotoxins Viral infections Ischemia Anoxia Direct trauma Activated proenzyme, (eg. Trypsin) • Trypsinogen • Chymotrypsinogen • Proelastase • Phospholipase A Source: p. 2006-2007

5. Three phases of Pancreatitis INITIAL PHASE • acinar cell injury due to intrapancreatic digestive enzyme activation • Zymogen activation mediated by lysosomal hydrolases e.g. cathepsin B Source: p. 2006-2007

6. Three phases of Pancreatitis SECOND PHASE • Intrapancreatic inflammation reaction • Due to activation, chemoattraction, and sequestration of neutrophils in the pancreas * This neutrophil sequestration can activate trypsinogen Source: p. 2006-2007

7. Three phases of Pancreatitis THIRD PHASE • Activated proenzymes, (esp. Trypsin) • Digest pancreatic and peripancreatic tissues • Activate other enzymes (i.e. elastase, phospholipase) • Due to effects of activated proteolytic enzymes and cytokines, released by inflamed pancreas, on distant organs, most notably the lungs • May result to SIRS and ARDS • Multiorgan failure Source: p. 2006-2007

8. The Third phase Source: p. 2006-2007

9. Clinical Manifestations

10. Abdominal pain • Major symptom • Vary from mild to severe, constant pain • Steady and boring in character • Located in epigastrium and periumbilical radiating to the back • Chest, flank and lower abdomen • Pain more intense on supine, relieved by sitting

11. Clinical Manifestations • Nausea, vomitting, abdominal distention • Low grade fever, tachycardia, hypotension • Shock • Jaundice • Erythematous skin nodules • In 10-20% of patients- basilar rales, atelectasis, and pleural effusion

12. Clinical Manifestations • Bowel sounds usually diminished or absent • Palpable enlarged pancreas, or a pseudocyst in the upper abdomen • Cullen’s Sign • Turner’s Sign

13. Diagnosis of Acute Pancreatitis

14. Diagnosis of Acute Pancreatitis • History and PE • Laboratory Tests • Imaging Studies

15. History and PE History • Severe and constant abdominal pain • Nausea, emesis • Fever, tachycardia PE • Abdominal tenderness, muscle rigidity • Diminished bowel sounds • Cullen’s sign, Turner’s sign

16. Laboratory Tests • Increased level of serum amylase • Elevated pancreatic isoamylase and lipase levels • Markedly increase levels of peritoneal or pleural fluid amylase [ >1500 nmol/ L (> 5000U/ dl)] • Leukocytosis (15,000-20,000 leukocytes/ microliter) • Hemoconcentration ( Hct > 44%) • Hyperglycemia • Hypocalcemia • Hypertriglyceridemia • Elevated LDH • ECG: ST segment and T wave abnormalities

17. IMAGING STUDIES • Abdominal plain films • Localized ileus, involving the jejunum • Generalized ileus with air- fluid levels • Colon cutt- off sign • Duodenal distention with air fluid levels • Mass, frequently a pseudocyst • Ultrasonography: enlarged pancreas; also evaluates gallbladder

18. CT SCAN: • confirms clinical impression of acute pancreatitis even with normal serum amylase • indicates severity and risk of morbidity and mortality

19. Course Fauci, et al., 2008. Principles of Internal Medicine, 17th ed. US:Mcgraw Hill

20. Complications • Key indicators of a severe attack of pancreatitis • Associated with organ failure and/or local complication • Clinical Manifestations • Organ Failure Fauci, et al., 2008. Principles of Internal Medicine, 17th ed. US:Mcgraw Hill

21. Complications • Key indicators of a severe attack of pancreatitis • Associated with organ failure and/or local complication • Clinical Manifestations • Obesity BMI >30 • Hemoconcentration (Hct >44%) • Age >70 • Organ Failure • Shock (Systolic BP <90 mmHg/ PR >130) • Pulmonary insufficiency ( PO2 <60) • Renal failure (Crea >2.0mg%) • GI Bleeding (>500ml/24hr) Fauci, et al., 2008. Principles of Internal Medicine, 17th ed. US:Mcgraw Hill

22. Complications Fauci, et al., 2008. Principles of Internal Medicine, 17th ed. US:Mcgraw Hill

23. Local Complications • Necrotizing pancreatitis • severe form of acute pancreatitis, • increasing abdominal pain, fever, marked leukocytosis, and bacteremia Cooper, D., et al. (2007) The Washington Manual of Medical Therapeutics 32nd Ed. Lippincott Williams & Wilkins,

24. Local Complications • Pancreatic fluid collections • Pancreatic abscess • Ill defined collection of pus • persistent fever, leukocystosis, and ileus • Pancreatic pseudocyst • Collections of tissue, fluid, debris, pancreatic enzymes, and blood • persistent pain or hyperamylasemia • Palpable, tender mass in the middle or LUQ of abdomen Fauci, et al., 2008. Principles of Internal Medicine, 17th ed. US:Mcgraw Hill

25. Local Complications • Pancreatic ascites • disruption of the main pancreatic duct, often by an internal fistula between the duct and the peritoneal cavity or a leaking presudocyst. • Hyperamylasemia Fauci, et al., 2008. Principles of Internal Medicine, 17th ed. US:Mcgraw Hill

26. Complications Fauci, et al., 2008. Principles of Internal Medicine, 17th ed. US:Mcgraw Hill

27. Systemic Complications • Pulmonary: ARDS • damage to the pulmonary surfactant layer by circulating phospholipase A and free fatty acids • Cardiovascular: Circulatory shock • a combination of volume depletion and hyperdynamic circulatory state with decreased peripheral vascular resistance Goldman, L., et al (2004).Cecil’s Textbook of Medicine 22nd ed.,

28. Systemic Complications • Renal: Acute renal failure • caused by circulatory shock and a selective increase in renal vascular resistance. • GI: Hemorrhage • erosion of the splenic or gastroduodenal arteries. • diffuse mucosal bleeding from the antrum and duodenum • perforation of peripancreatic inflammation into any portion of the gastrointestinal tract from esophagus to colon. • Splenic involvement by direct extension of the inflammatory process or, secondarily, by splenic vein thrombosis, which leads to gastric fundicvarices. Goldman, L., et al (2004).Cecil’s Textbook of Medicine 22nd ed.,

29. Acute Pancreatitis TREATMENT

30. Conventional Measures • Analgesics  pain • IV fluids & colloids  maintain normal intravascular volume • No oral alimentation • Usually, subsides spontaneously within 3 to 7 days after treatment

31. Diet and Management • IV fluids and fasting • Clear liquid diet: started on the 3rd to 6th day • Regular diet: 5th to 7th day • Reintroduction of oral intake based on: • ↓ or resolution of abdominal pain • Hungry patient • Resolved organ dysfunction (if present)

32. Antibiotic Prophylaxis • IMIPENEM-CILASTATIN • 500mg 3x/day for 7 days • Current recommendation in patients with necrotizing acute pancreatitis • Fungicide prophylaxis • Due to increase frequency of intraabdominal Candida infection

33. Infected Necrotizing Pancreatitis • Peritoneal Lavage • through percutaneous dialysis catheter • Necrosectomy • after confirmation of the presence of infected necrosis • Laparotomy + adequate drainage + removal of necrotic tissue • if conventional therapy does not halt the patient’s deterioration