22 acute pancreatitis

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22 acute pancreatitis

  1. 1. Acute Pancreatitis <ul><li>Xia, Zhongsheng </li></ul><ul><li>Department of Gastroenterology, </li></ul><ul><li>Sun Yat-sen Memorial Hospital, </li></ul><ul><li>Sun Yat-sen University. </li></ul>
  2. 2. Teaching Objective <ul><li>To know the etiology and pathogenesis of acute pancreatitis </li></ul><ul><li>To master the clinical features and key points of diagnosis for different types of acute pancreatitis </li></ul><ul><li>To master the therapy principles of acute pancreatitis </li></ul>
  3. 3. Definition <ul><li>Acute pancreatitis is a inflammation of the pancreas induced by the activation of the pancreatic enzymes derived from various causes. </li></ul>
  4. 4. Etiology <ul><li>Biliary duct diseases: gallstone, acute and chronic cholecystitis, ascariasis accompanied with inflammatory stricture at the level of the papilla. </li></ul><ul><li>Common channel hypothesis </li></ul><ul><li>Alcohol and/ or square meal </li></ul><ul><li>hyperlipidemia </li></ul><ul><li>Postoperation: post-ERCP, abdominal operation. </li></ul>
  5. 5. Etiology <ul><li>Metabolic diseases: hyperparathyroidism, hypercalcemia, etc. </li></ul><ul><li>Drugs: glucocorticords, diuretics, azathioprine, estrogen, etc. </li></ul><ul><li>Autoimmune diseases: SLE, RA, vasculitis, etc. </li></ul><ul><li>Viral infections: mumps, coxsackie virus , HIV, etc </li></ul><ul><li>Idiopathic pancreatitis. </li></ul>
  6. 6. Pathogenesis <ul><li>trypsinogen-> trypsin </li></ul><ul><li>trypsin ->pancreatic enzymes, complement system and kinin system </li></ul><ul><li>Pathophysiological changes: leukocyte chemotaxis, release of active agents, oxygenic stress, microcirculation disorder and bacteria transposal. </li></ul>
  7. 7. <ul><li>Trypsin activates other proenzymes and results in proteolysis, edema and vascular damage </li></ul><ul><li>Lipase produces extrapancreatic fat necrosis </li></ul><ul><li>Phospholipase degrades the lecithin into the lysolecithin which induces pancreatic necrosis and hemorrhage </li></ul><ul><li>Kallikrein and elastase cause vascular destruction </li></ul><ul><li>Bradykinin peptidase and vasoactive substance induce vasodilatation, increase vascular permeability and edema </li></ul><ul><li>Cytokine, oxygen free radicals, platelet activating factor, prostaglandins, blood circulation disturbance, systemic inflammation response syndrome (SIRS) </li></ul>
  8. 8. Pathology <ul><li>Mild form (interstitial or edematous pancreatitis) </li></ul><ul><li>focal or diffused edema </li></ul><ul><li>slight leukocyte infiltration </li></ul>
  9. 9. <ul><li>Severe form ( necrotic or hemorrhagic pancreatitis ) </li></ul><ul><li>marked acinar destruction with hemorrhage </li></ul><ul><li>extensive leukocyte infiltration </li></ul><ul><li>necrosis of parapancreatic fat </li></ul><ul><li>grossly an inflammatory tumor-like mass with diffused hemorrhagic change </li></ul><ul><li>secondary infection induces the formation of abscess or pseudocysts </li></ul>
  10. 10. <ul><li>Symptoms </li></ul><ul><li>abdominal pain: located in epigastrium and radiates to the back. The lateral kneel-chest position with the neck flexed may relieve the abdominal pain. </li></ul><ul><li>Nausea, vomiting, abdominal distention: 90% patients </li></ul><ul><li>Fever: low-grade fever in mild pancreatitis; high fever suggests coexisting infection. </li></ul><ul><li>Hypotension or shock: often in severe pancreatitis </li></ul>Clinical manifestations
  11. 11. Signs <ul><li>MAP: signs are mild. Abdominal tenderness and diminished bowel sounds are present. </li></ul><ul><li>SAP: </li></ul><ul><li>peritoneal irritation sign </li></ul><ul><li>bowel sounds are diminished or absent </li></ul><ul><li>ascites or shifting dullness </li></ul><ul><li>Grey-Turner sign </li></ul><ul><li>Cullen sign </li></ul><ul><li>jaundice </li></ul><ul><li>Pancreatic pseudocyst </li></ul>
  12. 12. Complications <ul><li>Local complications </li></ul><ul><li>Pseudocyst: occur 2 weeks after the onset. </li></ul><ul><li>Acute fluid collection: occur in the early stage. </li></ul><ul><li>Pancreatic abscess: after 4 weeks on the basis of pseudocyst </li></ul><ul><li>Pancreatic necrosis infection: usually after 2 weeks </li></ul>
  13. 13. Systemic complications <ul><li>ARDS </li></ul><ul><li>acute renal failure </li></ul><ul><li>heart failure and cardiac arrhythmia </li></ul><ul><li>gastrointestinal bleeding </li></ul><ul><li>Septicemia </li></ul><ul><li>disorders of hemostasis: thrombosis, DIC. </li></ul><ul><li>disorders of CNS: pancreatic encephalopathy </li></ul><ul><li>Hyperglycemia </li></ul><ul><li>disorders of water, electrolytes and acid-base balance </li></ul>
  14. 14. Laboratory Studies <ul><li>blood count: leukocytes count is more than 10,000/mm 3 </li></ul><ul><li>Hematocrit (Hct): is high (over 50%) because of loss of plasma into the retroperitoneal space </li></ul>
  15. 15. Amylase <ul><li>normal values of the serum amylase: </li></ul><ul><li>40 to 180 Somogyi units or 8 to 64 Winslow units </li></ul><ul><li>over 500 Somogyi units are strongly suggested acute pancreatitis. </li></ul><ul><li>there is no significant correlation between the severity of the pancreatitis and the levels of the serum amylase </li></ul><ul><li>normal values of urinary amylase: </li></ul><ul><li>< 256 Winslow units </li></ul><ul><li>over 256 Winslow units are suggested acute pancreatitis </li></ul>
  16. 16. <ul><li>False positive amylase elevation in serum or urine may occur in many conditions other than pancreatitis, such as the other acute abdominal diseases, proximal renal tubular malfunction, including thermal burns, diabetic acidosis and postoperative states or macroamylasemia. </li></ul>
  17. 18. <ul><li>Biochemical test </li></ul><ul><li>Hypocalcemia </li></ul><ul><li>Hyperglycemia </li></ul><ul><li>Hyperbilirubinemia </li></ul><ul><li>Hypoxemia </li></ul>
  18. 19. Imaging examination <ul><li>X-ray: </li></ul><ul><li>Abdominal X-ray </li></ul><ul><li>sentinel loop </li></ul><ul><li>colon cut-off </li></ul><ul><li>Chest X-ray: may reveal the complications of lung such as pleural effusion, pulmonary edema and interstitial inflammation. </li></ul>
  19. 20. <ul><li>Ultrasonography </li></ul><ul><li>It is a useful method to find an enlarged pancreas, a pseudocyst , ascites, biliary stone, dilated common bile duct and other pancreatic mass </li></ul>
  20. 21. <ul><li>CT & MRI </li></ul>Normal pancreas 正常胰腺 CT 平扫 肝右 叶 胰头 肠管 肾 腹主 动脉 下腔 静脉 胰腺体、 尾部 胆 囊 肝右 叶 脾 肠管 下腔 静脉 膈脚 腹主 动脉
  21. 22. Contrast CT showing pancreatic necrosis
  22. 23. Diagnosis- criteria <ul><li>symptoms: acute, severe constant epigastric pain. Nausea and vomiting. </li></ul><ul><li>Physical examination: epigastric tenderness with or without rebound tenderness. </li></ul><ul><li>Laboratory studies: elevated serum amylase (≥3 times of high limit of normal value) </li></ul><ul><li>Imaging examinations: morphological changes of pancreas or not </li></ul><ul><li>Excluding the other acute abdominal diseases. </li></ul>
  23. 24. <ul><li>Clinical manifestations </li></ul><ul><li>Scoring systems: Ranson </li></ul><ul><li>CT grading </li></ul><ul><li>Serum biomarkers: CRP, IL-6 </li></ul>Diagnosis- evaluation of patients’ condition
  24. 25. Diagnosis- classification <ul><li>MAP (mild acute pancreatitis): </li></ul><ul><li>Acute pancreatitis </li></ul><ul><li>No dysfunction of organ or local complications </li></ul><ul><li>Ranson’s score <3 </li></ul><ul><li>or CT grading: A, B, C or CTSI <2 </li></ul>
  25. 26. Diagnosis- classification <ul><li>SAP (severe acute pancreatitis): </li></ul><ul><li>Acute pancreatitis </li></ul><ul><li>Local complications </li></ul><ul><li>or organ failure </li></ul><ul><li>or Ranson’s score >3 </li></ul><ul><li>or CT grading: D, E or CTSI >3. </li></ul>
  26. 27. Differential diagnosis <ul><li>Perforated peptic ulcer </li></ul><ul><li>Acute calculous cholecystitis </li></ul><ul><li>Acute ileus </li></ul><ul><li>Mesenteric vascular embolism </li></ul><ul><li>Rupture of the spleen </li></ul><ul><li>Acute appendicitis </li></ul><ul><li>Angina pectoris </li></ul><ul><li>Acute myocardial infarction </li></ul>
  27. 28. Therapy- MAP <ul><li>Monitoring: should be monitored for at least 3 days. </li></ul><ul><li>Supportive treatment: volume repletion with crystalloids and colloids to keep balance. </li></ul><ul><li>Relieve severe pain: Dolantin is preferred over morphine. </li></ul><ul><li>inhibit excrine of the pancreas: </li></ul><ul><li>No oral alimentation and continuous nasogastric suction </li></ul><ul><li>H 2 RA or PPI </li></ul><ul><li>Somatostatin and its long-acting analogue (Sandostatin) </li></ul><ul><li>Antibiotics is required especially in infection of biliary duct. </li></ul>
  28. 29. Therapy- SAP <ul><li>Monitoring </li></ul><ul><li>Nutritional support: </li></ul><ul><li>parenteral nutrition->enteral nutrition </li></ul><ul><li>maintain balance of water, electrolytes and acid-base. </li></ul><ul><li>essential diet </li></ul><ul><li>Prevention of infection: </li></ul><ul><li>oral antibiotics </li></ul><ul><li>intravenous infusion of antibiotics </li></ul><ul><li>enteral feeding </li></ul>
  29. 30. <ul><li>inhibit excrine of pancreas and pancreatic enzymes: </li></ul><ul><li>No oral alimentation and continuous nasogastric suction </li></ul><ul><li>H 2 RA or PPI </li></ul><ul><li>Somatostatin and its long-acting analogue (Sandostatin) </li></ul>
  30. 31. <ul><li>Prevention and treatment of enteral failure </li></ul><ul><li>oral antibiotics </li></ul><ul><li>enteral microecological preparations </li></ul><ul><li>glutamine </li></ul><ul><li>enteral feeding </li></ul><ul><li>Treatment of multiple organs failure </li></ul>
  31. 32. <ul><li>Endoscopic therapy: ERCP+EST+ENBD </li></ul><ul><li>Surgical operation: indications </li></ul><ul><li>necrotic pancreatitis with infection </li></ul><ul><li>pancreatic abscess </li></ul><ul><li>early severe acute pancreatitis (ESAP) </li></ul><ul><li>abdominal compartment syndrome (ACS) </li></ul><ul><li>pancreatic pseudocyst: >6cm </li></ul><ul><li>diagnosis remain unclear and GI perforation is suggested </li></ul>
  32. 33. <ul><li>Emerging drugs: </li></ul><ul><li>CCK receptor antagonist: loxiglumide </li></ul><ul><li>Prostaglandins: PGE 1 </li></ul><ul><li>Platelet activating factor (PAF) antagonist </li></ul><ul><li>TNF monoclonal antibody: Infliximab </li></ul>
  33. 34. prognosis <ul><li>MAP: good </li></ul><ul><li>SAP: poor. 10~30% mortality </li></ul><ul><li>Risk factors: age, hypotension, hypoalbuminemia, hypoxemia, hypocalcemia, miscellaneous complications. </li></ul>
  34. 35. Questions <ul><li>What are the clinical manifestations of acute pancreatitis? </li></ul><ul><li>What is the diagnostic key points of acute pancreatitis? </li></ul><ul><li>What is the therapy of acute pancreatitis? </li></ul>
  35. 36. Thank you
  36. 38. necrotic pancreatitis
  37. 39. Grey-Turner sign
  38. 40. Cullen sign
  39. 41. jaundice
  40. 42. Pseudocyst of pancreas
  41. 43. Sentinel loop. A segment of air-filled small intestine
  42. 44. Colon cut-off sign. Supine abdominal radiograph obtained in a patient with acute pancreatitis shows an abrupt termination of air in the left side of the transverse colon (arrows).
  43. 45. Pseudocyst of pancreas Edematous pancreas
  44. 46. <ul><li>On admission: </li></ul><ul><li>Age >55 </li></ul><ul><li>Leukocyte count >16,000/mm 3 </li></ul><ul><li>Blood glucose >11mmol/L </li></ul><ul><li>LDH >350 IU/L </li></ul><ul><li>AST >250 </li></ul><ul><li>After 48 hours: </li></ul><ul><li>Hct increase >10% </li></ul><ul><li>BUN rise >5 mmol/L </li></ul><ul><li>Serum calcium <2 mmol/L </li></ul><ul><li>PaO 2 <60mmHg </li></ul><ul><li>Base deficit >4mmol/L </li></ul><ul><li>Estimated fluid sequestration >6 L </li></ul>Ranson’s scoring system
  45. 47. CT grading <ul><li>Grade A: normal pancreas </li></ul><ul><li>Grade B: enlargement of pancreas </li></ul><ul><li>Grade C: Grade B + peripancreatitis </li></ul><ul><li>Grade D: Grade C + one area of fluid collection </li></ul><ul><li>Grade E: multiple region of fluid collection </li></ul>

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