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Acute pancreatitis

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Gastroenterology

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Acute pancreatitis

  1. 1. Acute Pancreatitis
  2. 2. Acute Pancreatitis <ul><li>Sudden onset of unrelenting upper abdominal pain resulting from inflammation of the pancreas </li></ul><ul><li>Patients commonly present to ER due to severe abdominal pain </li></ul><ul><li>Requires admission to the hospital for medical management </li></ul>
  3. 3. Pathophysiology <ul><li>Release of kallikrein and chymotrypsin results in increased capillary membrane permeability, leading to leakage of fluid into the interstitium and development of edema and relative hypovolemia </li></ul><ul><li>Elastase is the most harmful in terms of direct cell damage, it causes dissolution of the elastic fibers of blood vessels and cuts, leading to hemorrhage </li></ul><ul><li>Phospholipase A destroys phosholipids of cell membranes causing severe pancreatic and adipose tissue necrosis </li></ul><ul><li>Lipase flows into damaged tissue and is absorbed into systemic circulation, resulting in fat necrosis of the pancreas and surrounding tissues </li></ul>
  4. 4. Acute Pancreatitis <ul><li>Inflammation of the pancreas that produces exocrine and endocrine dysfunction </li></ul><ul><li>Results from premature activation of pancreatic exocrine enzymes (trypsin, phospholipase A, and elastase) </li></ul>
  5. 5. Edematous (Interstitial) Pancreatitis <ul><li>Usually mild </li></ul><ul><li>Resolves in about 7 days </li></ul><ul><li>Results in fluid accumulation and swelling </li></ul>
  6. 6. Severe or Necrotizing Pancreatitis <ul><li>Associated with a high degree of complications and mortality </li></ul><ul><li>Caused by the release of cytokines and other proinflammatory mediators that produce a hyperinflammatory reaction, resulting in cell death and tissue damage </li></ul>
  7. 7. Causes of Acute Pancreatitis <ul><li>Ethanol abuse </li></ul><ul><li>Biliary diseases </li></ul><ul><ul><li>Gallstones </li></ul></ul><ul><ul><li>Choledocholithiasis </li></ul></ul><ul><ul><li>Biliary sludge </li></ul></ul><ul><ul><li>Microlithiasis </li></ul></ul><ul><li>Mechanical/structural injury </li></ul><ul><ul><li>Sphincter of Oddi dysfunction </li></ul></ul><ul><ul><li>Pancreas divisum </li></ul></ul><ul><ul><li>Trauma </li></ul></ul><ul><ul><li>Postendoscopic retrograde cholangiopancreatography </li></ul></ul><ul><ul><li>Pancreatic malignancy </li></ul></ul><ul><ul><li>PUD </li></ul></ul><ul><ul><li>IBD </li></ul></ul><ul><li>Medications </li></ul><ul><ul><li>Azathiprine/6-mercaptopurine </li></ul></ul><ul><ul><li>Dideoxyinosine </li></ul></ul><ul><ul><li>Pentamidine </li></ul></ul><ul><ul><li>Sulfonamides </li></ul></ul><ul><ul><li>Thiazide diuretics </li></ul></ul><ul><ul><li>ACEI </li></ul></ul><ul><li>Metabolic </li></ul><ul><ul><li>Hypertriglyceridemia </li></ul></ul><ul><ul><li>Hypercalcemia </li></ul></ul><ul><li>Infectious </li></ul><ul><ul><li>Viral </li></ul></ul><ul><ul><li>Bacterial </li></ul></ul><ul><ul><li>Parasitic </li></ul></ul><ul><li>Vascular </li></ul><ul><ul><li>Vasculitis </li></ul></ul><ul><li>Genetic predisposition </li></ul><ul><li>idiopathic </li></ul>
  8. 8. Acute Pancreatitis: Damage and Destruction <ul><li>Inflammation is caused by premature activation of enzymes which leads to tissue damage </li></ul><ul><li>If pancreatitis damages the islets of Langerhans, diabetes mellitus may result </li></ul><ul><li>Severe sudden pancreatitis causes massive hemorrhage and total destruction of the pancreas, manifested as diabetic acidosis, shock and coma </li></ul>
  9. 9. Clinical Presentation <ul><li>Upper abdominal pain rapidly increasing in severity, often within 60 minutes </li></ul><ul><li>Epigastric pain </li></ul><ul><li>Right-sided pain </li></ul><ul><li>Diffuse abdominal pain with radiation to back </li></ul><ul><li>Pain rarely only in left upper quadrant </li></ul><ul><li>Restless </li></ul><ul><li>Prefer to sit and lean </li></ul><ul><li>N/V </li></ul><ul><li>Fever </li></ul><ul><li>Tachycardia </li></ul>
  10. 10. Abdominal Examination <ul><li>Decreased or absent bowel sounds </li></ul><ul><li>Abdominal tenderness </li></ul><ul><li>Guarding </li></ul><ul><li>Palpable mass in epigastric area </li></ul><ul><li>Biliary colic </li></ul><ul><li>Jaundice if there’s obstruction of the bile duct </li></ul><ul><li>Cullen’s sign </li></ul><ul><li>Grey Turner’s Sign </li></ul>
  11. 11. Clinical Manifestations <ul><li>Abdominal distention </li></ul><ul><li>Abdominal guarding </li></ul><ul><li>Abdominal tympany </li></ul><ul><li>Hypoactive bowel sounds </li></ul><ul><li>Severe disease: peritoneal signs, ascites, jaundice, palpable abdominal mass, Grey Turner’s sign, Cullen’s sign, and signs of hypovolemic shock </li></ul>
  12. 12. Diagnostic Evaluation <ul><li>Patient’s history </li></ul><ul><li>Physical examination </li></ul><ul><li>Diagnostic findings </li></ul><ul><ul><li>Serum amylase levels greater than three times the upper limit </li></ul></ul><ul><ul><li>Serum amylase levels may be normal in patients with pancreatitis related to alcohol abuse or hypertriglyceridemia </li></ul></ul><ul><ul><li>Levels greater than five times the top normal value should be expected in patients with renal failure because amylase is cleared by the kidneys </li></ul></ul>
  13. 13. Imaging Modalities <ul><li>Plain abdominal x-rays for visualizing gallstones or a gas-filled transverse colon ending at the area of pancreatic inflammation </li></ul><ul><ul><li>colon cut-off sign </li></ul></ul><ul><li>Abdominal ultrasound </li></ul><ul><ul><li>Cholelithiasis, biliary sludge, bile duct dilation, and pseudocysts </li></ul></ul><ul><li>CT of abdomen </li></ul><ul><li>MRCP (magnetic resonance cholangiopancreatography) </li></ul>
  14. 14. Ranson’s Criteria <ul><li>The severity of acute pancreatitis is determined by the existence of certain criteria, called Ranson’s criteria </li></ul><ul><li>The more criteria met by the patient, the more severe the episode of pancreatitis </li></ul><ul><li>1% mortality: fewer than three </li></ul><ul><li>16%: three or four criteria </li></ul><ul><li>40% with five or six criteria </li></ul><ul><li>100%: seven or eight criteria </li></ul>
  15. 15. Ranson’s Criteria <ul><li>On admission </li></ul><ul><ul><li>Patient older than 55 </li></ul></ul><ul><ul><li>WBC > 16,000 </li></ul></ul><ul><ul><li>Serum glucose >200 </li></ul></ul><ul><ul><li>Serum lactate dehydrogenase >350 </li></ul></ul><ul><ul><li>Aspartate aminotransferase > 250 </li></ul></ul><ul><li>During initial 48 hours after admission </li></ul><ul><ul><li>10% decrease in Hct </li></ul></ul><ul><ul><li>BUN increase > 5 </li></ul></ul><ul><ul><li>Serum calcium < 8 </li></ul></ul><ul><ul><li>Base deficit > 4 </li></ul></ul><ul><ul><li>PaO2 < 60 </li></ul></ul><ul><ul><li>Estimated fluid sequestration > 6 liters </li></ul></ul>
  16. 16. Common Complications of Acute Pancreatitis <ul><li>Pulmonary </li></ul><ul><ul><li>Atelactasis </li></ul></ul><ul><ul><li>Pleural effusions </li></ul></ul><ul><ul><li>ARDS </li></ul></ul><ul><li>Cardiovascular </li></ul><ul><ul><li>Cardiogenic shock </li></ul></ul><ul><li>Neurologic </li></ul><ul><ul><li>Pancreatic encephalopathy </li></ul></ul><ul><li>Metabolic </li></ul><ul><ul><li>Metabolic acidosis </li></ul></ul><ul><ul><li>Hypocalcemia </li></ul></ul><ul><ul><li>Altered glucose metabolism </li></ul></ul><ul><li>Hematologic </li></ul><ul><ul><li>DIC </li></ul></ul><ul><ul><li>GI bleeding </li></ul></ul><ul><li>Renal </li></ul><ul><ul><li>Prerenal failure </li></ul></ul>
  17. 17. Management <ul><li>Fluid Management </li></ul><ul><li>Nutritional support </li></ul><ul><ul><li>Rest gut </li></ul></ul><ul><ul><li>TPN </li></ul></ul><ul><li>Pain management </li></ul><ul><li>Supporting other organ systems </li></ul>
  18. 18. Treatment <ul><li>IV replacement of fluids, proteins, and electrolytes </li></ul><ul><li>Fluid volume replacement and blood transfusions </li></ul><ul><li>Withholding food and fluids to rest the pancreas </li></ul><ul><li>NG tube suctioning </li></ul><ul><li>Drugs </li></ul><ul><li>Peritoneal lavage </li></ul><ul><li>Surgical drainage </li></ul><ul><li>Laparotomy to remove obstruction </li></ul>

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