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acute pancreatitis
Acute pancreatitis is a condition where pancreatic enzymes leak into the pancreas and cause its auto-digestion. Common causes include gallstones, alcohol use, and idiopathic factors. Patients present with epigastric pain radiating to the back that is exacerbated by eating or lying down. Lab tests show elevated pancreatic enzymes and imaging shows changes to the pancreas. Treatment is supportive with NPO, IV fluids, pain control and monitoring for complications like necrosis, pseudocysts, shock and respiratory failure. Severe cases may require ERCP, surgery or drainage procedures.
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acute pancreatitis
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- 2. Introduction • Acute pancreatitisis a condition in which activated pancreatic enzymes leak into the substance of the pancreas and initiate the auto-digestion of the gland. introduction
- 3. Etiology Common (90%) • Gallstones • Alcohol • Idopathic Rare • Metabolic: hypercalcemia, hypertrigyceridemia • Drugs: thiazide, azathioprine, sodium valporate, pentamidine • Infection: mumps, coxsackie virus • Post ERCP (due to back pressure of contrast into ductal system) • Trauma • Organ transplantation • Post surgical etiology
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- 6. Pathophysiology • The pancreassecretes the digestive enzymes as proenzymes which are activated in the intestinal lumen. • Acute pancreatitis may result when activation occurs in pancreatic duct system or acinar cells. May include edema or obstruction of the ampulla of Vater resulting in reflux of bile into pancreatic ducts or direct injury to the acinar cells. • The pancreas show edema and necrosis. The release of enzymes lead to fat necrosis both in the pancreas and in the peritoneal cavity. • Premature activation of trypsinogen into trypsin while it is still in pancreas. Resulting in auto digestion of the pancreas. pathophysiology
- 7. Proenzymes Activated proteolytic enzymes Defective intracellular transport and secretionof pancreatic zymogens Pancreatic duct obstruction (common bile duct stones, tumors) Acute pancreatitis Hyperstimulation of pancreas (alcohol, triglycerides) Reflux of infected bile or duodenal contents into pancreatic duct (sphincter of Oddi dysfunction) Pancreatic secretory trypsin inhibitors ++ + + - pathophysiology
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- 9. Clinical presentation • Midepigastricpain with tenderness. Sudden severe pain occurring often within 12-24 hours of a large meal or alcohol. The pain is persistent and radiates frequently through to the back to either shoulder or to one iliac fossa before spreading to involve the whole abdomen. Exacerbated on walking and lying supine. Relieved on sitting and leaning forward. • Nausea and vomiting has always been the presentation of acute pancreatitis in the majority of cases. • When pancreatitis is extremely severe, it mimics septic shock; fever, hypotension, respiratory distress from ARDS, elevation of the WBC and a rigid abdomen. clinical presentation
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- 11. Abdominal examination • Tendernessin epigastrium • Although severe pain, there may be little or no guarding of abdominal muscles at first. Later the upper abdomen becomes tender and rigid as peritoneal irritation increases. • Mild abdominal distention if paralytic ileus develops. • Severe advanced cases may develop bruising and discoloration in the left flank (Grey Turner’s sign due to tissue catabolism of Hb) and around the umbilicus (Cullen’s sign due to hemoperitoneum). These are the rare and late signs of extensive pancreatic destruction. abdominal examination
- 12. Cullen’s sign Grey Turner’ssign abdominal examination
- 13. Complications of acutepancreatitis Complications Causes and features Shock and renal failure Pancreatic failure is associated with leakage of fluid in the pancreatic bed also ileus with fluid filled loops of bowel leading to pre-renal azotemia and then acute tubular necrosis. Hypoxia ARDS due to micro thrombi in pulmonary vessels. Hyperglycemia Due to disruption of pancreatic islets. Hypocalcemia Sequestration of calcium in fat necrosis. Hypoalbuminemia Increased capillary permeability. complications
- 14. Complications of acutepancreatitis Pancreatic complications Causes and features Necrosis Abscess Rising fever, leukocytosis, localized tenderness and epigastric mass. It may be associated with left sided pleural effusion and enlarged spleen due to splenic vein thrombosis. Pseudocyst Encapsulated fluid collection with high enzyme content. Usually less than 6cm sized pseudocysts resolve spontaneously. They may become secondarily infected requiring drainage of abscess. Ascites Gradual increase in abdominal girth and persistent elevation of serum amylase in the absence of frank abdominal pain. It results from rupture of pancreatic duct or drainage of pseudocyst into the pancreatic cavity. complications
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- 17. Complications of acutepancreatitis Gastrointestinal complications Causes and features Upper GI bleeding Gastric or duodenal erosion Duodenal obstruction Compression by pancreatic mass Obstructive jaundice Compression of common bile duct complications
- 18. Investigations Serum amylase • Increasedlevel of 3-fold or more the normal value indicates acute pancreatitis, however other causes of elevation should be excluded such as mumps and perforation or infarction of the intestine. • Levels turn normal after 48-72 hrs even with the continuing of pancreatitis, serum lipase should also be sent that remains high for 7-14 days. • Persistent elevation suggests pseudocyst, pancreatic abscess or non pancreatic causes (intestinal obstruction, mumps, narcotics) investigations
- 19. Serum lipase • Remainselevated for 7-14 days. It is diagnostic. Other laboratory findings • WBC: 15000 – 30000 • Glucose : high • BUN: may be elevated • Serum calcium: low in 25% of cases • AST, bilirubin, alkaline phosphatase are transiently elevated. Serum albumin is low in 10% of patients and indicates severe pancreatitis. • Markedly elevated LDH (>500U/dl) suggests poor prognosis • Serial assessment of C-reactive is a good indicator of progress • ABGs show hypoxia investigations
- 21. Plain x-ray abdomen •It may show gall stones, sentinel loop, colon cut off sign, features of paralytic ileus, left pleural effusion or collapsing of lung CT scan • Useful in detecting large pancreas, pseudocyst, abscess, hemorrhagic pancreas • Presence of gas bubbles indicate abscess Ultrasound • To detect gallstone and biliary obstruction and serial assessment of pseudocysts, although in the earlier stages the gland may not be grossly swollen and may be missed on US. investigations
- 22. Acute exudative pancreatitisCT scan Acute necrotizing pancreatitis CT scan investigations
- 23. Differential diagnosis • Perforatedpeptic ulcer • Acute cholecystitis and biliary colic • Acute intestinal obstruction • Renal colic • Myocardial infarction • Vasculitis • Pneumonia • Diabetic ketoacidosis differential diagnosis
- 24. Management • In mostpatients it is a mild disease that subsides spontaneously within several days. Withhold food and liquids by mouth, bed rest and in patients with severe pain and ileus nasogastric suction. Supportive treatment • Bed rest NPO • IV fluids; saline or whole blood • Nasogastric suctioning; if severe nausea, vomiting or development of paralytic ileus • Pethidine 3-4 hourly to control pain, avoid morphine • Oxygen for hypoxia, ventilator may be required for ARDS • Dopamine may be required for shock nonresponsive to fluid management
- 25. • Calcium gluconateIV only if hypocalcemia is associated with tetany • Fresh frozen plasma for coagulopathy • Serum albumin for hypoalbuminemia • Insulin for hyperglycemia • Total parenteral nutrition for severe cases • Antibiotics; prophylactic broad spectrum antibiotic is given even in sterile pancreatitis to prevent infection • Imipenem 500mg IV 8 hourly or cefuroxime 1.5g IV 8 hourly • ERCP; when severe pancreatitis results from stone in biliary tract; particularly if there is jaundice or cholangitis ERCP with endoscopic sphincterotomy and stone extraction is indicated management
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- 27. Surgery • Cholecystectomy shouldbe undertaken within 2 weeks of resolution of pancreatitis. • Patients with necrotizing pancreatitis or abscess require urgent endoscopic or minimally invasive retroperitoneal pancreatic (MIRP) necrosectomy to debride all cavities of necrotic material. • Pancreatic pseudocysts can be treated by draining into stomach, duodenum or jejunum. Performed after 6 weeks, once capsule matures, by surgery or endoscopic cystogastrostomy. management
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- 30. References • Davidson’s principlesand practice of medicine 22nd edition • Short textbook of medical diagnosis and management 11th international edition (Inam Danish) • Kaplan medical USMLE step 2 CK internal medicine lecture notes references
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