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