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Source: Bolesta S, Montgomery PA. Pancreatitis. In: DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey LM, eds. Pharmacotherapy: A Pathophysiologic Approach. 8th ed. http://accesspharmacy.com/content.aspx?aid=7979530. Accessed June 22, 2012.

  • Inflammatory disorder of pancreas characterized by severe pain in upper abdomen and elevations of serum pancreatic enzymes.

  • Obstruction caused by gallstones
  • Alcohol abuse
  • Endoscopic retrograde cholangiopancreatography (ERCP)
  • End-stage kidney disease
  • Bacterial, viral, parasitic infections
  • Hypertriglyceridemia
  • Cystic fibrosis
  • Medications
  • Idiopathic

  • Premature activation of trypsinogen to trypsin within pancreas causes activation of digestive enzymes and autodigestion of gland.
  • Attraction of neutrophils and macrophages causes systemic inflammatory response.
  • Kinin release increases capillary permeability and promotes edema.
  • Pancreatic infection may result from increased intestinal permeability and translocation of colonic bacteria.
  • Local complications include:
    • Fluid collection
    • Pancreatic necrosis
    • Infection
    • Abscess
    • Pseudocyst formation
    • Pancreatic ascites
  • Systemic complications may include these abnormalities:
    • Cardiovascular
    • Renal
    • Pulmonary
    • Metabolic
    • Hemorrhagic
    • Central nervous system (CNS)

  • Prevalence in United States: <1%.
  • Increasing hospitalizations for acute pancreatitis due to gallstones associated with obesity.

  • Patient may have acute mild symptoms or present with severe acute attack with life-threatening complications.

Signs and Symptoms

  • Ranges from moderate abdominal discomfort to excruciating pain, shock, and respiratory distress.
  • Abdominal pain occurs in 95% of patients and is usually epigastric, often radiating to upper quadrants or back.
  • Onset usually sudden and knife-like in intensity.
  • Pain reaches maximum intensity within 30 minutes and may persist for hours or days.
  • Nausea and vomiting occur in 85% and usually follow onset of pain.
  • Signs may include:
    • Epigastric tenderness on palpation with rebound tenderness and guarding
    • Abdominal distention
    • Diminished or absent bowel sounds
    • Hypotension
    • Tachycardia
    • Dyspnea
    • Low-grade fever

Means of Confirmation and Diagnosis

  • Characteristic abdominal pain

Laboratory Tests

  • Elevation of serum amylase, lipase, or both to at least 3 times upper limit of normal.
    • Amylase rises 4–8 hours after symptom onset, peaks at 24 hours, and returns to normal over 8–14 days.
    • Lipase elevations parallel amylase increases but persist longer and can be detected after amylase has normalized.
    • Leukocytosis, hyperglycemia, and hypoalbuminemia may occur.
    • Hepatic transaminases, alkaline phosphatase, and bilirubin are usually elevated in gallstone pancreatitis and in intrinsic liver disease.
    • Marked hypocalcemia indicates severe necrosis and is poor prognostic sign.
    • Hematocrit may be normal or reflect hemoconcentration (e.g., from vomiting).
    • C-reactive protein (CRP) may be >150 mg/dL at 48–72 hours in severe disease.
    • Thrombocytopenia and increased International normalized ratio (INR) may occur with liver disease.

Imaging

  • Contrast-enhanced computed tomography (CECT) of abdomen
  • Ultrasonography alternative to CECT.

Differential Diagnosis

  • Acute cholecystitis
  • Perforated duodenal ulcer
  • Acute intestinal obstruction
  • Renal colic and acute mesenteric ischemia

  • Relieve abdominal pain and nausea.
  • Replace fluids.
  • Correct electrolyte, glucose, and lipid abnormalities.
  • Minimize systemic complications.
  • Prevent pancreatic necrosis and infection.

  • Nutritional support because catabolic state promotes nutritional depletion.
  • ERCP to remove biliary tract stones.
  • Surgery in patients with pancreatic pseudocyst ...

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