Pancreatitis, Acute

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.

• See Etiology

• 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.
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