Skip to Main Content

++

SOURCE

++

Source: Bolesta S, Montgomery PA. Pancreatitis. In: DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey LM, eds. Pharmacotherapy: A Pathophysiologic Approach. 10th ed. New York, NY: McGraw-Hill; 2017. http://accesspharmacy.mhmedical.com/content.aspx?bookid=1861&sectionid=146059813. Accessed April 18, 2017.

++

DEFINITION

++

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

++

ETIOLOGY

++

  • Obstruction caused by gallstones.

  • Alcohol abuse.

  • Endoscopic retrograde cholangiopancreatography (ERCP)

  • End-stage kidney disease.

  • Bacterial, viral, parasitic infections.

  • Hypertriglyceridemia.

  • Cystic fibrosis.

  • Trauma.

  • Medications.

  • Idiopathic.

++

PATHOPHYSIOLOGY

++

  • 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)

++

EPIDEMIOLOGY

++

  • Prevalence in the United States: <1%.

  • Increasing hospitalizations for acute pancreatitis due to gallstones associated with obesity.

++

RISK FACTORS

++

++

CLINICAL PRESENTATION

++

  • 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 min 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.

++

DIAGNOSIS

++
MEANS OF CONFIRMATION AND DIAGNOSIS
++

  • Characteristic abdominal pain.

++
LABORATORY TESTS
++

  • Elevation of serum amylase, lipase, or both to at least three 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 (eg, 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 ...

Pop-up div Successfully Displayed

This div only appears when the trigger link is hovered over. Otherwise it is hidden from view.