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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.
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- Inflammatory disorder of pancreas characterized by severe
pain in upper abdomen and elevations of serum pancreatic enzymes.
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- Obstruction caused by gallstones
- Alcohol abuse
- Endoscopic retrograde cholangiopancreatography (ERCP)
- End-stage kidney disease
- Bacterial, viral, parasitic infections
- Hypertriglyceridemia
- Cystic fibrosis
- Medications
- Idiopathic
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- 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)
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- Prevalence in United States: <1%.
- Increasing hospitalizations for acute pancreatitis due to
gallstones associated with obesity.
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++
- Patient may have acute mild symptoms or present with severe
acute attack with life-threatening complications.
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- 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
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Means of Confirmation
and Diagnosis
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- Characteristic abdominal pain
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- 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.
++
- 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
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- 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.
...