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TEXTBOOK PRESENTATION
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Patients with acute pancreatitis often complain of a constant and boring abdominal pain of moderate to severe intensity that develops in the epigastrium and may radiate to the back. Associated symptoms may include nausea, vomiting, low-grade fever, and abdominal distention.
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Etiology
Alcohol abuse (typically binge drinking) and choledocholithiasis (with concomitant obstruction of pancreatic outflow) cause 80% of acute pancreatitis cases.
15–25% of cases are idiopathic, many of which may be due to microlithiasis or sphincter of Oddi dysfunction.
34–67% of patients with idiopathic pancreatitis were found to have small gallstones on EUS or ERCP.
Sphincter of Oddi dysfunction may be particularly common in patients with prior cholecystectomy.
Post ERCP
Drugs commonly associated with pancreatitis include
Azathioprine
Didanosine
Estrogens
Furosemide
Hydrochlorothiazide
L-asparaginase
Metronidazole
Opioids
Pentamidine
Sulfonamides
Corticosteroids
Tamoxifen
Tetracycline
Valproate
Less common causes include
Trauma
Marked hypertriglyceridemia (> 1000 mg/dL)
Hypercalcemia
Ischemia
HIV infection, other infection
Pancreatic carcinoma
Pancreatic divisum
Autoimmune pancreatitis
Cystic fibrosis
Organ transplantation
Regardless of the inciting event, trypsinogen is activated to trypsin, which activates other pancreatic enzymes resulting in pancreatic autodigestion and inflammation (which may become systemic and lethal). Interleukins contribute to the inflammation.
Complications may be local or systemic. Severe pancreatitis develops in about 20% of patients and is complicated by significant morbidity and mortality.
Local complications
Pancreatic pseudocyst
Pancreatic necrosis
Infections: A variety of infections may develop. Bacterial translocation from the bowel may infect pancreatic pseudocysts or necrotic pancreatic tissue. Ascending cholangitis may develop in patients with GAP.
Systemic complications
Hyperglycemia
Hypocalcemia
Acute respiratory distress syndrome
Acute kidney injury
Disseminated intravascular coagulation
Death occurs in up to 4% of patients.
Usually occurs in patients with infected pancreatic necrosis and in patients in whom multiple organ dysfunction develops.
Several predictive scores have been developed including the Ranson criteria as well as the Glasgow and Apache II scores.
All use similar variables that increase the likelihood of organ failure, including increased age and elevated WBC, BUN, glucose, or lactate dehydrogenase.
Hypoxia and hypocalcemia are also associated with an increased risk.
Hemoconcentration (HCT ≥ 50%) on admission predicts severe pancreatitis; LR+, 7.5 (compared to LR–, of 0.4 for patients with HCT ≤ 45%).
CRP > 150 mg/L at 48 hours can also predict severe pancreatitis; sensitivity, 85–86%; specificity, 74–87%; LR+, 3.2–6.6; LR−, 0.16–0.2
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EVIDENCE-BASED DIAGNOSIS
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History and physical exam
Low-grade fevers (< 38.3°C) are common (60%).
Pain may radiate to the back (50%) and may be exacerbated in the supine position.
Nausea and vomiting are usually present (75%).
Rebound is rare on presentation; guarding is common (50%).
Periumbilical bruising (Cullen sign) is rare.
Pancreatitis (as well as other diseases) can lead to retroperitoneal bleeding and flank bruising (Grey Turner sign), which is a rare but valuable clue when present.
Laboratory studies
Lipase > 3 times the upper limit of normal
79% sensitive, 89% specific; LR+, 7.2; LR–, 0.2
Remains elevated longer than serum ...