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Key Clinical Updates in Acute Pancreatitis
Goal-directed therapy with moderate fluid resuscitation (a bolus of 10 mL/kg in patients with signs of hypovolemia followed by no more than 1.5 mL/kg/hour) may reduce the frequency of systemic inflammatory response syndrome and organ failure in this group of patients and appears to have the greatest benefit in patients with acute pancreatitis predicted to be mild in severity when started within 4 hours of the patient’s arrival at the hospital.
de-Madaria E et al. N Engl J Med. [PMID: 36103415]
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ESSENTIALS OF DIAGNOSIS
Abrupt onset of deep epigastric pain, often with radiation to the back.
History of previous episodes, often related to alcohol intake.
Nausea, vomiting, sweating, weakness.
Abdominal tenderness and distention and fever.
Leukocytosis, elevated serum amylase, elevated serum lipase.
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GENERAL CONSIDERATIONS
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The annual incidence of acute pancreatitis ranges from 110 to 140 per 100,000 population and has increased since 1990. Most cases of acute pancreatitis are related to biliary tract disease (45%) (a passed gallstone, usually 5 mm or less in diameter) or heavy alcohol intake (20%), with worldwide variations. The exact pathogenesis is not known but may include edema or obstruction of the ampulla of Vater, reflux of bile into pancreatic ducts, and direct injury of pancreatic acinar cells by prematurely activated pancreatic enzymes (eFigure 18–56). Among the numerous other causes or associations are (1) hyperlipidemias (chylomicronemia, hypertriglyceridemia, or both); (2) hypercalcemia; (3) abdominal trauma (including surgery); (4) medications (including azathioprine, mercaptopurine, asparaginase, pentamidine, didanosine, valproic acid, tetracyclines, dapsone, isoniazid, metronidazole, estrogen and tamoxifen [by raising serum triglycerides], sulfonamides, mesalamine, celecoxib, sulindac, leflunomide, thiazides, simvastatin, fenofibrate, enalapril, methyldopa, procainamide, sitagliptin, exenatide, possibly corticosteroids, and others); (5) vasculitis; (6) infections (eg, hepatitis viruses, mumps, cytomegalovirus, M avium intracellulare complex, SARS-CoV-2); (7) peritoneal dialysis; (8) cardiopulmonary bypass; (9) single- or double-balloon enteroscopy; (10) ERCP; and (11) a scorpion bite (rare). Medication-induced acute pancreatitis is generally dose-related and associated with worse outcomes than that due to other causes. In patients with pancreas divisum, a congenital anomaly in which the dorsal and ventral pancreatic ducts fail to fuse, acute pancreatitis may result from stenosis of the minor papilla with obstruction to flow from the accessory pancreatic duct, although concomitant gene variants, particularly in the cystic fibrosis transmembrane conductance regulator (CFTR) gene, may account for acute pancreatitis in these patients. Genetic mutations also predispose to chronic pancreatitis, particularly in persons younger than 30 years of age if no other cause is evident and a family history of pancreatic disease is present (see Chronic Pancreatitis). Acute pancreatitis may also result from an anomalous junction of the pancreaticobiliary duct (pancreaticobiliary malunion). Rarely, acute pancreatitis may be the presenting manifestation of a pancreatic or ampullary neoplasm or pancreatic cyst. Celiac disease appears to be associated with an increased risk of acute and chronic pancreatitis. Apparently “idiopathic” acute pancreatitis is often caused by occult biliary microlithiasis but unlikely ...