Pancreatite aguda

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American Journal of Gastroenterology C 2006 by Am. Coll. of Gastroenterology Published by Blackwell Publishing

ISSN 0002-9270 doi: 10.1111/j.1572-0241.2006.00856.x

Practice Guidelines in Acute Pancreatitis
Peter A. Banks, M.D., M.A.C.G.,1 Martin L. Freeman, M.D., F.A.C.G.,2 and the Practice Parameters Committee ∗ of the American College of Gastroenterology 1 Division of Gastroenterology,Center for Pancreatic Disease, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts; 2 Division of Gastroenterology, Hennepin County Medical Center, University of Minnesota, Minneapolis, Minnesota

(Am J Gastroenterol 2006;101:2379–2400)

INTRODUCTION
Guidelines for the diagnosis and treatment of acute pancreatitis were published by the American College ofGastroenterology in 1997 (1). These and subsequent guidelines (2–7) have undergone periodic review (6, 8–13) in accordance with advances that have been made in the diagnosis and treatment of acute pancreatitis. Guidelines for clinical practice are intended to apply to all health-care providers who take care of patients with acute pancreatitis and are intended to be flexible, and to suggest preferable (but notthe only) approaches. Because there is a wide range of choices in any health-care situation, the physician should select the course best suited to the individual patient and the clinical situation. These guidelines have been developed under the auspices of the American College of Gastroenterology and its Practice Parameters Committee, and approved by the Board of Trustees. The world literature inEnglish was reviewed using a MEDLINE search and also using the Cochrane Library. The ratings of levels of evidence for these guidelines are indicated in Table 1. The final recommendations are based on the data available at the time of the publication of this document and may be updated with appropriate scientific development at a later time. The following guidelines are intended for adult and notpediatric patients. The main diagnostic guidelines include an assessment of risk factors of severity at admission and determination of severity. The major treatment guidelines include supportive care, fluid resuscitation, transfer to intensive care unit, enteral feeding, use of antibiotics, treatment of infected pancreatic necrosis, treatment of sterile pancreatic necrosis, treatment of associatedpancreatic duct disruptions, and role of magnetic resonance cholangiopancreatography (MRCP), endoscopic ultrasound (EUS), and endoscopic retrograde cholangiopancreatography (ERCP) with biliary sphincterotomy for detection and treatment of choledocholithiasis in biliary pancreatitis.

PATHOPHYSIOLOGY
The pathophysiology of acute pancreatitis is generally considered in three phases. In the firstphase, there is premature activation of trypsin within pancreatic acinar cells. A variety of mechanisms have been proposed including disruption of calcium signaling in acinar cells (14–18), cleavage of trypsinogen to trypsin by the lysosomal hydrolase cathepsin-B, and decreased activity of the intracellular pancreatic trypsin inhibitor (17, 18). Once trypsin is activated, it activates a variety ofinjurious pancreatic digestive enzymes. In the second phase, there is intrapancreatic inflammation through a variety of mechanisms and pathways (16, 18–28). In the third phase, there is extrapancreatic inflammation including acute respiratory syndrome (ARDS) (16, 19–21, 29). In both phases, there are four important steps mediated by cytokines and other inflammatory mediators: 1) activation of inflammatorycells, 2) chemoattraction of activated inflammatory cells to the microcirculation, 3) activation of adhesion molecules allowing the binding of inflammatory cells to the endothelium, and 4) migration of activated inflammatory cells into areas of inflammation. In the majority of patients, acute pancreatitis is mild. In 10– 20%, the various pathways that contribute to increased intrapancreatic and...
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