Biliary acute pancreatitis:a review.
2000; National Institutes of Health; Volume: 6; Issue: 2 Linguagem: Inglês
10.3748/wjg.v6.i2.157
AutoresOsvaldo Tiscornia, Susana Hamamura, Enriqueta S. de Lehmann, Graciela Otero, Hipólito Waisman, Patricia Tiscornia‐Wasserman, Simmy Bank,
Tópico(s)Diet, Metabolism, and Disease
ResumoIt is axiomatic that the most effective and soundly based plan of treatment of any disorder is one aimed at the mechanism or mechanisms responsible for its development[1]. This basic notion, coupled with recent reports[2-11] in which, surprisingly there is a total lack of reference to the probable involvement of autonomic-arc-reflexes in the physiopathogenesis of biliary acute pancreatitis have prompted this presentation. Undoubtedly, this disease entity has numerous causes, an obscure physiopathology, few effective remedies, and, often, an unpredictable outcome. At the turn of the century, Opie[12,13] brought to light the association between gallstone migration and acute pancreatitis. When referring to the intimate evolving process, most authors steadily adhere to the Opie’s theories: chemical and physical. The former is linked to the common-channel or biliary-reflux mechanism. The latter, to the stone-elicited Wirsung duct obstruction, with the resultant hypertension in the pancreatic ductal tree. What is indeed surprising is the lack of speculation on the subsequent steps that necessarily must follow the initial chemical and/or physical injuries that end up in an episode of acute pancreatitis. The core of our contention is that the pathophysiology of biliary acute pancreatitis is centered on two basic mechanisms: the activation of autonomic arc reflexes and the disruption of the entero-pancreatic feedback loop. Superimposed on the aforementioned pivotal processes we must consider, in some cases, the aggravating role of alcoholism. In this presentation we will also try to point out those features that justify to consider the Pfeffer method, or of the closed-duodenal-loop, as an experimental surgical model suitable to mimic the clinical condition of acute pancreatitis. Furthermore, we will analyze the properties of local anesthetics that, according to our contention, are valuable agents to either prevent and/or treat efficaciously an episode of biliary acute pancreatitis.
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