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World Journal of Surgery

, Volume 21, Issue 2, pp 130–135 | Cite as

Natural course of acute pancreatitis

  • H. G. Beger
  • B. Rau
  • J. Mayer
  • U. Pralle
World Progress in Surgery-Acute Pancreatitis:Diagnosis and Treatment

Abstract

Acute pancreatitis comprises, in terms of clinical, pathologic, biochemical, and bacteriologic data, four entities. Interstitial edematous pancreatitis and necrotizing pancreatitis are the most frequent clinical manifestations; pancreatic pseudocyst and pancreatic abscess are late complications after necrotizing pancreatitis, developing after 3 to 5 weeks. Determinants of the natural course of acute pancreatitis are pancreatic parenchymal necrosis, extrapancreatic retroperitoneal fatty tissue necrosis, biologically active compounds in pancreatic ascites, and infection of necrosis. Early in the course of acute pancreatitis multiple organ failure is the consequence of various inflammatory mediators that are released from the inflammatory process and from activated leukocytes attracted by pancreatic injury. During the late course, starting the second week, local and systemic septic complications are dominant. Around 80% of deaths in acute pancreatitis are caused by septic complications. The infection of pancreatic necrosis occurs in 8% to 12% of acute pancreatitis and in 30% to 40% of patients with necrotizing pancreatitis. Bacteriologic analysis of intraoperative smears and aspirates reveals predominantly gram-negative germs deriving from the intestine, most frequently Escherichia coli. It has been confirmed that after necrotizing pancreatitis a considerable large group of patients suffer long-lasting exocrine and endocrine insufficiency.

Keywords

Pancreatitis Acute Pancreatitis Severe Acute Pancreatitis Pancreatic Necrosis Necrotizing Pancreatitis 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Résumé

Sous le terme de pancréatite aiguë se regroupe une large gamme d’entités pathologiques en termes de données cliniques, pathologiques, biochimiques et bactériologiques. La pancréatite oedémateuse interstitielle et la pancréatite nécrosante sont les variétés cliniques les plus fréquemment rencontrées. Les faux kystes et les abcès pancréatiques sont des complications tardives que l’on rencontre après évolution de la pancréatite nécrosante pendant 3 à 5 semaines. Dans l’évolution de la pancréatite aiguë, la nécrose du parenchyme, la nécrose des tissus graisseux rétropéritonéaux extrapancréatiques, la richesse en amylase de l’ascite pancréatique et l’infection de la nécrosc sont déterminants. La défaillance polyviscérale, conséquence de multiples médiateurs inflammatoires qui sont libérés à partir de l’inflammation et des leucocytes activés par la lésion pancréatique, est un facteur pouvant jouer un rôle très tôt dans l’évolution de la pancréatite. Plus tardivement, 15 jours environ après le début de la maladie, ce sont les complications infectieuses qui dominent. Environ 80% des décès dans la pancréatite aiguë sont en rapport avec des complications infectieuses. L’infection de la nécrose pancréatique se voit dans 8–12% des cas de pancréatite aiguë et chez 30–40% des patients ayant une nécrose pancréatique. L’analyse bactériologique des ensemencements provenant des prélèvements peropératoires révèlent des bactéries gram négatives en provenance de la lumière digestive et en particulier, l’E. Coli. On a confirmé également qu’après la pancréatite nécrosante, une large proportion des patients ont une insuffisance pancréatique exocrine et endocrine persistante.

Resumen

La pancreatitis aguda comprende, en términos de sus manifestaciones clìnicas, patológicas, bioquímicas y bacteriológicas, diferentes entidades de la enfermedad. La pancreatitis edematosa intersticial y la pancreatitis necrotizante son sus manifestaciones más frecuentes; el pseudoquiste y el absceso pancreático son complicaciones tardías de la pancreatitis necrotizante, las cuales se desarrollan a las 3–5 semanas. Factores determinantes del curso natural de la pancreatitis aguda son: la necrosis parenquimatosa del páncreas, la necrosis extrapancreética de los tejidos grasos retroperitoneales, la presencia de compuestos biológicamente activos en la ascitis pancreática y la infection de los tejidos necróticos. La falla orgánica múltiple que aparece en las fases tempranas de la pancreatitis aguda es la consecuencia de diversos mediadores inflamatorios generados por el proceso inflamatorio y por leucocitos activados que han sido atraídos por la lesión pancreática. Mas tardíamente en el curso de la enfermedad, comenzando en la segunda semana, son dominantes las complicaciones sépticas, tanto locales como sistémicas. La infección de la necrosis pancreática ocurre en 8–12% de los casos de pancreatitis aguda y en 30–40% de los pacientes con pancreatitis necrotizante. El análisis bacteriológico de frotis y de aspirados intraoperatorios revela predominancia de gérmenes gram-negativos derivados del intestino, especialmente de E.coli. Se ha confirmado que luego de una pancreatitis necrotizante, un grupo considerable de pacientes desarrolla insuficiencia pancreático exocrina y endocrina.

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Copyright information

© Springer-Verlag 1997

Authors and Affiliations

  • H. G. Beger
    • 1
  • B. Rau
    • 1
  • J. Mayer
    • 1
  • U. Pralle
    • 1
  1. 1.Department of General SurgeryUniversity of UlmUlmGermany

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