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Natural course of acute pancreatitis

  • World Progress in Surgery-Acute Pancreatitis:Diagnosis and Treatment
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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.

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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References

  1. Fitz, R.H.: Acute pancreatitis: a consideration of pancreatic hemorrhage, hemorrhagic, suppurative and gangrenous pancreatitis. Boston Med. Surg. J. 70:181, 1889

    Google Scholar 

  2. Ranson, J.H.C., Rifkind, K.M., Roses, D.F., Fink, S.D., Eng, K., Localio, S.A.: Objective early identification of severe acute pancreatitis. Am. J. Gastroenterol. 61:443, 1974

    PubMed  CAS  Google Scholar 

  3. Imrie, C.W.: Observations on acute pancreatitis. Br. J. Surg. 61:539, 1974

    Article  PubMed  CAS  Google Scholar 

  4. Knaus, W.A., Draper, E.A., Wagner, D.P., Zimmermann, J.E.: APACHE II: a severity of disease classification system. Crit. Care Med. 13:818, 1985

    Article  PubMed  CAS  Google Scholar 

  5. Wilson, C., Heath, D.I., Imrie, C.W.: Prediction of outcome in acute pancreatitis: a comparative study of APACE II, clinical assessment and multiple factor scoring systems. Br. J. Surg. 77:1260, 1990

    Article  PubMed  CAS  Google Scholar 

  6. Beger, H.G., Krautzberger, W., Bittner, R., Block, S., Büchler, M.: Results of surgical treatment of necrotizing pancreatitis. World J. Surg. 9:972, 1985

    Article  PubMed  CAS  Google Scholar 

  7. Beger, H.G., Kunz, R., Bittner, R.: Prognostic criteria in necrotizing pancreatitis. In Acute Pancreatitis, H.G. Beger, M. Büchler, editors. Springer, Berlin, 1987, pp. 198–200

    Google Scholar 

  8. Block, S., Maier, W., Bittner, R., Büchler, M., Malfertheiner, P., Beger, H.G.: Identification of pancreatic necrosis in severe acute pancreatitis: imaging procedures versus clinical staging. Gut 27:1035, 1986

    Article  PubMed  CAS  Google Scholar 

  9. Kivisaari, L., Schröder, T., Sainio, V., Somer, K., Standertskjöld-Nordenstam, C.-G.: CT evaluation of acute pancreatitis: 8 years clinical experience and experimental evidence. Acta Radiol., 377:20, 1987

    Google Scholar 

  10. Freeny, P.C.: Incremental dynamic bolus computed tomography of acute pancreatitis. Int. J. Pancreatol. 13:147, 1993

    PubMed  CAS  Google Scholar 

  11. Beger, H.G., Bittner, R., Block, S., Büchler, M.: Bacterial contamination of pancreatic necrosis. Gastroenterology 49:433, 1986

    Google Scholar 

  12. Bittner, R., Block, S., Büchler, M., Berger, H.G.: Pancreatic abscess and infected necrosis: different local septic complications in acute pancreatitis. Dig. Dis. Sci. 32:1082, 1987

    Article  PubMed  CAS  Google Scholar 

  13. Beger, H.G.: Surgery in acute pancreatitis. Hepatogastroenterology 38:92, 1991

    PubMed  CAS  Google Scholar 

  14. Bradley, E.L., III: A clinically based classification system for acute pancreatitis. Arch. Surg. 128:586, 1993

    PubMed  Google Scholar 

  15. Bockman, D.E.: Pathology of edematous (interstitial) pancreatitis. In: Acute Pancreatitis: Diagnosis and Therapy, E.L. Bradley, III, editor. New York, Raven, 1994, pp. 241–247

    Google Scholar 

  16. Klöppel, G., Maillet, B.: Pathology of acute and chronic pancreatitis. Pancreas 8:659, 1993

    PubMed  Google Scholar 

  17. Gerzof, S.G., Banks, P.A., Robbins, A.H., Johnson, W.C., Spechler, S.J., Wetzner, S.M., Snider, J.M., Langevin, R.E., Jay, M.E.: Early diagnosis of pancreatic infection by computed tomography-guided aspiration. Gastroenterology 93:1315, 1987

    PubMed  CAS  Google Scholar 

  18. Bradley, E.L., III, Allen, K.: A prospective longitudinal study of observation versus surgical intervention in the management of necrotizing pancreatitis. Am. J. Surg. 161:19, 1991

    Article  PubMed  Google Scholar 

  19. Grace, P.A., Williamson, R.C.N.: Modern management of pancreatic pseudocysts. Br. J. Surg. 80:573, 1993

    Article  PubMed  CAS  Google Scholar 

  20. Banks, P.A.: Acute pancreatitis: clinical presentation. In The Exocrine Pancreas, V.L.W. Go, F.P. Brooks, E.P. DiMagno, J.D. Gardner, E. Lebenthal, G.A. Scheele, editors, New York, Raven, 1986, pp. 475–479

    Google Scholar 

  21. Beger, H.G., Bittner, R., Büchler, M., Hess, W., Schmitz, J.E.: Hemodynamic data pattern in patients with acute pancreatitis. Gastroenterology 90:74, 1986

    PubMed  CAS  Google Scholar 

  22. Carey, L.C.: Extra-abdominal manifestations of acute pancreatitis. Surgery 86:337, 1979

    PubMed  CAS  Google Scholar 

  23. McFadden, D.W.: Organ failure and multiple organ system failure in pancreatitis. Pancreas 6(Suppl. 1):27, 1991

    Google Scholar 

  24. Widdison, A.L., Karanjia, N.D.: Pancreatic infection complicating acute pancreatitis. Br. J. Surg. 80:148, 1993

    Article  PubMed  CAS  Google Scholar 

  25. Renner, I.G., Savage, W.T., Pantoia, J.L., Renner, V.J.: Death due to acute pancreatitis: a retrospective analysis of 405 autopsy cases. Dig. Dis. Sci. 30:1005, 1985

    Article  PubMed  CAS  Google Scholar 

  26. Teerenhovi, O.: Fatal fulminant pancreatitis. Surg. Res. Commun. 3:207, 1988

    Google Scholar 

  27. Jimenez, G., Aldrete, J.S.: Clinical implications derived from the morphological classification of 89 patients with acute pancreatitis. J. Clin. Gastroenterol. 5:137, 1983

    Article  PubMed  CAS  Google Scholar 

  28. Uhl, W., Büchler, M., Malfertheiner, P., Isenmann, R., Martini, M., Beger, H.G.: Pancreatic necrosis develops within four days after the acute attack. Gastroenterology 100:A 123, 1991

    Google Scholar 

  29. Rau, B., Seifert, T., Schoenberg, M.H., Brambs, H.J., Beger, H.G.: Contrast enhanced CT: does it accentuate severity of necrotizing pancreatitis in humans? Pancreas 11:445, 1995

    Google Scholar 

  30. Balthazar, E.J., Robinson, D.L., Megibow, A.J.: Acute pancreatitis: value of CT in establishing prognosis. Radiology 174:331, 1990

    PubMed  CAS  Google Scholar 

  31. Foitzik, T., Bassi, D.G., Schmidt, J., Lewandrowski, K.B., Fernandez-del Castillo, C., Rattner, D.W., Warshaw, A.L: Intravenous contrast medium accentuates the severity of acute necrotizing pancreatitis in the rat. Gastroenterology 106:207, 1994

    PubMed  CAS  Google Scholar 

  32. Aldridge, M.C., Francis, N.D., Glazer, G., Dudley, H.A.F.: Colonic complications of severe acute pancreatitis. Br. J. Surg. 76:362, 1989

    Article  PubMed  CAS  Google Scholar 

  33. McMahon, M.J., Lankisch, P.G.: Peritoneal lavage and dialysis for the treatment of acute pancreatitis. In Acute Pancreatitis, H.G. Beger, M. Büchler, editors. Berlin, Springer, 1987, pp. 278–284

    Google Scholar 

  34. Büchler, M., Malfertheiner, P., Schädlich, H., Nevalainen, T.J., Friess, H., Beger, H.G.: Role of phospholipase A2 in human acute pancreatitis. Gastroenterology 97:1521, 1989

    PubMed  Google Scholar 

  35. Heath, D.I., Wilson, C., Gudgeon, A.M., Jehanli, A., Shenkin, A., Imrie, C.W.: Trypsinogen activation peptides (TAP) concentrations in the peritoneal fluid of patients with acute pancreatitis and their relation to the presence of histologically confirmed pancreatic necrosis. Gut 35:1311, 1994

    Article  PubMed  CAS  Google Scholar 

  36. Puolakkainen, P., Valtonen, V., Paananen, A., Schröder, T.: C-reactive protein (CRP) and serum phospholipase A2 in the assessment of the severity of acute pancreatitis. Gut 28:764, 1987

    Article  PubMed  CAS  Google Scholar 

  37. Uhl, W., Büchler, M., Malfertheiner, P., Martini, M., Beger, H.G.: PNM-elastase in comparison with CRP, antiproteases and LDH as indicators of necrosis in human acute pancreatitis. Pancreas 6:253, 1991

    Article  PubMed  CAS  Google Scholar 

  38. Torab, F., Berger, D., Uhl, W., Seidelmann, M., Büchler, M., Beger, H.G.: Clinical significance of endotoxin and interleukin-6 during acute pancreatitis. Int. J. Pancreatol. (1996, in press)

  39. Wilson, C., Heads, A., Shenkin, A., Imrie, C.W.: C-reactive protein, antiproteases and complement factors as objective markers of severity in acute pancreatitis. Br. J. Surg. 76:177, 1989

    Article  PubMed  CAS  Google Scholar 

  40. Gross, V., Leser, H-G., Heinisch, A., Schölmerich, J.: Inflammatory mediators and cytokines—new aspects of the pathophysiology and assessment of severity of acute pancreatitis. Hepatogastroenterology 40:522, 1993

    PubMed  CAS  Google Scholar 

  41. Bassi, C., Falconi, M., Girelli, R., Nifosi, F., Elio, A., Martini, N., Pederzoli, P.: Microbiological findings in severe pancreatitis. Surg. Res. Commun. 5:1, 1989

    Google Scholar 

  42. Rau, B., Pralle, U., Uhl, W., Schoenberg, M.H., Beger, H-G.: Management of sterile necrosis in instances of severe acute pancreatitis. J. Am. Coll. Surg. 181:259, 1995

    Google Scholar 

  43. Yeo, C.T., Bastidas, J.A., Lynch-Nyhan, A., Fishman, E.K., Zinner, M.J., Cameron, J.L.: The natural history of pancreatic pseudocysts documented by computed tomography. Surg. Gynecol. Obstet. 170: 411, 1990

    PubMed  CAS  Google Scholar 

  44. Schoenberg, M.H., Rau, B., Beger, H.G.: Diagnose und Therapie des primären Pankreasabszesses. Chirurg 66:588, 1995

    PubMed  CAS  Google Scholar 

  45. Mitchell, C.J., Playforth, M.J., Kellenher, J., McMahon, M.J.: Functional recovery of the exocrine pancreas after acute pancreatitis. Scand. J. Gastroenterol. 18:5, 1983

    Article  PubMed  CAS  Google Scholar 

  46. Büchler, M., Malfertheiner, P., Block, S., Beger, H.G.: Morphologische und funktioneile Veränderungen des Pankreas nach akuter nekrotisierende Pankreatitis. Z. Gastroenterol. 23:79, 1985

    PubMed  Google Scholar 

  47. Angelini, G., Cavallini, G., Pederzoli, P., Bovo, P., DiFrancesco, V., Frulloni, L., Sgabri, L., Talamini, G., Castagnini, A.: Long-term outcome of acute pancreatitis: a prospective study with 118 patients. Digestion 54:143, 1993

    Article  PubMed  CAS  Google Scholar 

  48. Beger, H.G., Büchler, M. Decision-making in surgical treatment of acute pancreatitis: operative or conservative management of necrotizing pancreatitis. Theor. Surg. 1:61, 1986

    Google Scholar 

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Beger, H.G., Rau, B., Mayer, J. et al. Natural course of acute pancreatitis. World J. Surg. 21, 130–135 (1997). https://doi.org/10.1007/s002689900204

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