Oláh A, Pardavi G, Belágyi T, Romics L
Department of Surgery, Petz Aladár Teaching Hospital, Gyor, Hungary.
Chirurgia (Bucur). 2007 Jul-Aug;102(4):383-8.
The diagram of the mortality of acute pancreatitis is characterized by two distinct peaks, in a similar manner to other generalized acute inflammatory responses. In the first phase, which is characterized by "hyper-inflammatory" mechanisms, death occurs due to overwhelming SIRS and subsequent multi-organ failure. The second peak of death is usually detected much later, at least two weeks after the onset of acute pancreatitis. Infection in necrotising pancreatitis is frequently observed in this so-called "compensatory antiinflammatory" phase. Since there has been no effective therapy evolved to prevent the activation of inflammatory and proteolytic cascades, the treatment of acute pancreatitis is merely symptomatic. Adequate fluid resuscitation and analgesia are the mainstays of treatment. In case of development of multi-organ failure, extensive medical and ventilatory supportive therapy is usually necessary. However, recent studies suggested certain methods might decrease the incidence of infection in pancreatic necrosis, which is usually due to bacterial translocation from the gut. Numerous attempts have been published in the literature to decrease the frequency of septic complications. Furthermore, the outcome of studies favouring antibiotic prophylaxis in acute pancreatitis were debatable. The development of multi-resistant strains of Gram-positive bacteria and Candida, due to long-term antibiotic use, is a strong argument against the indication of prophylactic antibiotic use. Recently, various clinical studies aimed to decrease bacterial translocation, including probiotic use and enteral feeding as part of the treatment. This paper provides a systematic review on data available in the evidence based literature on the use of antibiotics and the role of alternative and supportive therapy in the treatment of severe acute pancreatitis.
急性胰腺炎死亡率图表的特点是有两个明显的高峰,这与其他全身性急性炎症反应类似。在以“高炎症”机制为特征的第一阶段,死亡是由于严重的全身炎症反应综合征(SIRS)及随后的多器官功能衰竭。第二个死亡高峰通常在急性胰腺炎发病至少两周后才出现。在这个所谓的“代偿性抗炎”阶段,坏死性胰腺炎中经常会出现感染。由于尚未研发出有效的疗法来阻止炎症和蛋白水解级联反应的激活,急性胰腺炎的治疗仅仅是对症治疗。充分的液体复苏和镇痛是治疗的主要手段。如果出现多器官功能衰竭,通常需要广泛的医疗和通气支持治疗。然而,最近的研究表明某些方法可能会降低胰腺坏死感染的发生率,胰腺坏死感染通常是由于细菌从肠道移位所致。文献中已发表了许多降低脓毒症并发症发生率的尝试。此外,支持急性胰腺炎预防性使用抗生素的研究结果存在争议。由于长期使用抗生素导致革兰氏阳性菌和念珠菌多重耐药菌株的出现,这有力地反驳了预防性使用抗生素的指征。最近,各种临床研究旨在减少细菌移位,包括使用益生菌和将肠内营养作为治疗的一部分。本文对循证文献中关于抗生素使用以及替代和支持性疗法在重症急性胰腺炎治疗中的作用的现有数据进行了系统综述。