8 手術(shù)治療
重癥胰腺炎的治療選擇經(jīng)歷了一個由非手術(shù)、手術(shù)、“個性化方案”的發(fā)展過程,目前正處在手術(shù)和非手術(shù)2種治療并存的階段。一般地說在AP的急性反應期,要盡快去除病因,并爭取非手術(shù)治療。但是對需要通過手術(shù)治療祛除病因的病例或非手術(shù)療法無效的情況應考慮手術(shù)治療。經(jīng)過不同治療過渡到全身感染期和殘余感染期的病例是治療的初步成功。如果出現(xiàn)需要手術(shù)的情況,如壞死感染包裹、胰腺或胰周膿腫則要做出手術(shù)治療的選擇[23]。
目前,對于急性胰腺炎的發(fā)病機制尚未完全闡明,細胞因子網(wǎng)絡(luò)是如何互相作用并推動胰腺炎臨床病程的演進,其詳細機制并不十分清楚。細胞凋亡在胰腺組織損傷,遠隔器官并發(fā)癥產(chǎn)生中的詳盡作用并不十分清楚。臨床上正確判斷SIRS/CARS具體哪一個占優(yōu)勢,尚非常困難,且SIRS/CARS在MODS發(fā)病中消長關(guān)系也不完全清楚。致使臨床治療仍停留在病因和器官功能支持上,細胞因子及血液濾過等治療也只是剛剛起步,其具體作用機制并不十分清楚。故常常失去控制SIRS/CARS平衡的有利時機,難以明確改善預后。因此,現(xiàn)階段重點應對胰腺微循環(huán)障礙、炎性介質(zhì)和細胞因子作用等發(fā)病機制進行深入研究,并探討SIRS、CARS的平衡關(guān)系及尋找臨床判斷標準指標。力求及早阻斷SIRS的發(fā)展,預防MODS的發(fā)生,并為免疫調(diào)節(jié)治療奠定基礎(chǔ)。
【參考文獻】
1 Bogdan C,Vodovotz Y,Nathan C.Macrophage deactivation by inTERLEUKIN 10.Jexp Med,2006,91:104.
2 Olikowsky T,Wang ZQ,Dudhane A,et al.Two distinct path ways of human macrophage differentiation are mediated bt interferonr and interleukin10.Immunology,1997,91:104.
3 Osman MO,Kristensen JU,Jacobsen NO,et al.A monoclonal antiinterleukin 8 antibody(WS4)inhibits cytokin response and acute lung injury in experimental severe acute necrotising pancreatitis in rabbits.Gut,2007,43:232.
4 金牡丹,周智林,傅志泉.重癥急性胰腺炎大鼠白介素8和白介素10及核因子κB的表達.中國全科醫(yī)學,2008,11:577579.
5 Smeenk RJT,Wijdenes J,Aarden I.A ProstaglandinE2 is a potent inhibitor of human interleukin 12 production.J Exp Med,2005,181:775醫(yī)學全.在線payment-defi.com.
6 Meldrum D, Dinarello CA, Cleveland JC, et al. Hydrogen Peroxide induces tumor necrosis factor mediated cardiac injury by a p38 mitogenactivated protein kinasedependent mechanism.Surgery,2004,124:291.
7 Foitzik T,Hotz HG,Eibl G,et al.Therapy for microcirculatory disorders in severe acute pancreatitis:effectiveness of plateactivating factor receptor blockade vs. endothelin receptor blockade. J Gastrointest Surg,2003,3:244.
8 Janathan A,Taichman LB.Effect of TGFβ on recpithelization of human kerainocytes in vitro:an organotypic model.J Invest dermatol,2004,103:554555.
9 Marcus BC,Wyble CW,Hynes KL,et al.Cytokineinduced increases in endothelial permeability after adhesion molecule expression.Surg, 2006,120:411416.
10 Barnett CC,Moore EE, Moore FA, et al. Intercellular adhesion molecule1 promote neutrophilmediated cytoxicity. Surg, 2005,118:171175.