脓毒症患者毛细血管渗漏综合征的危险因素分析
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摘要
脓毒症是一种高患病率、高死亡率、高治疗费用的临床综合征,是危重病研究的热点和难点。毛细血管渗漏综合征(capillary leak syndrome,CLS)发病机制是因毛细血管内皮细胞损伤,血管通透性增加而引起毛细血管水肿,大量血浆蛋白渗透到组织间隙,从而出现低蛋白血症、低血容量休克、急性肾缺血等临床表现。部分脓毒症患者在病情恶化或治疗过程中出现低血压、低氧血症、低灌注、低蛋白、低血容量、少或无尿、全身水肿、多器官功能障碍综合征(MODS)等表现——即CLS,是疾病最凶险、最严重、最复杂的表现,并发症多,治疗矛盾多,直接影响患者的预后。脓毒症合并CLS,是否及时诊断及有效治疗将影响患者的预后。因此对脓毒症合并CLS的临床危险因素进行分析,以期改善脓毒症患者的预后,降低死亡率。
Sepsis is a clinical syndrome with high morbidity, high mortality and high cost of treatment, it is the hot and difficult problem in critical diseases. The pathogenesis of capillary leak syndrome(CLS) is the injury of capillary endothelial cell and the increased vascular permeability which caused the capillary edema. A large number of plasma protein penetrate into the tissue gap, resulting in hypoalbuminemia, hypovolemic shock,acute renal ischemia and other clinical manifestations. Some patients with sepsis in the process of deterioration or treatment appear low blood pressure, hypoxemia, hypoperfusion, hypoalbuminemia, hypovolemia,oliguria or anuria, anasarca, MODS and other performances — that is CLS.It is the most dangerous, the most serious, the most complex performance situation with more complications and more contradictions in treatment, it will directly influence the prognosis of patients. Whether we can diagnose sepsis with CLS timely and whether we can treat the patients perfectly will influence the prognosis. Therefore, this article will analyze the clinical risk factors of sepsis with CLS in order to improve the prognosis of patients and reduce the mortality rate.
Sepsis is a clinical syndrome with high morbidity, high mortality and high cost of treatment, it is the hot and difficult problem in critical diseases. The pathogenesis of capillary leak syndrome(CLS) is the injury of capillary endothelial cell and the increased vascular permeability which caused the capillary edema. A large number of plasma protein penetrate into the tissue gap, resulting in hypoalbuminemia, hypovolemic shock,acute renal ischemia and other clinical manifestations. Some patients with sepsis in the process of deterioration or treatment appear low blood pressure, hypoxemia, hypoperfusion, hypoalbuminemia, hypovolemia,oliguria or anuria, anasarca, MODS and other performances — that is CLS.It is the most dangerous, the most serious, the most complex performance situation with more complications and more contradictions in treatment, it will directly influence the prognosis of patients. Whether we can diagnose sepsis with CLS timely and whether we can treat the patients perfectly will influence the prognosis. Therefore, this article will analyze the clinical risk factors of sepsis with CLS in order to improve the prognosis of patients and reduce the mortality rate.
引文
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[11]武前枝,倪琛琛,张志红.机械通气对小鼠肺损伤的初步研究[J].安徽医科大学学报,2012,47(7):805-808.
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[13]CS Barbas.Acute lung injury and acute respiratory distress syndrome:diagnostic hurdles[J].J Bras Pneumol,2007,33(4):xxv-xxvi.
[14]魏海苓.脓毒症毛细血管渗漏的研究进展[J].感染、炎症、修复,2013,14(2):126-128.
[15]Marx G.Fluid therapy in sepsis with capillary leakage[J].Eur JAnaesthesiol,2003,20(6):429-442.
[16]Aman J,van der Heijden M,van Lingen A,et al.Plasma protein levels are markers of pulmonary vascular permeability and degree of lung injury in critically ill patients with or at risk for acute lung injury/acute respiratorydistress syndrome[J].Crit Care Med,2011,39(1):89-97.
[17]马丽君,秦英智.血管外肺水指数和肺毛细血管渗透性指数在肺水肿诊断中的意义[J].中国危重病急救医学,2008;20(2):111-114.
[18]梅华鲜,李永胜,陈正中,等.毛细血管渗漏指数在脓毒症并ARDS早期诊断中的应用[J].新医学,2016,47(10):681-685.
[19]Frost RA,Nystrom GJ,Lang CH.Lipopolysaecharide regulates proinflammatory cytokine expression in mouse myoblasts and skeletal muscle[J].Am J Physiol Regul Integr Comp Physiol,2002,283(3):R698-R709.
[20]David S,Mukherjee A,Ghosh CC,et al.Angiopoietin-2 may contribute to multi-organ dysfunction and death in sepsis[J].Crit Care Med,2012,40(11):3034-3041.
[21]温占兵,李真玉,刘健,等.血管生成素-2与严重脓毒症肺毛细血管渗漏的相关性研究[J].天津医科大学学报,2013,19(6):474-477.
[22]陈秋萍,冯永民,张媛莉,等.脓毒症患者血浆血管生成素2与(1,3)-β-D葡聚糖水平变化及其相关性分析[J].山东医药,2014,54(8):21-24.
[23]Tamion F,Camduchez V,Menard JF,et al.Erythropoietin and rennin as biologiclal markers in critical ill patients[J].Crit Care,2004,8(5):R328-R335.
[24]Suzuki Y,Ruiz-ortega M,Lorenzo O,et al.Inflammation and angiotensinⅡ[J].Int J Biochem Cell Biol,2003,35(6):881-900.
[25]Chang Y,Wei W.Angiotensin II in inflammation,immunity and rheumatoid arthritis[J].Clin Exp Immunol,2015,179(2):137-145.
[26]李士欣,翟建华,柴艳芬.液体复苏前后血浆血管紧张素Ⅱ水平对严重脓毒症患者的预后价值[J].中华危重症医学杂志(电子版),2015,8(1):8-11.
[27]苏俊,王锦权,陶晓根,等.毛细血管渗漏综合征的易患因素分析[J].中国急救医学,2011,31(10):872-875.
[2]CLARKSON B,THOMPSON D,HORWITH M,et al.Cyclical edema and shock due to increased capillary permeability[J].Am J Med,1960,29:193-216.
[3]景炳文,林兆奋.关于毛细血管渗漏综合征救治问题中有关问题的讨论[J].中国危重病急救医学,2009,21(12):705,后插4.
[4]邱海波,于凯江.重症医学[M].北京:人民卫生出版社,2013:106-108.
[5]隆彩霞,朱之尧,胥志跃,等.儿童脓毒症发生毛细血管渗漏综合征的临床危险因素分析[J].中国当代儿科杂志,2013,15(3):219-222.
[6]羊玲,钟丽花,张娅琴,等.新生儿重症监护室毛细血管渗漏综合征的危险因素[J].中国妇幼保健,2013,28(21):3448-3449.
[7]Dreyfuss D,Saumon G.Ventilator-induced lung injury:lessons from experimental studies[J].Am J Respir Crit Care Med,1998,157(1):294-323.
[8]Halbertsma FJ,Vaneker M,Pickkers P,et al.A single recruitment maneuver in ventilated critically ill children can translocate pulmonary cytokines into the circulation[J].J Crit Care,2010,25(1):10-15.
[9]Imanaka H,Shimaoka M,Matsuura N,et al.Ventilator induced lung injury is associated with neutrophil infiltration,macrophage activation,and TGF-beta 1 mRNA upregulation in rat lungs[J].Anesth Analg,2001,92(2):428-436.
[10]谭华,吴畏.肺保护性通气策略研究进展[J].西南国防医药,2017,27(2):212-214.
[11]武前枝,倪琛琛,张志红.机械通气对小鼠肺损伤的初步研究[J].安徽医科大学学报,2012,47(7):805-808.
[12]Hong CM,Xu DZ,Lu Q,et al.Low tidal volume and high positive end-expiratory pressure mechanical ventilation results in increased inflammation and ventilator-associated lung injury in normal lungs[J].Anesth Analg,2010,110(6):1652-1660.
[13]CS Barbas.Acute lung injury and acute respiratory distress syndrome:diagnostic hurdles[J].J Bras Pneumol,2007,33(4):xxv-xxvi.
[14]魏海苓.脓毒症毛细血管渗漏的研究进展[J].感染、炎症、修复,2013,14(2):126-128.
[15]Marx G.Fluid therapy in sepsis with capillary leakage[J].Eur JAnaesthesiol,2003,20(6):429-442.
[16]Aman J,van der Heijden M,van Lingen A,et al.Plasma protein levels are markers of pulmonary vascular permeability and degree of lung injury in critically ill patients with or at risk for acute lung injury/acute respiratorydistress syndrome[J].Crit Care Med,2011,39(1):89-97.
[17]马丽君,秦英智.血管外肺水指数和肺毛细血管渗透性指数在肺水肿诊断中的意义[J].中国危重病急救医学,2008;20(2):111-114.
[18]梅华鲜,李永胜,陈正中,等.毛细血管渗漏指数在脓毒症并ARDS早期诊断中的应用[J].新医学,2016,47(10):681-685.
[19]Frost RA,Nystrom GJ,Lang CH.Lipopolysaecharide regulates proinflammatory cytokine expression in mouse myoblasts and skeletal muscle[J].Am J Physiol Regul Integr Comp Physiol,2002,283(3):R698-R709.
[20]David S,Mukherjee A,Ghosh CC,et al.Angiopoietin-2 may contribute to multi-organ dysfunction and death in sepsis[J].Crit Care Med,2012,40(11):3034-3041.
[21]温占兵,李真玉,刘健,等.血管生成素-2与严重脓毒症肺毛细血管渗漏的相关性研究[J].天津医科大学学报,2013,19(6):474-477.
[22]陈秋萍,冯永民,张媛莉,等.脓毒症患者血浆血管生成素2与(1,3)-β-D葡聚糖水平变化及其相关性分析[J].山东医药,2014,54(8):21-24.
[23]Tamion F,Camduchez V,Menard JF,et al.Erythropoietin and rennin as biologiclal markers in critical ill patients[J].Crit Care,2004,8(5):R328-R335.
[24]Suzuki Y,Ruiz-ortega M,Lorenzo O,et al.Inflammation and angiotensinⅡ[J].Int J Biochem Cell Biol,2003,35(6):881-900.
[25]Chang Y,Wei W.Angiotensin II in inflammation,immunity and rheumatoid arthritis[J].Clin Exp Immunol,2015,179(2):137-145.
[26]李士欣,翟建华,柴艳芬.液体复苏前后血浆血管紧张素Ⅱ水平对严重脓毒症患者的预后价值[J].中华危重症医学杂志(电子版),2015,8(1):8-11.
[27]苏俊,王锦权,陶晓根,等.毛细血管渗漏综合征的易患因素分析[J].中国急救医学,2011,31(10):872-875.