烧伤后多脏器功能失常综合征的临床防治研究——27年临床诊治经验总结

目的：总结烧伤后多脏器功能失常综合征（ＭＯＤＳ）临床防治的经验。方法：将我科７０年代、８０年代和９０年代以来ＭＯＤＳ临床救治工作分为３个阶段，分析３个阶段ＭＯＤＳ监测技术和防治措施的进步对降低ＭＯＤＳ发生率和病死率的作用。结果：９０年代以来，由于我科采用了一系列新的监测技术和早期防治措施，烧伤ＭＯＤＳ总发生率以及总体表烧伤面积（ＴＢＳＡ）＞５０％伤员ＭＯＤＳ发生率均显著低于７０年代和８０年代（Ｐ＜０．０５或Ｐ＜０．０１）。９０年代以来，尽管ＭＯＤＳ脏器衰竭个数多于７０年代和８０年代，但ＴＢＳＡ＞３０％患者的病死率（４７．１％）却显著降低（Ｐ＜０．０１）。结论：烧伤休克后及时和充分复苏、清除坏死组织和控制伤后感染、加强脏器保护与支持是降低烧伤后ＭＯＤＳ发生率、提高治愈率的最重要措施     

多发创伤合并休克导致大鼠多器官功能障碍综合征的实验研究

目的：探讨造成大鼠一次打击型多器官功能障碍综合征（ＭＯＤＳ）所需的创伤条件。方法：５６只ＳＤ大鼠随机分为５组：假手术组（Ｎ）、低血容量性休克组（Ｓ）、２处创伤合并休克组（Ｂ）、４处创伤合并休克组（Ｃ）和６处创伤合并休克组（Ｄ）,用各脏器生化检测指标及脏器受损数来评价各组动物各脏器的功能。结果：Ｎ、Ｓ组复苏后７２小时内无一只动物死亡,不发生多器官损伤（ＭＯＩ）和衰竭（ＭＯＦ）;Ｂ、Ｃ组７２小时内极少死亡（仅Ｃ组死亡１只）,ＭＯＩ发生率分别为３７．５％和８７．５％,ＭＯＦ发生率分别为０和１２．５％;Ｄ组均于７２小时内死亡,复苏成功的动物平均存活（３２．３±９．３）小时,且全部发生ＭＯＩ,ＭＯＦ的发生率达９５．０％。结论：６处创伤合并休克可导致一次打击型ＭＯＤＳ。     

休克患者血浆肾上腺髓质素与血管阻力变化的关系

目的：观察休克患者血浆肾上腺髓质素（ＡＤＭ）与血管阻力变化,探讨其在休克病理生理过程中的作用。方法：应用放射免疫方法检测４６ 例休克患者血浆ＡＤＭ 浓度,无创胸导生物电阻抗方法测定平均动脉压（ＭＢＰ）、全身血管阻力（ＳＶＲＩ）和心排指数（ＣＩ）。结果：休克组治疗前血浆ＡＤＭ 浓度明显高于正常对照组（Ｐ＜０．０１）;感染性休克组高于非感染性休克组（Ｐ＜ ０．０５）;死亡组高于存活组（Ｐ＜ ０．０５）;感染性休克组ＳＶＲＩ较其他组明显降低,而ＣＩ较正常组略高,其他休克组则明显降低（Ｐ＜ ０．０５）。结论：ＡＤＭ 与血管阻力变化相关,并参与了休克的病理生理过程。     

感染性休克患者血流动力学和氧合功能的变化

目的：研究感染性休克患者血流动力学和氧合功能的变化。方法：因输液致感染性休克患者８ 例,入ＩＣＵ后置入Ｓｗａｎ Ｇａｎｚ导管测定中心静脉压（ＣＶＰ）、肺动脉平均压（ＭＰＡＰ）、肺毛细血管嵌压（ＰＣＷＰ）;用热稀释法测定心排血量（ＣＯ）,同时监测平均动脉压（ＭＡＰ）和心率。于入ＩＣＵ 后１、２、３、４ 和５ 日内进行血气分析,计算出氧输送（ＤＯ２ ）、氧耗量（ＶＯ２ ）、氧摄取率（Ｏ２ｅｘｔｒ）、肺内分流率（Ｑｓ／Ｑｔ）、肺泡 动脉血氧分压差〔Ｐ（Ａ－ ａ）Ｏ２ 〕、外周血管阻力指数（ＳＶＲＩ）、肺血管阻力指数（ＰＶＲＩ）和心排指数（ＣＩ）。结果：感染性休克患者入ＩＣＵ 后１ 日内ＭＡＰ和ＣＶＰ分别降低３８．５％ 和４２．８％ （Ｐ均＜ ０．０１）;入ＩＣＵ 后３ 日内ＰａＯ２ 降低３０．６％ ～４３．２％ ,〔Ｐ（Ａ－ ａ） Ｏ２ 〕和Ｏ２ｅｘｔｒ分别升高３８．８％ ～５０．３％ 和８．０％ ～３２．０％ （Ｐ均＜ ０．０１）;入ＩＣＵ 后５ 日内ＣＩ、ＰＶＲＩ、ＭＰＡＰ、ＤＯ２ 、ＶＯ２ 和Ｑｓ／Ｑｔ分别升高１２．０％ ～２２．３％ 、３５．３％ ～５８．２％ 、１７．２％ ～２４．８％ 、１１．９％ ～２０．９％ 、１４．９％     

去甲斑蝥素致大鼠多脏器功能失常综合征的动态观察

目的：探讨多脏器功能失常综合征（ＭＯＤＳ）病程中重要脏器功能的变化以及与氧自由基的关系。方法：用ＳＤ大鼠制作ＭＯＤＳ模型,动态检测脏器功能及血清超氧化物歧化酶（ＳＯＤ）、谷胱甘肽过氧化物酶（ＧＳＨ Ｐｘ）和丙二醛（ＭＤＡ）的变化。结果：血清丙氨酸氨基转移酶（ＡＬＴ）、肌酸激酶及其同工酶（ＣＫ 和ＣＫ ＭＢ）和肌酐（Ｃｒ）均明显升高,其中ＣＫ ＭＢ于１２ 小时明显升高,１８ 小时达到高峰（Ｐ＜ ０．０１）;ＣＫ于１２小时最先达到衰竭标准（Ｐ＜ ０．０１）;ＡＬＴ与Ｃｒ均在２４ 小时后达到衰竭标准（Ｐ＜ ０．０５）。同时ＳＯＤ、ＧＳＨ Ｐｘ活性降低和ＭＤＡ含量增多（Ｐ均＜ ０．０５）。ＭＤＡ与ＣＫ、ＡＬＴ和Ｃｒ之间呈正相关关系,ｒ值分别为０．８４７、０．６３４和０．５６７（Ｐ均＜ ０．０１）。结论：在去甲斑蝥素致大鼠ＭＯＤＳ的病程中,心功能衰竭出现在先,然后为肾和肝功能衰竭。器官功能受损与氧自由基有关。     

多脏器功能失常综合征合并胰腺炎患者肿瘤坏死因子和内皮素的测定及其意义

为探讨多脏器功能失常综合征（ＭＯＤＳ）中胰腺炎与细胞因子、炎性介质的关系。检测了８例由严重创伤并发休克或急性重症感染引起的ＭＯＤＳ患者（Ａ组）、５例ＭＯＤＳ并发胰腺炎患者（Ｂ组）和７例急性水肿型胰腺炎患者（Ｃ组）的肿瘤坏死因子（ＴＮＦ）和内皮素（ＥＴ）水平。发现Ａ组ＴＮＦ、ＥＴ水平明显高于Ｃ组（Ｐ＜０．００１）；Ｂ组ＴＮＦ水平明显高于Ａ组（Ｐ＜０．０５）；ＥＴ水平则呈升高趋势，但无显著统计学意义。提示：ＴＮＦ和ＥＴ的释放增多与ＭＯＤＳ的发病有重要意义；ＴＮＦ、ＥＴ释放的进一步增多（尤其是ＴＮＦ）可能导致更多脏器（包括胰腺）功能的损伤乃至衰竭     

APACHEⅡ评分在危重病患者治疗中的应用及其意义

目的：评价ＡＰＡＣＨＥⅡ评分在国内重症监护病房（ＩＣＵ）的适用性及对多脏器功能失常综合征（ＭＯＤＳ）的预测效果。方法：通过分析ＡＰＡＣＨＥⅡ评分对本组患者预测的校验力和辨析力来明确其适用性。比较ＭＯＤＳ患者预测死亡人数与实际死亡人数来评价其预测效果。结果：回顾性研究５５６例患者，其中ＭＯＤＳ患者７５例。ＬｅｍｅｓｈｏｗＨｏｓｍｅｒ拟合优度检验统计量Ｈ＝３．７８（Ｐ＞０．８０），Ｃ＝２．０２（Ｐ＞０．９８），受试者工作特性曲线下面积０．８６。ＭＯＤＳ患者预计死亡３１．１例，实验死亡５１例（Ｐ＜０．０００１）。结论：ＡＰＡＣＨＥⅡ评分适用于国内危重患者预后的估价，但对于ＭＯＤＳ患者的预测结果明显偏低。     

急性呼吸窘迫综合征患者病死危险因素的调查

目的：调查急性呼吸窘迫综合征（ＡＲＤＳ）的病死率及危险因素。方法：回顾性调查北京协和医院ＩＣＵ１９９１年～１９９６年的２１４例ＡＲＤＳ患者，进行单因素和多因素Ｌｏｇｉｓｔｉｃ回归分析。结果：ＡＲＤＳ总病死率为５１．４０％。以年龄（＞６０岁）、性别（男）、ＡＰＡＣＨＥⅡ评分（＞２０分）对病死率进行调整，调整后６年间病死率均无显著变化。多因素分析显示ＡＲＤＳ病死危险因素有：①肺外器官功能衰竭；②免疫功能低下；③慢性疾病史；④感染性休克；⑤ＡＰＡＣＨＥⅡ评分。未发生肺外器官功能衰竭者全部存活，而发生肺外器官功能衰竭者，病死率５７．２９％，衰竭器官数目越多，病死率越高。机械通气支持技术的进步使ＡＲＤＳ患者死于顽固性低氧血症仅１２．７３％；直接死于感染性休克者占４８．１８％。结论：该院９０年代以来ＡＲＤＳ病死率并未下降；防止全身性感染或创伤发展为感染性休克或多器官衰竭是降低ＡＲＤＳ病死率的关键     

急性出血性脑血管病并发多脏器功能失常综合征患者血浆内皮素-1及降钙素基因相关肽水平的观察

目的：探讨血浆内皮素１（ＥＴ１）和降钙素基因相关肽（ＣＧＲＰ）在急性出血性脑血管病（ＡＨＣＶＤ）并发多脏器功能失常综合征（ＭＯＤＳ）发病中的作用。方法：采用放射免疫法分别测定２１例ＡＨＣＶＤ合并ＭＯＤＳ患者（ＭＯＤＳ组）、２０例ＡＨＣＶＤ患者（ＡＨＣＶＤ组）及３０例正常人（正常对照组）血浆中ＥＴ１和ＣＧＲＰ水平。结果：ＭＯＤＳ组及ＡＨＣＶＤ组血浆ＥＴ１水平明显高于正常对照组（Ｐ均＜０．０１），ＭＯＤＳ组ＥＴ１水平又明显高于ＡＨＣＶＤ组（Ｐ＜０．０１）。ＡＨＣＶＤ组血浆ＣＧＲＰ水平高于正常对照组，但无显著性差异（Ｐ＞０．０５）。而ＭＯＤＳ组血浆ＣＧＲＰ水平明显低于正常对照组，ＥＴ１／ＣＧＲＰ（Ｅ／Ｃ）比值明显高于ＡＨＣＶＤ组及正常对照组（Ｐ均＜０．０１）。结论：血浆ＥＴ１水平升高、ＣＧＲＰ水平降低、Ｅ／Ｃ比值严重失衡与ＭＯＤＳ的发生相关；检测血浆ＥＴ１和ＣＧＲＰ水平对评估ＡＨＣＶＤ患者预后有一定意义     

参麦注射液在腹部外伤低血容量性休克致多脏器功能失常综合征中的防治作用

目的：探讨参麦注射液对腹部外伤并发低血容量性休克所致多脏器功能失常综合征（ＭＯＤＳ）的防治作用。方法：腹部外伤低血容量性休克患者６８例，随机分成２组。对照组３２例，采用手术及综合治疗；治疗组３６例，在手术及综合治疗基础上于休克发生后２４小时内加用参麦注射液静滴，每日１次。观察创伤后不同时间ＭＯＤＳ发生数和死亡数。结果：创伤后３日，治疗组ＭＯＤＳ发生数和死亡数与对照组比较无显著性差异（Ｐ＞０．０５），创伤后第５、７、１１、１５日治疗组的ＭＯＤＳ发生数和死亡数与对照组比较均有显著性差异（Ｐ＜０．０５和Ｐ＜０．０１）。结论：参麦注射液有扩张血管、改善微循环和调节免疫功能的作用。创伤发生后早期连续应用参麦注射液对腹部外伤并发低血容量性休克所致的ＭＯＤＳ具有预防作用。     

Development of multiple organ dysfunction in sepsis

The authors studied bioelectrical millivolt-range potentials (omega potential), followed up the health status by the SAPS II and APACHE III scales and organ dysfunction by the MODS scale in patients with sepsis verified by the classification described by R. C. Bone. It was established that in patients with sepsis from the systemic inflammatory response syndrome (SIRS) to the multiple organ dysfunction syndrome (MODS), three main functional groups could be identified with their characteristic clinical course, the level of a lesion, and estimated mortality. In septic patients, the severest condition was noted in a decompensated state when septic shock developed, which was equal to 83 (79.3/ 83) scores by the SAPS II scale. In the patients whose condition was defined as sepsis and severe sepsis in the presence of a subcompensated state, the severity was equal to 55 (51/56.3) scores by the SAPS II scale. The mildest severity (51 (46.8/53.4) scores characterized the development of SIRS or sepsis in the presence of a compensated state.     

急性中毒伴多器官功能障碍综合征的临床分析

目的:调查急性中毒伴多器官功能障碍综合征(MODS)的发病情况、临床特征和转归。方法:回顾性分析355例急性中毒患者,其中76例伴MODS。结果:76例伴MODS中,死亡17例,病死率22.4％。发生2、3、4、5或5个以上器官功能障碍者病死率分别为3.7％、12.0％、44.4％、83.3％。受累器官个数在死亡组和存活组的比较差异显著(X~2=99.81,P<0.005)。器官功能障碍发生率:脑(97.4％)、呼吸(94.7％)、循环(92.1％)、肝脏(55.3％)、肾脏(52.6％)、胃肠道(42.1％)、血液(31.6％)。各器官衰竭的构成比:呼衰47.1％、心衰29.4％、脑衰17.6％、肾衰5.9％。结论:不同中毒致MODS的病死率不同,且随器官障碍数目的增加而升高;不同中毒致MODS其器官障碍顺序不同,直接死亡原因也不同,这有助于临床医生早期诊断和干预可能发生的器官功能障碍,降低病死率。     

Elevated nucleosome levels in systemic inflammation and sepsis

OBJECTIVE: Multiple organ dysfunction syndrome is a frequent complication of severe sepsis and septic shock and has a high mortality. We hypothesized that extensive apoptosis of cells might constitute the cellular basis for this complication. DESIGN: Retrospective study. SETTING: Medical and surgical wards or intensive care units of two university hospitals. PATIENTS: Fourteen patients with fever, 15 with systemic inflammatory response syndrome, 32 with severe sepsis, and eight with septic shock. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: We assessed circulating levels of nucleosomes, specific markers released by cells during the later stages of apoptosis, with a previously described enzyme-linked immunosorbent assay in these 69 patients with fever, systemic inflammatory response syndrome, severe sepsis, or septic shock. Severity of multiple organ dysfunction syndrome was assessed with sepsis scores, and clinical and laboratory variables. Elevated nucleosome levels were found in 64%, 60%, 94%, and 100% of patients with fever, systemic inflammatory response syndrome, severe sepsis, or septic shock, respectively. These levels were significantly higher in patients with septic shock as compared with patients with severe sepsis, systemic inflammatory response syndrome, or fever, and in nonsurvivors as compared with survivors. In patients with advanced multiple organ dysfunction syndrome, nucleosome levels correlated with cytokine plasma levels as well as with variables predictive for outcome. CONCLUSIONS: Patients with severe sepsis and septic shock have elevated plasma levels of nucleosomes. We suggest that apoptosis, probably resulting from exposure of cells to excessive amounts of inflammatory mediators, might by involved in the pathogenesis of multiple organ dysfunction syndrome.     

Abdominal sepsis: the integral assessment of the severity of patient condition and of multiple organ dysfunction

Results of examinations of 247 patients with diffuse peritonitis and symptoms of abdominal sepsis are analyzed. Systemic inflammatory reaction in peritonitis patients can manifest by sepsis, severe sepsis, and infectious toxic (septic) shock. The severity of systemic inflammatory reaction syndromes can be evaluated by objective scores for evaluation of clinical states (APACHE II, SAPS) and the degree of multiple organ dysfunction/failure (MODS, SOFA). Application of objective scores for evaluation of clinical states provides clinical stratification of abdominal sepsis, helps predict the disease course and outcome, and improve treatment strategy.     

The cytokine storm and factors determining the sequence and severity of organ dysfunction in multiple organ dysfunction syndrome

Multiple organ dysfunction syndrome (MODS) is a major cause of morbidity and mortality in intensive care units. It is being encountered frequently in critically ill patients owing to advancements in organ-specific supportive technologies to survive the acute phase of severe sepsis and shock. It is now believed that MODS is the result of an inappropriate generalized inflammatory response of the host to a variety of acute insults. The pathologic mechanisms of MODS were reviewed, and factors determining the sequence and severity of organ dysfunction were discussed in depth. In the early phase of MODS, circulating cytokines cause universal endothelium injury in organs. In the later phase of MODS, overexpression of inflammatory mediators in the interstitial space of various organs is considered a main mechanism of parenchyma injury. The difference in constitutive expression and the upregulation of adhesion molecules in vascular beds and the density and potency of intrinsic inflammatory cells in different organs are the key factors determining the sequence and severity of organ dysfunction. By activating the intrinsic inflammatory cell in a distant organ, organ dysfunctions are linked in a positive feedback loop through circulating inflammatory mediators. Antagonists targeted at adhesion molecules may alleviate the severity of endothelial damage. And nonsteroidial anti-inflammatory drugs or steroids administered judiciously in the early phase of MODS may retard the progress of multiple organ failure.     

Outcomes of severe sepsis and septic shock patients after stratification by initial lactate value

BACKGROUND: In the setting of severe sepsis and septic shock, mortality increases when lactate levels are ≥ 4 mmol/L. However, the consequences of lower lactate levels in this population are not well understood. The study aimed to determine the in-hospital mortality associated with severe sepsis and septic shock when initial lactate levels are < 4 mmol/L.METHODS: This is a retrospective cohort study of septic patients admitted over a 40-month period. Totally 338 patients were divided into three groups based on initial lactate values. Group 1 had lactate levels < 2 mmol/L; group 2: 2-4 mmol/L; and group 3: ≥ 4 mmol/L. The primary outcome was in-hospital mortality.RESULTS: There were 111 patients in group 1, 96 patients in group 2, and 131 in group 3. The mortality rates were 21.6%, 35.4%, and 51.9% respectively. Univariate analysis revealed the mortality differences to be statistically significant. Multivariate logistic regression demonstrated higher odds of death with higher lactate tier group, however the findings did not reach statistical significance.CONCLUSION: This study found that only assignment to group 3, initial lactic acid level of ≥ 4 mmol/L, was independently associated with increased mortality after correcting for underlying severity of illness and organ dysfunction. However, rising lactate levels in the other two groups were associated with increased severity of illness and were inversely proportional to prognosis.     

The epidemiology of the systemic inflammatory response

Objective: To examine the incidence, risk factors, aetiologies and outcome of the various forms of the septic syndromes (the systemic inflammatory response syndrome [SIRS] sepsis, severe sepsis, and septic shock) and their relationships with infection.¶Design: Review of published cohort studies examining the epidemiology of the septic syndromes, with emphasis on intensive care unit (ICU) patients.¶Results: The prevalence of SIRS is very high, affecting one-third of all in-hospital patients, and > 50 % of all ICU patients; in surgical ICU patients, SIRS occurs in > 80 % patients. Trauma patients are at particularly high risk of SIRS, and most these patients do not have infection documented. The prevalence of infection and bacteraemia increases with the number of SIRS criteria met, and with increasing severity of the septic syndromes. About one-third of patients with SIRS have or evolve to sepsis. Sepsis may occur in approximately 25 % of ICU patients, and bacteraemic sepsis in 10 %. In such patients, sepsis evolves to severe sepsis in > 50 % of cases, whereas evolution to severe sepsis in non-ICU patients is about 25 %. Severe sepsis and septic shock occur in 2 %–3 % of ward patients and 10 %–15 % or more ICU patients, depending on the case-mix; 25 % of patients with severe sepsis have shock. There is a graded severity from SIRS to sepsis, severe sepsis and septic shock, with an associated 28-d mortality of approximately 10 %, 20 %, 20 %–40 %, and 40 %–60 %, respectively. Mortality rates are similar within each stage, whether infection is documented or not, and microbiological characteristics of infection do not substantially influence outcome, although the source of infection does. While about three of four deaths occur during the first months after sepsis, the septic syndromes significantly impact on long-term outcome, with an estimated 50 % reduction of life expectancy over the following five years. The major determinants of outcome, both short-term and long-term, of patients with sepsis are the severity of underlying diseases and comorbidities, the presence of shock and organ failures at onset of sepsis or evolving thereafter. It has been estimated that two-thirds of the overall mortality can be attributed to sepsis.¶Conclusions: The prevalence of sepsis in ICU patients is very high, and most patients have clinically or microbiologically documented infection, except in specific subset of patients. The prognosis of septic syndromes is related to underlying diseases and the severity of the inflammatory response and its sequelae, reflected in shock and organ dysfunction/failures.     

Plasma granulocyte colony-stimulating factor and granulocyte-macrophage colony-stimulating factor levels in critical illness including sepsis and septic shock: relation to disease severity, multiple organ dysfunction, and mortality

OBJECTIVE: To define the circulating levels of granulocyte colony-stimulating factor (G-CSF) and granulocyte-macrophage colony-stimulating factor (GM-CSF) during critical illness and to determine their relationship to the severity of illness as measured by the Acute Physiology and Chronic Health Evaluation (APACHE) II score, the development of multiple organ dysfunction, or mortality. DESIGN: Prospective cohort study. SETTING: University hospital intensive care unit. PATIENTS: A total of 82 critically ill adult patients in four clinically defined groups, namely septic shock (n = 29), sepsis without shock (n = 17), shock without sepsis (n = 22), and nonseptic, nonshock controls (n = 14). INTERVENTIONS: None. MEASUREMENT AND MAIN RESULTS: During day 1 of septic shock, peak plasma levels of G-CSF, interleukin (IL)-6, and leukemia inhibitory factor (LIF), but not GM-CSF, were greater than in sepsis or shock alone (p < .001), and were correlated among themselves (rs = 0.44-0.77; p < .02) and with the APACHE II score (rs = 0.25-0.40; p = .03 to .18). G-CSF, IL-6, and UF, and sepsis, shock, septic shock, and APACHE II scores were strongly associated with organ dysfunction or 5-day mortality by univariate analysis. However, multiple logistic regression analysis showed that only septic shock remained significantly associated with organ dysfunction and only APACHE II scores and shock with 5-day mortality. Similarly, peak G-CSF, IL-6, and LIF were poorly predictive of 30-day mortality. CONCLUSIONS: Plasma levels of G-CSF, IL-6, and LIF are greatly elevated in critical illness, including septic shock, and are correlated with one another and with the severity of illness. However, they are not independently predictive of mortality, or the development of multiple organ dysfunction. GM-CSF was rarely elevated, suggesting different roles for G-CSF and GM-CSF in human septic shock.     

Fluconazole improves survival in septic shock: a randomized double-blind prospective study

OBJECTIVE: To demonstrate whether fluconazole reduces multiple organ failure and mortality in early septic shock (<24 hrs). DESIGN: A prospective randomized double-blind study. SETTING: A medical and surgical adult intensive care unit in a tertiary referral center. PATIENTS: Values were obtained from 71 general adult intensive care unit patients. INTERVENTIONS: During a 2.5-yr period, December 1998-June 2001, 71 patients with septic shock attributed to either nosocomial pneumonia (n = 37) or intra-abdominal sepsis (n = 34) were admitted to our intensive care unit and met the criteria of early septic shock and were entered into this study. All patients were randomized by our clinical pharmacist to receive daily either 200 mg of fluconazole in isotonic saline (fluconazole group = 32) or isotonic saline alone (placebo group = 39) intravenously during the course of their septic shock. MEASUREMENTS AND MAIN RESULTS: All patients were closely monitored with pulmonary artery catheters and parameters to calculate daily organ dysfunction and Acute Physiology and Chronic Health Evaluation II scores. There was a highly significant increase in 30-day survival in the fluconazole-treated patients compared with the placebo patients (78% vs. 46%). However, fluconazole was found to be more effective in patients with septic shock attributed to intra-abdominal sepsis than to nosocomial pneumonia. Increased survival in the intra-abdominal sepsis clinical category was mirrored by a significantly lower number of organ failures in the treated group compared with the placebo group whereas the number of organ failures in the fluconazole group attributed to nosocomial pneumonia were not significantly increased compared with the control group. The septic shock state was considered in all cases to be attributed to bacterial and not to disseminated yeast infection with the exception of one patient in the control group who was admitted with candidemia. The mechanisms by which fluconazole exerts its protective effect against septic shock in patients is far from clear. However, fluconazole has been shown to enhance bactericidal activity of neutrophils and also to inhibit transmigration and adhesion of neutrophils in capillaries of distant organs. CONCLUSIONS: The development of organ failure and mortality in septic shock was significantly reduced by fluconazole given intravenously. The mechanism of action of fluconazole in reducing multiple organ dysfunction in this group of patients may be attributed to the ability of fluconazole to increase recruitment, improve bactericidal activity of neutrophils, and to contain microorganisms locally.     

脓毒性休克的临床流行病学调查——1087例全国多中心临床研究

目的：调查国内多器官功能障碍综合征（multiple organ dysfunction syndrome,MODS）患者脓毒性休克的发生、病死情况。方法：采用多中心、现况调查方法,分析2002年3月—2005年1月全国11省市、37家三级医院1 087例MODS患者的病例情况。结果：1087例患者中,发生脓毒性休克的患者占39.7%,28d住院病死率为60.4%,随着年龄的增长,病死率逐渐上升。结论：脓毒性休克具有较高的病死率。年龄≥55岁、黑便、粪便潜血阳性是MODS患者发生脓毒性休克的主要高危因素,而年龄≥50岁、血pH值〈7.35为MODS合并脓毒性休克的患者死亡的高危因素。