脓毒性休克早期液体复苏的临床研究

目的:探讨早期液体复苏容量对脓毒性休克的治疗意义。方法:定义正平衡即液体入量大于液体出量,负平衡即液体入量小于液体出量。回顾性分析80例脓毒性休克患者入院后24h和入院后72h液体复苏正平衡组及负平衡组的资料,分析两组间患者的预后。结果:入院后24h内负平衡组,负平衡液体量-218±21.4ml,死亡率显著低于正平衡组,正平衡液体量3206±57.9ml(P<0.01)。入院后72h内负平衡组,负平衡液体量-278±25.9ml,死亡率显著低于正平衡组,正平衡液体量5265±98.7ml(P<0.01)。结论:脓毒性休克患者早期液体复苏容量负平衡可以降低病死率。     

细胞因子、经皮氧分压/吸入氧浓度联合危重评分对脓毒症患者进展为脓毒性休克及预后的预测价值

目的探讨细胞因子、经皮氧分压(TcPO₂)/吸入氧浓度(FiO₂)及危重评分等对脓毒症患者短期进展为脓毒性休克及其28 d预后的预测价值。方法前瞻性选择2018年7月至2018年12月复旦大学附属中山医院急诊科收治的96例脓毒症患者,患者入院时均未休克。记录入院当天首次测定的TcPO₂/FiO₂、细胞因子、炎症标志物、肾功能、血乳酸等炎症及灌注相关指标;记录患者入院时急性生理学与慢性健康状况评分系统Ⅱ(APACHEⅡ)评分和序贯性器官功能衰竭评估(SOFA)评分。根据入院后7 d内是否进展为脓毒性休克分为休克组(n=14)和非休克组(n=82)。根据入院后28 d内是否死亡分为生存组(n=63)和死亡组(n=33)。采用logistic回归分析筛查脓毒症患者短期内进展为脓毒性休克和28 d内预后的危险因素,并采用受试者工作特征(ROC)曲线分析相关指标对脓毒症患者进展为脓毒性休克及28 d预后的预测价值。结果脓毒性休克组患者血白细胞计数、白介素(IL)-6、IL-8、IL-10、乳酸、血肌酐、TcP...     

液体复苏对创伤致严重脓毒症和脓毒性休克患者心肌损伤的影响

目的 观察液体复苏对创伤致严重脓毒症和脓毒性休克患者心肌损伤的影响,以及心肌损伤标志物对液体复苏的指导作用.方法 78例复合伤致严重脓毒症和脓毒性休克患者,急性生理学与慢性健康状况评分系统Ⅱ(APACHEⅡ)评分18 ～ 35分;记录治疗前及治疗3d、5d血清心肌肌钙蛋白Ⅰ(cTnI)、N末端-心室利钠肽前体(NT-proBNP)及血流动力学参数,并进行相关性分析.结果 62.8％(49/78)的严重脓毒症和脓毒性休克患者出现血清cTnI升高,73.5％(36/49)升高值大于界限值的2倍以上,30.6％( 15/49)超过界限值的4倍以上.入院时血清NT-proBNP升高者占46.2％(36/78),经液体复苏后继续升高者达74.4％(58/78).存活组(55例)治疗后血清cTnI、NT-proBNP、肺动脉楔压(PAWP)及心排血指数(CI)均明显改善;死亡组(23例)各指标无明显变化,且死亡组血清cTnI(μg/L)和NT-proBNP(ng/L)水平显著高于存活组(cTnI 3 d:2.09±1.00比1.57±0.93,5 d:1.78±0.67比0.72±0.51;NT-proBNP 3 d:3.52±0.73比3.16±0.65,5 d:3.21±0.66比2.66±0.58),CI( ml· s-1· m-2)明显低于存活组(3 d:57.6±6.2比68.3±5.6,5 d:40.5±4.7比80.7±6.8,均P＜0.05).46例液体复苏达目标值的患者cTnI水平(μg/L)低于32例未达标者(1.16±0.62比1.97±0.76,P＜0.05),且CI(ml ·s-1 ·m-2)明显增加(61.2±6.4比49.3±6.1,P＜0.05),液体复苏是否达到目标值与血清NT-proBNP、PAWP无关.血清cTnI与NT-proBNP呈正相关(r=0.865,Y=2.069+ 0.695X,P＜0.01),NT-proBNP与PAWP呈正相关(r=0.762,Y=1.125+ 4.929X,P＜0.01),cTnI与CI呈负相关(r=-0.891,Y=50.623 -6.114X,P＜0.01).结论 创伤致严重脓毒症和脓毒性休克患者有明显的心肌损伤,液体复苏可改善心肌损伤;血清cTnI和NT-proBNP与患者预后有关,NT-proBNP用于指导液体复苏的意义尚不能确定.     

PCT与NT-proBNP在老年脓毒症及脓毒性休克预后评估中的应用

目的探讨降钙素原(PCT)与N末端B型利钠肽原(NT-proBNP)在老年严重脓毒症和脓毒性休克患者的病情和预后评估中的作用。方法选择我院住院治疗的老年严重脓毒症和脓毒性休克患者96例,入院后予PCT、NT-proBNP和心脏超声等检查,并予急性生理学及慢性健康状况评分系统(APACHEⅡ)评分。比较死亡组和存活组、严重脓毒症组和脓毒性休克组PCT、NT-proBNP和APACHEⅡ评分,分析NT-proBNP与左室射血分数(LVEF)的相关性。结果死亡组PCT、NT-proBNP和APACHEⅡ评分均大于存活组,差异有统计学意义(P<0.05);严重脓毒症组PCT、NT-proBNP和APACHEⅡ评分均小于脓毒性休克组,差异有统计学意义(P<0.05),NT-proBNP与LVEF呈负相关(r=-0.64,P<0.05)。结论 PCT和NT-proBNP能有效评估老年严重脓毒症和脓毒性休克的预后和病情,PCT和NT-proBNP升高提示预后不良。     

suPAR及PCT对脓毒症患者病情严重程度及预后的评判价值

目的 探讨血浆可溶性尿激酶型纤溶酶原激活物受体(suPAR)及降钙素原(PCT)对脓毒症患者病情严重程度及预后的评判价值.方法 采用前瞻性研究方法,将上海交通大学附属新华医院收治的77例脓毒症患者按照病情严重程度分为脓毒症组、严重脓毒症组和脓毒性休克组,测定患者入院后24 h内PCT、suPAR水平,并进行APACHEⅡ评分及SOFA评分,比较suPAR、PCT和APACHEⅡ、SOFA评分的差异.后再根据28 d的结局比较suPAR、PCT和APACHEⅡ、SOFA评分的差异.结果 脓毒症组患者血浆suPAR为(7.9 ±6.5) ng/mL,低于严重脓毒症组[(8.4±4.5) ng/mL]和脓毒性休克组[(13.9±8.0) ng/mL],但脓毒症组和严重脓毒症组之间的差异没有统计学意义,而严重脓毒症组低于脓毒性休克组,差异具有统计学意义.脓毒症组患者血浆PCT为(6.3±3.5) ng/mL,低于严重脓毒症组[(23.7±3.9) ng/mL]和脓毒性休克组[(25.7±4.3) ng/mL],差异具有统计学意义,但是严重脓毒症组和脓毒性休克组之间的差异无统计学意义.死亡组患者血浆suPAR水平及APACHEⅡ、SOFA评分高于生存组,差异具有统计学意义,而PCT水平在生存组和死亡组之间的差异没有统计学意义.根据受试者工作特征曲线(ROC曲线)分析,PCT的ROC曲线下面积(AUC)为0.61 (P ＞0.05),suPAR的AUC为0.803 (P＜0.05),APACHEⅡ评分的AUC为0.832 (P ＜0.05),SOFA评分的AUC为0.767 (P ＜0.05).其截断值suPAR为9.905 ng/mL.结论 监测脓毒症患者入院当天血浆suPAR及APACHEⅡ评分有助于早期对脓毒症患者进行预后评估和病情严重程度的判断.     

英国国家早期预警评分对急诊老年严重脓毒症及脓毒症休克患者预后的评估价值

目的探讨英国国家早期预警评分(NEWS)对急诊老年严重脓毒症及脓毒性休克患者病情及预后的评估。方法收集首都医科大学宣武医院急诊老年严重脓毒症和脓毒性休克患者116例,就诊后采集患者的常规生理生化指标,并行NEWS评分,APACHEⅡ评分和SOFA评分,随访28 d,根据患者预后分为死亡组和存活组,分别比较死亡组和存活组NEWS评分,APACHEⅡ评分及SOFA评分区别;比较脓毒性休克和严重脓毒症组的NEWS评分,APACHEⅡ评分及SOFA评分的区别;NEWS评分与APACHEⅡ评分。SOFA评分的相关性分析;通过分析ROC曲线下面积(AUC)确定NEWS评分对老年严重脓毒症和脓毒性休克患者预后的评估价值。结果脓毒性休克组患者NEWS评分;APACHEII评分和SOFA评分大于严重脓毒症组;死亡组NEWS评分;APACHEII评分和SOFA评分均显著大于存活组(P<0.05);NEWS评分水平与APACHEⅡ评分。SOFA评分具有显著相关性(r=0.807、0.883,P<0.05),NEWS评分;APACHEII评分和SOFA评分预测死亡ROC曲线下面积分别为0.870、880、0.865(P>0.05)。结论 NEWS评分对急诊老年严重脓毒症和脓毒性休克患者的病情和预后具有重要的评估价值,评分愈高提示患者预后愈差。     

降钙素原和乳酸动态变化对急诊老年严重脓毒症和脓毒性休克患者预后的评估价值

目的研究血浆降钙素原(Procalcitonin,PCT)和动脉血乳酸动态变化情况对老年严重脓毒症及脓毒性休克患者病情和预后的评估作用。方法收集首都医科大学宣武医院急诊监护室老年严重脓毒症和脓毒性休克患者163例,入院后给予PCT和动脉血乳酸等检查,并给与APACHEⅡ评分(Acute Physiology and Chronic Health EvaluationⅡ)。入院后6h复查血乳酸,5d复查PCT,随访28d根据预后患者分为死亡组和存活组,分别比较死亡组和存活组PCT和乳酸区别和2组乳酸和PCT的变化情况;比较脓毒性休克和严重脓毒症组的PCT,乳酸和APACHEⅡ评分的区别;用ROC曲线下面积(AUC)分析PCT和动脉血乳酸预测老年严重脓毒症和脓毒性休克患者死亡的价值。结果脓毒性休克组患者PCT、乳酸和APACHE II评分大于严重脓毒症组;死亡组PCT和乳酸均大于存活组(P0.05),6h乳酸和5d的PCT的差别更明显,死亡组乳酸和PCT前后比较无显著性差异(P0.05),存活组乳酸和PCT较前明显下降(P0.01);PCT预测死亡ROC曲线下面积为0.803,动脉血乳酸曲线下面积为0.796,两者比较无统计学差异(P0.05)。结论 PCT和动脉血乳酸对急诊老年严重脓毒症和脓毒性休克患者的病情和预后具有重要的评估价值,PCT和乳酸含量持续保持高水平的提示预后差。     

严重脓毒症和脓毒性休克患者复苏治疗与血糖控制的非线性相关分析研究

目的 研究严重脓毒症和脓毒性休克患者复苏治疗与应用胰岛素强化治疗应激性高血糖之间的关系,探讨非线性观点在脓毒症患者治疗中的价值.方法 回顾性分析129例严重脓毒症和脓毒性休克患者的住院资料,根据充分复苏标准完成所需时间(每6 h一组)分为8组,采用非线性最小二乘法比较各复苏组充分复苏完成所需时问与单位时间胰岛素用量之间的关系.结果 各复苏组充分复苏完成所需时间与单位时间胰岛素用量之间存在指数回归关系,指数曲线方程(^y)=e0.7393-0.0152x(a=0.739 3,b=0.015 2),且拟合度甚佳(R2=0.976 943 6).结论 在严重脓毒症和脓毒性休克患者的治疗过程中,复苏治疗完成的时问与机体紊乱的内分泌系统恢复有密切的关系,符合非线性观点.因此治疗上重在帮助机体重建已紊乱的网络,恢复其正常的生理谐振;而不仅仅是给予受损器官充分的支持和修复.     

严重脓毒症和脓毒性休克患者复苏治疗与血糖控制的非线性相关分析研究

目的 研究严重脓毒症和脓毒性休克患者复苏治疗与应用胰岛素强化治疗应激性高血糖之间的关系,探讨非线性观点在脓毒症患者治疗中的价值.方法 回顾性分析129例严重脓毒症和脓毒性休克患者的住院资料,根据充分复苏标准完成所需时间(每6 h一组)分为8组,采用非线性最小二乘法比较各复苏组充分复苏完成所需时问与单位时间胰岛素用量之间的关系.结果 各复苏组充分复苏完成所需时间与单位时间胰岛素用量之间存在指数回归关系,指数曲线方程(^y)=e0.7393-0.0152x(a=0.739 3,b=0.015 2),且拟合度甚佳(R2=0.976 943 6).结论 在严重脓毒症和脓毒性休克患者的治疗过程中,复苏治疗完成的时问与机体紊乱的内分泌系统恢复有密切的关系,符合非线性观点.因此治疗上重在帮助机体重建已紊乱的网络,恢复其正常的生理谐振;而不仅仅是给予受损器官充分的支持和修复.     

严重脓毒症和脓毒性休克患者复苏治疗与血糖控制的非线性相关分析研究

目的 研究严重脓毒症和脓毒性休克患者复苏治疗与应用胰岛素强化治疗应激性高血糖之间的关系,探讨非线性观点在脓毒症患者治疗中的价值.方法 回顾性分析129例严重脓毒症和脓毒性休克患者的住院资料,根据充分复苏标准完成所需时间(每6 h一组)分为8组,采用非线性最小二乘法比较各复苏组充分复苏完成所需时问与单位时间胰岛素用量之间的关系.结果 各复苏组充分复苏完成所需时间与单位时间胰岛素用量之间存在指数回归关系,指数曲线方程(^y)=e0.7393-0.0152x(a=0.739 3,b=0.015 2),且拟合度甚佳(R2=0.976 943 6).结论 在严重脓毒症和脓毒性休克患者的治疗过程中,复苏治疗完成的时问与机体紊乱的内分泌系统恢复有密切的关系,符合非线性观点.因此治疗上重在帮助机体重建已紊乱的网络,恢复其正常的生理谐振;而不仅仅是给予受损器官充分的支持和修复.     

Hemorrhagic shock in the dog

A prerequisite elucidating the pathomechanism of hemorrhagic shock are reproducible experimental models, leading to a predictable outcome. Two concepts have been reported to be a good predictor for the outcome both employing a fixed hypotension level: total oxygen deficit and shed blood volume uptake. To correlate these two models we subjected 31 dogs to a standardized hemorrhagic shock procedure. Besides determination of acid-base status, hematocrit, mean arterial pressure, and cardiac output, these two parameters were measured continuously. Seventeen dogs survived the shock procedure, 14 died within 24 h. During shock, neither oxygen deficit nor any other parameter mentioned above correlated with the final outcome of the shock state. The only significant difference between surviving and non-surviving animals during this period was the amount of uptake. The non-surviving dogs exhibited a higher uptake volume, indicating an incipient collapse of the microcirculation. Terminating the duration of hypotension at an uptake volume of 5% of the maximum shed blood, all animals survived, while after an uptake volume of 15% about 50% of the dogs died. Using uptake volumes of various degrees in a hemorrhagic shock model as the endpoint of the hypotensive stress, it seems possible to produce reliable survival rates.     

Hemorrhagic shock in the dog

Oxygen consumption, hemodynamics, and regional blood flow (with the radioactive microspheres technique) were determined in 12 anesthetized dogs subjected to hemorrhagic shock. The animals were kept in hypotension at 40 mmHg, until 15% of the maximum shed blood had been infused to keep arterial pressure stable, whereafter all the shed blood was retransfused. Cardiac output (CO) decreased to 33% and 25% of preshock values in survivors (S) and nonsurvivors (NS), respectively, and after retransfusion it was significantly higher in S. After retransfusion, NS showed a higher arterial pCO2 than S adding a respiratory component to the metabolic acidosis that occurred during and after hemorrhage. Blood flow to the brain was not impeded during shock, but as CO decreased the fraction delivered to the brain was increased 2.6-3.3-fold. Myocardial blood flow decreased to about 28% of preshock values immediately after hemorrhage, and increased to about 54% at the end of hemorrhage. After retransfusion S had a higher myocardial flow than NS. The flow to the gut paralleled the decrease in CO during hemorrhage and immediately after retransfusion NS exhibited an overperfusion in ileum and colon compared to the preshock values. Kidney blood flow fell progressively during the course of hypotension, similarly in S and NS. After retransfusion it was normalized in S but not in NS. The preshock flow to pancreas was significantly higher in S than in NS, but during and after shock the blood flow did not differ between S and NS.     

Problems in the treatment of septic shock

A small review is presented on the problems encountered in the treatment of septic shock. The discussion is focussed on haemodynamic problems. At least three and possibly four haemodynamic mechanisms seem to be involved: peripheral pooling, increased vascular permeability, myocardial failure (right and/or left heart failure) and probably peripheral vascular failure. A method is indicated to study some of these mechanisms.     

Considerations in the therapy of septic shock

In summary, gram-negative sepsis is unique among infectious illnesses in that it is a disorder that recruits endogenous physiologic processes to mediate tissue injury. This host damage frequently occurs in the absence of microbial invasion of affected organs. The resultant hypotension, coagulation defects, and organ dysfunction may be associated with serious morbidity or may contribute to mortality. Ultimately, however, mortality in patients with septic shock depends on the nature of the infectious process and the severity of the underlying illnesses. Unfortunately, attempts to aggressively treat septic patients with a formidable array of antimicrobial and pharmaceutical agents have not remarkably reduced mortality. Nor does it seem likely that future elucidation of the inflammatory mechanisms of sepsis will lead to the generation of therapeutic agents that will significantly improve survival. On the other hand, prophylactic or therapeutic modalities that deter colonization or invasion by pathogenetic organisms or that alter the ability of pathogens to evoke adverse host responses may be more likely to impact on the incidence and morbidity of gram-negative bacillary infections. Until modifications in the initial interactions of gram-negative pathogens with human hosts can be realized, the mortality of gram-negative sepsis is likely to remain high.     

Reality shock in the nurse educator

The nurse educator, as with many other nursing roles, is a prime target for reality shock. The nurse educator who is aware of reality shock and the possible ways it may be exhibited in her current position, can also identify strategies to assist her through this transition. Graduate schools and universities hiring new clinical instructors and nurse educators can work together to alleviate this problem. The goal of this article is to make nurse educators, graduate schools, and universities hiring neophyte instructors aware of reality shock and to assist in this transitional period. Preliminary exposure of graduate students to stresses they may be experiencing during the early years as a clinical instructor, may assist universities assigning a mentor for the new clinical instructor, so she can have a consistent, nonthreatening source of feedback. Discussing these new feelings and being reassured they are normal, may serve as a preventive measure for developing reality shock. And lastly, the nurse educator has to realize that along with the exhilaration of finally holding a faculty position, comes change and new challenges which she must accept. As the neophyte becomes seasoned, these triumphant challenges will become a part of the position she has struggled for and deserves.     

Septic shock in the oncology patient

Septic shock is an infrequent but not uncommon oncologic emergency. An understanding of the risk factors, pathophysiology, and current issues in the management of septic shock can contribute to better patient care through early recognition and prompt and knowledgeable intervention. This article reviews the epidemiology, predisposing risk factors, causative organisms, and pathophysiology of septic shock. Medical and nursing interventions illustrate the necessary teamwork involved in managing this life-threatening problem. Investigational approaches are discussed as well as the importance of identifying at-risk patients and initiating preventative measures.     

Age shock index,shock index,and modified shock index for predicting postintubation hypotension in the emergency department

IntroductionHypotension after emergent ETI is a relatively common complication during and after emergency airway management. We aimed to evaluate SI, MSI, and age SI to predict PIH in patients who presented to the emergency department. Moreover, which factors would be better for predicting the event or similar to the others.MethodsA retrospective, standardized chart review of consecutive ED patients requiring intubation at an urban, tertiary-care teaching hospital, from January 2011 to December 2016. PIH was defined as any recorded SBP <90 mmHg or MAP <65 mmHg within the 60-minute period after intubation.ResultsHypotension after emergent ETI was observed in 130 (29.7%) patients. The ROC-AUC of age SI, MSI, and SI before intubation for prediction of PIH were 0.676 (95% CI 0.63–0.72), 0.614 (95% CI 0.567–0.66), and 0.611 (95% CI 0.564–0.657). The prognostic performance of age SI for prediction of PIH was better than MSI and SI (p = 0.006 for age SI versus MSI, p = 0.005 for age SI versus SI).ConclusionsPreintubation age SI, MSI, and SI are all independent predictors of PIH in patients who need emergent intubation. Aong these parameters, age SI is the best marker to predict the outcome. Calculation of these indexes are simple and could be an guide of implement to prevent hypotension after ETI.