乌司他丁对感染性休克患者影响的临床研究

目的　探讨乌司他丁 (UTI)对感染性休克患者是否有治疗作用。方法　 18例感染性休克的患者入ICU后立即将UTI 2 0万U溶于 2 0mL 0 9%生理盐水中静脉注射 (约 10min) ,分别于静脉注射UTI前后 1h采集血样品 ,并测试TNF -α、IL - 6、IL - 8和MDA的含量以及β -GCD活性和SOD活力。 结果　与治疗前相比 ,UTI治疗后其TNF -α、IL - 6、IL - 8、MDA的含量以及β-GCD活性均下降 (P均 <0 0 1～ 0 0 5 ) ,而SOD活力明显增加 (P <0 0 1)。结论　乌司他丁可通过抑制机体炎性细胞因子TNF -α、IL - 6和IL - 8生成和释放 ,降低β -GCD活性及MDA含量 ,保持SOD活力 ,从而达到对感染性休克的治疗作用。     

乌司他丁治疗感染性休克的临床疗效观察

目的：观察并探讨乌司他丁(UTI)对感染性休克患者的治疗效果。方法：将61例感染性休克患者随机分为治疗组(30例)和对照组(31例)，对照组予扩容、抗感染、血管活性药物应用等常规治疗，治疗组从入ICU后开始在常规治疗基础上加用鸟司他丁10万U+生理盐水100mL，静脉点滴，每8h1次，连续用药7d；检测两组第1、4、7天的血清肿瘤坏死因子(TNF-α)、白细胞介素-1、6(IL-1、IL-6)的浓度，并观察比较发生多器官功能障碍(MODS)的病例数，ICU的住院天数。结果：治疗组的第4、7天所测血TNF-α、IL-1和IL-6值，较对照组明显降低(P<0．05)；UTBI治疗组MODS的发生率、ICU的住院天数均少于对照组(P<0．01)。结论：UTI对感染性休克致炎细胞因子TNF-α、IL-1和IL-6有明显的抑制作用，减轻组织器官损伤，缩短患者在ICU的住院天数。     

乌司他丁联合还原型谷胱甘肽治疗感染性休克的有效性和安全性

目的 探究乌司他丁联合还原型谷胱甘肽治疗感染性休克的有效性和安全性.方法 将100例感染性休克患者根据治疗方案的不同分为对照组(还原型谷胱甘肽)和试验组(乌司他丁联合还原型谷胱甘肽),每组50例.比较两组的治疗效果.结果 试验组的治疗有效率高于对照组,MODS发生率及病死率均低于对照组(P<0.05);两组的不良反应总...     

参麦注射液联合乌司他丁治疗感染性休克患者临床疗效

目的分析参麦注射液联合乌司他丁治疗感染性休克的临床疗效。方法选取我院收治的感染性休克患者63例,分为对照组(31例)和联合组(32例),对照组患者在常规治疗基础上给予乌司他丁治疗,联合组患者在对照组治疗基础上联合参麦注射液治疗。比较两组患者治疗前后临床疗效。结果治疗3d后,联合组患者MAP、CI、SVRI、SvO_2水平均高于对照组(P0.05);联合组患者PCT、TNF-α、IL-6及CRP水平均低于对照组患者(P0.05);治疗1周后,联合组患者CK-MB、cTnI、MYO、NT-ProBNP水平均低于对照组患者(P0.05);两组恶心呕吐发生率和病死率比较无统计学差异(P0.05),联合组MODS发生率低于对照组,差异有统计学意义(P0.05)。结论参麦注射液联合乌司他丁治疗感染性休克疗效明显,可降低心肌损伤和炎症反应,改善血流动力学,且安全性高。     

乌司他丁联合血必净辅助治疗感染性休克的临床观察

目的 探讨乌司他丁联合血必净辅助治疗感染性休克的临床效果及安全性.方法将60例感染性休克患者随机分为观察组和对照组,每组各30例,两组患者均给予常规抗休克治疗,观察组加用乌司他丁联合血必净,观察患者临床症状变化及肝肾功能等.结果 治疗72h后,观察组患者总有效率为93.33%,明显高于对照组的73.33%,差异有统计学意义(P＜0.05);治疗前两组患者血清AST、ALT、Cr、BUN、hs-CRP和乳酸水平比较,差异无统计学意义(P＞0.05),治疗72h后各项指标水平均下降,但是观察组患者下降幅度更大(P＜0.05).结论 乌司他丁联合血必净辅助治疗感染性休克可以显著改善患者的病情,降低炎性反应程度,促进肝肾功能恢复,值得临床推广应用.     

乌司他丁治疗失血性休克鼠的疗效观察

目的：观察乌司他丁治疗大鼠失血性休克的疗效。方法：采用Chaudry方法（略作改动）制作大鼠失血性休克模型，休克60min后用回输血液和生理盐水进行复苏，其中一半则加用乌司他丁治疗。观察复苏前后大鼠的收缩压、舒张压、平均压、心率的变化及光镜下回肠粘膜组织的形态学改变。结果：加用乌司他丁治疗后，失血性休克大鼠的血压、心率得到明显改善，回肠粘膜组织的损伤明显减轻。结论：乌司他丁能够有效的辅助治疗失血性休克。     

甲泼尼龙联合乌司他丁治疗感染性休克的临床疗效

目的：探讨甲泼尼龙联合乌司他丁治疗感染性休克的临床效果。方法：选择2019年11月~2021年5月收治的86例感染性休克患者,采用掷硬币分组法分为对照组及观察组,每组43例。对照组在常规治疗基础上采用甲泼尼龙治疗,观察组在对照组基础上采用乌司他丁治疗,两组均连续治疗7 d。比较两组患者治疗效果、治疗前后病情危重程度[急性生理学及慢性健康状况Ⅱ（APACHEⅡ）评分],记录并比较两组住院时间、住院费用及30 d生存率。结果：观察组治疗效果优于对照组,治疗总有效率较对照组高（P＜0.05）;治疗7 d后,两组APACHEⅡ评分较治疗前降低,且观察组较对照组低（P＜0.05）;观察组住院费用较对照组少,住院时间较对照组短（P＜0.05）,两组30 d生存率对比,差异无统计学意义（P＞0.05）。结论：甲泼尼龙联合乌司他丁治疗感染性休克可提高疗效,减轻病情危重程度,且住院时间短,费用低。     

乌司他丁治疗创伤后急性肺损伤40例临床观察

目的 观察乌司他丁对创伤后急性肺损伤（ALI）患者呼吸功能及预后的影响。方法分别设乌司他丁观察组及对照组各40例，观察治疗前后呼吸频率、氧合指数、PaCO2、胸片变化及预后情况。结果观察组患者呼吸频率、氧合指数、PaCO2、胸片及预后情况均比对照组有显著改善。结论乌司他丁有助于改善ALI患者的呼吸功能及预后。     

乌司他丁通过抑制炎症反应及激活Nrf2/ARE通路提高感染性休克患者临床疗效的研究

目的:探讨乌司他丁对感染性休克患者的保护作用及其作用机制。方法:选择近2年徐州医科大学附属淮安医院ICU收治的40例感染性休克患者,随机分为对照组、观察组,对照组予常规治疗,观察组在常规治疗基础上加用乌司他丁。所有患者入院后第24、72、120小时,分别抽取静脉血,采用酶联免疫吸附法(ELISA)测血清TNF-α、IL-6、NF-E2相关因子2(Nrf2)、血红素加氧酶(HO-1)、超氧化物歧化酶(SOD)、丙二醛(MDA)浓度,并观察两组患者休克改善时间、ICU住院时间。结果:与对照组相比,观察组血清TNF-α、IL-6、MDA浓度明显降低,Nrf2、HO-1、SOD浓度明显升高,休克改善时间提前、ICU住院时间缩短,差异均具有统计学意义(P0.05)。结论:乌司他丁能抑制感染性休克患者的炎症反应,并激活Nrf2/ARE通路,减轻氧化应激反应,从而提高感染性休克患者的临床疗效。     

乌司他丁联合纳洛酮治疗急性心肌梗死合并心源性休克的效果观察

目的 观察乌司他丁联合纳洛酮对急性心肌梗死(AMI)合并心源性休克患者的临床治疗效果.方法 80例AMI合并心源性休克患者随机分为常规治疗组19例、乌司他丁组20例、纳洛酮组21例、乌司他丁联合纳洛酮组20例.检测患者入院及治疗1周后心肌肌钙蛋白I (cTnI)、脑钠肽(BNP)、肿瘤坏死因子-α (TNF-α)、白细胞介素-6(IL-6)的浓度;同时观察休克恢复时间、住院天数及28 d病死率.比较各组患者上述指标间的差异.结果 4组患者治疗后cTnI[常规治疗组(2.06±0.15) ng/L、乌司他丁组(1.59±0.16) ng/L、纳洛酮组(1.97±0.14) ng/L、乌司他丁联合纳洛酮组(1.04±0.17)ng/L]、BNP[常规治疗组(261.07±71.43) ng/L、乌司他丁组(203.46±65.73) ng/L、纳洛酮组(252.96±68.85) ng/L、乌司他丁联合纳洛酮组(143.21±56.94) ng/L]、TNF-α[常规治疗组(31.21±12.32) ng/L、乌司他丁组(20.39±11.08) ng/L、纳洛酮组(28.98±11.76) ng/L、乌司他丁联合纳洛酮组(13.42±8.93)ng/L]、IL-6[常规治疗组(80.46±27.15) ng/L、乌司他丁组(59.84±20.72) ng/L、纳洛酮组(76.15±26.45)ng/L、乌司他丁联合纳洛酮组(37.58±11.14) ng/L]的浓度较治疗前均下降(P均＜0.01),其中乌司他丁联合纳洛酮组各指标下降幅度大于常规治疗组、乌司他丁组和纳洛酮组(P均＜0.01).乌司他丁联合纳洛酮组休克恢复时间(7.16±1.52)d、住院时间(15.03±3.23)d及28 d病死率(41.62％)明显低于乌司他丁组[(8.05±1.81)d、(18.93±3.97)d、50.74％]、纳洛酮组[(8.74±1.98)d、(19.21±3.94)d、52.31％]和常规治疗组[(11.43±2.40)d、(22.64±4.18)d、61.20％],差异均有统计学意义(P均＜0.01).结论 乌司他丁联合纳洛酮能有效减轻AMI合并心源性休克患者的心肌损伤及炎症反应,促进循环功能恢复并改善其预后.     

乌司他丁对脓毒性休克患者细胞因子的影响

目的探讨乌司他丁(UTI)对脓毒性休克患者细胞因子的影响。方法采用前瞻对照研究。78例脓毒性休克患者随机分为对照组和治疗组各39例,两组均行常规抗休克和病因治疗。治疗组用乌司他丁20万U溶于20 ml 0．9%生理盐水中静脉注射,每24 h一次,连续3 d;对照组则以等量生理盐水作为安慰对照。分别于不同时相(静脉注射UTI前、后24 h、48 h和72 h)测试血清肿瘤坏死因子-α(TNF-α)、IL-1、IL-6、IL-8和SOD水平。结果与对照组相比,治疗组应用乌司他丁后不同时相点的TNF-α、IL-1、IL- 6、IL-8均明显降低(P＜0．05,P＜0．01),而SOD显著增加(P＜0．05,P＜0．01)。结论乌司他丁可降低脓毒性休克患者TNF-α、IL-1、IL-6和IL-8的水平并提高SOD活性,从而达到保护器官的作用。     

Steroid therapy of septic shock

Steroid therapy in patients with septic shock has been controversial for decades. Although treatment with high-doses of corticosteroids for patients with septic shock has been shown not to be beneficial, it was believed that therapy with low-doses would be helpful. Recent studies document that steroids are beneficial only in adult septic shock patients whose blood pressure is poorly responsive to fluid resuscitation and vasopressor therapy. For the majority of septic shock patients, corticosteroids should not be used, as the benefit of reversing shock is not worth the complications of superinfection, new sepsis, and septic shock. Finally, steroid therapy should not be guided by corticotropin test results.     

特利加压素在脓毒血症难治性休克中的应用价值

目的旨在探讨特利加压素(Terlipressin)对脓毒血症难治性休克的临床应用价值。方法对12例经多巴胺、去甲肾上腺素治疗无效的脓毒血症休克患者改用特利加压素2μg/(kg·h),并分别观察用药后6、12、24h心率、平均动脉压、休克指数和尿量变化。结果特利加压素使用6h后平均动脉压明显上升、休克指数明显下降,使用12h后心率、尿量明显改善。结论对严重脓毒血症难治性休克,特利加压素具有一定的临床应用价值。     

盐酸戊乙奎醚(长托宁)治疗脓毒性休克的临床研究

目的观察盐酸戊乙奎醚(长托宁)在脓毒性休克治疗中的作用。方法收集40例符合脓毒性休克诊断标准的ICU住院患者,随机分为A,B,C,D四组,分别为654—2组,长托宁2 mg每小时重复一次,长托宁2 mg每6 h重复一次及长托宁6 mg每6 h一次,直至“莨菪化”或末梢开始改善后逐渐减量。观察给药后1 h、6 h、12 h时点患者心率、平均动脉压、瞳孔、末梢转暖时间、脉搏血氧饱和度、神志、肠鸣音及血乳酸含量变化。结果长托宁可明显改善休克患者微循环,给药次数少,几乎不增加心率、不抑制肠蠕动。结论长托宁是脓毒性休克患者较理想的血管活性药。     

早期应用血必净对感染性休克患者血清降钙素原的影响

目的 观察早期加用血必净对感染性休克患者血清降钙素原(PCT)的影响.方法 将65例感染性休克患者按随机数字表分为两组,对照组给予抗生素+早期液体复苏+纠正酸中毒等基础治疗,血必净组在此基础上全程加用血必净注射液50 ml +0.9％氯化钠注射液100 ml静脉滴注,2次/d,共7d.分别于患者进入ICU当天和治疗1、3、5d采集静脉血5ml检测血清C反应蛋白(CRP)和PCT,分别于治疗前和治疗5、7d进行APACHEⅡ评定,观察两组疗效.结果 (1)两组患者入组时基础心率、平均动脉压、PCT、CRP、APACHEⅡ评分等比较差异均无统计学意义(P均＞0.05).(2)与对照组比较,血必净组治疗1 d PCT和CRP差异均无统计学意义(P均＞0.05);治疗3d血必净组PCT和CRP均低于对照组[(12.88±3.76)、(16.96±3.96) μg/L,(80.46±14.97)、(86.57±15.84) mg/L],差异均有统计学意义(P均＜0.05);治疗5d血必净治疗组PCT和CRP均低于对照组[(7.37±2.58)、(12.25±3.32) μg/L,(64.32±11.12)、(72.37±12.42) mg/L],差异均有统计学意义(P均＜0.05).(3)对照组治疗前和治疗5、7d的APACHEⅡ评分分别为(20.48±4.41)、(16.52±3.45)、(12.78±2.91)分,血必净组治疗前和治疗5、7d的APACHEⅡ评分分别为(20.74±4.73)、(12.48±2.76)、(9.24±6.67)分,两组组内不同时间APACHEⅡ评分两两比较差异均有统计学意义(P均＜0.05).(4)治疗7d对照组好转15例,迁延10例,死亡8例,有效率为75.8％(25/33);血必净组好转22例,迁延5例,死亡5例,有效率为84.8％(27/32),两组有效率比较差异有统计学意义(x2=7.27,P=0.03).结论 早期应用血必净能降低感染性休克患者体内的PCT水平,促进患者的转归.     

The pathophysiology of septic shock

Septic shock remains a significant challenge for clinicians. Recent advances in cellular and molecular biology have significantly improved our understanding of its pathogenetic mechanisms. These improvements in understanding should translate to better care and improved outcomes for these patients.     

短程脉冲式高容量血滤治疗感染性休克的临床应用与护理

目的通过对19例感染性休克患者在使用短程脉冲式高容量血液滤过（PHVHF）治疗期间的观察和护理,为此治疗方法提供护理、抗感染等依据。方法对19例需行CRRT治疗的感染性休克患者进行PHVHF6～8h治疗,记录患者的年龄、性别、诊断、APACHEII评分等一般资料,观察治疗前后患者的血流动力学、血管活性药物、氧合、对预后的影响以及在PHVHF操作中出现护理问题进行观察及处理。结果19例患者共行40例次PHVHF,APACHE1I评分为22．4±3．5,预计病死率为（56．2±11．8％）;感染源肺部9例,腹腔6例,胰腺炎3例,1例为骨盆碾压后坏死组织感染,最终病死率52．9％。结论在PHVHF治疗中及治疗后能改善并维持患者的血流动力学及氧合状态,并可减少去甲肾上腺素用量。在PHVHF治疗过程中有针对性的严密监护,并进行精心、细致、周到的护理,对感染性休克预后有重要作用。     

High-volume hemofiltration as salvage therapy in severe hyperdynamic septic shock

Objectives To evaluate the effect of short-term (12-h) high-volume hemofiltration (HVHF) in reversing progressive refractory hypotension and hypoperfusion in patients with severe hyperdynamic septic shock. To evaluate feasibility and tolerance and to compare observed vs. expected hospital mortality.Design and setting Prospective, interventional, nonrandomized study in the surgical-medical intensive care unit of an academic tertiary center.Patients Twenty patients with severe septic shock, previously unresponsive to a multi-intervention approach within a goal-directed, norepinephrine-based algorithm, with increasing norepinephrine (NE) requirements (> 0.3 μg kg^–1 min^–1) and lactic acidosis.Interventions Single session of 12-h HVHF.Measurements and results We measured changes in NE requirements and perfusion parameters every 4 h during HVHF and 6 h thereafter. Eleven patients showed decreased NE requirements and lactate levels (responders). Nine patients did not fulfill these criteria (nonresponders). The NE dose, lactate levels, and heart rates decreased and arterial pH increased significantly in responders. Hospital mortality (40%) was significantly lower than predicted (60%): 67% (6/9) in nonresponders vs. 18% (2/11) in responders. Of 12 survivors 7 required only a single 12-h HVHF session. On logistic regression analysis the only statistically significant predictor of survival was theresponse to HVHF (odds ratio 9).Conclusions A single session of HVHF as salvage therapy in the setting of a goal-directed hemodynamic management algorithm may be beneficial in severe refractory hyperdynamic septic-shock patients. This approach may improve hemodynamics and perfusion parameters, acid-base status, and ultimately hospital survival. Moreover, it is feasible, and safe.Electronic supplementary material The electronic reference of this article is . The online full-text version of this article includes electronic supplementary material. This material is available to authorised users and can be accessed by means of the ESM button beneath the abstract or in the structured full-text article. To cite or link to this article you can use the above reference.     

Inotrope and vasopressor therapy of septic shock

The ultimate goals of hemodynamic therapy in shock are to restore effective tissue perfusion and to normalize cellular metabolism. In sepsis, both global and regional perfusion must be considered. In addition, mediators of sepsis can perturb cellular metabolism, leading to inadequate use of oxygen and other nutrients despite adequate perfusion; one would not expect organ dysfunction mediated by such abnormalities to be corrected by hemodynamic therapy. Despite the complex pathophysiology of sepsis, an underlying approach to its hemodynamic support can be formulated that is particularly pertinent with respect to vasoactive agents. Both arterial pressure and tissue perfusion must be taken into account when choosing therapeutic interventions and the efficacy of hemodynamic therapy should be assessed by monitoring a combination of clinical and hemodynamic parameters. It is relatively easy to raise blood pressure, but somewhat harder to raise cardiac output in septic patients. How to optimize regional blood and microcirculatory blood flow remains uncertain. Specific end points for therapy are debatable and are likely to evolve. Nonetheless, the idea that clinicians should define specific goals and end points, titrate therapies to those end points, and evaluate the results of their interventions on an ongoing basis remains a fundamental principle. The practice parameters were intended to emphasize the importance of such an approach so as to provide a foundation for the rational choice of vasoactive agents in the context of evolving monitoring techniques and therapeutic approaches.     

Terlipressin as a rescue therapy for catecholamine-resistant septic shock in children

Objective To evaluate the effect of terlipressin on oxygenation, PaO₂/FIO₂, heart rate, mean arterial pressure, and mortality in children with septic shock refractory to high doses of dopamine/dobutamine and adrenaline. Design and setting A randomized, nonblind study in the pediatric intensive care unit of a university hospital. Patients and measurements We studied 58 children with septic shock and refractory hypotension despite fluid loading and high doses of catecholamines, randomly enrolled to terlipressin (TP, n = 30) or control (n = 28). TP was administered as intravenous bolus doses of 20 μg/kg every 6 h for a maximum of 96 h. Hemodynamic changes, PaO₂/FIO₂ rates, length of stay, and mortality rate in PICU were recorded prospectively. Results Mean arterial pressure and PaO₂/FIO₂ significantly increased, and heart rate significantly decreased 30 min after each TP treatment, but mortality did not differ from control (67.3% vs. 71.4%). Mean stay in the PICU was shorter in the TP group (13.4 ± 7.9 vs. 20.2 ± 9.7 days and was longer among nonsurvivors of the TP group vs. control (10.4 ± 6.9 vs. 6.2 ± 3.4 days). Blood urea nitrogen, creatinine, AST, ALT, and urine output of patients in the TP group did not change after terlipressin. Conclusions Although terlipressin infusion had no effect on mortality, it significantly increases mean arterial pressure, PaO₂/FIO₂, and survival time in nonsurvivors. Terlipressin seems to cause no adverse effect but warrants further evaluation as a rescue therapy in refractory septic shock.