感染性休克液体复苏治疗

脓毒症,尤其合并感染性休克时,是引起多器官功能衰竭的重要原因之一。早期恰当处理是降低脓毒症和感染性休克病人病死率的关键。在2016版国际脓毒症和感染性休克管理指南中,感染性休克的定义更新为脓毒症状态下经过充分液体复苏仍不能纠正的组织低灌注和低血压,通常指血乳酸>2mmol/L和平均动脉压<65mmHg(1mmHg=0.133 kPa)。     

感染性休克液体复苏策略

感染性休克的病死率为30%～60%,位列ICU致死病因第10位,感染性休克治疗中液体复苏一直被作为最基本、最重要的原则,早期液体复苏是治疗感染性休克重要内容之一。     

液体复苏对感染性休克患者继发肺水肿的影响

背景 有效循环血量减少是休克的核心病理生理过程,这也决定了液体复苏在休克治疗中的重要地位.但液体复苏在恢复有效循环血量同时可能会导致肺水肿加重,往往使休克的治疗面临进退两难的窘境.目的 现就感染性休克患者易发肺水肿的机制,如何针对感染性休克的病理生理过程制定液体复苏策略进行综述.内容 感染性休克患者易发肺水肿,液体复苏...     

液体复苏对感染性休克患者继发肺水肿的影响

背景 有效循环血量减少是休克的核心病理生理过程,这也决定了液体复苏在休克治疗中的重要地位.但液体复苏在恢复有效循环血量同时可能会导致肺水肿加重,往往使休克的治疗面临进退两难的窘境.目的 现就感染性休克患者易发肺水肿的机制,如何针对感染性休克的病理生理过程制定液体复苏策略进行综述.内容 感染性休克患者易发肺水肿,液体复苏可能加重肺水肿,需要根据休克不同时期的病理生理特征实施不同的液体管理策略.趋向 根据休克不同时期的病理生理特征实施不同的液体管理策略.     

感染性休克液体复苏研究进展

感染性休克是指由病原微生物及其毒素在人体内引起的一种微循环障碍状态，致组织缺氧、代谢紊乱、细胞损害甚至多器官功能衰竭，病死率极高。在休克的病理生理学分类它归在容量分布异常性休克，国外通常用severe sepsis和septic shock来描述它。严重的感染病人往往经过积极液体复苏后仍然存在着无法解释的急性循环衰竭的表现。     

早期液体复苏综合疗法治疗感染性休克的临床观察

目的 评价以早期液体复苏为中心的综合疗法治疗感染性休克的临床效果.方法 将282例感染性休克患者分为早期复苏组(n=177)和常规治疗组(n=105),同时根据治疗开始时患者脏器功能受损程度分为轻度、中度和重度,分别比较两组患者治疗前后的APACHE Ⅱ评分以及病死率.结果 轻度脏器功能受损早期复苏组患者治疗后24 h的APACHE Ⅱ评分和病死率明显低于常规治疗组(P<0.01),而在中度和重度水平上两组差异无统计学意义.结论 早期液体复苏能较显著地改善早期感染性休克患者的生存和预后情况.     

早期液体复苏对感染性休克患者血流动力学的影响

目的 分析早期液体复苏对感染性休克患者血流动力学的影响。方法 选取2011年1月至2012年4月我院ICU收治的26例感染性休克患者作为研究对象,随机分为对照组和试验组,各13例。两组患者均采用PICCO监测,并根据早期复苏目标导向疗法（early goal directed therapy,EGDT）进行早期液体复苏治疗。对照组和试验组复苏液分别为林格液和6%羟乙基淀粉130/0.4氯化钠溶液。分别于复苏开始时（0 h）、8 h和24 h收集患者的血流动力学参数。结果 试验组和对照组的CVP、CI、ITBVI及GEDVI水平均随着时间的增加上升（P＜0.05）,但EVLWI在对照组明显增加（P＜0.05）,而试验组无明显变化。除试验组EVLWI外,与开始复苏（0 h）相比较,试验组和对照组的CVP、CI、ITBVI、GEDVI及对照组的EVLWI与开始复苏（0 h）相比较均有明显差异（P＜0.05）。经重复测量资料的方差分析发现,试验组CVP和GEDVI较对照组上升水平明显,对照组EVLWI较试验组上升水平明显,差异均具有统计学意义（P＜0.05）。结论 感染性休克患者根据EGDT方案使用6%羟乙基淀粉130/0.4氯化钠溶液进行复苏,能更好地改善患者的血流动力学指标。     

感染性休克复苏液体的选择和指导液体治疗的监测指标

感染性休克被2012年的脓毒症治疗指南定义为适当补液治疗仍未能纠正的持续性脓毒症引起的低血压。尽管随着医疗水平的飞速发展,不断完善诊断技术和治疗方法使感染性休克的预后及死亡率有所改善,但高达40%~50%的死亡率仍旧严重威胁着全球人类健康。因此,用于治疗感染性休克患者的液体复苏疗法,不仅本身有着举足轻重的地位,而伴随在整个液体治疗过程中的每一环节也十分重要。     

临床路径对感染性休克患者心肺复苏效果影响的研究

目的探讨临床路径对感染性休克患者心肺复苏效果的影响,为心跳呼吸骤停患者复苏提供一定的临床依据。方法选择2011至2013年于本院实施救治的感染性休克所致心脏骤停的患者共90例为研究对象,其中对照组30例,实施常规救治,观察组60例,实施临床路径救治;比较两组患者的救治程序,包括基础生命支持复苏程序（BLS）和高级生命支持复苏程序（ALS）,以及救治疗效。结果两种复苏方法全部进行胸外按压,差异无统计学意义,其中实施人工呼吸常规方法者27例,占90.0%,临床路径全部实施,差异具有统计学意义（χ^2=4.143,P=0.043）,实施开放通道和置口咽管临床路径均显著高于常规复苏方法,差异具有统计学意义（χ^2=17.244、54.784,P=0.000、0.000）;常规方法对伴有急性肾功能衰竭、急性心功能不全、急性肺功能衰竭及其他疾病患者成功的例数分别为1、1、0和1例,临床路径成功复苏的例数为12、5、2和2例;对治疗伴有急性肾功能衰竭方面,两种方法疗效差异具有统计学意义（χ^2=5.121,P=0.027）;两种方法在伴有急性心功能不全及急性肺功能衰竭方面,具有显著性统计学意义（χ^2=12.070、11.224,P=0.001、0.001）,其他疾病复苏成功率一致;两种方法在立即复苏、5 min以内及5～8 min以内复苏方面比较差异具有统计学意义（χ^2=24.982、10.244、6.772,P=0.000、0.002、0.009）,8 min以上成功率一致,均无复苏成功者。结论按临床路径实施救治能显著提高感染性休克所致心脏骤停的患者复苏成功率。     

限制性与充分性液体复苏治疗失血性休克患者的效果观察

目的探讨限制性与充分性液体复苏治疗失血性休克的效果。方法将90例失血性休克患者随机分为两组,A组(46例)采用充分性液体复苏治疗。B组(44例)采用限制性液体复苏治疗,比较两组红细胞压积、血清乳酸水平、血气剩余碱值,并记录两组患者输液量及失血量。结果两组患者治疗前后红细胞压积、血清乳酸水平及血气剩余碱值等各项指标比较差异有统计学意义(P<0.05);患者均在30~60 min内止血,A组输液量及失血量均多于B组,两组比较,差异有统计学意义(P<0.05);B组病死率(11.36%)低于A组(19.56%)但两组比较,差异无有统计学意义(P>0.05)。结论限制性液体复苏比充分性液体复苏治疗失血性休克患者更具优势,在维持组织灌注压的基础上,可避免对正常内环境及代偿机制的干扰,值得在临床上推广应用。     

Direct peritoneal resuscitation as adjunct to conventional resuscitation from hemorrhagic shock: a better outcome

BACKGROUND: Conventional resuscitation (CR) from hemorrhagic shock often culminates in multisystem organ failure and death, commonly attributed to a progressive splanchnic vasoconstriction and hypoperfusion, a gut-derived systemic inflammatory response (SIR), and fluid sequestration. Direct peritoneal resuscitation (DPR) produces a sustained state of tissue hyperperfusion in splanchnic and distant organs. In this study we evaluated the therapeutic potential of DPR on the SIR and fluid sequestration as parameters of treatment outcome. METHODS: Anesthetized nonheparinized rats continuously monitored for hemodynamics were bled to 40% of mean arterial pressure for 60 minutes. Animals were randomized for CR or CR plus DPR under aseptic conditions. Sham nonhemorrhaged rats served as control. Qualitatively, animals were blindly observed for body weight, illness score, or death for 72 hours. Tissues were harvested from survivors, and SIR was measured by interleukin (IL)-6, IL-10, tumor necrosis factor-alpha, and enzyme-linked immunosorbent assay, and fluid sequestration was measured by dry weight/wet weight ratio (DW/WW). RESULTS: Adjunct DPR caused a marked increase (P >.01 by analysis of variance) in the immunoregulator IL-10 in the liver (10,990 +/- 1,470 pg/g) and gut (1815 +/- 640 pg/g), compared to CR rats (6450 +/- 1000 pg/g and 1555 +/- 590, respectively), which is associated with down-regulation of IL-6 and tumor necrosis factor-alpha in liver and gut, from 57 +/- 4 and 20 +/- 3 pg/g, respectively, to 42 +/- 4 and 9 +/- 2 pg/g in DPR-treated animals. CR animals had a lower DW/WW ratio in liver (-36%), spleen (-22%), and lung (-24%) compared to DPR (P <.05), where the DW/WW ratio did not differ from control animals. This fluid sequestration is consistent with a 12% and 5% gain in prehemorrhage body weight at 24 and 72 hours after treatment in the CR animals. Thirty percent of CR animals died within 24 hours, and survivors were squeaking, cold, and pale in eyes and ears and oliguric despite features of fluid overload. In comparison, DPR animals exhibited normal appearance by 24 hours and demonstrated a 100% survival at 72 hours. CONCLUSIONS: This study demonstrates that DPR as adjunct to CR has beneficial effects on the pathophysiology of resuscitated hemorrhagic shock. In addition to restoration of tissue perfusion, DPR has immunomodulation and anti-fluid sequestration effects. These modulations result in improved outcome.     

Therapeutic effect of cisapride on gastric injury following hemorrhagic shock resuscitation in rats

Whenshockandtraumaoccur, stomachisoneofthetargetorganswhichcaneasilybeharmed,1acutegastricmucosalesionisalatentandfatalthreattothoseclinicalcriticallyillpatients.Aresearchshowsthattreatmentofgastricmotilityishelpfultoreducedeathrateofcriticallyillpatients…     

Direct peritoneal resuscitation from hemorrhagic shock: effect of time delay in therapy initiation

BACKGROUND: After conventional resuscitation from hemorrhagic shock, splanchnic microvessels progressively constrict, leading to impairment of blood flow. This occurs despite restoration and maintenance of central hemodynamics. The authors' recent studies have demonstrated that topical and continuous ex vivo exposure of the gut microvasculature to a glucose-based clinical peritoneal dialysis solution (Delflex), as a technique of direct peritoneal resuscitation (DPR), can prevent these postresuscitation events when initiated simultaneously with conventional resuscitation. This study aimed to determine whether DPR applied after conventional resuscitation reverses the established postresuscitation intestinal vasoconstriction and hypoperfusion. METHODS: Male Sprague-Dawley rats were bled to 50% of baseline mean arterial pressure and resuscitated intravenously over 30 minutes with the shed blood returned plus two times the shed blood volume of saline. Initiation of ex vivo, topical DPR was delayed to 2 hours (group 1, n = 8), or to 4 hours (group 2, n = 8), respectively, after conventional resuscitation. Intravital microscopy and Doppler velocimetry were used to measure terminal ileal microvascular diameters of inflow A1 and premucosal A3 (proximal pA3, distal dA3) arterioles and blood flow in the A1 arteriole, respectively. Maximum arteriolar dilation capacity was obtained from the topical application, in the tissue bath, of the endothelium-independent nitric oxide-donor sodium nitroprusside (10M). RESULTS: Hemorrhagic shock caused a selective vasoconstriction of A1 (-24.1% +/- 2.15%) arterioles from baseline, which was not seen in A3 vessels. This caused A1 blood flow to drop by -68.6% of the prehemorrhage value. Conventional resuscitation restored and maintained hemodynamics in all the animals without additional fluid therapy. In contrast, there was a generalized and progressive postresuscitation vasoconstriction of A1 (-21.7%), pA3 (-18.5%), and dA3 (-18.7%) vessels. The average postresuscitation A1 blood flow was -49.5% of the prehemorrhage value, indicating a persistent postresuscitation hypoperfusion. Direct peritoneal resuscitation reversed the postresuscitation vasoconstriction by 40.9% and enhanced A1 blood flow by 112.9% of the respective postresuscitation values. CONCLUSIONS: Delayed DPR reverses the gut postresuscitation vasoconstriction and hypoperfusion regardless of the initiation time. This occurs without adverse effects on hemodynamics. Direct peritoneal resuscitation-mediated enhancement of tissue perfusion results from the local effects from the vasoactive components of the Delflex solution, which are hyperosmolality, lactate buffer anion, and, to a lesser extent, low pH. The molecular mechanism of this vasodilation effect needs further investigation.     

Hypertonic saline solution-hetastarch for fluid resuscitation in experimental septic shock

Hypertonic colloid solutions have been found efficacious in the resuscitation from hemorrhagic/traumatic shock. The present study investigated the hemodynamic, gasometric, and metabolic effects of hypertonic colloids in endotoxic shock in the dog. Thirty minutes after administration of 3 mg/kg normal body weight of Escherichia coli endotoxin, dogs were randomly assigned to receive 10 mL/kg hydroxyethylstarch (HES) either in 0.9% NaCl (HES, 10 dogs) or in 7.5% NaCl (HT-HES, 10 dogs) in 30 min. Thereafter, 0.9% NaCl solution was administered in volumes adequate to maintain pulmonary artery balloon-occluded pressure at baseline levels. Total fluid administered averaged 64 +/- 30 mL/kg (mean +/- SD) in the HES group and 73 +/- 34 mL/kg in the HT-HES group. As these differences were not statistically significant, total sodium load was higher in the HT-HES group. The persistent volume effect was associated with persistently lower hematocrit and protein levels in the HT-HES group. Initial fluid resuscitation with HT-HES resulted in arterial pressure, cardiac filling pressures, cardiac output, stroke volume, and rates of oxygen delivery and oxygen consumption that were greater than those with HES. Vascular resistances were similar. Analysis of left ventricular function curves also indicated an improvement in cardiac performance. However, these effects almost completely vanished during the remainder of the study. In the HT-HES group, serum sodium and osmolality levels increased to 167 +/- 4 mEq/L and 344 +/- 4 mOsm/kg H2O, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)     

早期复苏对严重脓毒血症和脓毒性休克的脏器功能影响

目的：探讨严重脓毒血症和脓毒性休克病人早期充分复苏对脏器功能和后续治疗反应的影响。方法：2004年6月至2005年8月，我院外科监护病房和呼吸监护病房连续收治的严重脓毒血症和脓毒性休克病人共28例，进行及时充分复苏治疗。根据复苏达标时间是否超过12h将病人分为早期复苏组（12例）和晚期复苏组（16例），较两组病人对后续治疗的反应和脏器功能影响。结果：晚期复苏组需再次复苏治疗者占68．8％，早期复苏组为16．7％（P〈0．01）。复苏后第7天，早期复苏组血AST、ALT、Cr均显著低于晚期复苏组（P〈0．05）；复苏后，早期复苏组各时点心率（HR）均显著低于晚期复苏组（P〈0．05）；复苏7d后，早期复苏组PaO2和PaO2／FiO2均显著高于晚期复苏组（P〈0．05）。比较院内死亡率，晚期复苏组为43．8％，早期复苏组8．3%（e〈0．05）。结论：早期充分复苏治疗可明显增强严重脓毒血症和脓毒性休克病人对后续治疗的敏感性，并减轻对重要脏器功能的损害，从而降低其死亡率。     

不同液体腹腔复苏对失血性休克大鼠肠道炎性反应的影响

目的 探讨不同液体腹腔复苏对失血性休克大鼠肠道炎性反应的影响.方法 清洁级健康雄性SD大鼠50只,体重200～250 g,随机分为5组(n=10):假手术组(S组)仅行手术操作,不制备失血性休克模型;采用股动脉置管放血法制备大鼠失血性休克模型,常规静脉复苏组(CVR组)失血性休克1 h后,经左侧股静脉匀速回输自体血及相当于2倍失血量的生理盐水行常规静脉复苏;不同液体腹腔复苏组(DPR1～3组)行常规静脉复苏,同时分别腹腔输注生理盐水、6%羟乙基淀粉130/0.4、2.5%腹膜透析液20 ml行腹腔复苏.输注时间均为30 min.右颈总动脉连接多功能监测仪持续监测平均动脉压;于复苏后2 h时股动脉采血,测定乳酸浓度,取小肠组织检测髓过氧化物酶(MPO)活性,采用免疫组化法检测小肠组织肿瘤坏死因子α(TNF-α)表达水平,光镜下观察小肠黏膜组织形态,计算小肠黏膜上皮损伤指数.结果 与S组比较,其余各组大鼠复苏后平均动脉压差异无统计学意义(P>0.05),动脉血乳酸浓度、小肠组织MPO活性、TNF-α表达水平及小肠黏膜上皮损伤指数升高(P<0.05或0.01);与CVR组比较,DPR3组动脉血乳酸浓度、小肠组织MPO活性、TNF-α表达水平及小肠黏膜上皮损伤指数降低(P<0.05).结论 采用2.5%腹膜透析液20 ml行腹腔复苏可有效抑制肠道炎性反应,从而对失血性休克大鼠产生保护作用.