PiCCO指导脓毒症心肌抑制患者液体复苏的临床研究

目的探讨PiCCO指导脓毒症心肌抑制患者液体复苏的效果。方法选取2016年12月~2017年12月入住惠州市中心医院重症医学科的脓毒症患者100例,根据PICCO监测的GEF分为心肌抑制组(56例)和正常组(44例),3h内给予30mL/kg的积极液体复苏,比较两组患者液体复苏后血流动力学参数的变化。结果 (1)治疗前,两组患者MAP、HR、CVP、CI、EVLWI及GEDVI差异无统计学意义(P0.05);心肌抑制患者SVI、GEF、LVSWI及dPmx均较正常组患者降低,差异有统计学意义(P0.05)。(2)经液体复苏后,两组患者的液体输注量差异无统计学意义(P0.05);两组患者MAP、HR、CVP及CI均较治疗前有所改善,两组患者治疗后差异无统计学意义(P0.05);治疗后心肌抑制组患者EVLWI和GEDVI均显著高于正常值患者,差异有统计学意义(P0.05);治疗后心肌抑制患者SVI、GEF、LVSWI及d Pmx仍然较正常组患者降低,差异有统计学意义(P0.05)。结论脓毒症心肌抑制患者需要更少的液体输注量,可以根据GEDVI的变化值来指导脓毒症患者如何实施液体复苏治疗,保证足够的液体参与血液循环,并且血管外肺水合适,从而明显改善患者的临床状况及预后。     

血浆脑钠肽水平与重症脓毒症患者预后的相关性研究

目的：探讨血浆脑钠肽(BNP)水平与重症脓毒症患者预后的相关性研究。方法90例脓毒症患者,将所有患者按进院14 d预后状况分为存活组70例和死亡组20例,存活组根据APACHEⅡ评分分为轻度组20例,中度组30例,重度组20例。比较各组血乳酸、血浆BNP、APACHEⅡ评分及左室射血分数(LVEF)情况。结果存活组血乳酸、血浆BNP、APACHEⅡ评分及LVEF优于死亡组,差异有统计学意义(P<0.05),轻度组LVEF和BNP与中度组对比差异无统计学意义(P>0.05),轻度组血乳酸和APACHEⅡ与中度组对比,差异有统计学意义(P<0.05);轻度组和中度组各项指标与重度组对比,差异有统计学意义(P<0.05)。结论脓毒症患者血浆BNP水平升高不但能够知道患者心肌已经受到一定程度的损坏,而且可以作为脓毒症患者危险分层以及预后的重要的指标。     

磷酸肌酸对脓毒症相关性心肌损伤患者心脏功能的保护作用

目的：探讨磷酸肌酸对脓毒症相关性心肌损伤患者心脏功能的保护作用。方法将240例因肠穿孔合并腹腔感染导致严重脓毒症患者随机分为观察组和对照且各120例。所有患者均给予原发病手术治疗,术后入ICU监护。观察组术前及术后3d连续给予磷酸肌酸注射液静脉滴注。术后第3天分析2组患者肌酸激酶同工酶（Ck-MB）、肌钙蛋白I（cTnI）、钠尿肽（BNP）水平变化,利用心脏超声测定左心室射血分数（LVEF）、心室舒张功能：E/A、E/Ea比值。结果治疗后,观察组Ck-MB、cTnI、BNP较对照组明显减少,差异均有统计学意义（ P＜0.05）;2组LVEF值差异无统计学意义（ P＞0.05）;观察组E/A比值较对照组明显增加,E/Ea比值较对照组明显减少,差异均有统计学意义（ P＜0.05）。结论严重脓毒症可以导致明显的心肌损伤,影响心脏舒张功能,用磷酸肌酸治疗可减轻心肌损伤,保护心脏功能。     

不同剂量阿托伐他汀治疗冠心病慢性心力衰竭的临床分析

目的观察不同剂量阿托伐他汀治疗冠心病慢性心力衰竭的临床效果。方法以我院收治的75例冠心病慢性心力衰竭患者为研究对象,将患者按照随机分组的原则分为对照组和实验组,两组患者均给予常规治疗。对照组37例,阿托伐他汀用量为20 mg,1天1次,晚上服用;实验组38例,阿托伐他汀用量为40 mg,1天1次,晚上服用。两组均用药8周。两组患者治疗后测量患者左室舒张末期内径(LVEDD)、左室收缩末期内径(LVESD)、左室射血分数(LVEF)、6 min步行距离、超敏C反应蛋白水平。结果两组治疗前后LVEDD、LVESD、LVEF进行比较,治疗前两组各项指标比较差异无统计学意义(P>0.05),治疗后,实验组LVESD与LVEDD显著低于对照组,LVEF显著高于对照组,差异均具有统计学意义(P<0.05)。治疗前两组6 min步行距离与超敏C反应蛋白比较差异无统计学意义(P>0.05),治疗后,实验组两项指标均优于对照组,差异具有统计学意义(P<0.05)。结论冠心病慢性心力衰竭患者服用阿托伐他汀用药剂量40mg/d治疗效果更优,值得在临床中推广应用。     

左西孟旦治疗充血性心力衰竭的疗效观察

目的评价左西孟旦治疗充血性心力衰竭的临床疗效。方法选择充血性心力衰竭患者52例,随机分为观察组和对照组,分别予左西孟旦和米力农治疗。比较两组患者治疗前后临床疗效、B型脑利钠肽(BNP)、左室射血分数(LVEF)、左室舒张末期内径(LVEDD)等指标的变化。结果治疗前两组LVEF、LVEDD、BNP水平差异无统计学意义(P>0.05),治疗后两组LVEF、LVEDD、BNP水平明显改善,对照组患者改善更明显,组内及组间差异有统计学意义(P<0.05);观察组总有效率92.8%,对照组66.8%,两组疗效比较,差异有统计学意义(P<0.05)。治疗后两组患者BNP水平和LVEF、LVEDD均得到明显改善(P<0.05),观察组患者改善更明显(P<0.05)。结论左西孟旦在治疗CHF方面临床疗效确切。     

超声心动图联合HbA1 c和MOP检测对脓毒症心肌损伤风险的评估价值

目的 观察超声心动图联合糖化血红蛋白(HbA1c)及髓过氧化物酶(MOP)检测对脓毒症心肌损伤风险的评估价值.方法 84例脓毒症患者按诊断分为3组,分别为脓毒症组30例、严重脓毒症组28例和脓毒性休克组26例,另选体检正常者30例为对照(正常组).4组患者均于入院后24 h内行超声心动图检查,测量左心房内径(LAD)、左心室舒张末内径(LVEDD)、左心室射血分数(LVEF)、短轴缩短率(FS).检测清BNP和cTnI水平、血浆髓过氧化物酶(MOP)及糖化血红蛋白(HbA1c),评估患者急性生理和慢性健康状况评分Ⅱ(APACHEⅡ)分值.结果脓毒症组、严重脓毒症组、脓毒性休克组患者LAD、LVEDD均较正常组增加,HbA1c、MOP、BNP、cTnI水平升高,A-PACHEⅡ评分增加,LVEF及FS降低,差异均有统计学意义(P<0.05),且3组组间两两比较差异有统计学意义(P<0.05).提示随着脓毒症病情的加重,心脏功能受损也越严重.相关性分析统计结果显示,HbA1c、MOP水平与A-PACHEⅡ评分、BNP及cTnI水平均有相关性(P<0.05),其中LVEF、FS与APACHEⅡ评分、BNP及cTnI水平呈负相关,LVEDD、LAD、HbA1c、MOP呈正相关性.结论 超声心动图联合MPO、HbA1C检测可以更好的预测脓毒症心肌损伤发生的风险,评估心肌损伤的程度.     

比较平衡盐溶液与生理盐水对脓毒症患者急性肾损伤的影响

目的比较平衡盐溶液与生理盐水对脓毒症患者急性肾损伤的影响。方法前瞻性选取2019年2-8月山西医科大学第一医院重症医学科(ICU)收治的90例脓毒症患者,随机分为试验组和对照组,每组45例。试验组给予平衡盐溶液(钠钾镁钙葡萄糖注射液)用于液体复苏治疗,对照组给予生理盐水,连续用药5 d,余常规治疗不予干预。比较两组患者用药期间肾功能情况、急性生理学和慢性健康状况评分(APACHEⅡ评分)、序贯器官衰竭估计评分(SOFA评分)、急性肾损伤(AKI)发生率、高氯血症发生率、连续肾脏替代疗法(CRRT)使用时间、有创呼吸机使用时间、住ICU时间及住院时间、研究液使用量、用药结束后28 d生存率等。结果试验组高氯血症发生率、AKI发生率明显低于对照组,差异有统计学意义(P<0.05);试验组CRRT使用时间、有创呼吸机使用时间、住ICU时间及住院时间等短于对照组,差异有统计学意义(P<0.05);试验组血清肌酐下降程度整体优于对照组,入组第2天(D2)和第3天(D3)两组比较差异有统计学意义(P<0.05);试验组SOFA评分改善、APACHEⅡ评分改善明显优于对照组,差异有统计学意义(P<0.05);两组研究液使用量比较,差异无统计学意义(P>0.05);试验组28 d生存率明显高于对照组,差异有统计学意义(P<0.05)。结论使用平衡盐溶液用于脓毒症患者的液体复苏,可有效降低入住ICU脓毒症患者的AKI发生率,且能够有效减轻入住ICU时已经合并AKI患者的肾损伤程度,延缓患者病情进展,缩短住院日,改善预后。     

米力农注射液治疗高血压性心脏病伴心力衰竭的临床观察

目的:观察米力农注射液治疗高血压性心脏病伴心力衰竭的疗效及安全性。方法:将120例高血压性心脏病伴慢性心力衰竭患者按随机数字表法分为对照组与观察组,各60例。对照组患者接受常规治疗,包括控制血压、抗心力衰竭等对症处理;观察组患者在对照组基础上加用米力农注射液0.3 mg/kg,微量持续泵入,qd,连续5 d为1个疗程,每月治疗1个疗程,连续治疗6个月。两组患者均随访1年。观察两组患者治疗前,治疗3、6个月及治疗后1年6min步行距离(6MWD)、血浆脑钠肽(BNP)、左室射血分数(LVEF)、心脏指数(CI)、左室舒张末期内径(LVEDD)、静息心率、坐位收缩压、坐位舒张压、再住院、心血管病死发生情况,并比较两组患者心功能改善疗效及不良反应发生率。结果:治疗前,两组患者6MWD、BNP、LVEF、CI、LVEDD、静息心率、坐位收缩压、坐位舒张压比较,差异均无统计学意义(P>0.05)。治疗3、6个月及治疗后1年,两组患者6MWD、LVEF、CI均显著上升,BNP、LVEDD、静息心率、坐位收缩压、坐位舒张压均显著下降,且观察组改善程度显著优于对照组,差异有统计学意义(P<0.05)。观察组患者心功能改善总有效率为90.00%,显著高于对照组的63.33%,差异有统计学意义(P<0.05)。随访1年,观察组患者再住院率显著低于对照组,差异有统计学意义(P<0.05);心血管病死率比较,差异无统计学意义(P>0.05)。两组患者不良反应发生率比较,差异无统计学意义(P>0.05)。结论:米力农注射液治疗高血压性心脏病伴心力衰竭的疗效显著,能明显降低患者BNP和再住院率,改善预后,且安全性较好。     

微量白蛋白尿对脓毒症早期诊断及预后价值

目的 研究危重症患者微量白蛋白尿(MA)能否早期诊断脓毒症及评估其预后.方法 2013年1月至2014年12月入住本院ICU 206例危重症患者入选本研究,分别检测入ICU时尿白蛋白肌酐比值(ACR1)、乳酸(LAC1)及入ICU 6 h时ACR(ACR2)、乳酸(LAC2)等,追踪28 d病死率.比较脓毒症与非脓毒症ACR1,应用受试者工作特征(ROC)曲线测定ACR1对脓毒症诊断界值,应用Logistic回归分析脓毒症28 d病死的独立危险因素.结果 脓毒症组ACR1显著高于非脓毒症组(P＜0.01),ROC曲线分析提示ACR1诊断脓毒症界值为105 mg/g.脓毒症组28 d死亡患者ACR2显著高于生存者(P＜0.01).ACR2与LAC2是脓毒症患者28 d病死的独立危险因素(P＜0.01),两者死亡预测价值无统计学差异(P＞0.05).结论 入ICU时MA升高可能提示脓毒症.入ICU 6 h时MA与乳酸升高可能是脓毒症28 d病死的独立危险因素.     

靶剂量酒石酸美托洛尔对老年糖尿病并慢性心力衰竭患者心功能的影响

目的:观察靶剂量酒石酸美托洛尔对老年糖尿病并慢性心力衰竭患者心功能的影响。方法:104例老年糖尿病并慢性心力衰竭患者按随机数字表法均分为对照组和观察组。对照组患者给予吸氧、胰岛素或口服降糖药、血管紧张素转换酶抑制剂、利尿药、硝酸酯类药物等常规治疗;观察组患者在对照组治疗的基础上给予酒石酸美托洛尔片,初始剂量6.25 mg,口服,bid,视病情改善情况每14 d增加1次剂量,前3次每次增加6.25 mg,此后每次增加6.25¹2.5 mg,至靶剂量100 mg,口服,bid。两组患者疗程均为6个月。观察两组患者治疗前后左室收缩末期内径(LVESD)、左室舒张末期内径(LVEDD)、左室射血分数(LVEF)、6 min步行距离、空腹血糖(FBG)、糖化血红蛋白(HbA1c)、急性心力衰竭加重率、病死率及不良反应发生情况。结果:治疗前两组患者LVESD、LVEDD、LVEF、6 min步行距离比较,差异无统计学意义(P>0.05)。治疗后两组患者LVESD、LVEDD显著低于同组治疗前,且观察组低于对照组,LVEF、6 min步行距离显著高于同组治疗前,且观察组高于对照组,差异有统计学意义(P<0.05)。两组患者治疗前后FBG、HbA1c比较,差异无统计学意义(P>0.05)。两组患者急性心力衰竭加重率、病死率比较,差异均无统计学意义(P>0.05)。观察组患者不良反应发生率显著高于对照组,差异有统计学意义(P<0.05)。结论:靶剂量酒石酸美托洛尔可有效改善老年糖尿病并慢性心力衰竭患者的心功能,延缓心肌重构,虽然不良反应发生率较高,但患者均可耐受。     

Neonatal sepsis

A two year retrospective study of 242 neonates with a clinical diagnosis of neonatal sepsis was undertaken. The neonates on whom blood culture results were available for analysis were categorized into "proven" or "presumptive" sepsis. A changing pattern in aetiological pathogens is identified. The conspicuous absence of Group B Streptococcal (GBS) sepsis is discussed. The overall mortality rate was 37% but the mortality rate in the bacteraemic patients was only 22.6%. This discrepancy is discussed in detail and further prospective study suggested.     

Surviving sepsis campaign: a project to change sepsis trajectory

Sepsis is an acute and severe disease associated with early and late high mortality, high and growing prevalence, and impressive costs. In October 2002, during the European Society of Intensive Care Medicine annual congress, the Surviving Sepsis Campaign was launched through a "Barcelona Declaration" -- a document calling critical care providers, governments, health agencies and lay people to join the fight against sepsis. The aim of the campaign was to reduce the sepsis mortality rate by 25% within 5 years (actually, this deadline has been ended from 2007 to 2009). In 2003, a group of international critical care and infectious disease experts in the diagnosis and management of infection and sepsis met to develop guidelines that the bedside clinician could use to improve the outcome of severe sepsis and septic shock. A comprehensive document created from the committee's deliberations was published in prestigious journals. Thus, the SSC is a global, multi-organizational initiative to fight sepsis and undoubtedly, this campaign is a historic step for critical care medicine. This paper highlights the recommendations and the strategies proposed by SSC to implement them in intensive care units.     

他汀类与败血症

近来若干动物与临床试验表明,他汀类用于败血症的治疗可获得出乎意料的良好效果。该文总结了相关试验,并分析其作用机制可能为保护心脏功能,抑制内皮功能失调与凋亡,抗急性期反应及抗氧化应激等。     

Statins in sepsis

Sepsis is a common intensive care unit event occurring in approximately 750 000 patients annually, with a case mortality rate approaching 50%. Sepsis is characterized by a chaotic and excessive release of inflammatory cytokines and procoagulants including tumor necrosis factor, interleukin (IL)-1, IL-6, IL-8, platelet-activating factor, and tissue factor. Efforts to inhibit individual cytokines in order to modify poor outcomes have been generally disappointing, suggesting the need to target multiple inflammatory mediators to obtain clinical benefit. Statins lower lipids by inhibiting 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase, which in turn inhibits the rate-limiting step in cholesterol biosynthesis. In addition to lowering total cholesterol, statins have pleiotropic effects on inflammation and immunity. Instead of impacting a single entity in the sepsis syndrome, statins may have positive effects on multiple inflammatory, immunomodulating, and coagulation targets involved in the development of infection and sepsis. There have been a number of institutional- and population-based studies that have evaluated the impact of statins in patients with infection and sepsis. Most of these studies, but not all, have demonstrated a number of positive outcomes in patients with statins, including reduction in mortality. Based on these data, statins are a promising therapy in the management of patients with sepsis and warrant larger and more rigorous clinical trials.     

Immunosuppression in sepsis

The often fatal sepsis syndrome is characterized by the systemic release of inflammatory mediators, which is regulated and counterbalanced by the coordinated expression of anti-inflammatory molecules. The magnitude of sepsis-induced tissue injury and subsequent risk of infectious complications is dictated by the balance between the expression of pro- and anti-inflammatory mediators. As our understanding of the pathophysiology of sepsis continues to evolve, we have gained a greater appreciation for the profound effects that sepsis and similar states of overwhelming stress have on host innate and adaptive immunity. Impaired leukocyte function in sepsis has important clinical consequences, as high mortality rates have been observed in patients who display evidence of sepsis-induced immune dysregulation. Functional defects in leukocytes isolated from patients with sepsis include diminished expression of important cell surface molecules, dysregulated cytokine production, alterations in antigen-presenting ability, and accelerated apoptosis. In this article, we review the current literature supporting the notion that dysregulation of host immunity occurs during sepsis syndrome, and describe novel therapeutic interventions directed at augmenting host immunity during sepsis.     

Coagulation and sepsis

Sepsis is a complex disease and coagulation derangements are part of this context. The inflammatory storm is ultimately responsible for coagulation derangements. It is characterized by exacerbated coagulation, impaired anticoagulation and decreased fibrin removal. These derangements are implicated in the generation of microcirculation thrombosis, with deposition of microclots and obstruction of circulation, impairing blood flow and contributing to tissue hypoperfusion and consequently, organ dysfunction. This review will address the main issues regarding coagulation disorders in the context of sepsis.     

The epidemiology of sepsis

Sepsis is a common and devastating syndrome that represents a significant healthcare burden worldwide. The average annual cost to care for patients with sepsis has been estimated to being $16.7 billion. Uniform definitions have been developed for the spectrum of sepsis syndrome, including the systemic inflammatory response syndrome (SIRS), sepsis, severe sepsis and septic shock. SIRS describes the clinical manifestations derived from an acute yet nonspecific illness, whereas an infectious etiology is required for the diagnosis of sepsis. As sepsis progresses, organ system dysfunction becomes apparent (severe sepsis) with the final development of fluid refractory cardiovascular dysfunction (septic shock). Pulmonary, gastrointestinal, genitourinary, and primary bloodstream infections account for the majority of infectious sources in septic patients. Since 1987, gram positive bacteria have become the most common organisms responsible for the development of sepsis. Several risk factors for the development of sepsis have been identified including male sex, race, age, comorbid medical conditions, alcohol abuse, and a lower socioeconomic status. Seasonal variations also exist, with sepsis being more common in the winter months. Fortunately, the case fatality rates for both sepsis and severe sepsis have diminished over the last two decades. However, patients who survive their episode of sepsis continue to have increased morbidity and mortality up to five years after their initial illness.     

Adrenal insufficiency in sepsis

The role of the hypothalamic-pituitary adrenal axis in the host response to infection is crucial. The initial inflammatory response to sepsis activates the endogenous release of cortisol, which in turn modulates the synthesis and release of both pro- and anti-inflammatory mediators to restrict inflammation in infected tissues. However, a number of factors, including vascular or ischemic damage, inflammation and apoptosis within the hypothalamic-pituitary adrenal axis, as well as use of drugs that alter cortisol metabolism, may cause adrenal insufficiency. One major problem ICU physicians are faced with is the diagnosis of sepsis-induced adrenal insufficiency at the bedside. A multidisciplinary international task force has recently recommended that sepsis induced adrenal insufficiency is best recognized by basal cortisol of less than 10 microg/dl or change in cortisol of less than 9 microg/dl after administration of corticotrophin. The diagnostic value of measuring salivary free cortisol in this setting remains to be investigated. While sepsis adrenal insufficiency is undoubtedly associated with a poor prognosis, the indication and practical modalities of corticosteroids therapy remained controversial. Based on the two largest randomised, placebo-controlled trials, many investigators, myself included, contend that septic shock patients with hypotension poorly responsive to fluid replacement and vasopressors should receive a seven day treatment with the combination of hydrocortisone at a dose of 200 mg per day and fludrocortisone at the dose of 50 microg per day.     

Advances in sepsis therapy

During the past 3 years new insights have been gained into the fundamental elements that underlie the pathogenesis of sepsis, and after years of frustrating failures, progress in the basic understanding of sepsis has translated into successful new therapies. These new treatment strategies have significantly improved the outcome of patients experiencing the puzzling syndrome of severe sepsis. More effective supportive therapies with early, goal-oriented therapy including volume resuscitation, catecholamine therapy and transfusion improve the chances for survival in septic shock. Novel endocrine management with hydrocortisone replacement therapy for relative adrenal insufficiency in septic shock patients and strict blood glucose control provide a survival advantage in critically ill patients. Administering appropriate antimicrobial therapy, nutritional support and ventilation protocols with low tidal volumes have now been shown to benefit septic patients. Finally, human recombinant activated protein C (drotrecogin alfa), which ameliorates sepsis-induced disseminated intravascular coagulation and exerts several other favourable effects on endothelial cells, has been shown to reduce mortality in patients with severe sepsis. On the basis of newly discovered pathophysiological mechanisms of sepsis, several other adjuvant therapies for sepsis are in various stages of preclinical and clinical development. Individualised and optimal supportive care with efforts to reverse the precipitating cause of sepsis remains the mainstay of therapy for severe sepsis. How these new and often expensive regimens will fit into the standard treatment approach to sepsis remains to be defined by future clinical investigations.