强化胰岛素治疗脓毒血症的疗效

脓毒血症患者由于炎症介质和细胞因子大量失控释放,容易导致一系列炎症反应和代谢紊乱,多数会出现反应性高血糖和胰岛素抵抗。高血糖被认为是脓毒血症患者死亡的独立危险因素[1]。强化胰岛素治疗被认为是控制危重症患者应激性高血糖的标准治疗,强化胰岛素治疗可以更好地抑制机体的炎性反应,改善免疫功能,提高生存率,     

胰岛素强化治疗在外伤后应激性高血糖的最新研究进展

外伤后应激性高血糖比较常见,明显影响患者的预后.近年胰岛素强化治疗(IIT)目标血糖值较前有所提高,主要原因是预防严重低血糖的发生.胰岛素强化治疗能改善外伤后高血糖及毒性症状,降低发病率和死亡率;能降低患者炎症因子,减少感染的发生;能明显改善患者免疫功能;能降低患者凝血系统功能紊乱.     

早期强化及适度胰岛素治疗重症急性胰腺炎的疗效观察

重症急性胰腺炎（severe acute pancreatitis， SAP）为急性胰腺炎的一种特殊类型，病情凶险，并发症多、病死率高。SAP 多由胆道结石、酗酒或暴饮暴食损害胰腺功能引起［1］。SAP 以胰腺局部出血坏死为主要特征，伴全身多器官炎症反应［2］。近年来，有报道采用胰岛素强化治疗可降低 SAP 患者多脏器功能不全的发生率及病死率［3］。本科对 SAP 患者早期采取胰岛素强化及适度胰岛素治疗，取得良好效果。报告如下。     

危重症高血糖患者胰岛素强化治疗及护理现状

危重症患者由于手术、创伤、感染、急性应激等因素,无论有无糖尿病史常合并高血糖存在,后者不仅被视为预后不良的预警指标,更是病情进展、恶化的原因之一。胰岛素强化治疗不仅能控制高血糖而且能降低感染的发生率、改善机体的能量代谢及预后,在临床实践中越来越受到重视。现就危重症高血糖患者胰岛素强化治疗的护理现状进行综述。     

严重创伤患者早期胰岛素强化治疗对预后的影响

目的 探讨胰岛素强化治疗对严重创伤患者预后的影响，研究其对危重患者脏器的保护作用。方法 选择64例严重创伤患者，分为胰岛素强化治疗组和对照组，分别给予胰岛素强化治疗和常规治疗，在入院后0、2、4、6、8d留取外周静脉血，同时每日行APACHEⅡ评分，并记录反映脏器功能的生化指标和预后主要指标。结果 胰岛素强化治疗实施的安全性良好。强化治疗严格控制血糖后，心功能、肝功能、肾功能不全发生率显著下降，APACHEⅡ评分降低，两组患者死亡率、院内感染发生率比较差异具有统计学意义。结论 胰岛素强化治疗能有效降低ICU中危重患者脏器功能不全等并发症的发生，既降低死亡率，又减少感染出现。     

短期胰岛素强化治疗危重症应激性高血糖的临床观察

目的:探讨短期胰岛素强化控制应激性高血糖对危重症临床疗效及预后的影响.方法:将172例合并应激性高血糖危重病患者随机分成胰岛素强化治疗组(治疗组)与常规胰岛素治疗组(对照组),对照组当血糖11.9 mmol/L时,使用胰岛素将血糖控制在10～11.1 mmol/L;治疗组当血糖6.1 mmol/L,使用胰岛素将血糖控制在4.0～6.1 mmol/L.强化治疗期为7天,7天后血糖控制及其处理均同对照组.结果:治疗组院感发生率、MODS发生率、死亡率较对照组明显降低;ICU住院时间较对照组明显缩短.结论:短期胰岛素强化治疗能有效提高危重症的治愈率,减少危重症并发症的发生,降低危重症的死亡率,并能缩短ICU住院时间,降低医疗费用.     

严重创伤后早期胰岛素强化治疗的临床价值

目的 严重危重患者应激性高血糖的发生极为普遍.应激性高血糖主要由下丘脑-垂体-肾上腺皮质轴及细胞因子激活导致,严重影响创伤后的救治效果,增加了患者的死亡率.早期胰岛素强化治疗能有效减少感染,显著降低血清炎性介质的水平,增加患者的免疫功能,从而降低患者并发症的发生率及死亡率.     

全身炎症反应综合征患者胰岛素强化治疗对血清炎症介质的影响

目的研究全身炎症反应综合征患者(SIRS)施行胰岛素强化治疗对体内肿瘤坏死因子-α(TNF-α)和白细胞介素-6(IL-6)等早期炎症介质的影响。方法68例发生应激性高血糖(血糖超过9.00mmol/L)的SIRS患者,配对后随机分为胰岛素强化治疗组和常规治疗组,分别在治疗前和治疗后第1、2和3天抽取肘静脉血3ml,采用酶联免疫吸附法(ELISA)测定血浆TNF-α与IL-6水平,并测定C-反应蛋白(CRP)变化以评估炎症程度。结果胰岛素强化治疗显著降低了SIRS患者血清TNF-αI、L-6和CRP水平,与常规治疗组比较差异有显著性,(P<0.05或P<0.01)。结论胰岛素强化治疗可拮抗SIRS患者高炎症状态,抗炎效应可能是除降血糖、促合成代谢作用之外胰岛素强化治疗又一改善SIRS患者预后的重要机制。     

髓源性抑制细胞在脓毒症免疫抑制中的研究进展

脓毒症是指由宿主对感染的反应失调引起的威胁生命的器官功能障碍, 常继发于严重创伤后的感染和各种化脓性感染, 致病菌数量多、病菌毒性强以及宿主免疫功能低下均可导致脓毒症发生。现阶段对脓毒症患者的治疗主要由早期复苏、抗微生物治疗、感染源控制以及其他辅助治疗部分组成。但进一步的研究发现与脓毒症早期因感染所导致的机体炎症功能亢进、细胞炎症因子风暴暴发等损伤机制不同, 在脓毒症后期会因多种机制的作用而导致机体免疫功能处于低下、抑制甚至失能的状态。这种免疫功能的抑制状态将导致机体发生二次感染等预后不良事件, 因此, 对脓毒症幸存患者的免疫抑制机制的研究逐渐浮上水面。     

免疫功能抑制患者的血行性感染:临床处理有何不同?

血行性感染是免疫功能抑制患者最常见的感染性并发症之一,罹患率和致死率很高。革兰阴性杆菌(尤其多重耐药革兰阴性杆菌)是最常见的致病微生物。由于免疫功能抑制患者炎症反应减弱,血行性感染的临床表现缺乏特异度,往往需要结合生物标志物进行综合判断。免疫功能抑制患者发生血行性感染后,其抗生素治疗疗程应适当延长。     

A patient with severe acute pancreatitis successfully treated with a new critical care procedure.

It has been accepted widely that excessive humoral mediators play important roles in the pathogenesis of organ failure in patients with severe acute pancreatitis (SAP) and that infection of the pancreas due to bacterial translocation (BT) is the most frequent cause of death in SAP. On the other hand, it has been reported that continuous hemodiafiltration (CHDF) removes humoral mediators on hypercytokinemic patients such as those with systemic inflammatory response syndrome. Furthermore, several clinical studies have demonstrated that selective digestive decontamination (SDD) effectively eliminates aerobic Gram-negative bacteria from the intestinal tract and reduces the incidence of septic complications in SAP. Herein we report a case of SAP who was treated successfully with intensive care including CHDF and SDD. Thus, this case report suggests that CHDF aimed at removing causative humoral mediators and SDD for the prevention of BT are useful new tools for the management of SAP.     

胰岛素强化治疗对严重创伤患者炎症介质和外周血核转录因子κB的影响

目的:探讨胰岛素强化治疗对临床严重创伤患者应激性高血糖的炎症介质、外周血核转录因子κB的影响。方法:分别通过ELISA和PCR检测TNF-α、IL-6和NF-κB。结果:胰岛素强化治疗能降低血清炎症介质TNF-α、IL-6水平,能显著降低NF-κB表达。结论:胰岛素强化治疗可有效下调创伤后炎症介质水平,降低NF-κB的转录水平。     

Inflammatory response and immune regulation of high mobility group box-1 protein in treatment of sepsis

Sepsis is an infection induced systemic inflammatory response syndrome and is a major cause of morbidity as well as mortality in intensive care units. A growing body of evidence suggests that the activation of a proinflammatory cascade is responsible for the development of immune dysfunction, susceptibility to severe sepsis and septic shock. The present theories of sepsis as a dysregulated inflammatory response and immune function, as manifested by excessive release of inflammatory mediators such as high mobility group box 1 protein (HMGB1), are supported by increasing studies employing animal models and clinical observations of sepsis. HMGB1, originally described as a DNA-binding protein and released passively by necrotic cells and actively by macrophages/monocytes, has been discovered to be one of essential cytokines that mediates the response to infection, injury and inflammation. A growing number of studies still focus on the inflammation-regulatory function and its contribution to infectious and inflammatory disorders, recent data suggest that HMGB1 formation can also markedly influence the host cell-mediated immunity, including T lymphocytes and macrophages. Here we review emerging evidence that support extracellular HMGB1 as a late mediator of septic complications, and discuss the therapeutic potential of several HMGB1-targeting agents in experimental sepsis. In addition, with the development of traditional Chinese medicine in recent years, it has been proven that traditional Chinese herbal materials and their extracts have remarkable effective in treating severe sepsis. In this review, we therefore provide some new concepts of HMGB1-targeted Chinese herbal therapies in sepsis.KEY WORDS: Sepsis, Inflammatory mediators, High mobility group box 1 protein     

Immunologic changes in obesity

A growing body of literature suggests multifaceted alterations to the immune function in obese patients compared with a lean cohort. Although treatment in the intensive care unit has an associated risk of infectious complications, which, if any, of these immunologic alterations are causal is unclear. Obesity clearly causes abundant alterations to the immune system. Overall, the aggregate effect seems to be chronic activation of inflammatory mediators.     

Science review: Extracellular acidosis and the immune response: clinical and physiologic implications

Metabolic acidosis is among the most common abnormalities seen in patients suffering from critical illness. Its etiologies are multiple and treatment of the underlying condition is the mainstay of therapy. However, growing evidence suggests that acidosis itself has profound effects on the host, particularly in the area of immune function. Given the central importance of immune function to the outcome of critical illness, there is renewed interest in elucidating the effects of this all too common condition on the immune response. In this review we concentrate on the effects of extracellular acids on production and release of inflammatory mediators, and we demonstrate that different acids produce different effects despite similar extracellular pH. Finally, we discuss potential clinical implications.     

Genetic predisposition for development of complications in multiple trauma patients

The care of multiple trauma patients has been improved through advances made in preclinical treatment, surgical procedures, and intensive care medicine. However, posttraumatic complications such as systemic inflammatory response syndrome, multiple organ dysfunction syndrome, and sepsis remain a major problem following multiple trauma. Components of the innate immune system and other inflammatory mediators (e.g., procalcitonin) play a pivotal role in the pathophysiology of posttraumatic complications. Studies investigating the genetic predisposition for complications after multiple trauma have provided evidence for a genetic heterogeneity in the posttraumatic immune response. The differences in response to multiple trauma associated with single-nucleotide polymorphisms may contribute to the development of new genetically tailored diagnostic and therapeutic interventions improving outcome in this patient population. In addition, detrimental adverse effects of adjuvant therapy could be avoided in other patients who, by genotype, are predicted not to benefit.     

重症急性胰腺炎的治疗进展

重症急性胰腺炎(SAP)是临床常见的危重疾病,其病情凶险,病死率高。随着对SAP发病机制认识的不断深入,治疗观念已从20世纪中期提倡的早期手术治疗变为早期内科综合治疗,采取早期液体复苏、营养支持、预防和控制感染、抑制胰酶分泌及活性、腹腔灌洗、血液滤过控制和减少全身炎症反应综合征(SIRS)对器官的损伤、免疫治疗、中医中药治疗、必要时手术治疗。开展综合性个体治疗提高了治愈成功率,代替了以往一律采用手术治疗的方案,并建立了多学科综合诊疗体系,重症医学的发展为SAP治疗创造了条件。重症监护成为治疗SAP的主要手段,外科手术是SAP治疗的坚强后盾。     

清胰汤对SA哈并感染患者单核细胞HLA—DR表达的影响

目的探讨清胰汤对重症急性胰腺炎（SAP）并发感染患者单核细胞HLA—DR表达的影响。方法33例SAP合并感染患者随机分成3组：SAP并发感染组（Ⅱ组）、GM-CSF治疗组（Ⅲ组）、清胰汤治疗组（Ⅳ组）;选取7例SAP未并发感染患者为对照组（Ⅰ组）;各组均予常规治疗,Ⅲ、Ⅳ组在常规治疗基础上加用GM-CSF或清胰汤治疗,一周后检测外周血WBC,血淀粉酶,ET,CRP,IL-6以及单核细胞HLA—DR表达率。结果Ⅱ、Ⅲ、Ⅳ组患者在各项血清学指标均高于Ⅰ组,单核细胞HLA-DR表达水平低于Ⅰ组（P〈0．05）;而Ⅲ、Ⅳ组患者各项指标较Ⅱ组明显改善（P〈0．05）。结论SAP并发感染患者存在单核细胞免疫功能缺陷,而清胰汤治疗能够改善这种免疫功能障碍以及过度炎症反应。     

血液灌流联合连续性静脉-静脉血液滤过治疗重症急性胰腺炎临床观察

目的探讨血液灌流（HP）联合连续性静脉-静脉血液滤过（CVVH）治疗重症急性胰腺炎（SAP）的临床疗效。方法选择本院2011年1月-2013年6月我院急诊重症监护室（EICU）收治的16例SAP患者,给予常规治疗同时予HP联合CVVH治疗,观察治疗后临床指标的动态变化及治疗效果。结果治疗24h后患者体温、心率、呼吸、平均动脉压（MAP）、血肌酐（Cr）、尿素氮（殴州）、血淀粉酶（AMS）、血清C反应蛋白（cRP）及APACHEII评分均较治疗前明显改善,差异有统计学意义（P〈0．05）;P02、WBC计数在治疗48h后较治疗前明显改善,差异有统计学意义（P〈0．05）;16例SAP患者中12例患者最终好转出院,死亡4例,死亡率为25．0％。结论HP联合CVVH治疗SAP可有效清除炎症介质,减轻全身炎症反应,并遏制由此引起炎性介质对机体组织器官的再次损害,改善患者的临床症状,是治疗SAP的有效措施。