不同血糖水平对体外循环心脏手术围术期患者血乳酸以及康复进程的影响

目的:探讨体外循环(CPB)心脏手术围术期患者不同血糖水平对血乳酸值及术后康复进程的影响。方法:选择2016年3月至2018年5月在我院行CPB心脏手术的患者78例为研究对象,根据术前血糖水平分为糖尿病组(术前空腹血糖≥7.0 mmol/L)33例和非糖尿病组(术前空腹血糖7.0 mmol/L)45例,于术前2h(T_1)、麻醉后(T_2)、CPB转机后5 min(T_3)、主动脉阻断后5 min(T_4)、停止CPB时(T_5)、手术结束时(T_6)、术后2h(T_7)、4h(T_8)、6h(T_9)、8h(T_(10))、12h(T_(11))、24h(T_(12))及48h(T_(13))监测两组血糖及血液乳酸水平,比较两组康复进程指标及并发症发生情况。结果:糖尿病组患者围手术期各时间点血糖及血乳酸水平均高于非糖尿病组,且两组血糖与血乳酸水平呈正相关(P0.05);两组各时间点血糖及血乳酸水平均高于T_1时刻(P0.05)。非糖尿病组患者呼吸机辅助通气时间、ICU停留时间、术后住院时间均短于糖尿病组(P0.05)。非糖尿病组并发症发生率为4.44%(2/45),与糖尿病组的15.15%(5/33)比较无统计学差异(P0.05)。结论:CPB心脏手术患者围术期血糖及血乳酸水平明显升高,二者呈正相关关系,但术前糖尿病患者围手术期血糖及血乳酸水平波动更明显,控制围手术期血糖水平有助于加快康复进程。     

心脏术后急性肾损伤的研究进展

急性肾损伤（Acute Kidney Injury,AKI）是心脏术后较常见且较严重的并发症,明显增加患者的住院费用,并且增加手术死亡率。研究发现术前肾功能不全、糖尿病、及外周血管疾病等是术后AKI的危险因素。最新的研究发现一些新的生物学标准物可以为我们早期诊断心脏术后AKI的发生的提供帮助。而一旦出现AKI,选择适当药物治疗和肾脏替代治疗,可以保护肾功能,改善AKI患者的预后。     

围术期应用他汀类药物对冠状动脉旁路移植术并发急性肾损伤疗效的研究进展

急性肾损伤是冠状动脉旁路移植术后常见并且严重的并发症,目前临床治疗主要以对症治疗和肾脏替代治疗为主。作为调节冠心病患者血脂的他汀类药物,其对于行冠状动脉旁路移植术患者肾脏的作用也成为了学者研究的热点问题。目前虽已有充分证据表明他汀类药物可以降低行冠状动脉旁路移植术患者院内死亡率,但是尚不清楚其能否降低患者术后急性肾损伤的发生率。对于在冠状动脉旁路移植术围手术期应用他汀类药物,其应用的时间窗以及应用的剂量学者们仍未达成统一意见。本文通过分析他汀类药物在冠心病整体防治中的作用机理机制,以及总结近几年关于他汀用药时间窗,用药剂量对于行CABG患者术后肾脏影响的相关文献,对围手术期应用他汀类药物对于行CABG患者术后急性肾损伤的影响展开综述。     

患儿体外循环直视心脏术后高尿酸血症分析

目的：探讨体外循环心脏术后24h患儿高尿酸血症发生的原因、影响因素和预后。方法：以2006年9～12月我院心脏外科收治的106例体外循环心脏手术患儿为研究对象,收集其年龄、体外循环时间、尿量、预后资料和心脏术后24h血尿酸、尿素氮、肌酐、胱抑素、血糖、总胆红素、直接胆红素等生化指标数据;以空腹血尿酸为标准,将患儿分为无高尿酸血症组和高尿酸血症组,用SPSS11．0软件分析两组之间临床资料的差异、高尿酸血症组血尿酸与其他指标的相关性及影响患者预后的因素。结果：患儿术后高尿酸血症组患者53例（50％）,与无高尿酸血症组相比P〈0．01,除年龄因素外,其他临床指标均有统计学意义;高尿酸血症组的血尿酸与血糖、总胆红素无相关性,与年龄、尿量呈显著负相关,与转流时间、尿素氮、肌酐、胱抑素、直接胆红素含量呈极显著正相关;在预后良好组与死亡组的比较中,转流时间、血尿酸、尿素氮、肌酐含量有统计学意义。结论：患儿体外循环心脏术后高尿酸血症的发生较常见,血尿酸水平对患者术后肾功能状态及预后具有重要临床意义,连续监测术后血尿酸、尿素氮、肌酐水平是及时判断患者临床状况以采取相应措施改善预后的重要方法;低心排血量综合征是引起患者死亡的危险因素之一,通过提高体外循环心脏手术水平,尽量缩短转流时间,加强围手术期监护,可有效减少术后并发症,降低死亡率。     

骨折合并糖尿病围手术期护理

骨折手术创伤大。并发症多,对合并糖尿病的患者,手术治疗风险大。术后伤口愈合与感染的几率与血糖的高低密切相关,故围手术期血糖的监测与护理直接关系到手术成功率及术后愈合情况。我科2008年8月～2009年1月收治骨折伴糖尿病手术患者20例．通过加强血糖的控制,手术治疗及围手术期的护理,获得满意效果．现将护理体会报告如下。     

高血压脑出血术后血糖值测定的意义

目的 探讨高血压脑出血术后血糖值的水平与死亡的关系。方法 检测38例非糖尿病病人在手术后48小时内空腹血糖,并根据血糖值高低分为高血糖组和非高血糖组,观察两组间与死亡的关系,进行统计学分析。结果 高血糖组死亡发生率明显高于非高血糖组,两组有显著差异(p<0.05)。结论 高血糖脑出血术后出现高血糖现象,病人死亡率明现增加,故应尽量避免各种引起血糖增高的因素,并尽早尽快的采取治疗措施。     

吸入麻醉药预处理心肌保护作用的临床研究进展

心肌梗死是围术期最严重的并发症之一,所以减少围术期心肌梗死的风险对于围术期麻醉十分重要。大量实验研究证明,吸入麻醉药预处理可以有效减轻心肌的缺血/再灌注损伤,减少心肌梗死范围,促进心脏功能的恢复。麻醉药预处理是一个复杂的过程,这一过程触发了两个不同的时相。第一,简称为早期预处理(E预处理),包括心肌细胞内有保护作用的酶的激活;第二,称为晚期预处理(L预处理),依赖于新的心肌保护蛋白的从头合成。虽然早期预处理和晚期预处理对心肌细胞的影响是挥发性麻醉药心脏保护作用的关键,但他们对冠状动脉内皮细胞的影响也很重要,这一机制可能改善了冠状动脉手术患者的长期预后。挥发性麻醉药,对改善围术期有心肌梗死风险的非心脏手术患者的预后,尚没有得到有明确意义的证实。     

急性脑梗死患者血糖、糖化血红蛋白水平与临床关系的研究(附152例报告)

目的 探讨急性脑梗死患者血糖、糖化血红蛋白水平与临床的关系。方法 根据152例患者入院时的空腹血糖水平分为正常血糖组、高血糖I组、高血糖Ⅱ组和高血糖Ⅲ组,在治疗前、治疗后的第7天、第14天、第21天、第28天,对神经系统缺损进行评分,并观察血糖、糖化血红蛋白、年龄、既往病史积分、并发病积分和临床的关系。结果 急性脑梗死患者的血糖水平越高。其并发病和神经系统缺损评分也越高,其临床疗效也越差。结论 高血糖尤其伴高糖化血红蛋白会增加急性脑梗死神经系统损伤和并发症,控制糖尿病可能会提高急性脑梗死的临床疗效。而积极预防和治疗高血糖是预防脑梗死的有力措施之一。     

肝移植术后营养治疗

近30多年来,肝移植技术已逐步成熟,并迅速发展成为治疗终末期肝病的首选方法。随着肝移植例数的增加,手术经验的积累,手术技巧的提高,与手术相关的并发症逐渐减少。而许多围手术期因素成为影响肝移植成败的关键。适宜的肝移植围手术期营养治疗,可以提高手术成功率,降低术后并发症,促进受体和移植肝功能的恢复,从而改善预后,提高受体与移植肝的近远期存活率。     

膀胱全切原位回肠代膀胱术围手术期的护理进展

在膀胱全切原位回肠代膀胱术围手术期,患者的生理心理会产生巨大改变。围手术期护理对保证手术成功率、减少并发症、加速患者康复等具有重要作用。目前,临床上尚未制订膀胱全切原位回肠代膀胱术围手术期护理的标准指南,本研究总结和分析近来年膀胱全切原位回肠代膀胱术围手术期护理的研究现状,旨在为其临床应用研究与其临床护理工作提供指导参考。     

Reversal of anemia with allogenic RBC transfusion prevents post-cardiopulmonary bypass acute kidney injury in swine

Anemia during cardiopulmonary bypass (CPB) is strongly associated with acute kidney injury in clinical studies; however, reversal of anemia with red blood cell (RBC) transfusions is associated with further renal injury. To understand this paradox, we evaluated the effects of reversal of anemia during CPB with allogenic RBC transfusion in a novel large-animal model of post-cardiac surgery acute kidney injury with significant homology to that observed in cardiac surgery patients. Adult pigs undergoing general anesthesia were allocated to a Sham procedure, CPB alone, Sham+RBC transfusion, or CPB+RBC transfusion, with recovery and reassessment at 24 h. CPB was associated with dilutional anemia and caused acute kidney injury in swine characterized by renal endothelial dysfunction, loss of nitric oxide (NO) bioavailability, vasoconstriction, medullary hypoxia, cortical ATP depletion, glomerular sequestration of activated platelets and inflammatory cells, and proximal tubule epithelial cell stress. RBC transfusion in the absence of CPB also resulted in renal injury. This was characterized by endothelial injury, microvascular endothelial dysfunction, platelet activation, and equivalent cortical tubular epithelial phenotypic changes to those observed in CPB pigs, but occurred in the absence of severe intrarenal vasoconstriction, ATP depletion, or reductions in creatinine clearance. In contrast, reversal of anemia during CPB with RBC transfusion prevented the reductions in creatinine clearance, loss of NO bioavailability, platelet activation, inflammation, and epithelial cell injury attributable to CPB although it did not prevent the development of significant intrarenal vasoconstriction and endothelial dysfunction. In conclusion, contrary to the findings of observational studies in cardiac surgery, RBC transfusion during CPB protects pigs against acute kidney injury. Our study underlines the need for translational research into indications for transfusion and prevention strategies for acute kidney injury.     

The Association Between Glycemic Control and Clinical Outcomes after Kidney Transplantation

ObjectiveTo analyze the relationship between glycemic control after renal transplantation and subsequent graft function and complications.MethodsWe conducted a retrospective chart review of 202 consecutive patients undergoing kidney transplantation to analyze the association between perioperative and chronic glycemic control and clinical outcomes of rejection, infection, and hospital readmission during the first year after kidney transplantation.ResultsMean in-hospital blood glucose (BG) was 157 ± 34.5 mg/dL. Mean hemoglobin A1c (HbA1c) during the first 12 months posttransplantation was 6.84 ± 1.46%. Fiftyfour patients (27%) were treated for acute or chronic rejection, 88 (44%) for infection, and 149 (74%) patients were readmitted at least once within the first year after transplantation. There were no significant differences in the risks for rejection, infection, or readmission across the 5 mean initial inpatient BG or subsequent HbA1c quintiles. In addition, there was no significant relationship between the percentage of BG measurements that fell in the “tight control” range of 80 to 110 mg/dL for each patient and any of the outcomes.ConclusionWe did not find an association between glycemic control (perioperative or chronic) and the outcomes of graft rejection, infection, or hospital readmission in the first 12 months after renal transplantation. Our results suggest that “near normal” glycemic targets are not necessary for managing hyperglycemia after renal transplantation. (Endocr Pract. 2014;20:894-900)     

Amelioration of acute kidney injury in lipopolysaccharide-induced systemic inflammatory response syndrome by an aldose reductase inhibitor, fidarestat

Background

Systemic inflammatory response syndrome is a fatal disease because of multiple organ failure. Acute kidney injury is a serious complication of systemic inflammatory response syndrome and its genesis is still unclear posing a difficulty for an effective treatment. Aldose reductase (AR) inhibitor is recently found to suppress lipopolysaccharide (LPS)-induced cardiac failure and its lethality. We studied the effects of AR inhibitor on LPS-induced acute kidney injury and its mechanism.

Methods

Mice were injected with LPS and the effects of AR inhibitor (Fidarestat 32 mg/kg) before or after LPS injection were examined for the mortality, severity of renal failure and kidney pathology. Serum concentrations of cytokines (interleukin-1β, interleukin-6, monocyte chemotactic protein-1 and tumor necrosis factor-α) and their mRNA expressions in the lung, liver, spleen and kidney were measured. We also evaluated polyol metabolites in the kidney.

Results

Mortality rate within 72 hours was significantly less in LPS-injected mice treated with AR inhibitor both before (29%) and after LPS injection (40%) than untreated mice (90%). LPS-injected mice showed marked increases in blood urea nitrogen, creatinine and cytokines, and AR inhibitor treatment suppressed the changes. LPS-induced acute kidney injury was associated with vacuolar degeneration and apoptosis of renal tubular cells as well as infiltration of neutrophils and macrophages. With improvement of such pathological findings, AR inhibitor treatment suppressed the elevation of cytokine mRNA levels in multiple organs and renal sorbitol accumulation.

Conclusion

AR inhibitor treatment ameliorated LPS-induced acute kidney injury, resulting in the lowered mortality.     

Comparative analysis of urinary biomarkers for early detection of acute kidney injury following cardiopulmonary bypass

The purpose of this study was to compare the performance of six candidate urinary biomarkers, kidney injury molecule (KIM)-1, N-acetyl-β-D-glucosaminidase (NAG), neutrophil gelatinase-associated lipocalin (NGAL), interleukin (IL)-18, cystatin C and α-1 microglobulin, measured 2?h following cardiopulmonary bypass (CPB) for the early detection of acute kidney injury (AKI) in a prospective cohort of patients undergoing cardiac surgery. A total of 103 subjects were enrolled; AKI developed in 13%. Urinary KIM-1 achieved the highest area under-the-receiver-operator-characteristic curve (AUC 0.78, 95% confidence interval 0.64–0.91), followed by IL-18 and NAG. Only urinary KIM-1 remained independently associated with AKI after adjustment for a preoperative AKI prediction score (Cleveland Clinic Foundation score; p?=?0.02), or CPB perfusion time (p?=?0.006). In this small pilot cohort, KIM-1 performed best as an early biomarker for AKI. Larger studies are needed to explore further the role of biomarkers for early detection of AKI following cardiac surgery.     

Method used to establish a large animal model of drug-induced acute kidney injury

Acute kidney injury is a serious health hazard disease due to its complex etiology and lack of effective treatments, resulting in high medical costs and high mortality. At present, a large number of basic research studies on acute kidney injury have been carried out. However, acute kidney injury models established in rodents sometimes do not simulate the course of human disease well. Research in large animal models of acute kidney injury is relatively rare, and methods to build a mature model of acute kidney injury have failed. Because its kidney anatomy and morphology are very similar to those in humans, the mini pig is an ideal animal in which to model kidney disease. Nephrotoxic drug-induced acute kidney injury has a high incidence. In this study, we established models of acute kidney injury induced by two drugs (gentamicin and cisplatin). Finally, the model of cisplatin-induced acute kidney injury was developed successfully, but we found the model of gentamycin-induced acute kidney injury was not reproducible. Compared to other models, these models better represent acute kidney injury caused by antibiotics and chemotherapeutic drugs and provide a basis for the study of new treatments for acute kidney injury in a large animal model.     

Diabetic kidney disease in FVB/NJ Akita mice: temporal pattern of kidney injury and urinary nephrin excretion

Akita mice are a genetic model of type 1 diabetes. In the present studies, we investigated the phenotype of Akita mice on the FVB/NJ background and examined urinary nephrin excretion as a marker of kidney injury. Male Akita mice were compared with non-diabetic controls for functional and structural characteristics of renal and cardiac disease. Podocyte number and apoptosis as well as urinary nephrin excretion were determined in both groups. Male FVB/NJ Akita mice developed sustained hyperglycemia and albuminuria by 4 and 8 weeks of age, respectively. These abnormalities were accompanied by a significant increase in systolic blood pressure in 10-week old Akita mice, which was associated with functional, structural and molecular characteristics of cardiac hypertrophy. By 20 weeks of age, Akita mice developed a 10-fold increase in albuminuria, renal and glomerular hypertrophy and a decrease in the number of podocytes. Mild-to-moderate glomerular mesangial expansion was observed in Akita mice at 30 weeks of age. In 4-week old Akita mice, the onset of hyperglycemia was accompanied by increased podocyte apoptosis and enhanced excretion of nephrin in urine before the development of albuminuria. Urinary nephrin excretion was also significantly increased in albuminuric Akita mice at 16 and 20 weeks of age and correlated with the albumin excretion rate. These data suggest that: 1. FVB/NJ Akita mice have phenotypic characteristics that may be useful for studying the mechanisms of kidney and cardiac injury in diabetes, and 2. Enhanced urinary nephrin excretion is associated with kidney injury in FVB/NJ Akita mice and is detectable early in the disease process.     

Comparison of Plasma and Urine Biomarker Performance in Acute Kidney Injury

Background

New renal biomarkers measured in urine promise to increase specificity for risk stratification and early diagnosis of acute kidney injury (AKI) but concomitantly may be altered by urine concentration effects and chronic renal insufficiency. This study therefore directly compared the performance of AKI biomarkers in urine and plasma.

Methods

This single-center, prospective cohort study included 110 unselected adults undergoing cardiac surgery with cardiopulmonary bypass between 2009 and 2010. Plasma and/or urine concentrations of creatinine, cystatin C, neutrophil gelatinase-associated lipocalin (NGAL), liver fatty acid-binding protein (L-FABP), kidney injury molecule 1 (KIM1), and albumin as well as 15 additional biomarkers in plasma and urine were measured during the perioperative period. The primary outcome was AKI defined by AKIN serum creatinine criteria within 72 hours after surgery.

Results

Biomarkers in plasma showed markedly better discriminative performance for preoperative risk stratification and early postoperative (within 24h after surgery) detection of AKI than urine biomarkers. Discriminative power of urine biomarkers improved when concentrations were normalized to urinary creatinine, but urine biomarkers had still lower AUC values than plasma biomarkers. Best diagnostic performance 4h after surgery had plasma NGAL (AUC 0.83), cystatin C (0.76), MIG (0.74), and L-FAPB (0.73). Combinations of multiple biomarkers did not improve their diagnostic power. Preoperative clinical scoring systems (EuroSCORE and Cleveland Clinic Foundation Score) predicted the risk for AKI (AUC 0.76 and 0.71) and were not inferior to biomarkers. Preexisting chronic kidney disease limited the diagnostic performance of both plasma and urine biomarkers.

Conclusions

In our cohort plasma biomarkers had higher discriminative power for risk stratification and early diagnosis of AKI than urine biomarkers. For preoperative risk stratification of AKI clinical models showed similar discriminative performance to biomarkers. The discriminative performance of both plasma and urine biomarkers was reduced by preexisting chronic kidney disease.     

Acute pancreatic beta cell apoptosis by IL-1β is responsible for postburn hyperglycemia: Evidence from humans and mice

Background

Acute hyperglycemia is regarded as a risk factor for critically ill patients; however, insufficient understanding of its nature and underlying mechanisms hinders widespread adoption of glycemic control in critical care units.

Effects of remote ischemic preconditioning in high-risk patients undergoing cardiac surgery (Remote IMPACT): a randomized controlled trial

Background:Remote ischemic preconditioning is a simple therapy that may reduce cardiac and kidney injury. We undertook a randomized controlled trial to evaluate the effect of this therapy on markers of heart and kidney injury after cardiac surgery.Methods:Patients at high risk of death within 30 days after cardiac surgery were randomly assigned to undergo remote ischemic preconditioning or a sham procedure after induction of anesthesia. The preconditioning therapy was three 5-minute cycles of thigh ischemia, with 5 minutes of reperfusion between cycles. The sham procedure was identical except that ischemia was not induced. The primary outcome was peak creatine kinase–myocardial band (CK-MB) within 24 hours after surgery (expressed as multiples of the upper limit of normal, with log transformation). The secondary outcome was change in creatinine level within 4 days after surgery (expressed as log-transformed micromoles per litre). Patient-important outcomes were assessed up to 6 months after randomization.Results:We randomly assigned 128 patients to remote ischemic preconditioning and 130 to the sham therapy. There were no significant differences in postoperative CK-MB (absolute mean difference 0.15, 95% confidence interval [CI] −0.07 to 0.36) or creatinine (absolute mean difference 0.06, 95% CI −0.10 to 0.23). Other outcomes did not differ significantly for remote ischemic preconditioning relative to the sham therapy: for myocardial infarction, relative risk (RR) 1.35 (95% CI 0.85 to 2.17); for acute kidney injury, RR 1.10 (95% CI 0.68 to 1.78); for stroke, RR 1.02 (95% CI 0.34 to 3.07); and for death, RR 1.47 (95% CI 0.65 to 3.31).Interpretation:Remote ischemic precnditioning did not reduce myocardial or kidney injury during cardiac surgery. This type of therapy is unlikely to substantially improve patient-important outcomes in cardiac surgery. Trial registration: ClinicalTrials.gov, no. {"type":"clinical-trial","attrs":{"text":"NCT01071265","term_id":"NCT01071265"}}NCT01071265.Each year, 2 million patients worldwide undergo cardiac surgery. For more than 25% of these patients, the surgery is complicated by myocardial infarction (MI) and/or acute kidney injury, both of which are strongly associated with morbidity and mortality.^1–3 Preventing MI and acute kidney injury after cardiac surgery would improve survival.An important cause of MI and acute kidney injury in patients undergoing cardiac surgery is ischemia–reperfusion injury.^4,5 This type of injury begins as ischemia, which is then exacerbated by a systemic inflammatory response upon restoration of organ perfusion.⁶ Remote ischemic preconditioning may mitigate ischemia–reperfusion damage. It is accomplished by inducing, before surgery, brief episodes of ischemia in a limb, which lead to widespread activation of endogenous cellular systems that may protect organs from subsequent severe ischemia and reperfusion.^7–9Small randomized controlled trials evaluating the efficacy of remote ischemic preconditioning have had mixed results.^10–17 Interpretation of their data is difficult because of small sample sizes and heterogeneity in the preconditioning procedures and patient populations (e.g., few trials have evaluated patients at high risk of organ injury and postoperative death). Whether remote ischemic preconditioning effectively mitigates ischemia–reperfusion injury therefore remains uncertain. We undertook the Remote Ischemic Preconditioning in Cardiac Surgery Trial (Remote IMPACT) to determine whether this procedure reduces myocardial and kidney injury. We proposed that a large trial to determine the effect on clinically important outcomes would be worthwhile only if a substantial effect on myocardial or kidney injury, or both, were observed in the current study.