胰岛素强化治疗对高血糖患者手术后的治疗观察

将88例收治于综合ICU的高血糖开腹手术后的患者随机分为传统组、强化组各44例。传统组血糖控制在8.1～11.1mmol/L;强化组4.4～8.0mmol/L。观察每天血糖、肾功能损害(血肌酐221μmol/L)及高心肌酶发生例数、伤口感染例数及住院20天后死亡例数。结果①传统组发生肾功能有损害(11例)多于强化组(3例)。发生心肌损伤(8例)多于强化组(2例)。②伤口感染率(13.65%)高于强化组(4.55%)。病死率(22.73%)高于强化组(6.82%),有显著性差异(P0.05)。结论强化治疗能减少高血糖患者手术后的心肌损作和肾损伤,并能减少他们的伤口感染率和病死率。     

肝移植术后激素冲击治疗急性排斥反应诱发1例高渗性非酮症高血糖昏迷

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60例重型颅脑损伤并高血糖患者行胰岛素强化治疗护理体会

2003年1月～2006年1月，我们对60例例重型颅脑损伤并发高血糖患者实行了胰岛素强化治疗。现将护理体会介绍如下。     

门冬胰岛素和人胰岛素强化治疗内科危重症高血糖患者的疗效

<正>高血糖症的发生在危重症患者中较常见,是导致患者死亡的一个危险因素〔1〕。内科危重症病人因处于强烈的应激反应致使糖代谢紊乱,血糖升高,高血糖可引起人体水电解质紊乱促进了炎症反应,增加感染机会,造成器官功能损害,使病情加重影响预后。近年来对危重症患者高血糖状态的研究越来越多,相关研究表明,采用强化胰岛素治疗的方法治疗危重症患     

胰岛素强化治疗对高血糖危重症患者抢救成功率的影响

目的观察胰岛素强化治疗对高血糖危重症患者抢救成功率的影响，并探讨其可能的机制。方法将收入ICU监护病房的110例高血糖危重症患者随机分为胰岛素强化治疗组（血糖控制在4．4～6．1mmol／L）和胰岛素常规治疗组（血糖控制在8．0～11．1mmol／L）。观察两组患者并发症发生率、ICU停留时间、死亡率等，并于人院后24h、4天、10天通过EMSA、流式细胞仪和ELISA法对外周血单核细胞NF—kB活性、单核细胞HLA—DR表达及血浆CRP水平进行动态检测。结果（1）强化治疗组死亡率（19．6％VS27．8％，P〈0．05）明显低于常规治疗组。（2）强化治疗组人院后24h、4天、10天各时点NF—kB活性、CRP水平均显著低于常规治疗组（P〈0．05）。（3）强化治疗组HLA—DR表达显著高于常规治疗组（P〈0．05）。结论胰岛素强化治疗能降低高血糖危重症患者死亡率，缩短ICU停留时间，降低医疗费用等，这与胰岛素严格控制血糖能够改善机体免疫状态、减轻全身炎症反应有关。     

门冬胰岛素和人胰岛素强化治疗内科危重症高血糖疗效比较

目的 比较门冬胰岛素和人胰岛素强化治疗内科危重症高血糖的有效性和安全性.方法 选取中南大学湘雅二医院老年病科符合全身炎症反应综合征诊断标准的内科危重患者186例,入组时空腹血糖水平为(10.8±2.3)mmoL/L,根据患者入组时恢复进食情况分为多次皮下注射胰岛素组(MDI,n=90)和持续皮下注射胰岛素组(CSⅡ,n=96),2组均随机分为门冬胰岛素和人胰岛素亚组.MDI组中门冬胰岛素和人胰岛素亚组分别为44、46例,CSⅡ组分别为46、50例.MDI组餐前大剂量采用门冬胰岛素或人胰岛素,基础量均采用甘精胰岛素,CSⅡ组餐前大剂量及基础量均采用门冬胰岛素或人胰岛素.根据多点指尖血糖监测结果调整胰岛素用量,强化胰岛素治疗疗程7 d,使血糖控制在4.4～8.3 mmol/L,7 d后改为常规胰岛素治疗,使血糖控制在4.4～11.1 mmol/L,观察各哑组患者基线及第7天日内平均血糖水平、日内血糖标准差、日内血糖极差(最高和最低血糖之差)、血清C反应蛋白(CRP)水平、急性生理与慢性疾病评分(APACHE Ⅱ),统计7 d内低血糖发生率、严重低血糖发生率、日平均胰岛素用量及28 d内各组死亡率.统计学分析采用t检验和x~2检验.结果 (1)MDI及CSⅡ组的门冬胰岛素亚组和人胰岛素亚组强化治疗各项指标差异无统计学意义.(2)强化治疗后第7天门冬胰岛素哑组较人胰岛素组日内平均血糖水平更低,MDI组:(6.2±1.3)mmol/L比(7.6±1.6)mmol/L;CSⅡ组:(6.0±1.2)mmol/L比(7.4±2.5)mmol/L,均P＜0.05.(3)门冬胰岛素亚组血糖标准差更小,MDI组:(1.54±0.27)mmol/L比(1.92±0.38)mmol/L;CSⅡ组:(1.24±0.27)mmol/L比(1.83±0.45)mmol/L,均P＜0.05.(4)门冬胰岛素亚组极差更小,MDI组:(3.0±0.5)mmoL/L vs(3.9±1.1)mmoL/L;CSⅡ组:(3.1±0.6)mmol/L vs(3.9±1.0)mmol/L,均P＜0.05.(5)门冬胰岛素业组7 d内日平均胰岛素用量更少,低血糖发生率及严重低血糖发生率更低.同时,门冬胰岛素亚组7 d内血清CRP?     

早期改良强化胰岛素序贯治疗在ICU中的应用

目的 探讨强化胰岛素治疗在重症监护室(ICU)的临床运用.方法 将所选病例随机分成强化治疗组1、组2和常规血糖控制组,组1将血糖控制在4.4～6.1 mmol/L(80～110 mg/dl)之间,组2将血糖控制在6.1～7.8 mmol/L(110～140 mg/dl)之间,而常规血糖控制组,血糖控制在10.0～11.0 mmoL/L(180～198 mg/dl)之间.比较三组的院内感染发生率、并发症发生率、住ICU时间、机械通气时间及3个月死亡率.结果 强化组1、组2及常规组治疗后的血乳酸值(mmol/L)分别为(0.74±0.33、0.68±0.19、0.96±0.29),强化组1及强化组2与常规组比较均有显著差异(P=0.000).强化组1及组2的院内感染发生率、并发症发生率、住ICU时间、机械通气时间与常规组比较无显著性差异(P>0.05).强化组1及强化组2与常规组的3个月死亡率比较无显著差异(P>0.05).强化组1的低血糖发生率(6.67%)与常规组(0%)比较有显著性差异(P<0.05);强化组2的低血糖发生率(3.33%)与常规治疗组比较无显著性差异(P>0.05).结论 对于危重症高血糖患者进行正确地血糖控制对改善危重病人的临床症状有重要的意义,推荐血糖控制在6.1～7.8 mmol/L之间.     

胰岛素强化治疗在呼吸机相关性肺炎并高血糖中的应用分析

目的探讨胰岛素强化治疗在呼吸机相关性肺炎(VAP)并高血糖中的疗效及预后。方法入选2008年1月~2013年12月我院收治的VAP合并高血糖患者90例,分为胰岛素强化治疗组(观察组)与传统治疗组(对照组)。观察两组患者使用呼吸机时间、低血糖发生率、多器官功能障碍综合征(MODS)发生率以及死亡率。此外,对治疗前后患者体温、白细胞(WBC)水平、血清降钙素原(PCT)、血清淀粉样蛋白A(SAA)水平进行记录分析。结果观察组MODS发生率及死亡率分别为42.22%、33.33%,明显低于对照组的22.22%、15.56%,差异具有显著性(P0.05);观察组呼吸机时间明显少于对照组(P0.05);治疗后,观察组体温、WBC、血清PCT、SAA水平等均明显优于对照组,差异均具有统计学意义(均P0.05)。结论VAP合并高血糖患者给予胰岛素强化治疗具有较好疗效,能够缩短呼吸机使用时间,降低MODS发生率与死亡率,可以改善相关炎症指标,值得临床推广。     

肝移植术后相关高血糖症的调查分析

有研究表明,糖代谢异常可增加肝移植术后患者发生心血管疾病、感染以及神经系统病变等的危险性,是肝移植术后患者病死率的独立预测因素[1].因此,如何预防和控制肝移植术后糖代谢异常在移植术后患者的随访中显得日益重要.现就我院肝移植术后1年发生血糖代谢异常的患者进行回顾性分析,报道如下.     

Management of biliary complications after liver transplantation

Biliary complications(BC) currently represent a major source of morbidity after liver transplantation. Although refinements in surgical technique and medical therapy have had a positive influence on the reduction of postoperative morbidity, BC affect 5% to 25% of transplanted patients. Bile leak and anastomotic strictures represent the most common complications. Nowadays, a multidisciplinary approach is required to manage such complications in order to prevent liver failure and retransplantation.     

Management of early hepatic artery occlusion after liver transplantation with failed rescue

Hepatic artery thrombosis is a serious complication after liver transplantation which often results in biliary complications, early graft loss, and patient death. It is generally thought that early hepatic artery thrombosis without urgent re-vascularization or re-transplantation almost always leads to mortality, especially if the hepatic artery thrombosis occurs within a few days after transplantation. This series presents 3 cases of early hepatic artery thrombosis after living donor liver transplantation, in which surgical or endovascular attempts at arterial re-vascularization failed. Unexpectedly, these 3 patients survived with acceptable graft function after 32 mo, 11 mo, and 4 mo follow-up, respectively. The literatures on factors affecting this devastating complication were reviewed from an anatomical perspective. The collective evidence from survivors indicated that modified nonsurgical management after liver transplantation with failed revascularization may be sufficient to prevent mortality from early hepatic artery occlusion. Re-transplantation may be reserved for selected patients with unrecovered graft function.     

Management of recurrent hepatitis C virus after liver transplantation

Chronic hepatitis C virus(HCV) infection is the leading cause of death from liver disease and the leading indication for liver transplantation(LT) in the United States and western Europe. LT represents the best therapeutic alternative for patients with advanced chronic liver disease caused by HCV or those who develop hepatocarcinoma. Reinfection by HCV of the graft is universal and occurs in 95% of transplant patients. This reinfection can compromise graft function and patient survival. In a few cases, the histological recurrence is minimal and non-progressive; however, in most patients it follows a more rapid course than in immunocompetent persons, and frequently evolves into cirrhosis with graft loss. In fact, the five-year and ten-year survival of patients transplanted because of HCV are 75% and 68%, respectively, compared with 85% and 78% in patients transplanted for other reasons. There is also a pattern of recurrence that is very severe, but rare(< 10%), called fibrosing cholestatic hepatitis, which often involves rapid graft loss. Patients who present a negative HCV viremia after antiviral treatment have better survival. Many studies published over recent years have shown that antiviral treatment of post-transplant HCV hepatitis carried out during the late phase is the best option for improving the prognosis of these patients. Until 2011, PEGylated interferon plus ribavirin was the standard of care, resulting in a sustained virological response in around 30% of recipients. The addition of protease inhibitors, such as boceprevir or telaprevir, to the standard of care, or the use of other direct-acting antiviral drugs may involve therapeutic changes in the context of HCV recurrence. This may result a better prognosis for these patients, particularly those with severe recurrence or factors predicting rapid progression of fibrosis. However, the use of these agents in LT still requires clarification in terms of safety and efficacy.     

Hepatic venous outflow obstruction after piggyback liver transplantation by an unusual mechanism： Report of a case

INTRODUCTIONHepatic venous outflow obstruction after piggybackorthotopic liver transplantation is a rare complication[1,2]. However, failure of early recognition and treatment of this complication can result in graft failure and even death of patients. We…     

肝移植术后早期肝功能不全影响因素的研究进展

肝移植作为终末期肝病最有效的治疗手段,术后往往会出现早期移植物功能不全。肝移植术后早期肝功能不全已成为肝移植术后的并发症之一,严重影响移植物和患者生存。因此,减少其发生可作为改善肝移植术后受体预后的重要手段。现就肝移植术后受体早期肝功能不全的定义、影响因素、预后、预测模型等研究进展作一论述,以期为更好地防治移植术后早期肝功能不全,进一步提高肝移植手术成功率,改善患者预后提供有效参考。     

Comprehensive risk assessment for early neurologic complications after liver transplantation

AIM: To determine risk factors for early neurologic complications(NCs) after liver transplantation from perspective of recipient, donor, and surgeon. METHODS: In all, 295 adult recipients were enrolled consecutively between August 2001 and February 2014 from a single medical center in Taiwan. Any NC in the first 30 d post-liver transplantation, and perioperative variables from multiple perspectives were collected and analyzed. The main outcome was a 30-d NC. Generalized additive models were used to detect the non-linear effect of continuous variables on outcome, and to determine cut-off values for categorizing risk. Risk factors were identified using multiple logistic regression analysis. RESULTS: In all, 288 recipients were included, of whom 142(49.3%) experienced at least one NC, with encephalopathy being the most common 106(73%). NCs prolonged hospital stay(35.15 ± 43.80 d vs 20.88 ± 13.58 d, P 0.001). Liver recipients' age 29 or ≥ 60 years, body mass index 21.6 or 27.6 kg/m~2, Child-Pugh class C, history of preoperative hepatoencephalopathy or mental disorders, day 7 tacrolimus level 8.9 ng/m L, and postoperative intraabdominal infection were more likely associated with NCs. Novel risk factors for NCs were donor age 22 or ≥ 40 years, male-to-male gender matching, graftrecipient weight ratio 0.9%-1.9%, and sequence of transplantation between 31 and 174. CONCLUSION: NCs post- liver transplantation occurs because of factors related to recipient, donor, and surgeon. Our results provide a basis of risk stratification for surgeon to minimize neurotoxic factors during transplantation.     

Long-term antiviral treatment for recurrent hepatitis C after liver transplantation

Background and aims

The management of patients treated for hepatitis C recurrence after liver transplantation and not achieving virological response following treatment with interferon plus ribavirin is controversial.

Methods

A retrospective analysis of the outcomes of 70 patients non-responders to antiviral treatment after liver transplantation was performed. Twenty-one patients (30.0%; Group A) were treated for ≤12 months and 49 (70.0%; Group B) for more than 12 months.

Results

The 2 groups were comparable for main demographic, clinical and pathological variables. Median duration of antiviral treatment was 8.2 months in Group A and 33.4 months in Group B. No patient achieved a complete virological response. The 5-year patient hepatitis C-related survival rate was 49.2% in Group A and 88.3% in Group B (P = 0.002), while the 5-year graft survival rate was 49.2% in Group A and 85.9% in Group B (P = 0.007). The median yearly fibrosis progression rate was 1.21 per year in Group A and 0.40 per year in Group B (P = 0.001).

Conclusions

Prolonged antiviral treatment showed an overall beneficial effect in transplanted patients with a recurrent hepatitis C infection and not responding to conventional therapy. The treatment should be continued as long as it is permitted, in order to improve clinical and histological outcomes.     

Management of hepatitis B virus infection after liver transplantation

Chronic hepatitis B virus(HBV) infection is responsible for up to 30% of cases of liver cirrhosis and up to 53% of cases of hepatocellular carcinoma. Liver transplantation(LT) is the best therapeutic option for patients with end-stage liver failure caused by HBV. The success of transplantation, though, depends on receiving prophylactic treatment against post-transplant viral reactivation. In the absence of prophylaxis, liver transplantation due to chronic hepatitis B(CHB) is associated with high rates of viral recurrence and poor survival. The introduction of treatment with hepatitis B immunoglobulins(HBIG) during the 1990 s and later the incorporation of oral antiviral drugs have improved the prognosis of these patients. Thus, LT for CHB is now a universally accepted option, with an estimated 5 years survival of around 85% vs the 45% survival seen prior to the introduction of HBIG. The combination of lamivudine plus HBIG has for many years been the most widely used prophylactic regimen. However, with the appearance of new more potent oral antiviral agents associated with less resistance(e.g., entecavir and tenofovir) for the treatment of CHB, new prophylactic strategies are being designed, either in combination with HBIG or alone as a monotherapy. These advances have allowed for more personalized prophylaxis based on the individual risk profile of a given patient. In addition, the small pool of donors has required the use of anti-HBc-positive donors(with the resulting possibility of transmitting HBV from these organs), which has been made possible by suitable prophylactic regimens.     

New-onset hyperglycemia immediately after liver transplantation: A national survey from China Liver Transplant Registry

Background: New-onset hyperglycemia(NOH) is a common phenomenon after liver transplantation(LT),but its impact on clinical outcomes has not yet been fully assessed. We aimed to evaluate the etiology and prognosis of NOH within 1 month after LT.Methods: The data of 3339 adult patients who underwent primary LT from donation after citizen death between January 2010 and June 2016 were extracted from China Liver Transplant Registry database and analyzed. NOH was defined as fasting blood glucose ≥7.0 mmol/L confirmed on at least two occasions within the first post-transplant month with or without hypoglycemic agent.Results: Of 3339 liver recipients, 1416(42.4%) developed NOH. Recipients with NOH had higher incidence of post-transplant complications such as graft and kidney failure, infection, biliary stricture, cholangitis,and tumor recurrence in a glucose concentration-dependent manner as compared to non-NOH recipients(P 0.05). The independent risk factors of NOH were donor warm ischemic time 10 min, cold ischemic time 10 h, anhepatic time 60 min, recipient model for end-stage liver disease score 30, moderate ascites and corticosteroid usage(P 0.05). Liver enzymes(alanine aminotransferase and gammaglutamyltranspeptidase) on post-transplant day 7 significantly correlated with NOH(P 0.001).Conclusions: NOH leads to increased morbidity and mortality in liver recipients. Close surveillance and tight control of blood glucose are desiderated immediately following LT particularly in those with delayed graft function and receiving corticosteroid. Strategic targeting graft ischemic injury may help maintain glucose homeostasis.