肾移植术后肺部感染致呼吸衰竭应用无创机械通气患者的护理

总结应用无创机械通气治疗的12例肾移植术后肺部感染致呼吸衰竭患者的临床资料及护理方法.无创机械通气治疗前及治疗2 h后血气分析结果比较,差异有显著性意义(P＜0.05);无1例发生呼吸机相关性肺炎等严重并发症.认为在机械通气尤其是无创机械通气的过程中,有效的心理护理及正确的指导,保持呼吸道通畅,密切观察病情,加强并发症的预防护理及基础护理等措施,对提高肾移植术后肺部感染致呼吸衰竭患者的治愈率有重要的作用.     

肾移植术后肺部感染致呼吸衰竭应用无创机械通气患者的护理

总结应用无创机械通气治疗的12例肾移植术后肺部感染致呼吸衰竭患者的临床资料及护理方法。无创机械通气治疗前及治疗2h后血气分析结果比较，差异有显著性意义（P〈0．05）；无1例发生呼吸机相关性肺炎等严重并发症。认为在机械通气尤其是无创机械通气的过程中，有效的心理护理及正确的指导，保持呼吸道通畅，密切观察病情，加强并发症的预防护理及基础护理等措施，对提高肾移植术后肺部感染致呼吸衰竭患者的治愈率有重要的作用。     

无创正压机械通气治疗肾移植术后巨细胞病毒肺炎所致急性呼吸窘迫综合征

目的 探讨肾移植术后巨细胞病毒(CMV)肺炎合并急性呼吸窘迫综合征(ARDS)无创正压机械通气治疗效果. 方法 肾移植术后CMV肺炎合并ARDS患者10例.早期应用无创正压机械通气治疗及抗病毒、调整免疫抑制剂、加强营养支持的综合治疗.比较分析患者通气治疗前后动脉血气、生命指标及移植肾功能变化. 结果 10例患者中治愈7例.1例脱机时发生张力性气胸及广泛皮下气肿死亡;另2例治疗中病情加重改有创机械通气,治疗5、18 d无效死亡.7例治愈患者上机前与上机后、脱机前的动脉血气分析血氧分压、血氧饱和度、血二氧化碳分压比较差异有统计学意义(P<0.05);治疗前后患者血肌酐(平均15625对101.85 μmol/L)、血尿素氮(平均11.93对6.55 mmol/L)比较差异有统计学意义(P<0.05). 结论 早期应用无创正压机械通气辅以抗病毒为主的综合治疗,是提高重症CMV肺炎治愈率的重要措施.     

开胸术后发生急性呼吸窘迫综合征的病因探讨及治疗

目的 探讨开胸术后发生急性呼吸窘迫综合征(ARDS)的原因及防治措施。方法 回顾分析1993年7月～2001年4月,31例开胸患者术后发生ARDS的发病特点,可能的原因及防治方法。结果 有长期慢性肺部疾患、大量吸烟、原发性高血压病的患者,术后容易发生ARDS。肺部感染、休克和手术肺损伤是发生ARDS的3大诱因。治疗应积极清除呼吸道分泌物、保持气道通畅、控制感染、利尿减轻肺水肿,尤其是尽早行气管插管或气管切开机械辅助通气是抢救成功的关键。结论 开胸术后患者发生ARDS的原因复杂,其中肺部感染、休克和手术肺损伤可能是主要原因,早期积极的治疗有望降低ARDS患者的病死率。     

机械通气治疗腹部外科术后急性呼吸衰竭的临床研究

目的探讨腹部外科术后发生急性呼吸衰竭的诱因及影响机械通气疗效的因素。方法回顾性分析91例患者腹部外科术后发生急性呼吸衰竭的基础疾病、诱因及机械通气治疗的效果。结果诱因包括术后发生肺部感染53例，严重腹腔感染或急性重症胰腺炎导致的急性呼吸窘迫综合征(ARDS) 38例。其中合并慢性阻塞性肺病(COPD)38例，重度营养不良32例，低钾血症14例。呼吸衰竭发生在术后(4.08±2.45)d，机械通气维持时间(21.66±21.42)d。死亡33例（36.3%），撤机成功58例（63.7%）。结论腹部外科术后发生急性呼吸衰竭时，应合理实施机械通气并调整撤机策略，避免机械通气依赖。及时处理原发病，有效控制腹腔感染，积极进行对症与支持治疗是影响机械通气成败的因素。     

机械通气在胸部肿瘤术后急性呼吸衰竭治疗中的应用

目的总结胸部肿瘤患者术后发生急性呼吸衰竭（ARF）行机械通气治疗的经验。方法根据64例胸部肿瘤患者术后发生ARF的情况，如原发病、手术后的肺疾病、呼吸肌力和手术并发症等进行不同的机械通气治疗，其中61例进行有创通气治疗，3例进行无创性正压通气。对12例肺不张或严重肺部感染者进行床旁纤维支气管镜吸痰、支气管肺泡灌洗（BAL）。结果64例ARF中54例治愈，10例死亡。12例肺不张或严重肺部感染者经纤维支气管镜治疗均有效；随访54例，随访时间2个月，无ARF复发。结论胸部肿瘤患者术后发生ARF应选择恰当的通气模式，进行个性化机械通气治疗，良好的机械通气有利于治疗术后并发症；对有肺不张或严重肺部感染者进行纤维支气管镜吸痰和BAI。治疗效果良好。     

老年患者术后急性呼吸衰竭12例分析

本文对12例老年患者术后呼吸衰竭分析结果表明,老年患者因其脏器存在潜在功能障碍,如果术前准备不充分,术中生命体征不平稳,特别是逾量补液时易发生呼吸衰竭。其发生率为4.5％,呼吸衰竭发生后及时给予氧疗,同时应给予脱水利尿药物、低分子右旋糖苷及皮质激素可减轻肺水肿。上述治疗失败后应及时进行机械通气。维持术中、术后血压稳定,防治肺部感染是预防术后呼吸衰竭的主要措施。     

机械通气对食管癌术后呼吸衰竭患者血气分析指标及预后的影响

目的探讨机械通气治疗食管癌术后呼吸衰竭患者的效果及其对血气分析指标及预后的影响。方法 2011年1月至2014年1月选取80例行食管癌根治手术后发生呼吸衰竭的患者为研究对象,根据随机数字表分为观察组及对照组各40例,对照组术后给予有创机械通气,观察组应用无创机械通气辅助治疗,对比分析两组患者治疗前后血气分析指标、并发症及预后的情况。结果两组治疗后PaCO2、PaO2、SaO2、pH值较术前有明显改善(P0.05),治疗后观察组与对照组比较无显著差异(P0.05)。观察组并发症发生率及死亡率均低于对照组,观察组ICU时间及机械通气时间显著短于对照组,差异有统计学意义(P0.05)。结论对食管癌术后并发呼吸衰竭患者应用机械通气辅助治疗能有效改善患者血气分析指标,促进患者预后。     

影响经面罩机械通气治疗慢性阻塞性肺病呼吸衰竭的因素分析

目的:探讨影响经面罩机械通气治疗慢性阻塞性肺病呼吸衰竭发生急性呼吸窘迫综合征的因素。方法:选择慢性阻塞性肺病呼吸衰竭患者120例,都采用影响经面罩机械通气治疗,观察急性呼吸窘迫综合征发生情况与影响因素。结果:治疗中与治疗后发生呼吸窘迫综合征12例,发生率为8.0%。单因素分析显示pH值、严重感染、呼衰指数、肺顺应性是导致急性呼吸窘迫综合征的危险因素(P<0.05)。多因素分析显示严重感染、pH值、肺顺应性为主要的危险因素(P<0.05)。结论:经面罩机械通气治疗慢性阻塞性肺病呼吸衰竭有很好的效果,但是容易出现急性呼吸窘迫综合征,为此要对应加强预防处理。     

呼吸机辅助呼吸治疗肾移植术后重症肺炎的体会并文献复习

目的探讨呼吸机辅助呼吸对肾移植术后重症肺炎并发呼吸衰竭患者的治疗价值。方法 4例患者中男3例,女1例,平均年龄50岁。除给予常规治疗外,使用纽邦E360呼吸机给予辅助呼吸。有创通气2例,无创通气2例。有创通气采用同步间歇指令+压力支持通气模式;无创通气采用压力支持通气加呼吸末正压通气。严密观察患者病情变化,注意气管插管深度、气囊状态、面罩漏气程度等,及时给予调整呼吸机参数。同时积极治疗原发病,患者全身状况得到改善,体温正常,营养状态改善,导致呼吸衰竭的原发病因已解除或得到控制,肺部分泌物减少,呼吸肌力恢复较好,血液循环状态稳定后,从逐渐撤机过渡到完全撤机。结果 4例患者经治疗后,3例痊愈出院,1例死亡。3例痊愈患者的通气时间平均为15 d,其动脉血气分析指标、呼吸频率、心率均较通气前明显改善。在机械通气过程中,1例发生气胸,经予胸腔闭式引流后治愈。1例死亡患者合并糖尿病、肾癌等病史,有延误诊治史。结论经呼吸机辅助呼吸治疗肾移植术后重症肺炎并发呼吸衰竭患者疗效较好。     

Nitric oxide inhalation in the treatment of primary graft failure following heart transplantation.

BACKGROUND: Primary graft failure from right or left ventricular insufficiency remains a serious cause of early death following heart transplantation. Inhaled nitric oxide (NO) is a potent pulmonary vasodilator that could decrease pulmonary pressure and improve right ventricular function. METHODS: Two cases of early graft failure following orthotopic heart transplantation were treated with NO inhalation. The treatment consisted of inhalation of 20 ppm of NO, introduced 4 to 6 hours following transplantation, in 2 patients supported with high doses of inotropic agents and vasopressors in addition to the intra-aortic balloon pump. RESULTS: In the first and second cases, NO inhalation resulted in a decrease in pulmonary artery pressure, in a decrease in pulmonary vascular resistance and in an increase in cardiac index. In the second patient, systemic oxygenation improved markedly 30 minutes after initiation of NO. In the 2 patients, NO inhalation, mechanical ventilation and the intra-aortic balloon pump were weaned 4 days following transplantation. CONCLUSION: Primary graft failure from donor ischemic damage, reperfusion injury or pulmonary hypertension remains a serious complication. The use of an intra-aortic balloon pump, inotropic agents and of inhaled NO appears to offer the best support for recovery of donor heart function. Primary graft failure from right or left ventricular insufficiency remains a serious cause of early mortality following heart transplantation. Ischemic damage of donor heart, reperfusion injury or pulmonary hypertension are the main causes of early graft failure. Although the cause is multifactorial, treatment of primary organ failure remains difficult with dismal results. The objective of the present study was to review the result of 2 patients with donor right heart failure following heart transplantation treated with inhaled nitric oxide (NO).     

Lung retrieval from non-heart beating cadavers with the use of a rat lung transplant model.

BACKGROUND: Lungs retrieved from cadavers after death and circulatory arrest may alleviate the critical shortage of lungs for transplant. We report a rat lung transplantation model that allows serial measurement of arterial blood gases after left single lung transplantation from non-heart beating donors. METHODS: Twelve Sprague-Dawley rats underwent left lung transplantation with a vascular cuff technique. Donor rats were anesthetized with intraperitoneal injection of pentobarbital, heparinized, intubated via tracheotomy, and then killed with pentobarbital. Lungs were retrieved immediately or after 2 hours of oxygen ventilation after death (tidal volume 1 mL/100 g, rate 40/min FIO2 = 1.0, positive end-expiratory pressure 5 cm H2O). Recipient rats were anesthetized, intubated, and ventilated. The carotid artery and jugular vein were cannulated for arterial blood gases and infusion of Ringer's lactate (4 mL/h). Anesthesia was maintained with halothane 0.2%, and recipient arterial blood gases were measured at 4 and 6 hours after lung transplantation after snaring the right pulmonary artery for 5 minutes. Animals were put to death 6 hours after lung transplantation, and portions of transplanted lungs were frozen in liquid nitrogen and assayed for wet/dry ratio, myeloperoxidase as a measure of neutrophil infiltration, and conjugated dienes as a measure of free radical-mediated lipid peroxidation. RESULTS: Arterial PO2 and wet/dry ratio were not significantly different in recipients of non-heart beating donor lungs retrieved immediately after death or after 2 hours of oxygen ventilation. Significant neutrophil infiltration was observed in recipients of non-heart beating donor lungs retrieved 2 hours after death from oxygen-ventilated donors. CONCLUSIONS: Strategies to ameliorate reperfusion injury may allow for successful lung transplantation from non-heart beating donors.     

Risk factors for acute respiratory failure after liver transplantation

OBJECTIVES: To study the risk factors for acute respiratory failure during recovery after liver transplantation. PATIENTS AND METHODS: We prospectively studied 340 consecutive liver transplant operations. Patient data was grouped according to whether acute respiratory failure developed (group I) or not (group II). Acute respiratory failure was defined by the need for mechanical ventilation longer than 5 days after transplantation or by the need for an inspired oxygen fraction of over 50% for 72 hours. We evaluated demographic characteristics, stage of liver disease before the transplant, comorbidity, immunosuppressant treatment administered, and complications during and after surgery. RESULTS: Sixty-six patients were placed in group I and 274 in group II. Univariate analysis showed significant differences between the groups for age, sex, Child-Pugh functional stage, preoperative renal failure, type of immunosuppression, and postoperative complications such as atrial fibrillation, pleural effusion, pulmonary edema, ascites, postoperative acute renal failure, brain dysfunction, early graft dysfunction, and respiratory infection. Multivariate analysis by logistic regression, taking the development or not of acute respiratory failure as the dependent variable, gave a model with 6 variables that accounted for 94% of the cases. The variables entering into the model, with their respective odds ratios (OR) were female sex (OR, 5.5), stage C liver function (OR, 3.9), pulmonary edema (OR, 16.3), postoperative acute renal failure (OR, 9), cerebral dysfunction (OR, 4.5), and respiratory infection (OR, 62). CONCLUSIONS: The development of acute respiratory failure after liver transplantation is affected by the following factors: female sex, Child-Pugh class, pulmonary edema, postoperative acute renal failure, cerebral dysfunction, and respiratory infection.     

Postoperative pulmonary complications: pneumonia and acute respiratory failure

Postoperative pulmonary complications (atelectasis, pneumonia, pulmonary edema, acute respiratory failure) are common, particularly after abdominal and thoracic surgery, pneumonia and atelectasis being the most common. Postoperative pneumonia is associated with increased morbidity, length of hospital stay, and costs. Few institutions have pneumonia prevention programs for surgical patients, and these should be strongly considered. Acute respiratory failure is a life-threatening pulmonary complication that requires institution of mechanical ventilation and admission to the intensive care unit, and is associated with increased risk for ventilator-associated pneumonia. This article discusses epidemiology, risk factors, diagnosis, treatment, and prevention of these pulmonary complications in surgical patients.     

Ecstasy-induced brain death and acute hepatocellular failure: multiorgan donor and liver transplantation

BACKGROUND: Ecstasy is a neurotoxic and hepatotoxic drug. Brain edema and fulminant hepatic failure are two of the most serious complications associated with the consumption of ecstasy. Acute ecstasy intoxication can transform a patient into an organ donor or a hepatic graft recipient. MATERIALS AND METHODS: In the last 5 years in our centers, we have had two multiorgan donors who died from ecstasy-induced brain edema and three patients who required urgent orthotopic liver transplantation for treatment of severe acute hepatocellular failure induced by this drug. We performed eight transplantations using the organs of these two brain-dead donors: one heart, one bipulmonary, three kidneys, one kidney-pancreas, and two livers. RESULTS: Toxicity caused by ecstasy was not observed in any of the eight patients who underwent transplantation. The clinical state and the graft function of the heart, two liver, renopancreatic, and three kidney recipients were normal for a follow-up period that ranged between 7 months and 4.5 years. The lung recipient died from multiorgan failure secondary to bilateral pneumonia 5 days after the transplantation, and one of the kidney transplant patients died as a result of intestinal lymphoma 6 months after transplantation. The three liver transplantations in the three patients with ecstasy-induced fulminant hepatic failure were performed successfully using orthotopic transplantation. These three recipients are asymptomatic and have normal-functioning hepatic grafts after follow-up of 3.5 years, 15 months, and 11 months, respectively. CONCLUSIONS: The thoracic and abdominal organs of people dying from ecstasy intoxication can be viable for transplantation. The short- and medium-term survival of the graft and of the recipient have been similar to that of other organ donors. Urgent liver transplantation is an effective therapeutic option in patients with ecstasy-induced acute hepatocellular failure.     

Anesthetic management of infants receiving an adult kidney transplant

Renal transplantation in infants has been associated with a high incidence of acute tubular necrosis and of renal artery thrombosis. Since 1978, 24 infants who received an adult kidney transplant at the University of Minnesota have had aggressive administration of intravenous colloids to increase the central venous pressure to 16-20 mm Hg before renal reperfusion. Acute tubular necrosis developed in only two infants, and there were no cases of renal artery thrombosis. Chest radiographic evidence of pulmonary edema was present in the recovery room in seven patients (29%) and within the first four postoperative days in five patients (21%). Yet, only two infants (8.3%) required postoperative mechanical ventilation beyond 24 h to manage fluid overload. With aggressive intravenous colloid administration, infants in renal failure can receive an adult kidney transplant with a low incidence of active tubular necrosis or renal artery thrombosis, but pulmonary edema may develop requiring ventilatory support.     

介入诊疗技术在肾移植临床上的应用(附14例报告)

目的：探讨介入诊疗技术在肾移植临床上的应用。方法：回顾性分析14例肾移植术后患者接受介入诊疗的临床资料．其中肾移植术后肾功能丧失8例。移植肾动脉血栓形成2例．移植肾动脉狭窄2例。假性动脉瘤和术后并发重症高血压各1例。结果：对8例移植肾失功能者进行动脉造影。3例显示血管堵塞未予处置，另5例进行移植。肾动脉栓塞。其中3例栓塞术后完全停用免疫抑制剂．1例用小剂量激素维持．1例手术切除移植肾。1例重症高血压者经自体肾动脉栓塞．血压得到很好控制。接受肾动脉栓塞术患者均出现“栓塞后综合征”。2例移植肾动脉血栓形成患者溶栓成功．但。肾功能未恢复。2例移植肾动脉狭窄患者．1例放置支架失败。仅进行球囊扩张，术后血压控制良好。肾功能恢复。但6个月后血压再次升高、肾功能严重受损而行栓塞治疗，1例未处置。术后高血压得到控制。1例移植肾假性动脉瘤者经动脉造影证实后手术切除。结论：移植肾或自体肾动脉栓塞可替代手术切除移植肾和治疗肾移植术后重症高血压；移植肾动脉血栓形成可作溶栓治疗；移植肾动脉狭窄进行球囊扩张远期效果不佳。     

肾移植术后早期死亡原因分析

目的:分析肾移植术后早期(6个月内)死亡原因,总结经验,提高和改善移植效果。方法:回顾性分析2000年1月~2005年2月施行433例尸体肾移植患者的临床资料,对其中19例术后早期死亡原因及相关因素进行探讨。结果:术后早期死亡病因包括感染7例,占36.8%;急性心力衰竭4例,占21.1%;肾破裂致失血性休克3例,占15.8%;弥漫性血管内凝血2例,占10.5%;暴发性肝功能衰竭1例、急性心肌梗死1例、肺动脉栓塞1例,各占5.3%。除暴发性肝功能衰竭患者于术后118天死亡外,其余均在术后1个月内死亡。结论:感染是肾移植术后早期死亡最常见的原因,与术后免疫抑制过度、营养不良及术后并发症等有关,其中以肺部和泌尿系感染最重要;心血管疾病是引起移植术后早期死亡的另一重要因素,尤其是高龄和糖尿病患者;肾移植早期死亡与肾功能延迟恢复(包括急性排斥反应和急性肾小管坏死)有密切关系,积极合理的治疗对预防肾移植术后早期死亡具有重要意义。     

肺移植治疗儿童肺动脉高压的临床疗效

目的 探讨同种异体肺移植治疗儿童肺动脉高压(PAH)的临床疗效.方法 受者例1、2为特发性肺动脉高压( IPAH)患儿,均经右心导管术确诊为IPAH,术前心功能不全Ⅳ级,肺动脉收缩压、平均压分别为110、70 mm Hg(1 mm Hg =0.133 kPa)和148、72 mm Hg,在全麻体外膜肺氧合(ECMO)支持下行序贯式双侧单肺移植术,术中ECMO支持时间分别为550 min和450 min,出血量分别为3000 ml和1200 ml.受者例3为先天性心脏病室间隔缺损合并艾森曼格综合征心内直视探查术后,超声心动图(UCG)提示先天性心脏病室间隔缺损,双向分流,肺动脉收缩压、平均压为110、60 mm Hg,在全麻低温体外循环(CPB)下行室间隔缺损修补术同期右侧单肺移植术,术中CPB时间244 min.3例受者与供者体型较匹配,ABO血型相同.结果 受者例1、2术后ECMO分别维持16h、13 h后撤离,术后第3、4天均出现不同程度的血流动力学不稳定,诊断为急性左心衰,均于术后第3、6天行气管切开呼吸机辅助正压通气,经强心、利尿、扩血管等治疗,分别于术后第33天、12天脱离呼吸机.受者例3术后3天内移植肺出现中等程度再植反应性肺水肿,术后第7天气管切开,第12天撤离呼吸机;术后第14天出现急性排斥1次,治疗后缓解.3例受者术后UCG提示心脏形态和心功能明显改善,受者例3室间隔缺损修补完整,无残余分流.分别于术后第93天、32天、62天康复出院,心功能均达Ⅰ级,肺动脉收缩压、平均压分别降为54、32 mm Hg,60、36 mm Hg和53、39 mm Hg.术后已随访41、21、82个月,患儿正常工作学习,至今生活质量良好.结论 对终末期经内科保守治疗效果欠佳的PAH患儿行肺移植能很好改善生活质量.