肾移植术后肺部感染致急性呼吸窘迫综合征抢救9例护理体会

目的 探讨肾移植术后肺部感染致急性呼吸窘迫综合征（ARDS）的病情观察，早期提供呼吸支持及护理。方法 对9例肾移植术后肺部感染致ARDS的临床资料进行了回顾性分析，总结抢救护理体会。结果 抢救成功5例，死亡3例，放弃治疗1例，死亡率达37．5％。结论 针对肾移植术后肺部感染致急性呼吸窘迫综合征（ARDS），应综合性治疗，及时调整免疫抑制剂，采取相应护理措施，加强整体护理、基础护理、心理护理，及早提供呼吸支持，正确使用呼吸机，均是提高抢救成功率的关键。     

肾移植术后重症肺部感染致急性呼吸窘迫综合征18例报告

目的：探讨肾移植术后重症肺部感染致急性呼吸窘迫综合征（ARDS）的临床特点和诊断与治疗。方法：对本院2002年1月-2006年4月收治的18例重症肺部感染致ARDS患者的临床资料进行分析。结果：18例患者中，治愈8例（44．5％），死亡10例（55．6％）。结论：肾移植术后重症肺部感染病情发展迅速，发展为ARDS后治疗难度加大，预后差，早期诊治、注重自身抵抗力的提高、合理及时调整免疫抑制方案及使用激素是救治成功的关键。     

肾移植术后并发重症肺部感染的原因与护理

目的探讨肾移植术后并发重症肺部感染的原因与护理。方法回顾性分析29例肾移植术后并发重症肺部感染患者的临床资料。结果29例重症肺部感染患者中17例（58．6％）救治成功,12例（41．4％）因合并急性呼吸窘迫综合征抢救无效死亡。结论重症肺部感染是肾移植受者术后近期死亡的主要原因之一;果断减少或停用免疫抑制剂、早期联合用药抗感染治疗、制定个体化护理措施、积极配合医师的诊断与治疗等对患者的成功救治至关重要。     

肺挫伤所致急性呼吸窘迫综合征的预防

目的：探讨降低肺挫伤患者并发急性呼吸窘迫综合征的经验。方法：1999－2001年肺挫伤患者448例在处理过程中保持呼吸通畅，充分给氧、早期使用抗生素、合理使用呼吸机。结果：全组448例肺挫伤患者32例并发肺炎，4例并发急性呼吸窘迫综合征（ARDS）。4例并发ARDS患者2例死亡，另2例痊愈。结论：预防ARDS的关键于正确的伤情评估，预防和早期治疗肺部感染，合理应用呼吸支持治疗和适当的支持治疗。     

肾移植术后肺部感染致急性呼吸窘迫综合征的护理

目的探讨肾移植术后重症肺部感染致急性呼吸窘迫综合征（ARDS）的护理措施。方法回顾性分析24例肾移植术后重症肺部感染致ARDS患者的临床护理措施。结果本组24例患者,15例痊愈出院,2例放弃治疗,7例抢救无效死亡。结论肾移植术后肺部感染致ARDS患者应密切观察病情,严格执行消毒隔离制度,及早提供呼吸支持,加强心理护理、基础护理及营养支持,这些对提高抢救成功率极为关键。     

肾移植术后肺部感染的诊治

目的提高肾移植术后肺部感染的诊疗水平。方法回顾性分析总结36例肾移植术后并发肺部感染患者的临床资料及诊治情况。结果29例患者找到病原体47例次，7例未找到确切的病原体；并发急性肺损伤／急性呼吸窘迫综合征者共20例，其中12例行机械通气治疗，10例（83．3％）治愈；19例患者行纤维支气管镜（纤支镜）介入诊疗，其中16例（84．2％）明确了病原体，12例患者经纤支镜介入治疗后，临床症状均有不同程度改善；本组36例患者中，32例（88．9％）治愈，2例死亡，2例因经济原因放弃治疗自动出院。结论肾移植术后肺部感染患者应积极进行病原学的检测，重视影像学检查的意义；早期经验性治疗能否覆盖可能感染的病原体是治疗能否成功的关键；纤支镜介入诊疗对于提高肾移植术后肺部感染（尤其是莺症肺部感染）的治愈率有重要作用。     

健康教育预防肾移植术后肺部感染的效果观察

肾移植是目前救治慢性肾衰竭最有效的方法，但肾移植术后由于免疫抑制剂的使用及病人预防感染意识缺乏等原因，易导致肺部感染的发生，特别是严重肺部感染并发急性呼吸窘迫综合征（ARDS），症状严重，病情复杂，进展迅猛，处理棘手，现已成为肾移植术后致病人死亡的最主要原因。     

开胸术后并发急性呼吸窘迫综合征的相关因素分析

目的:分析开胸术后发生急性呼吸窘迫综合征(ARDS)的可能原因及防治措施方法:回顾分析2004年1月至2008年12月43例开胸术后发生ARDS的43例病例资料.结果:开胸术后ARDS患者大多数手术较为复杂,时间偏长,术中输血较多,高龄患者占多数.术后33例并发肺部感染.结论:对于手术时间偏长、术中输血较多、高龄的患者,术后发生ARDS的风险较大,而手术创伤、肺部感染是发生ARDS的直接诱因.重视和加强ARDS高风险人群的围手术期处理,减少手术创伤有助于开胸术后ARDS的防治.     

创伤性休克患者院前救治与术后急性肺损伤/急性呼吸窘迫综合征发生的相关性调查

目的 调查分析创伤性休克患者院前救治与术后急性肺损伤（ALI）／急性呼吸窘迫综合征（ARDS）的相关性及其临床意义。方法 随机双盲法抽取1995年10月-2005年10月符合调查条件的创伤性休克患者600例，其中院前进行综合治疗184例（A组），单纯液体复苏治疗305例（B组），未治疗111例（C组）。对比各组全身炎症反应综合征（SIRS）、ALI／ARDS、多器官功能障碍综合征（MODS）确诊率及预后；并以入院1h及术后24、48、96和144h相关数据进行SIRS评分。结果 600例患者中524例诊断为SIRS（占87．33％），其中A组73．37％（135／184例），B组91．48％（279／305例），C组99．10％（110／111例）；SIRS分值A组各时间点均显著低于B组和C组（P均〈O．01），B组又低于C组（P均〈O．01）；且A组术后96h基本正常，而B组术后144h才接近正常。ALI确诊率A组为5．98％（11／184例），发生ARDS1例，MODS1例，无死亡；B组为10．49％（32／305例），发生ARDS7例，MODS3例，死亡3例；C组则为20．72％（23／111例），发展为ARDS8例，MODS5例，死亡5例。结论 创伤性休克院前救治与术后ALI密切相关，院前综合治疗有助于降低术后ALI／ARDS的发生率。     

71例肾移植受者术后肺部感染的诊治体会

目的探讨肾移植术后肺部感染发病特点、诊治及预防措施。方法回顾性分析71例肾移植术后肺部感染患者临床资料。结果71例患者中肺部感染发生于肾移植术后〈4个月54例（76．06％）,4-6个月12例（16．9％）,〉6个月5例（7．04％）。临床表现均有发热,23例为固定时间发热,52例感胸闷,19例迅速进展出现急性呼吸紧迫综合征（ARDS）,3例死亡。混合感染者36例,细菌感染16例,巨细胞病毒（HCMV）感染13例,结核感染2例,肺孢子虫感染1例,不明原因3例。结论肾移植后肺部感染多为细菌为主的混合感染,病情进展迅速而危重,早期就诊,针对病原体合理抗菌治疗,及时调整免疫治疗方案和加强综合治疗是治疗成功的关键。     

Pneumothorax in patients with acute respiratory distress syndrome: pathophysiology, detection, and treatment

Pneumothorax is a frequent and potentially fatal complication of mechanical ventilation in patients with acute respiratory distress syndrome (ARDS). Prompt recognition and treatment of pneumothoraces is necessary to minimize morbidity and mortality. The radiologic and clinical signs of pneumothoraces in ARDS patients may have unusual and subtle features. Furthermore, small pneumothoraces in these patients can cause severe hemodynamic or pulmonary compromise. Sparse clinical literature exists on when or how to treat pneumothoraces once they develop in patients with ARDS. In this article, the authors review the pathogenesis, radiologic signs, clinical significance, and treatment of pneumothoraces in ARDS patients. Treatment options include traditional tube thoracostomy, open thoracotomy, and image-guided percutaneous catheters.     

纤溶酶原激活物抑制物-1与急性脑梗死并发急性肺损伤/急性呼吸窘迫综合征的相关性研究

目的探讨急性脑梗死并发急性肺损伤/急性呼吸窘迫综合征患者血清纤溶酶原激活物抑制物-1(PAI-1)水平变化及临床意义。方法采用前瞻性研究方法,收集急性脑梗死并发ALI/ARDS患者28例,单纯ALI/ARDS患者26例,健康对照组20例。根据脑梗死部位不同,A组被进一步分为前循环区组(5例)、后循环区组(15例)、分水岭区组(8例)。所有研究对象均已行头颅CT/MRI检查。A、B组行APACHEⅡ评分。检测所有患者血清PAI-1水平,比较各组PAI-1水平变化及其与A-PACHEⅡ评分相关性。结果脑梗死并发ALI/ARDS组、单纯ALI/ARDS组PAI-1水平高于对照组(P<0.01),脑梗死并发ALI/ARDS组高于单纯ALI/ARDS组(P<0.05)。后循环梗死患者ALI/ARDS发生率最高(53.57%)。血清PAI-1水平与A-PACHEⅡ评分呈正相关(P<0.01)。结论 ALI/ARDS存在凝血纤溶功能障碍,脑梗死(尤其后循环区梗死)更易致ALI/ARDS的发生,PA-I1水平可预示疾病的严重程度。     

Sequential production of leukaemia inhibitory factor by blood cell culture in patients with ARDS

Objective: Leukaemia inhibitory factor (LIF) is a polyfunctional cytokine integrated in cytokine networks and its concentration has been shown to be elevated in bronchoalveolar lavage fluid of patients with the acute respiratory distress syndrome (ARDS). The aim of our study was to evaluate the production of LIF by culturing blood cells from patients with ARDS. Patients: 8 patients with ARDS, 8 patients with pneumonia and 5 healthy subjects. Measurements and results: The blood samples were taken on day 1 after onset of ARDS. LIF was measured, in the cell-free supernatant, with an enzyme-linked immunosorbent assay after 24 h, 48 h and 72 h of blood cell culture. LIF was detectable in some patients in the ARDS group: at i) at 24 h and 48 h: in 2 patients ii) at 72 h in 4/5 patients (140 ± 231 pg/ml). Only in the 4 patients in whom LIF was measured at 72 h was ARDS associated with the multiple organ dysfunction syndrome. Furthermore, among the 5 patients with ARDS who subsequently died, 4 had a detectable LIF. Conclusions: We have observed that LIF was produced only in ARDS, but not in all patients. The production of LIF seems to be a good indicator of the severity of ARDS. These preliminary results must be confirmed by a larger study. Received: 31 July 1997 Accepted: 13 January 1998     

Evaluation of the -26G>A CC16 polymorphism in acute respiratory distress syndrome

OBJECTIVE: Different risk factors are presumably involved in the pathogenesis of acute respiratory distress syndrome (ARDS) including genetic factors. Clara cell protein 16 (CC16) is a potential candidate gene for ARDS susceptibility because reduced levels of the anti-inflammatory CC16 have been observed in bronchoalveolar lavage fluids or serum of patients with different inflammatory lung diseases. Furthermore, CC16 potently inhibits phospholipase A2, which plays a major role in ARDS pathophysiology. A functional polymorphism (-26G>A) was previously identified and related to decreased CC16 levels, asthma, and asthma severity. DESIGN: Observational study. SETTINGS: Adults with ARDS were recruited from intensive care units in two university medical centers. SUBJECTS: We evaluated the role of this genetic variant in 117 German patients with ARDS and 373 German controls. MEASUREMENTS: The CC16 -26G>A polymorphism was analyzed by melting-curve analysis using a pair of fluorescence resonance energy transfer probes. MAIN RESULTS: CC16 genotype frequencies in ARDS patients did not differ from those seen in controls. Also, the allele frequencies were identical in patients compared with controls (0.66 and 0.34). Moreover, only one of the patients who died (n = 27) was homozygous for the -26A allele. CONCLUSIONS: The CC16 -26G>A polymorphism does not affect the susceptibility to and the outcome of ARDS.     

Incidence and mortality of adult respiratory distress syndrome: a prospective analysis from a large metropolitan hospital

We examined the incidence and mortality of adult respiratory distress syndrome (ARDS) in patients receiving emergency medical care at a large metropolitan medical center. The patients were classified into eight high-risk categories and monitored prospectively until discharge or death. Over a period of 12 months, 11,112 such patients entered the emergency room. Of 4926 who were admitted to the hospital acutely ill, 90 (2%) developed ARDS. Thirty-six percent of these survived. ARDS occurred in 25% of patients admitted with acquired immune deficiency syndrome and Pneumocystis carinii pneumonia, and mortality in these patients was 86%. Aspiration pneumonia was the primary cause of ARDS in 37% of the patients, who also had a similar mortality rate (85%). Mortality was also high in patients with multisystem organ failure or with ARDS and disseminated intravascular coagulation. These results indicate that there probably is a relatively low incidence of ARDS among hospital patients admitted with high-risk diagnoses.     

Postoperative Acute Respiratory Distress Syndrome in Patients With Previous Exposure to Bleomycin

ObjectiveTo determine the incidence and risk factors for postoperative acute respiratory distress syndrome (ARDS) in a large cohort of bleomycin-exposed patients undergoing surgery with general endotracheal anesthesia.Patients and MethodsFrom a Mayo Clinic cancer registry, we identified patients who had received systemic bleomycin and then underwent a major surgical procedure that required more than 1 hour of general anesthesia from January 1, 2000, through August 30, 2012. Heart, lung, and liver transplantations were excluded. Postoperative ARDS (within 7 days after surgery) was defined according to the Berlin criteria.ResultsWe identified 316 patients who underwent 541 major surgical procedures. Only 7 patients met the criteria for postoperative ARDS; all were white men, and 6 were current or former smokers. On univariate analysis, we observed an increased risk of postoperative ARDS in patients who were current or former smokers. Furthermore, significantly greater crystalloid and colloid administration was found in patients with postoperative ARDS. We also observed a trend toward longer surgical duration and red blood cell transfusion in patients with postoperative ARDS, although this finding was not significant. Intraoperative fraction of inspired oxygen was not associated with postoperative ARDS. In bleomycin-exposed patients, the incidence of postoperative ARDS after major surgery with general anesthesia is approximately 1.3% (95% CI, 0.6%-2.6%). For first major procedures after bleomycin therapy, the incidence is 1.9% (95% CI, 0.9%-4.1%).ConclusionThe risk of postoperative ARDS in patients exposed to systemic bleomycin appears to be lower than expected. Smoking status may be an important factor that modifies the risk of postoperative ARDS in these patients.     

Complement activation and increased alveolar-capillary permeability after major surgery and in adult respiratory distress syndrome

The concentrations of C3a des Arg were measured in bronchoalveolar fluid (BAL) and plasma from 12 patients with adult respiratory distress syndrome (ARDS). Compared with 32 controls, all patients had increased BAL fluid levels (p less than .001), and nine of 12 had increased plasma levels (p less than .001) of this split product from the third complement component. Reduced total hemolytic activity (CH50) in serum was seen in five patients (p less than .01). As an indication of damage to the alveolar-capillary barrier, ten of the 12 ARDS patients had elevated albumin concentrations in BAL fluid (p less than .001). These signs of complement activation and lung tissue damage are not specific for ARDS. Thus, in 15 patients investigated preoperatively and postoperatively, we found that major surgery induced a significant increase of BAL fluid C3a (p less than .01) and plasma C3a (p less than .02), a significant reduction of CH50 (p less than .001), and a significant increase of BAL fluid albumin (p less than .02). Similar values of CH50 and plasma C3a were seen in ARDS and after surgery (p greater than .05). Of the 12 ARDS patients, eight had increased BAL fluid concentrations of C3a (p less than .001), and ten had increased BAL fluid levels of albumin (p less than .001) compared with the post-surgical patients. Measuring complement consumption in blood by these techniques is of limited value in ARDS due to the lack of specificity. BAL fluid albumin has a similar degree of sensitivity and specificity for ARDS as does BAL fluid C3a.(ABSTRACT TRUNCATED AT 250 WORDS)     

Ventilator-associated pneumonia and ICU mortality in severe ARDS patients ventilated according to a lung-protective strategy

ABSTRACT: INTRODUCTION: Ventilator-associated pneumonia (VAP) may contribute to the mortality associated with acute respiratory distress syndrome (ARDS). We aimed to determine the incidence, outcome, and risk factors of bacterial VAP complicating severe ARDS in patients ventilated by using a strictly standardized lung-protective strategy. METHODS: This prospective epidemiologic study was done in all the 339 patients with severe ARDS included in a multicenter randomized, placebo-controlled double-blind trial of cisatracurium besylate in severe ARDS patients. Patients with suspected VAP underwent bronchoalveolar lavage to confirm the diagnosis. RESULTS: Ninety-eight (28.9%) patients had at least one episode of microbiologically documented bacterial VAP, including 41 (41.8%) who died in the ICU, compared with 74 (30.7%) of the 241 patients without VAP (P = 0.05). After adjustment, age and severity at baseline, but not VAP, were associated with ICU death. Cisatracurium besylate therapy within 2 days of ARDS onset decreased the risk of ICU death. Factors independently associated with an increased risk to develop a VAP were male sex and worse admission Glasgow Coma Scale score. Tracheostomy, enteral nutrition, and the use of a subglottic secretion-drainage device were protective. CONCLUSIONS: In patients with severe ARDS receiving lung-protective ventilation, VAP was associated with an increased crude ICU mortality which did not remain significant after adjustment.