Managing acute respiratory failure during exacerbation of chronic obstructive pulmonary disease

Exacerbations of chronic obstructive pulmonary disease (COPD) are a major health problem, causing more than half a million hospital admissions per year in the United States. Although overall mortality is low, it is substantially higher with severe exacerbations that require intensive care and mechanical ventilation. The majority of COPD exacerbations result from infection, with typical bacterial organisms most commonly identified. Numerous randomized controlled trials and meta-analyses have documented the benefits of antibiotics, low-flow oxygen, and systemic corticosteroids, and the therapeutic equivalency of the major classes of bronchodilators (short-acting beta-agonist and anticholinergics). Randomized controlled trials also demonstrate that noninvasive ventilation can decrease the incidence of intubation, shorten stay, reduce infectious complications, and improve survival. Although patients who require intubation have the worst prognosis, the vast majority of them can be successfully liberated from mechanical ventilation. For invasively ventilated patients the clinical emphasis should be on improving patient-ventilator interaction and avoiding dynamic hyperinflation (intrinsic positive end-expiratory pressure).     

慢性阻塞性肺疾病和支气管哮喘生理评分在疾病急性加重期护理中的应用价值

目的 探讨慢性阻塞性肺疾病和支气管哮喘生理评分(the COPD and Asthma Physiology Score,CAPS)能否正确评估慢性阻塞性肺疾病急性加重期(AECOPD)患者病情的严重性和预后,指导治疗和护理计划的制定.方法 对我科2008年9月～2010年5月住院的AECOPD患者进行回顾性分析和CA...     

Mechanisms of acute exacerbation of respiratory symptoms in chronic obstructive pulmonary disease

Exacerbations of chronic obstructive respiratory disease (ECOPD) are acute events characterized by worsening of the patient's respiratory symptoms, particularly dyspnoea, leading to change in medical treatment and/or hospitalisation. AECOP are considered respiratory diseases, with reference to the respiratory nature of symptoms and to the involvement of airways and lung. Indeed respiratory infections and/or air pollution are the main causes of ECOPD. They cause an acute inflammation of the airways and the lung on top of the chronic inflammation that is associated with COPD. This acute inflammation is responsible of the development of acute respiratory symptoms (in these cases the term ECOPD is appropriate). However, the acute inflammation caused by infections/pollutants is almost associated with systemic inflammation, that may cause acute respiratory symptoms through decompensation of concomitant chronic diseases (eg acute heart failure, thromboembolism, etc) almost invariably associated with COPD. Most concomitant chronic diseases share with COPD not only the underlying chronic inflammation of the target organs (i.e. lungs, myocardium, vessels, adipose tissue), but also clinical manifestations like fatigue and dyspnoea. For this reason, in patients with multi‐morbidity (eg COPD with chronic heart failure and hypertension, etc), the exacerbation of respiratory symptoms may be particularly difficult to investigate, as it may be caused by exacerbation of COPD and/or ≥ comorbidity, (e.g. decompensated heart failure, arrhythmias, thromboembolisms) without necessarily involving the airways and lung. In these cases the term ECOPD is inappropriate and misleading.     

慢性阻塞性肺疾病急性加重的临床意义

慢性阻塞性肺疾病（COPD）急性加重（AECOPD）特征是患者的呼吸困难、咳嗽和（或）咯痰出现了超常的变化，需要对治疗进行调整。COPD患者常经历急性加重，每一次发作将加重疾病并促进疾病的发展，AECOPD的程度和频率均可以加重基础疾病，COPD患者1年内平均出现1～3次急性加重，可导致患者病死率增高。因此，AECOPD是COPD的重要评价指标，对急性加重预防和医疗资源利用的评估是COPD治疗的重要目标。     

Administration of acute exacerbation of chronic obstructive pulmonary disease

We have to consider the exacerbation of chronic obstructive pulmonary disease(COPD) may be caused not only by infection, but also by acute exacerbation of chronic heart failure, pulmonary embolism, pneumothorax, or other cardiopulmonary complications. Because it is characteristic that the exacerbation of COPD is often recurensive, the most important thing is the administration during stable status. Approximately 40% of pathogens of the acute infectious exacerbation of COPD are Haemophilus influenzae, Streptococcus pneumoniae, Moraxella catarrhalis, Pseudomonas aeruginosa, Staphylococcus aureus, and Echelisia coli. Also, approximately 15% is exacerbated by atypical pathogens such as Chlamydia pneumoniae and approximately 30% is by viral infection. We should contemplate the possibility of pathogens according to the statistics, when we choose antibiotics empirically.     

呼吸道合胞病毒感染对慢性阻塞性肺疾病急性加重期患者的影响

目的:分析慢性阻塞性肺疾病急性加重(AECOPD)患者有无合并呼吸道合胞病毒(RSV)感染的临床资料,观察RSV感染的临床表现及其对AECOPD患者病情的影响。方法:2009年1月至6月瑞金医院呼吸科急诊留院观察符合AECOPD诊断标准病例80例,采用直接免疫荧光及酶联免疫吸附试验双重方法进行RSV感染定性检测,纳入阳性组12例,阴性组45例,比较两组间血浆和痰上清液肿瘤坏死因子α(TNF-α)水平、入院48h内入住ICU比率等临床资料。结果:①RSV阳性组和RSV阴性组AECOPD患者男女构成比、年龄、体质量指数(BMI)、第1秒用力呼气容积(FEV1)/用力肺活量(FVC)、FEV1占预计值(%)、吸烟史、本次就诊前1年慢性阻塞性肺疾病急性加重频率、本次加重天数无统计学意义(P均>0.05)。入院后首次血常规各类细胞计数、动脉血pH值、动脉血二氧化碳分压(PaCO2)、血TNF-α、痰上清液TNF-α在两组间差异无统计学意义(均P>0.05)。②12例RSV阳性组48h内入住ICU有5例,45例RSV阴性组入住ICU有6例,RSV阳性组较RSV阴性组入住ICU比率较高(P=0.03)。相关性分析示RSV阳性组痰上清液TNF-α与血清TNF-α呈正相关(r=0.66,P=0.02),RSV阴性组两指标无显著相关(P>0.05)。结论:合并RSV感染的AECOPD患者发病初期气道与全身炎症应答相关联可能是RSV感染的表现,合并RSV感染的患者入院48h内入住ICU的比率较高,提示RSV感染有导致AECOPD急性危重倾向。     

雾化布地奈德治疗慢性阻塞性肺疾病急性加重期临床观察

目的比较慢性阻塞性肺疾病急性加重期(AECOPD)吸入布地奈德与静脉滴注甲强龙的临床疗效及卫生经济学。方法回顾性分析山西医科大学第一医院住院的AECOPD患者121例,根据糖皮质激素应用情况分为:布地奈德低剂量组(3 mg/d,A组)33例,布地奈德高剂量组(6 mg/d,B组)32例,甲强龙组(40 mg/d,C组)28例,对照组(未用糖皮质激素,D组)28例,观察各组有效率、血气指标、不良反应、住院天数及费用并进行统计学分析。结果与D组比较,A、B、C组临床总有效率增高,差异均有统计学意义(均P<0.05),各治疗组间比较差异均无统计学意义(均P>0.05)。治疗后血气指标比较,与D组比较,A、B、C组动脉血氧分压(Pa O2)升高,动脉血二氧化碳分压(PCO2)降低;与A组比较,B、C组Pa O2升高,PCO2降低,差异均有统计学意义(均P<0.05);B组与C组比较差异均无统计学意义(均P>0.05)。与C组比较,A、B、D组不良反应降低,差异均有统计学意义(均P<0.05)。与D组比较,A、B、C组的住院天数、费用均减少;与A组比较,B、C组的住院天数、费用均减少,差异均有统计学意义(均P<0.05);B与C组比较差异无统计学意义(P>0.05)。结论 AECOPD吸入布地奈德6 mg/d疗效可靠,糖皮质激素的不良反应发生率低,患者的经济负担轻。     

慢性阻塞性肺病急性加重期的循证治疗

1 病例 男性,68岁,因“反复咳嗽,咯痰40~ 年,气促2~ 年,复发伴加重1周”入院,入院前40年,患者感冒受凉后出现咳嗽、咯痰,经对症治疗后好转,此后上述症状反复发作,有时伴有喘息。入院前2~ 年,患者开始出现活动后气促。入院前1周,患者出现咳嗽、咯痰、喘息,气促症状加重,入我院就诊。     

血清淀粉样蛋白A水平在慢性阻塞性肺疾病急性加重期的临床意义

目的探讨慢性阻塞性肺疾病急性加重期(AECOPD)患者血清淀粉样蛋白A(SAA)水平变化的临床意义。方法选取AECOPD住院患者40例,依据2011年慢性阻塞性肺疾病全球倡议(GOLD)标准分为A组6例、B组11例、C组8例、D组15例,记录患者CAT评分、缓解期肺功能,采用酶联免疫吸附法(ELISA)测定SAA。观察各组急性期与缓解期血清SAA水平、白细胞计数及中性粒细胞百分比的变化;分析血清SAA水平与第1秒用力呼气容积占预计值百分比(FEV1)、白细胞计数及中性粒细胞比例的相关性。结果 A、B、C、D各组急性期血清SAA水平显著高于缓解期,差异有统计学意义(P<0.01);急性期血清SAA水平在A、B、C、D各组间差异显著(P<0.01),且呈递增趋势;AECOPD患者血清SAA水平与FEV1%预计值呈负相关(r=-0.746,P<0.01);与白细胞计数(r=0.783,P<0.01)、中性粒百分比(r=0.621,P<0.01)呈正相关。结论SAA弥补了单独运用FEV_1%预计值或CAT评分作为AECOPD患者病情评估指标的不足;SAA比白细胞计数及中性粒细胞比例有更好的诊断价值,可能为探索AECOPD的炎症机制提供一个新的视角和手段。     

The role of respiratory infection in exacerbation of chronic obstructive pulmonary disease

Periods of acute deterioration known as exacerbations significantly lower the quality of life and health status of patients with chronic obstructive pulmonary disease (COPD), thus making treatment of these patients more expensive. Understanding of the pathogenesis of COPD exacerbations and their influence on the clinical course and prognosis of this disease has greatly improved during the last decades. Some aspects of the interrelation between the infectious pathogen and the host organism have been studied. According to modern data, respiratory infections present one of the main causes of exacerbations of the disease. The role of respiratory viruses, especially rhinoviruses and respiratory syncytial virus, which often precede secondary bacterial infections, have been found to be important in the etiology of COPD exacerbation. The main bacterial etio-pathogens of COPD exacerbations--the non-capsulated bacteria H. influenzae, S. pneumoniae, and M. catarrhalis, which in 25 to 50% of cases colonize the lower respiratory tract (LRT)--have been isolated. Colonization of the LRT of infectious agents (viruses and bacteria) results in chronization of the inflammatory process and progress of the disease. Besides, colonization correlates with the severity of the disease. A "vicious circle" theory has been put forward to explain the pathogenesis of COPD exacerbations. Etiological diagnostics of a COPD exacerbation will allow adequate choice of effective etiotropic therapy making it possible to eradicate the pathogen or lower microbial load in the respiratory tract, which will decrease the risk of recurrence and improve the prognosis of the disease.     

慢性阻塞性肺疾病急性加重期下呼吸道感染病原学检测及耐药分析

目的探讨慢性阻塞性肺疾病(COPD)患者急性加重期下呼吸道感染的病原菌分布情况及其耐药特点,为临床合理使用抗生素治疗提供依据。方法回顾性分析本院2008年1~12月呼吸科92例COPD患者急性加重期下呼吸道病原学和细菌耐药性特点。结果共培养阳性菌101株,革兰阴性细菌占主导地位,主要包括铜绿假单胞菌(31.24%)、大肠埃希菌(24.56%)、鲍曼不动杆菌(14.85%);革兰阳性菌中金黄色葡萄球菌(9.78%)、表皮葡萄球菌(4.72.%);白色假丝酵母菌(6.75%);部分致病菌呈多重耐药。结论 COPD急性加重期下呼吸道感染病原菌以革兰阴性菌占优势,部分致病菌呈多重耐药,临床应合理使用抗生素防止细菌耐药。     

七叶皂苷钠对慢性阻塞性肺疾病急性加重期氧化应激和肺功能的影响

目的探讨七叶皂苷钠对慢性阻塞性肺疾病（COPD）急性加重期氧化应激和肺功能的影响。方法120例符合COPD纳入标准的患者随机分为对照组60例和治疗组60例。所有患者均给予常规抗感染、吸氧、化痰和平喘等对症治疗,治疗组在常规对症治疗基础上加用七叶皂苷钠。两组均于治疗前及治疗后2周测定血清超氧化物歧化酶（SOD）、丙二醛（MDA）、谷胱甘肽过氧化物酶（GSH—Px）以及总抗氧化能力（T—AOC）,同时进行肺功能和6min步行距离（6MWD）检测,并与60名健康体检者（健康组）进行比较。结果治疗组总有效率91．67％（55／60）,对照组总有效率76．67％（46／60）,差异有统计学意义（χ^2=5．065,P〈0．05）。治疗前对照组血清MDA（9．25±1．55）μmoL／L和治疗组（9．74±1．50）μmoL／L较健康组（2．06±0．29）μmoL／L高,差异均有统计学意义（P均〈0．001）,而血清SOD[对照组（91．14±9．54）kU／L、治疗组（90．61±8．01）kU／L]、GSH-Px[对照组（139．38±36．56）U／L、治疗组（137．57±34．19）U／L]、T-AOC[对照组（6．48±1．15）kU／L、治疗组（6．39±1．13）kU／L]水平较健康组[（116．63±6．57）kU／L、（189．34±35．54）U／L、（13．34±1．23）kU／L]低,差异均有统计学意义（P均〈0．001）。治疗后两组各指标较治疗前均有所改善（P〈0．001）,但治疗后治疗组血清MDA[（4．56±1．39）μmol/L]与对照组[（5．85±1．37）μmoL／L]比较明显下降,差异有统计学意义（t=6．517,P〈0．001）,血清SOD[（103．85±7．07）kU／L]、GSH-Px[（169．65±34．51）U／L]、T-AOC[（10．52±1．09）kU／L]水平,第1秒用力呼气容秽用力肺活量（FEV1／FVC）[（60．49±6．11）％],FEV1占预计值％[（76．62±6．35）％]以及6MWD[（394．83±10．11）m]与对照组[分别为（97．99±6．24）kU／L、（156．33±38．31）U／L、（8．82±1．41）kU／L、（53．84±2．97）％、（67．86±4．58）％、（331．19±11．03）m]比较明显升高,差异有统计学意义（t值分别为6．574、2．738、7．137、6．574、6．517、21．198,P均〈0．001）。结论氧化应激参与了COPD急性加重期的病理生理过程,七叶皂苷钠可能通过减轻COPD急性加重期患者氧化应激水平改善肺功能。     

无创正压通气治疗慢性阻塞性肺疾病急性加重并发肺性脑病临床研究

慢性阻塞性肺疾病（COPD）急性加重（AECOPD）时由于气道阻力显著增加，以及内源性呼气末正压（PEEPi）存在。患者常可并发严重Ⅱ型呼吸衰竭。由于严重的CO2潴留而并发肺性脑病，传统的方法是在常规药物治疗基础上应用呼吸兴奋剂或建立人工气道机械通气，前者疗效不理想，后者则治疗护理复杂、要求高、并发症多．在基层医院尚未普及重症加强治疗病房（ICU）条件下，应用受到限制。     

布地奈德在慢性阻塞性肺疾病急性加重期的临床疗效观察

目的评价局部吸入布地奈德治疗慢性阻塞性肺疾病急性加重期的疗效及安全性。方法选择60例COPD急性加重期住院患者随机均分为3组:①布地奈德组给予布地奈德雾化液雾化吸入2 mg/次,每8小时1次;②泼尼松组给予口服泼尼松片30 mg/次,每日1次;③空白对照组不使用任何糖皮质激素。观察3组患者治疗后呼吸困难评分、肺功能和动脉血气变化。结果与空白对照组比较,布地奈德组、泼尼松组在治疗后呼吸困难评分、动脉血气及肺功能的改善有显著性差异(P0.05)。布地奈德组与泼尼松组在提高FEV1、PaO2,改善呼吸困难评分方面无显著性差异(P0.05)。但在PaCO2值下降方面,在治疗7 d后布地奈德组下降(4.4±1.5)mmHg,泼尼松组下降(5.3±2.2)mmHg,两组比较有显著性差异(P0.05)。布地奈德组的不良反应少于泼尼松组。结论布地奈德组的疗效明显优于空白对照组,但与泼尼松组的无显著性差异。局部吸入布地奈德溶液是COPD急性加重期有效选择。     

布地奈德在慢性阻塞性肺疾病急性加重期的临床疗效观察

目的评价局部吸入布地奈德治疗慢性阻塞性肺疾病急性加重期的疗效及安全性。方法选择60例COPD急性加重期住院患者随机均分为3组：①布地奈德组给予布地奈德雾化液雾化吸入2 mg/次,每8小时1次;②泼尼松组给予口服泼尼松片30 mg/次,每日1次;③空白对照组不使用任何糖皮质激素。观察3组患者治疗后呼吸困难评分、肺功能和动脉血气变化。结果与空白对照组比较,布地奈德组、泼尼松组在治疗后呼吸困难评分、动脉血气及肺功能的改善有显著性差异（P〈0.05）。布地奈德组与泼尼松组在提高FEV1、PaO2,改善呼吸困难评分方面无显著性差异（P〉0.05）。但在PaCO2值下降方面,在治疗7 d后布地奈德组下降（4.4±1.5）mmHg,泼尼松组下降（5.3±2.2）mmHg,两组比较有显著性差异（P〈0.05）。布地奈德组的不良反应少于泼尼松组。结论布地奈德组的疗效明显优于空白对照组,但与泼尼松组的无显著性差异。局部吸入布地奈德溶液是COPD急性加重期有效选择。     

慢性阻塞性肺疾病急性发作期病原菌及耐药性分析

目的:总结我院慢性阻塞性肺疾病急性发作期(AECOPD)患者下呼吸道感染病原菌分布和耐药性特点,指导抗生素应用。方法:对我院2003年7月1日至2004年12月31日呼吸科收治的258例AECOPD患者行痰液细菌培养,药敏采用纸片扩散法。结果:258例AECOPD患者痰细菌培养分离出251株致病菌,以革兰阴性杆菌居首位(77.3%),真菌第2位(12.4%),革兰阳性球菌第3位(10.4%)。革兰阴性杆菌中以铜绿假单胞菌(38.1%)、嗜麦芽窄食单胞菌(16.0%)、不动杆菌(12.9%)、洋葱伯克霍尔德氏菌(7.2%)为主要致病菌。革兰阳性球菌中以金黄色葡萄球菌(34.6%)、表皮葡萄球菌(23.1%)、肺炎链球菌(19.2%)为主要致病菌。药敏发现,对铜绿假单胞菌抗菌活性较强的有头孢他啶、头孢哌酮/舒巴坦;对嗜麦芽窄食假单胞菌抗菌活性较强的有环丙沙星、头孢哌酮/舒巴坦;对不动杆菌较敏感的有泰能、美罗培南、哌拉西林/他唑巴坦、头孢哌酮/舒巴坦;对洋葱伯克霍尔德氏菌敏感的有复方新诺明、泰能。阿米卡星、万古霉素对大部分革兰阳性球菌敏感。结论:AECOPD下呼吸道致病菌以革兰阴性杆菌为主,且耐药率较高。AECOP...