Surgical therapies for chronic obstructive pulmonary disease

Surgical procedures for treating emphysema were first developed nearly 100 years ago. Despite a wide range of surgical procedures performed over the years, only three appear to have true clinical benefit: bullectomy, lung volume reduction surgery (LVRS), and lung transplantation. Lung volume reduction surgery has been reintroduced in the past decade and is currently under active research. A recent large, multicenter trial showed LVRS to improve quality of life, exercise capacity, and even survival in certain highly selected patients. Some individuals with emphysema may be candidates for either LVRS or lung transplantation. Patient-selection criteria for these procedures are being developed.     

Noninvasive ventilation for chronic obstructive pulmonary disease

Noninvasive positive-pressure ventilation (NPPV) should be considered a standard of care to treat COPD exacerbations in selected patients, because NPPV markedly reduces the need for intubation and improves outcomes, including lowering complication and mortality rates and shortening hospital stay. Weaker evidence indicates that NPPV is beneficial for COPD patients suffering respiratory failure precipitated by superimposed pneumonia or postoperative complications, to allow earlier extubation, to avoid re-intubation in patients who fail extubation, or to assist do-not-intubate patients. NPPV patient-selection guidelines help to identify patients who need ventilatory assistance and exclude patients who are too ill to safely use NPPV. Predictors of success with NPPV for COPD exacerbations have been identified and include patient cooperativeness, ability to protect the airway, acuteness of illness not too severe, and a good initial response (within first 1-2 h of NPPV). In applying NPPV, the clinician must pay attention to patient comfort, mask fit and air leak, patient-ventilator synchrony, sternocleidomastoid muscle activity, vital signs, hours of NPPV use, problems with patient adaptation to NPPV (eg, nasal congestion, dryness, gastric insufflation, conjunctival irritation, inability to sleep), symptoms (eg, dyspnea, fatigue, morning headache, hypersomnolence), and gas exchange while awake and asleep. For severe stable COPD, preliminary evidence suggests that NPPV might improve daytime and nocturnal gas exchange, increase sleep duration, improve quality of life, and possibly reduce the need for hospitalization, but further study is needed. There is consensus, but without strong supportive evidence, that COPD patients who have substantial daytime hypercapnia and superimposed nocturnal hypoventilation are the most likely to benefit from NPPV. Adherence to NPPV is problematic among patients with severe stable COPD.     

推拿治疗慢性阻塞性肺疾病的疗效

目的:观察推拿治疗慢性阻塞性肺疾病、改善肺功能的效应。方法:选择2003-07/2005-08来自上海交通大学附属第一人民医院呼吸科和推拿科收治的缓解期的慢性阻塞性肺疾病患者30例,男28例,女2例,随机分为两组,推拿组和对照组各15例,所有患者均给予常规按需治疗。推拿组患者给予每周5次推拿,每次20min,共8周。头面部及项部操作:①从头顶部到枕部用五指拿法,从枕部到项部用三指拿法。②推桥弓穴。③面部分法。④扫散法。躯干部操作:①横擦前胸部。②横擦肩背、腰部。③斜擦两肋。上肢操作:①直擦上肢。②拿上肢。③运肩关节,理手指,最后搓抖上肢。④重复头面部操作,加震百会、大椎、命门穴。按揉心俞、肺俞、脾俞、肾俞、命门,擦肾俞、命门。治疗前后给予测定肺功能(第1秒用力呼出量、用力肺活量、一秒率);呼吸困难分级评分;6min步行距离实验。结果:30例均进入结果分析,无脱落者。①两组患者康复治疗前后呼吸功能变化:推拿组呼吸困难减轻的有效率明显高于对照组(67%,40%)。②两组患者康复治疗前后肺功能变化:推拿组治疗后第1秒用力呼气量,用力肺活量比治疗前升高犤(1.419±0.953),(1.248±0.743)L;(2.628±0.921),(2.311±0.875)L,P<0.01犦,对照组的升高差异没有显著性。推拿组治疗后肺功能改善情况明显高于对照组(P<0.05)。③两组患者康复治疗前后6min步行距离实验的变化:两组患者6min步行距离实验均有增加,对照组的增加差异不显著(由328m增加到346m),推拿治疗前后差异显著(由330m增加到389m,P<0.01),而且治疗后推拿组较对照组差异有显著性(P<0.05)。结论:推拿治疗缓解期的慢性阻塞性肺疾病,可改善肺功能、减轻呼吸困难,增强运动耐力,值得推广。     

推拿治疗慢性阻塞性肺疾病的疗效

目的：观察推拿治疗慢性阻塞性肺疾病、改善肺功能的效应。方法：选择2003—07／2005—08来自上海交通大学附属第一人民医院呼吸科和推聿科收治的缓解期的慢性阻塞性肺疾病患者30例，男28例，女2例，随机分为两组，推拿组和对照组各15例，所有患者均给予常规按需治疗。推拿组患者给于每周5次推拿，每次20min，共8周。头面部及项部操作：①从头顶部到枕部用五指拿法，从枕部到项部用三指拿法。②推桥弓穴。③面部分法。④扫散法。躯干部操作：①横擦前胸部。②横擦肩背、腰部。③斜擦两肋。上肢操作：①直擦上肢。②拿上肢。③运肩关节，理手指，最后搓抖上肢。④重复头面部操作，加震百会、大椎、命门穴。按揉心俞、肺俞、脾俞、肾俞、命门，擦肾俞、命门。治疗前后给予测定肺功能（第1秒用力呼出量、用力肺活量、一秒率）；呼吸困难分级评分；6min步行距离实验。结果：30例均进入结果分析，无脱落者。①两组患者康复治疗前后呼吸功能变化：推拿组呼吸凼难减轻的有效率明显高于对照组（67％，40％）。②两组患者康复治疗前后肺功能变化：推拿组治疗屙第1秒用力呼气最，用力肺活量比治疗的升高[（1．419&;#177;0.953），（1．248&;#177;0．743）L；（2．628&;#177;0．921），（2.311&;#177;0．875）L，P＜0．01]，对照组的升高差异没有显著性。推拿组治疗后肺功能改善情况明屁高于对照组（P〈0．05）。③两组患者康复治疗前后6min步行距离实验的变化：两组患者6min步行距离实验均有增加，对照组的增加差异不显著（由328111增加到346111），推拿治疗前后差异显著（由330m增加到389m，P＜0．01），而且治疗后推拿组较对照组差异有显著性（P＜0．05）。结论：推拿治疗缓解期的慢性阻塞性肺疾病，可改善肺功能、减轻呼吸困难，增强运动耐力，值得推广。     

β受体阻滞剂应用于慢性阻塞性肺疾病治疗的Meta分析

目的评价心脏选择性β受体阻滞剂对于慢性阻塞性肺疾病患者肺功能的影响。方法计算机检索PUBMED(1980年至2011年7月)、Cochrane Library(2011年第3期)等西文数据库及中国知网(1990年至2011年7月)、万方数据库(1990年至2011年7月)等中文数据库,收集心脏选择性β受体阻滞剂用于慢性阻塞性肺疾病患者的相关文献,按纳入与排除标准筛选随机对照试验。评价质量及提取资料后,采用RevMan 5.1软件对数据进行Meta分析。结果共检索到文献61篇,经筛选最终纳入7篇,共378例慢性阻塞性肺疾病患者。各研究间无异质性,采用固定效应模型进行效应量合并。Meta分析结果显示,用药后,β受体阻滞剂组的FEV1值(一秒用力呼气容积)较安慰剂组降低0.03 L[95%CI(-0.07,0.02)],FEV1占预计值百分比(FEV1%)值较安慰剂组升高0.89%[95%CI(-1.26,3.04)],两组间差异无统计学意义。讨论心脏选择性β受体阻滞剂不会对慢性阻塞性肺疾病患者的呼吸功能产生不利的影响。     

Exercise and chronic obstructive pulmonary disease

Patients with chronic obstructive pulmonary disease have abnormal respiratory mechanics, respiratory muscle function, gas exchange, and cardiovascular function during exercise. Their impaired exercise tolerance is at least partly due to altered respiratory mechanics, but factors that increase ventilation during exercise indirectly contribute to exercise limitation. Clinical exercise testing is a very important tool in the assessment of exercise capacity, assessment of factors that contribute to exercise limitation, and differential diagnosis of cardiopulmonary disease.     

Management of chronic obstructive pulmonary disease

Original Article Chronic obstructive pulmonary disease (COPD) is a major cause of mortality and morbidity throughout the world. It is the only cause of death among the top 10 causes that is increasing and is expected to become the third leading cause of death in the world by 2020. A diagnosis of COPD should be considered in any patient with previous exposure to risk factors for the disease and/or the presence of chronic cough, sputum production, or dyspnea. Patients with COPD are categorized into five stages based on their pulmonary function tests and symptoms. Smoking cessation is the single most effective way to halt the progression of COPD and prolong life. Pharmacological management of stable COPD includes the use of bronchodilators (Β2 agonists, anticholinergics and methylxanthines) and inhaled corticosteroids. Other adjunctive measures include vaccination, oxygen therapy, pulmonary rehabilitation, and certain surgical measures like bullectomy and lung transplantation. Management of acute exacerbations includes the use of systemic steroids, antibiotics, bronchodilators, and oxygen therapy. During very severe exacerbations, patients may need ventilatory support.     

Pathogenesis of chronic obstructive pulmonary disease

The current epidemic of chronic obstructive pulmonary disease (COPD) has produced a worldwide health care burden, approaching that imposed by transmittable infectious diseases. COPD is a multidimensional disease, with varied intermediate and clinical phenotypes. This Review discusses the pathogenesis of COPD, with particular focus on emphysema, based on the concept that pulmonary injury involves stages of initiation (by exposure to cigarette smoke, pollutants, and infectious agents), progression, and consolidation. Tissue damage entails complex interactions among oxidative stress, inflammation, extracellular matrix proteolysis, and apoptotic and autophagic cell death. Lung damage by cigarette smoke ultimately leads to self-propagating processes, resulting in macromolecular and structural alterations - features similar to those seen in aging.     

Exacerbations of chronic obstructive pulmonary disease

Exacerbations of chronic obstructive pulmonary disease (COPD) cause morbidity, hospital admissions, and mortality, and strongly influence health-related quality of life. Some patients are prone to frequent exacerbations, which are associated with considerable physiologic deterioration and increased airway inflammation. About half of COPD exacerbations are caused or triggered primarily by bacterial and viral infections (colds, especially from rhinovirus), but air pollution can contribute to the beginning of an exacerbation. Type 1 exacerbations involve increased dyspnea, sputum volume, and sputum purulence; Type 2 exacerbations involve any two of the latter symptoms, and Type 3 exacerbations involve one of those symptoms combined with cough, wheeze, or symptoms of an upper respiratory tract infection. Exacerbations are more common than previously believed (2.5-3 exacerbations per year); many exacerbations are treated in the community and not associated with hospital admission. We found that about half of exacerbations were unreported by the patients, despite considerable encouragement to do so, and, instead, were only diagnosed from patients' diary cards. COPD patients are accustomed to frequent symptom changes, and this may explain their tendency to underreport exacerbations. COPD patients tend to be anxious and depressed about the disease and some might not seek treatment. At the beginning of an exacerbation physiologic changes such as decreases in peak flow and forced expiratory volume in the first second (FEV(1)) are usually small and therefore are not useful in predicting exacerbations, but larger decreases in peak flow are associated with dyspnea and the presence of symptomatic upper-respiratory viral infection. More pronounced physiologic changes during exacerbation are related to longer exacerbation recovery time. Dyspnea, common colds, sore throat, and cough increase significantly during prodrome, indicating that respiratory viruses are important exacerbation triggers. However, the prodrome is relatively short and not useful in predicting onset. As colds are associated with longer and more severe exacerbations, a COPD patient who develops a cold should be considered for early therapy. Physiologic recovery after an exacerbation is often incomplete, which decreases health-related quality of life and resistance to future exacerbations, so it is important to identify COPD patients who suffer frequent exacerbations and to convince them to take precautions to minimize the risk of colds and other exacerbation triggers. Exacerbation frequency may vary with the severity of the COPD. Exacerbation frequency may or may not increase with the severity of the COPD. As the COPD progresses, exacerbations tend to have more symptoms and take longer to recover from. Twenty-five to fifty percent of COPD patients suffer lower airway bacteria colonization, which is related to the severity of COPD and cigarette smoking and which begins a cycle of epithelial cell damage, impaired mucociliary clearance, mucus hypersecretion, increased submucosal vascular leakage, and inflammatory cell infiltration. Elevated sputum interleukin-8 levels are associated with higher bacterial load and faster FEV(1) decline; the bacteria increase airway inflammation in the stable patient, which may accelerate disease progression. A 2-week course of oral corticosteroids is as beneficial as an 8-week course, with fewer adverse effects, and might extend the time until the next exacerbation. Antibiotics have some efficacy in treating exacerbations. Exacerbation frequency increases with progressive airflow obstruction; so patients with chronic respiratory failure are particularly susceptible to exacerbation.     

Therapy of chronic obstructive pulmonary disease

Chronic obstructive pulmonary disease is one of the commonest causes of morbidity and mortality in the world, and is increasing in prevalence. Current therapies are not very effective, and no current treatment prevents the relentless progression of airflow limitation that characterizes this disease. Smoking cessation is the only strategy that reduces this decline in lung function, and although bupropion is the most effective aid to quitting, more effective treatments of nicotine addiction are needed. The mainstay of treatment is bronchodilators for symptom relief, and inhaled anticholinergics and beta(2)-agonists are useful by reducing hyperinflation of the lungs. A new once-daily inhaled anticholinergic is the most effective bronchodilator, but long-acting inhaled beta(2)-agonists are also useful. Theophylline is used as an additional bronchodilator in more severe patients, and may have some anti-inflammatory action. In contrast, inhaled corticosteroids are poorly effective and do not reduce disease progression, although recent studies with combination inhalers (corticosteroid + long-acting beta(2)-agonist) have shown better effects. Long-term oxygen therapy is needed by patients with pulmonary hypertension and right heart failure. There is a pressing need to develop new classes of therapy, and several new drugs are current in development, including interleukin-8 antagonists, phosphodiesterase-4 inhibitors, protease inhibitors, and antioxidants.     

慢性阻塞性肺疾患的康复

近年来 ,随着发病率和致残率的不断升高 ,慢性阻塞性肺疾患已成为中国及一些西方发达国家前 5位的死亡原因。慢性阻塞性肺疾患 (ｃｈｒｏｎｉｃｏｂｓｔｒｕｃｔｉｖｅｐｕｌ ｍｏｎａｒｙｄｉｓｅａｓｅ ,ＣＯＰＤ)的主要症状之一是呼吸困难 ,因此而引起的并发症是致残的主要原因。肺康复的主要内容即是针对ＣＯＰＤ的。根据我国 6 0 0 0多万人口的普查 ,不同地区ＣＯＰＤ的发病率最低为 0 .6 %,最高为 4 .3%,严重地影响了人民群众的健康。康复训练和治疗对于预防ＣＯＰＤ发展为慢性肺源性心脏病和右心衰竭 ,改善患者的健康状况、提高患者…     

骨质疏松与慢性阻塞性呼吸系统疾病

目的:分析慢性阻塞性呼吸系统疾病继发骨质疏松的病因及发病途径,为其预防及治疗提供理论依据。资料来源:应用计算机检索Medline,Pubmed和Ovid数据库1990-01/2006-06有关慢性阻塞性呼吸系统疾病和骨质疏松关系的文章。检索词为“COPD or chronic obstructive pulmonary disease,osteoporosis,pathogenesis,treatment”,限定文章语言种类为English。同时计算机检索中国期刊全文数据库(CNKI)1990-01/2006-06有关慢性阻塞性呼吸系统疾病和骨质疏松关系的文章,检索词为“慢性阻塞性肺病,骨质疏松,发病机制,治疗”,限定文章语言种类为中文。资料选择:对资料进行初审,筛除非随机的研究。纳入标准:①随机对照临床研究。②前后对照临床研究。排除标准:①重复性研究。②综述文献。资料提炼:共收集到45篇有关慢性阻塞性呼吸系统疾病和骨质疏松症关系的文章,其中36篇符合纳入标准。资料综合:36篇文献中包括27个随机对照临床研究和9个前后对照临床研究,提示慢性阻塞性呼吸系统疾病继发骨质疏松症的病因主要是吸烟、户外运动减少、缺氧与营养不良、激素作用及一些相关的细胞因子和蛋白酶,对其治疗除了积极治疗慢性阻塞性呼吸系统疾病外,还应减少香烟的吸入,适当加强户外运动,增加营养,对于严重者可适当给予治疗骨质疏松的中西医药物。结论:对于慢性阻塞性呼吸系统疾病继发骨质疏松,要定期进行骨密度等测定,及时发现,及早治疗,防止其发生和发展,将有利于提高老年肺病患者的生活质量。     

Genes and chronic obstructive pulmonary disease

Although much remains to be done, recent advances and the advent of new methodologies are promising and should yield increased understanding of the genetic and epigenetic mechanisms influencing the pathogenesis of COPD, both related and unrelated to severe AAT deficiency. Such understanding should ultimately be translated into novel approaches to prevent, diagnose, and treat COPD.