Wedzicha Jadwiga A, Donaldson Gavin C
Academic Unit of Respiratory Medicine, St Bartholomew's and Royal London School of Medicine and Dentistry, Dominion House, St Bartholomew's Hospital, London EC1A 7BE, United Kingdom.
Respir Care. 2003 Dec;48(12):1204-13; discussion 1213-5.
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.
慢性阻塞性肺疾病(COPD)急性加重会导致发病、住院及死亡,并对健康相关生活质量产生重大影响。一些患者容易频繁急性加重,这与相当程度的生理功能恶化及气道炎症增加有关。约一半的COPD急性加重主要由细菌和病毒感染(感冒,尤其是鼻病毒引起的感冒)导致或触发,但空气污染也可能促使急性加重的发生。1型急性加重表现为呼吸困难加重、痰液量增加及痰液脓性增加;2型急性加重表现为后两种症状中的任意两种;3型急性加重表现为其中一种症状并伴有咳嗽、喘息或上呼吸道感染症状。急性加重比之前认为的更为常见(每年2.5 - 3次急性加重);许多急性加重在社区进行治疗,与住院无关。我们发现,尽管大力鼓励患者报告,但约一半的急性加重未被患者报告,而是仅通过患者的日记卡才得以诊断。COPD患者习惯了频繁的症状变化,这可能解释了他们少报急性加重的倾向。COPD患者往往对疾病感到焦虑和抑郁,一些人可能不寻求治疗。在急性加重开始时,诸如峰值流速和第一秒用力呼气量(FEV(1))下降等生理变化通常较小,因此对预测急性加重并无帮助,但峰值流速较大幅度下降与呼吸困难及有症状的上呼吸道病毒感染有关。急性加重期间更明显的生理变化与更长的急性加重恢复时间相关。前驱期呼吸困难、普通感冒、喉咙痛和咳嗽显著增加,表明呼吸道病毒是重要的急性加重触发因素。然而,前驱期相对较短,对预测发病并无帮助。由于感冒与更长、更严重的急性加重相关,患感冒的COPD患者应考虑早期治疗。急性加重后的生理恢复往往不完全,这会降低健康相关生活质量并削弱对未来急性加重的抵抗力,因此识别频繁急性加重的COPD患者并说服他们采取预防措施以尽量降低感冒及其他急性加重触发因素的风险非常重要。急性加重频率可能随COPD严重程度而变化。急性加重频率可能随COPD严重程度增加,也可能不增加。随着COPD进展,急性加重往往症状更多,恢复时间更长。25%至50%的COPD患者存在下呼吸道细菌定植,这与COPD严重程度及吸烟有关,并引发上皮细胞损伤、黏液纤毛清除功能受损、黏液分泌过多、黏膜下血管渗漏增加及炎症细胞浸润的循环。痰液白细胞介素 - 8水平升高与更高的细菌载量及更快的FEV(1)下降相关;细菌会增加稳定期患者的气道炎症,这可能加速疾病进展。口服糖皮质激素2周疗程与8周疗程效果相同,但不良反应更少,且可能延长至下次急性加重的时间。抗生素在治疗急性加重方面有一定疗效。急性加重频率随气流阻塞进展而增加;因此慢性呼吸衰竭患者尤其易发生急性加重。