What is COPD Is it to do with cough and sputum

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'Chronic bronchitis' was the term commonly used throughout the UK in the 1950s for the syndrome we would now describe as chronic obstructive pulmonary disease (COPD). The Americans were inclined to describe it as 'emphysema', and there were many other synonyms in use until, in the last decade, general agreement developed that we should use the umbrella term 'COPD' and accept that it includes a series of subsidiary components (Table 3.1). It is important to recognize that some of the early studies worked with definitions that are different from those we use today and that therefore one must be cautious before extrapolating some of the earlier studies to current practice.

The productive cough that occurred particularly in smokers and in those working in dusty jobs was shown in the 1950s to be primarily a large-airway problem. Several studies demonstrated an increase in mucosal goblet cells, and the Reid index defined the increased thickness of the mucosa pathologically [1]. The definition of chronic bronchitis used today is that produced by the Medical Research Council (MRC) for epidemiological surveys and not for clinical purposes [2]. The definition restricted chronic bronchitis to 'a productive cough for more than 3 months of the year in each of two successive years'. Thus, chronic bronchitis is related to the productive cough and not to any level of airflow limitation. This symptomatic definition has been used in many epidemiological studies, in which it has been of considerable value, but it is less helpful in managing individuals in clinical practice. For example, patients with bronchiectasis and/or with chronic asthma—very different pathological processes—would be included. However, this is of little consequence in large, population-based surveys, since bronchiectasis is sufficiently uncommon for it not to confound the results unduly.

Cough and sputum are common in smokers. The prime cause is the need to clear the increased inhaled particulate load from the airways and to respond to the toxic chemicals within the smoke. Cigarette smoke consists of a particu-late fume containing particles of less than 0.5 mm in size [3], as well as many highly irritant chemicals. The 'full-strength' cigarettes of the 1950s contained 40 mg per cigarette or more, while the lowest-tar filter cigarettes of the 1990s had as little as 1 mg. Smokers are much more likely to fulfil the MRC definition, with the incidence rising from 10% in young adults to over 50% in those aged over 50years. Dusty occupations such as mining yield dust that contains mostly larger particulates, of which only the minority smaller than 10 mm are inhaled. The effects of smoking and dust inhalation on the prevalence of cough are additive at all ages [4]. In many cases, those who cease to be exposed to dust or who stop smoking stop having a productive cough [5]. But do the cough and sputum represent disease, or are they simply a normal lung defence against the increased particulate and toxic burden in the large airways? In other words, does the reported symptom help to define the disease or simply describe a potential cause of the disease?

The Global Initiative for Obstructive Lung Disease (GOLD) initiative suggests that chronic sputum production is an early part of the COPD process and should be used to define an at-risk population. Cough and sputum indicate a cohort who should be targeted for lung function measurements. They are also a marker of the prevalence of cigarette smoking and thus a useful public health measure.

It is still unclear whether cough and sputum are part of the process that leads to obstruction or an entirely separate phenomenon. Physiologically, the mucosal thickening in the large airways contributes little to the overall limitation of airflow [6] — and in most patients with moderate to severe reductions in their forced expiratory volume in 1s (FEV1), it is widespread small-airway disease [7] and loss of elastic recoil leading to expiratory collapsibility of the subsegmental airways in those with emphysema [8] that is responsible.

Fletcher and Peto suggested that chronic sputum production does not affect life expectancy and by implication should be considered a separate process from conditions leading to airflow limitation, which does reduce both the quality and quantity of life [9]. More recently, Vestbo et al., in a large population study in Copenhagen [10], showed that those with cough and sputum do suffer some loss of life expectancy, suggesting that the separation is less than complete. There are small but quite subtle changes in lung mechanics and airflow in patients with chronic sputum production [11], but it is not known whether these are permanent or whether they reverse on ceasing exposure.

However, when applied to the individual patient, a label of 'chronic bronchitis' is less helpful. It is possible to have a cough and regular sputum production without any decrement in airflow, and it is also true that a third or more of patients with severe airflow obstruction have no sputum [12]. Detecting a non-specific symptom should make the clinician consider COPD, but only in the context of a differential diagnosis that may include many other conditions. On the other hand, the absence of cough and sputum is not helpful in exclud ing COPD. Symptoms are not a substitute for measuring airflow in all cases of suspected COPD.

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