Differentiating and treating COPD

Dr Richard Costello of Beaumont Hospital, Dublin, writes that although COPD is difficult to diagnose, there are a growing number of treatments available to tackle the condition

The detection of chronic obstructive pulmonary disease (COPD) starts with suspicion. In clinical practice, it can be extremely hard to detect, and therefore manage, COPD. In some cases, the patient presents with exertional dyspnoea, while other patients present with respiratory infections and are relatively well between times.
Furthermore, some patients with the condition — even with quite advanced COPD — may not have any symptoms. None of these clinical types are closely related to the severity on spirometry; however spirometry is a vital test, as it demonstrates the presence of the condition.
The current approach of focusing on the results of spirometry tests alone seems, to me, not to help the clinician in practice. The aim of this article is to give an approach to the different presentations of COPD.
Exertional dyspnoea
Exertional dyspnoea is an extremely hard symptom to accurately evaluate, because there are several causes of dyspnoea. In addition, people often report distances that precipitate dyspnoea very inaccurately.
There are at least four different conditions that can lead to shortness of breath: lack of fitness (deconditioning); cardiac limitation due to insufficient cardiac output; pulmonary limitation due to defects in the lungs; or weakness in the peripheral muscles, which do not use oxygen well.
In a GP practice, many patients may attend with shortness of breath. Many of these may also be middle-aged, inactive smokers or may have a completely different cause for their shortness of breath. This shows how difficult the diagnosis of COPD can be to make. Hence, there is rarely one explanation for a patient who presents with dyspnoea and so a rapid systematic evaluation is suggested.
Establishing the diagnosis starts with evaluation of the severity of dyspnoea. It is well established that all people, including doctors, are very poor at judging distance walked in yards or metres. So, instead of asking how far a patient can walk, I suggest the following: quantify by features familiar to the patient – for example, how far can you walk? Around the house? Up the stairs, without stopping? To the shops? These accurately relate to much more sophisticated exercise tests.
Secondly, a smoking history of more than 20 pack-years, a low peak flow or the detection of wheeze or reduced air entry on examination should prompt a spirometry test. I recommend the spirometry because this test alone can identify the presence of COPD and its severity. The spirometry and level of dyspnoea gives a rough guide to the patient’s prognosis, as well as the diagnosis.
Dyspnoea, regardless of the cause, leads to deconditioning. Deconditioning is not always associated with obesity, although if this is also present it can worsen exercise capacity. In other words, among patients with a primary heart or lung disease, the lack of exercise itself leads to a vicious circle of events.
Postponed exercise
Dyspnoea leads to postponed exercise, which itself leads to further wasting of muscles and so to a further decline in exercise capacity. It is the purpose of pulmonary rehabilitation to break this pattern, and even those doctors without access to rehabilitation should still promote exercise.
Improving fitness will always lead to reduced dyspnoea and improved exercise capacity, regardless of the underlying cause. The advice is worthy but people do struggle to take this message on board, and this is where rehabilitation classes, gyms and local groups may help.
Once a diagnosis is made, the relationship of FEV1 (forced expiratory volume in one second) on the spirometry test relates the disease severity.
Bearing in mind that improving exercise in patients is hard to achieve, it is important to target the respiratory aspect to the dyspnoea in patients with COPD. Improving dyspnoea can be directly achieved with bronchodilators.
In the past, salbutamol/ipratropium were the only inhalers available. However, there are now several new long-lasting bronchodilators available for the treatment of dyspnoea. These have the advantage of being easy to use and also being convenient. It is now strongly recommended that these be used in preference to either short-acting bronchodilators or nebulisers.
Infections or exacerbations
In term of exacerbations, there is a clear relationship between infections and subsequent changes of airway inflammation and worsening of symptoms. There is a complete inconsistency in the types of inflammation observed in the exacerbations, suggesting that there are several causes of an exacerbation.
The epidemiological results suggest 25 per cent are viral, and there is a clear seasonal variation in the occurrence of these exacerbations. Some 25 per cent are bacterial, while another 25 per cent are due to both types of infections. The rest may be due to pollutants and/or unidentified causes.
A recent study has shown that an experimentally delivered viral infection leads to an exacerbation, and in half of these, a second bacterial infection subsequently develops. Hence, there is almost always a bacterial component to a respiratory infection in COPD.
The heterogeneity in inflammation may result because of differences between the type of viral and bacterial colonisation, the continuation of smoking and the patient gene type, and the severity of COPD. There is thus likely to be, in time, multiple types of treatment approaches to infection as data on the different types of infection become clearer.
Among patients with COPD, there is a recognised type of clinical course separate from the breathless-type term called ‘frequent exacerbators’. This type of clinical presentation appears to be a stable phenotype, meaning that they both settle into this pattern and remain in this pattern.
In clinical terms, they often have more cough and sputum; in the old classification, these patients were the ‘chronic bronchitis’ types of COPD patient. In immunological terms, the frequent exacerbators have more inflammation, a more rapid decline in lung function (and so probably lower life expectancy), have more sub clinical depression and are less active.
There is no clear relationship between continued smoking and the tendency to be a frequent exacerbator. Among patients with frequent exacerbators, there is a tendency for the exacerbations to cluster together.
These clusters could be seasonal or aetiological, e.g. due to an initial moderate viral infection and a subsequent bacterial infection. This means that, in practice, people returning for repeated courses of antibiotics, year on year, or in particular for several courses in quick succession, should be thought of as having COPD.
What next?
So what should we do about this information? Firstly, we need to identify the patients and track their progress so that we can intervene. This group of patients benefit from bronchodilator therapy and anti-inflammatory therapy with inhaled corticosteroids long-term and long-acting bronchodilators, in both the form of long-acting beta agonists and long-acting antimuscarinic agents and early administration of oral antibiotics and steroids for the exacerbations.
Self-care and action management plans, as used in asthma, are also of value in COPD. Studies clearly show that self-management does not lead to abuse of medicines, but does help prevent unscheduled visits and exacerbations. However, it does not help with the severity of the exacerbations. This is an important development in thinking with regard to clinical practice in primary care.
Several recent relatively small-scale studies of asymptomatic smokers have shown that up to 30 per cent may have moderate or advanced COPD. It remains to be seen if these individuals were on the cusp of presenting with COPD or if, as seems likely, there is a small group of patients who present only when the condition is at an advanced stage. It is logical that this group should be targeted with smoking cessation efforts and appropriate vaccination.
Summary
In an ironic turn of the circle, there is an emerging trend to classify patients with COPD as ‘breathless types’, whereas they were termed ‘emphysematous type’ patients a generation ago. Also, those with frequent cough, phlegm and chest infections, who were termed ‘chronic bronchitis’ a generation ago, are now recognised as a subset of COPD patients.
We have added the diagnostic tool of spirometry and the use of a combination of long-acting bronchodilator and long acting anti-inflammatory drugs to help join up these two groups of patients who have smoking-related lung disease.
References available on request.