Chronic obstructive pulmonary disease: underdiagnosed, underinvestigated, inappropriately managed?

To the Editor:

The article of Rennard et al. 1 and the accompanying editorial by Dekhuijzen 2 proposed that chronic obstructive pulmonary disease (COPD) is not only underdiagnosed and underinvestigated but also that the morbidity is underestimated. The evidence on which they base this hypothesis lacks two essential components. These are independent assessments of exercise tolerance and objective measurement of lung function. If disability is primarily to be attributed to COPD then it must be associated with a commensurate physiological abnormality, which is a reduction in after-bronchodilator forced expiratory volume in one second (FEV₁) or at least abnormality of the flow/volume loop. In medico-legal practice, I have been seeing large numbers of subjects managed principally in general practice with COPD or symptoms wrongly attributed to it. Too frequently, limitation of exercise cannot be explained by the objective reduction in pulmonary function. My previous clinical practice leads me to believe that this is not confined to any particular group of patients and certainly not related to litigation. The vast majority of patients have access to appropriate medication and use it in at least the prescribed dose, so there is little room for improvement in the pharmaceutical approach. Nevertheless there is much perceived and real morbidity. The tragedy is that much of the associated disability is not only accepted too passively, but is also unnecessary.

The diagnosis may be made on the basis of no pulmonary function tests or tests of poor quality. Often, the mere presence of cough and sputum or an industrial history leads to the diagnosis, which is then indelibly reproduced in the notes without thought as to its validity, even if subsequent pulmonary function tests are normal. Too often, a history of breathlessness is accepted at face value as objective evidence of disability due to respiratory disease. The perceived level of exercise limitation probably does reflect actual activity, but is rarely objectively confirmed either explicitly or opportunistically as, for example, by comparison with performance on the Bruce protocol. Overdiagnosis is only part of the problem. Many of these subjects do have mild COPD as demonstrated by minor changes in FEV₁ or the shape of the flow/volume loop, but with disproportionate exercise limitation. The clinician accepts the diagnosis, maybe rightly, but attributes disability directly to it, usually wrongly.

The problem arises because breathlessness is incorrectly regarded as the prime symptom reflecting impairment associated with cardiorespiratory dysfunction. This, however, is not the case. It is exercise limitation itself that is the proper measure of cardiorespiratory dysfunction. If cardiorespiratory dysfunction is the direct cause of this exercise limitation then it must be associated with changes in carbon dioxide or acid-based balance causing fatigue or the legs to give out. This is well recognised in athletes who accept breathlessness as incidental. It should apply equally to those with COPD, particularly when the disease is mild. In practice it is the dislike of breathlessness itself and the consequent vicious circle of increasing perceived breathlessness, exercise restriction and muscle weakness that is the prime cause of disability in COPD and not the actual impairment of lung function. Whether or not the COPD itself contributes to the perception of breathlessness is immaterial.

Management must involve acceptance by the patient of the true cause of disability, a message often difficult to convey in these days of patient autonomy, followed by rehabilitation to reverse the vicious circle. The approach might include: 1) taking history, directed first at the extent of disability and then at the associated symptoms, with the least reliable, breathlessness, last in the list; 2) objective assessment of exercise tolerance in all cases; 3) an absolute requirement for a physiological confirmation of the diagnosis by spirometry, including flow/volume loops (most unhelpful in this respect is the concept of stage 0 COPD as cough and sputum; it should be normal FEV₁ with abnormality of the flow/volume loop); 4) development of tables of optimal rather than average exercise tolerance against FEV₁ % predicted, stratified by the shape of the flow/volume loop; and 5) immediate intervention with low-tech rehabilitation in primary care, with the triple benefit of preventing unnecessary morbidity, ensuring that those whose disease does subsequently decline are already in the best position to cope with it, and reducing the impact of COPD as comorbidity in other conditions.

By addressing the underlying problem of inability to cope with breathlessness, this physiological approach might substantially reduce the burden of COPD, which is indeed excessive, but not always for the reasons suggested by Rennard et al. 1 and Dekhuijzen 2.