COPD is a very prevalent lung disease characterised by narrowing of the airways in response to chronic exposure to inhaled inflammatory agents. In the developed world this is largely accounted for by smoking cigarettes, but in the developing world contamination of the home environment by biomass fuels for cooking accounts for about 50 per cent of cases. COPD causes considerable morbidity and is the third leading cause of death worldwide. If patients do not modify their risk factors, the disease is progressive.
As well as day-to-day symptoms, most patients suffer from exacerbations, which are usually acute episodes of bronchitis caused by viruses and bacteria. These episodes have short- and long-term health consequences. They cause an abrupt worsening of symptoms, including reduced exercise capacity and may require hospitalisation. The acute mortality from hospitalisation is 7 per cent (18 per cent if the patient has pneumonia). A vicious cycle can develop whereby infections damage the airways leading to further airflow obstruction, which in turn leads to more infections.
In the last few years the idea that there are three phenotypes of COPD has gained traction. These are: 1. The smoking asthmatic-termed asthma/COPD overlap (ACO), where patients have a hybrid of COPD and asthma; 2. Eosinophilic COPD, where there is elevated eosinophil counts in sputum and blood; and 3. Standard COPD.
This article focuses on diagnosis, mechanisms of dyspnoea in COPD, symptom and exacerbation management and discussion of ACO and eosinophilic COPD.
The diagnosis of COPD is based on chronic exposure to a noxious agent, having transient or chronic respiratory symptoms and demonstration of fixed airflow obstruction (FEV1/FVC ratio <0.7) on spirometry following administration of salbutamol. This sounds quite straightforward, but there are a very large number of undiagnosed patients and up to nearly one-third of COPD patients are only diagnosed when they already have severe disease.
<h3><strong>Why are there so many undiagnosed COPD patients? (see </strong>Table 1<strong>)</strong></h3>
A very important question is whether there should be a national screening programme for COPD. To my knowledge this does not exist at present in any country. If we look at standard screening criteria:
Very prevalent (12 per cent of the population > age 40 years) √
Causes huge morbidity, comorbidity and mortality √
Massive healthcare expenditure √
Reduces the workforce – carers often leave the workforce too √
Safe, cheap, non-invasive diagnostic test that can detect early disease √
Preventable risk factors?
Unfortunately, mass screening of, for example, 40-year-old people who have smoked more than 20 pack years may fall at this last hurdle as we do not know what patients, many of whom will be asymptomatic, will do regarding risk factors if diagnosed earlier with COPD. There are also very few smoking cessation clinics in Ireland, particularly in primary care. In the GOLD 2018 guidelines there is an emphasis on opportunistic smokers aged >35 years with at least one chronic respiratory symptom. In these patients, studies have picked up a new detection rate of COPD of nearly 25 per cent.
<h3><strong>Mechanisms of dyspnoea in COPD</strong></h3>
1. Dynamic hyperinflation – Pleural pressures can have a differential effect on airway calibre. Negative pressure on inspiration helps to splint the airways open, but cycling to positive pleural pressure on expiration causes further dynamic airway compression.
When the patient walks and needs to increase their respiratory rate they do not have time to exhale fully the previous breath before they need to breathe in again with the result that the end-respiratory volume increases in real-time causing further descent of the diaphragms and reduction of tidal volume. Another interesting phenomenon is that when COPD patients are admitted with pneumonia, pulmonary embolus, CCF, pneumothorax or metabolic acidosis, the acute increase in their breathing frequency will also result in dynamic hyperinflation.
2. Emphysema – COPD is often accompanied by some degree of emphysema. This reduces the oxygen transfer capability of the lungs and also the ability to exhaust carbon dioxide.
3. Deconditioning of leg muscles – patients with COPD are usually not very active and often avoid exercise due to breathlessness. This results in reduction of aerobic capacity due to ‘sick’ myocytes and diminished mitochondrial function. Premature release of lactic acid promotes increased ventilation and this, in turn, causes worsening dynamic hyperinflation.
4. High BMI – Due to limited exercise a number of COPD patients are overweight, which increases the work of breathing and can cause concomitant lung restriction. On smoking cessation the average COPD patient gains about 7kg in weight.
<h3><strong>Gauging severity of COPD</strong></h3>
The GOLD 2018 guidelines recommend dividing patients into four classes, A to D, based on severity markers (see <strong>Figure 1</strong>):
1. FEV1 per cent predicted.
2. Exacerbation frequency ≤1 in the previous year – low frequency exacerbator. Exacerbation frequency ≥2 or ≥1 hospitalisation in the previous year – high frequency exacerbator.
3. COPD Assessment Test questionnaire – eight questions rated 0-5 – score under 10 = good symptom control, >10 = poor symptom control.
4. Modified Medical Research Council Dyspnoea (mMRCD) score – 0. normal exercise tolerance, 1. shortness of breath on inclines or walking fast, 2. can’t keep up with peers walking on the flat, 3. unable to walk >100 yards in one go, 4. housebound.
<h3><strong>Treatment of COPD</strong></h3>
The main focus is on management of symptoms and exacerbations although the two are intimately connected. High frequency exacerbators have the worst prognosis with accelerated decline in FEV1, lower quality-of-life and increased mortality.
<strong><em>Non-pharmacological therapy for COPD</em></strong>
1. Smoking cessation – attenuates the accelerated loss of FEV1 and reduces exacerbation frequency.
2. Daily activity – walking >30 minutes/daily for at least five days per week maintains leg conditioning and reduces severe exacerbation risk by two-thirds.
3. Pulmonary rehabilitation – a proven outpatient intervention where patients attend twice weekly and are exposed to progressively more intense aerobic exercise over eight weeks. Leg muscle adaption takes place such that the anaerobic threshold is raised, less lactic acid is produced with less drive to breathing. This improves exercise capacity, quality-of-life and dyspnoea. The benefits last 18-24 months. There is strong evidence that acute pulmonary rehabilitation if started within four weeks of discharge following a COPD exacerbation reduces the risk of further exacerbations.
4. Endobronchial valve therapy has shown early potential for relief of dyspnoea, improved exercise capacity and quality-of-life. Success depends on careful selection of non-exacerbating, hyperinflated patients with intact lung fissures as collateral ventilation can prevent the desired atelectasis.
5. High BMI – Reduction in weight is very important in control of dyspnoea. Exacerbation control is critical to maintain activity and reduce exposure to oral corticosteroids.
6. Low BMI – Usually a marker of severe disease. Smoking cessation, exacerbation avoidance and calorie augmentation are all key issues.
7. Anxiety and depression – this is very common in COPD and may be a major barrier to management concordance. Specialist referral to physiotherapists, psychologists and psychiatrists may be necessary.
1. See <strong>Figure 2</strong> for recommended therapy according to GOLD class. The main changes from previous guidelines is that a long-acting beta-2 agonist (LABA)/long-acting antimuscarinic agent (LAMA) combination is now first-line treatment for class D patients and are superior to an inhaled corticosteroid (ICS)/LABA in terms of exacerbation reduction, lung function and safety.
2. Yearly influenza vaccination and pneumovax once < age 65 and once > age 65 with at least 10 years in between.
3. Smoking cessation – nicotine replacement therapy doubles long-term quit rates. Bupropion can achieve quit rates of about 15 per cent and varenicline, a partial nicotine agonist, can achieve 40 per cent quit rates at three months and 20 per cent at one year. E-cigarettes cause less short-term harm than tobacco, but there is no long-term safety data.
4. Long-term oxygen therapy is a critical treatment for patients with chronic hypoxia with a PO2 consistently below 7.3kPa and will double survival if worn more than 16 hours per day
5. Lung transplantation is a potential treatment for very carefully selected severe COPD patients usually in chronic respiratory failure. There are better outcomes achieved with double rather than single lung transplants.
<h3><strong>Asthma/COPD overlap (ACO)</strong></h3>
This applies to the smoking asthmatics who have an overlap of asthma and COPD. Like COPD patients they have smoked >10 pack years and have chronic airflow obstruction. ACO does not have a discreet diagnostic profile so its exact prevalence is unclear. Features that may suggest ACO include having been previously diagnosed as asthmatic; a high prevalence of self-reported allergies including hay fever; a long history of inhaler usage; frequent exacerbations and previous significant reversibility in FEV1 (>400ml). The reason to diagnose ACO is that these patients, because of the asthma component, respond better to initial treatment with ICS/LABA combination rather than an ICS-free regime.
About one-third of stable COPD patients exhibit an increase in airway and blood eosinophils. For ease, a blood eosinophil count >2 per cent is the accepted cut-off value. Previous studies revealed that eosinophilic patients with GOLD 2-3 disease had less moderate/severe exacerbations if treated with an ICS/LABA rather than non-ICS-based therapy. The recent FLAME study, however, where patients with an FEV1 of <60 per cent predicted were given either a LABA/LAMA or an ICS/LABA for one year revealed that dual bronchodilator therapy was superior at reducing exacerbations compared to the ICS group no matter what the eosinophil count. My personal practice is not to treat these patients differently than non-eosinophilic COPD patients at present.
A huge amount of work needs to be done regarding earlier diagnosis and the whole area of smoking cessation. There has been an explosion of new drugs for COPD in the last number of years and the role of ICS has been relegated to add-on therapy in GOLD class D patients who continue to exacerbate on LAMA/LABAs or patients with ACO.
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