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Key Questions on COPD

Posted on: 14 Feb 2019

Learning Objectives

This module will update your knowledge of COPD, including:

  • The role of spirometry in diagnosis
  • When to start LAMAs
  • How to help patients use home rescue packs appropriately
  • Indications for long-term oxygen therapy

Dr Jay Suntharalingam is a Consultant Respiratory Physician at the Royal United Hospitals Bath Foundation Trust and the Trust’s clinical lead for COPD.

In the UK smoking is by far the commonest cause of COPD – typically patients present in their 50s and 60s having accumulated >20 pack year history of smoking (where one pack year = 20 cigarettes a day for a year). Rarely, some patients do present at an earlier age with a less extensive smoking history. These patients are likely to have a genetic basis for their disease, although at present only one genetic abnormality, alpha 1 antitrypsin deficiency, can be routinely tested for. Given this, it is worth having a lower threshold for performing spirometry on younger patients who have a strong family history of early onset COPD. In younger patients where there are no clear genetic risk factors, it is also prudent to enquire about recreational drug abuse as inhaled recreational drugs can be associated with significant emphysematous damage.1

Finally, some never-smokers can present with fixed airflow obstruction at a later stage in life. Often these patients have a history of severe asthma during childhood when their lungs were developing. Although strictly speaking these patients fulfill the criteria for a diagnosis of COPD, I tend to label these patients as having ‘chronic asthma with fixed airflow obstruction,’ as they may benefit from asthma-specific therapies such as LTRAs, high dose inhaled corticosteroids etc.2

While spirometry is considered the gold standard for diagnosing COPD there are a few issues to consider. Firstly, spirometry should be carried out by a trained healthcare professional who can ensure the patient performs the procedure well – for example, an incomplete FVC manoeuvre can lead to an apparent restrictive picture on spirometry, therefore missing a diagnosis of COPD. Secondly, spirometry has to be interpreted within the right clinical context – a reduced FEV1/FVC ratio due to airflow obstruction can be seen in a number of other pathologies (e.g. asthma, bronchiectasis, bronchiolitis obliterans, increasing age etc.) and so patient demographics, smoking status and clinical presentation must all be considered in addition to spirometry to make a diagnosis of COPD. Finally, patients can occasionally present with COPD with a predominant emphysematous phenotype. These patients can have reasonably preserved spirometry values but still have severe disease, manifesting itself through significant emphysematous changes, visible only on CT.

While spirometry can help stage disease severity, patients’ level of disability can often correlate poorly with the values obtained at spirometry. This is probably down to a number of factors, including the degree of emphysematous damage, the degree of hyperinflation, the presence of additional comorbidities and the presence of deconditioning and motivational status. Therefore, while spirometry can help guide staging disease severity it should not be relied upon in isolation.

Both COPD and lung cancer share smoking as a common risk factor, while the presence of COPD itself acts as an additional independent risk factor for lung cancer. Given this, all patients presenting with an apparent new diagnosis of COPD should undergo a baseline chest X-ray to ensure their symptoms are not instead due to a first presentation of lung cancer. Clinicians should also be constantly alert for ‘red flag’ symptoms in their COPD population, particularly looking out for unexplained haemoptysis, dysphonia, chest pain or weight loss.

While a chest X-ray can identify most lung cancers some small tumours can be missed, particularly if located close to the mediastinum or behind the cardiac silhouette. With this in mind, if the clinical suspicion for malignancy remains high then a ‘staging’ CT thorax should be considered. Depending on your local service this could be ordered directly from primary care or via the local two week wait respiratory service. A normal CT thorax is very reassuring and essentially rules out an underlying lung malignancy. The only exception to this is in patients presenting with haemoptysis, where some respiratory specialists would still go on to perform a bronchoscopy to exclude a small endobronchial tumour that may be potentially missed on CT.

The only two interventions that have been proven to improve long term survival in COPD are smoking cessation and the use of long term oxygen therapy (LTOT) in chronically hypoxic patients. With this in mind it is crucial to encourage current smokers to quit, regardless of how severe their disease is or however late they have presented. I always try to explain this to patients, discussing how smoking cessation will both improve their lifespan and reduce their rate of decline in FEV1, helping them to maintain their quality of life in the longer term. In certain patients whose disease may be amenable to more advanced intervention techniques (e.g. domiciliary oxygen, lung volume reduction surgery, endobronchial valve placement or transplantation), I also add that treatment options tend to be limited in the presence of ongoing smoking.

The harmful effects of smoking mainly relate to the hundreds of other constituents that make up a tobacco cigarette, rather than the nicotine itself. Given this, I am more than happy for ongoing smokers to use nicotine replacement therapy (NRT) if this helps them cut down their smoking habit. Similarly I would prefer that a patient switch to e-cigarettes rather than continue to smoke tobacco cigarettes.

Long acting muscarinic antagonists (LAMAs) have been shown in various studies to improve many clinically relevant parameters including FEV1, symptom burden, exercise tolerance, quality of life and exacerbation frequency. LAMAs are typically started early in the disease, when patients first become symptomatic, and are then often continued throughout the disease course. Up until recently the only available LAMA was tiotropium, delivered via either the Handihaler or the Respimat device. Now, however, a number of other LAMAs are available, including aclidinium, umeclidinium and glycopyrronium. As there is no robust head to head data available to make a fair comparison between these various LAMAs, it is difficult to recommend one over the others on efficacy grounds alone. However, the range of drugs and devices that are now available does mean that it’s easier to marry an individual patient to a drug and device that suits him or her best. In my practice, patient choice tends to be the main driver to which device, and therefore which drug, I choose.

The addition of inhaled corticosteroids (ICS) to a long-acting beta agonist (LABA) in a combination device (i.e. a LABA/ICS inhaler) in advanced COPD (FEV1<50% predicted) has been shown to improve a number of parameters, particularly exacerbation frequency.3 As a result, many patients have ended up on ‘triple therapy’, a LABA/ICS and LAMA, within a few months of being diagnosed with COPD. There has been, however, increasing evidence that ICS are associated with a significant risk of pneumonia, possibly in a dose dependent manner. In addition a recent study has suggested that the newer LAMA/LABA inhalers may offer similar protection from exacerbations without the additional risk of pneumonia. My approach now is to reserve use of ICS for those patients who have moderate to severe COPD (FEV1<50%) who continue to have frequent exacerbations (≥2/year) despite optimal bronchodilatation with a LAMA/LABA device.

Some patients with COPD can have quite marked reversibility present at spirometry. But I would be wary of diagnosing these patients with co-existent asthma in the absence of any clinical history to suggest this, such as personal history of asthma in childhood or early adulthood, family history of asthma, atopic background or presence of diurnal variability to symptoms.

As only a proportion of COPD exacerbations are triggered by a bacterial organism, antibiotic therapy may not be indicated in every exacerbation. Unfortunately, sputum cultures cannot be relied upon in this setting due to poor sensitivity and slow turnaround times. Given this, the decision to start an antibiotic is an empirical one. Typically I suggest that patients start antibiotics if their sputum has become more purulent and if they have experienced more sputum production or more breathlessness than usual. The choice of antibiotic will depend on local resistance patterns but in our area it is either amoxicillin or doxycycline, depending on what allergies the patient may have.

There is no good evidence that home rescue packs can contribute to increased antimicrobial resistance although clearly this will always be a concern. It would be good practice, however, to monitor patients’ use of home rescue packs, with a view to reconsidering this in patients who appear to be overusing their packs.

Use of oral steroids can help shorten the duration of a COPD exacerbation, typically by around a day. However, there is no evidence to suggest any benefit from using oral steroids long term, although patients will often ask for this. Given this, I try to keep steroid courses as short as possible (i.e. 5-7 days). With this approach I am usually able to avoid having to use reducing courses of prednisolone – patients who require more than two courses of steroids a month, however, should be reduced to avoid adrenal suppression. Again, where patients appear to be inappropriately overusing their rescue packs it may be necessary to reconsider whether this is the right approach for that particular patient.

Long-term studies examining the use of regular mucolytics have shown variable results and so current guidance suggests there is no role for the routine use of mucolytics in stable COPD. But at an individual level, patients who have difficulties expectorating may benefit from using mucolytics as needed for symptom control – this can also be particularly helpful during an exacerbation.

Although theophylline does have a modest bronchodilator action it is not as effective as modern inhaled bronchodilators or as well tolerated. Theophylline levels are also affected by many other drugs, including macrolides, which can exacerbate their poor side-effect profile. Given this, I would typically only reserve theophylline for those patients unable to use inhaled bronchodilators effectively, for example due to poor inhaler technique. Similarly, there are no studies that have convincingly shown vitamin D supplementation to have a positive effect on COPD exacerbations and I would not routinely prescribe this either.

Patients recruited to a pulmonary rehabilitation programme are typically offered 1-2 sessions a week, run over 6-10 contiguous weeks. Although pulmonary rehabilitation programmes vary widely, they all tend to offer supervised exercise training as well as education on smoking cessation, dyspnoea management, exacerbation self-management and end of life issues. Robust evidence exists that pulmonary rehab programmes can improve exercise capacity, quality of life and perception of breathlessness while also reducing hospitalisation rates and rates of anxiety and depression. Furthermore, comparative data suggests that pulmonary rehab delivers similar, if not better, value for money than inhaler therapy (£2,000-£8,000/QALY for pulmonary rehab vs £7,000/QALY for LAMA monotherapy, £8,000/QALY for LABA monotherapy and £35,000-£187,000/QALY for ‘triple’ LAMA/LABA/ICS therapy).

Despite this, patients often receive rapidly escalating inhaler therapy rather than pulmonary rehab early in their disease course. At present both NICE guidance and BTS guidance suggest that only patients with an MRC dyspnea score ≥3 are offered pulmonary rehab.  I try to promote exercise as much as possible in patients with milder disease. Some programmes will also take patients with milder disease onto their PR programmes.. There is also increasing recognition that patients can benefit from pulmonary rehab when provided within four weeks of discharge from hospital with an exacerbation.

Specialist respiratory teams are usually happy to see any patient in which there are concerns over the diagnosis or long-term management. Specialist teams have access to a number of investigations (e.g. full lung function testing, CT scanning) and complex interventions (e.g. domiciliary oxygen, lung volume reduction surgery, endobronchial valve placement) that can help certain patient groups. Patients in whom a referral should definitely be considered include:

  • Young (i.e. <40 years old) patients, or those with a family history of alpha 1 antitrypsin deficiency
  • Suspected COPD asthma overlap syndrome (CAOS)
  • Where there is diagnostic uncertainty
  • Where symptoms seem disproportionate to spirometry findings
  • Where FEV1 is rapidly declining
  • Potential candidates for lung volume reduction surgery or lung transplantation
  • Suspected hypercapnoeic respiratory failure
  • Potential candidates for long term oxygen therapy (LTOT)

LTOT, oxygen administered for ≥15 hours per day for patients who are chronically hypoxaemic, remains the most evidence-based form of domiciliary oxygen in use. As LTOT is one of the only two interventions known to improve survival in COPD, it is important that potential candidates for LTOT are screened and referred appropriately. Patients with severe COPD should therefore be screened with oximetry at every annual COPD assessment. Those found to have resting saturations of ≤92% on air should be referred on to their local home oxygen service for a formal assessment with arterial blood gas sampling. LTOT should only be prescribed by a dedicated specialist team after a comprehensive review and is not something that should be initiated in primary care.

While it is important to identify patients who require LTOT early, this should be balanced against the risk of overprescribing LTOT to ‘unstable’ patients who have not yet fully recovered from an exacerbation. Patients should therefore not be screened for LTOT until they are ≥eight weeks clear of an exacerbation.

It is also important to weigh up the potential risks and benefits of LTOT in those who continue to smoke. Although it is unclear whether or not current smokers receive the full benefits of LTOT compared with non-smokers, it is known that LTOT has the potential for great harm, not only to the individual but also to carers, co-habitants and others around them. Up to 25% of all oxygen and smoking related domestic fires result in death, and 33% in serious injury. As a result most home oxygen services would avoid offering LTOT to those who continue to smoke.

Unlike some other conditions such as lung cancer it is difficult to anticipate when a patient with COPD may finally succumb to their disease. Often patients will deteriorate gradually over many years, with superimposed stepwise falls in their functional status following each exacerbation. Ultimately all patients will fail to survive an exacerbation, but predicting which exacerbation will be the final one for any given patient is impossible to judge. As a result, it is also impossible to clearly predict the time point at which to involve palliative care services. As a rule though, once symptoms become intrusive and inadequately controlled with conventional COPD interventions (e.g. inhaler therapy, pulmonary rehab etc.) then a more symptom-based approach is required, often with the help of the palliative care team.

Patients with disabling breathlessness may benefit from input from a physiotherapist to help manage their symptoms. Where drug therapy is warranted, regular low dose opiates (e.g. oramorph 2.5mg qds) or benzodiazepines (e.g. diazepam 2mg tds) can help keep symptoms at bay. Sublingual lorazepam 0.5-1.0mg can also be used as needed to help manage breakthrough acute attacks of breathlessness. Patients with excessive secretions ideally need to expectorate effectively to maintain good bronchial hygiene. Again a physiotherapist can help deliver this in a non-pharmacological way. Where medication is required, oral mucolytics and nebulized bronchodilators may be helpful. In the final stages hyoscine can be used to try and reduce secretion production.

Dr Jay Suntharalingam is a consultant respiratory physician at the Royal United Hospitals Bath Foundation Trust and the Trust’s clinical lead for COPD.

  1. Respirology. 2014 Jul;19(5):655-62. doi: 10.1111/resp.12298. Epub 2014 May 15. Cannabis smoking and respiratory health: consideration of the literature. Gates P, Jaffe A, Copeland J.
  2. BMJ. 2017 Sep 25;358:j3772. doi: 10.1136/bmj.j3772. Asthma-COPD overlap syndrome: pathogenesis, clinical features, and therapeutic targets. Leung JM1, Sin DD1
  3. NEJM 2007. Feb;356(8):775-789. Salmeterol and Fluticasone Propionate and survival in Chronic Obstructive Pulmonary Disease. Calverley et al.

Further reading

NICE guidance: Chronic Obstructive Pulmonary Disease in over 16s: Diagnosis and Management 2010 [CG101].

GOLD guidance: Global strategy for the diagnosis, management and prevention of Chronic Obstructive Pulmonary Disease: Updated 2016.

Indacaterol-Glycopyrronium versus Salmeterol-Fluticasone for COPD. Wedzicha JA, Banerji D, Chapman KR, Vestbo J, Roche N, Ayers RT, Thach C, Fogel R, Patalano F, Vogelmeier CF; FLAME Investigators. N Engl J Med. 2016 Jun 9;374(23):2222-34. doi: 10.1056/NEJMoa1516385. Epub 2016 May 15.

British Thoracic Society guidelines for home oxygen use in adults. Hardinge M, Annandale J, Bourne S, Cooper B, Evans A, Freeman D, Green A, Hippolyte S, Knowles V, MacNee W, McDonnell L, Pye K, Suntharalingam J, Vora V, Wilkinson T; British Thoracic Society Home Oxygen Guideline Development Group; British Thoracic Society Standards of Care Committee. Thorax. 2015 Jun;70 Suppl 1:i1-43. doi: 10.1136/thoraxjnl-2015-206865.

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