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Chronic obstructive pulmonary disease (COPD) encompasses chronic bronchitis, emphysema, and chronic airflow obstruction. It is characterised by persistent respiratory symptoms and airflow limitation that is not fully reversible.

COPD is associated with a range of pathological changes in the lung. The airflow limitation is usually progressive and associated with an inflammatory response to inhaled noxious particles or gases.1,2

Symptoms include cough, sputum production, shortness of breath, and wheeze. At first, these are often ascribed to “a smokers cough”, “getting old” or being “unfit”. Cough and sputum production may precede wheeze by many years. Symptoms may worsen and become severe and chronic, but not all of those with cough and wheeze advance to progressive disease.

Patients with COPD often have exacerbations, when symptoms become much worse and require more intensive treatment. These exacerbations have a significant mortality.

Many patients have extra-pulmonary effects and important co-morbidities that contribute to the severity of the disease. Important co-morbidities include asthma, bronchiectasis, lung cancer and heart disease. COPD can lead to debilitation, polycythaemia, osteoporosis, cachexia, depression and anxiety.

COPD is often confused with asthma. They are separate diseases, although some asthmatics develop irreversible airflow obstruction and some patients with COPD have a mixed inflammatory pattern. Asthma–COPD overlap (ACO) may be present when it can be difficult to distinguish between the diseases, or in patients who have both conditions.3

Guidelines review

The following documents were reviewed to formulate this Quick Reference Guide: COPD-X Australian and New Zealand Guidelines 20201 and the Global Initiative for Chronic Obstructive Lung Disease (GOLD) 2020.2 A systematic review was not performed, although relevant references were reviewed when necessary. Readers are referred to the COPD-X and GOLD documents for the more comprehensive detail and references that they provide. References are only provided when they differ from the COPD-X guidelines.

Grading

No levels of evidence grades are provided, due to the format of the Quick Reference Guide. Readers are referred to the above documents for the level of evidence on which the recommendations in this Quick Reference Guide are based.

Guideline development group

This group included representatives from a range of professions and disciplines relevant to the scope of the guidelines. The group did not include consumer representation.

Robert J Hancox, Stuart Jones, Christina Baggott, James Fingleton, Jo Hardy, Syed Hussain, and Justin Travers are respiratory physicians. Robert Young is a general physician. David Chen is a respiratory physiotherapist. Cheryl Davies is manager of the Tu Kotahi Maori Asthma Trust. Nicola Corna and Betty Poot are respiratory nurse practitioners. Jim Reid is a general practitioner. Joanna Turner is a pharmacist and research and education manager at the Asthma and Respiratory Foundation of New Zealand.

Peer review

The draft guidelines were peer-reviewed by a wide range of respiratory health experts and representatives from key professional organisations, including representatives from Asthma New Zealand, the Australian College of Emergency Medicine, Hutt Valley District Health Board, the Medical Research Institute of New Zealand, the New Zealand Medical Association, the New Zealand Nurses Organisation Te Rūnanga o Aotearoa, the NZNO College of Respiratory Nurses, Physiotherapy New Zealand, the Royal New Zealand College of General Practitioners, the New Zealand branch of the Thoracic Society of Australia and New Zealand, and Wellington Free Ambulance.

Dissemination plan

The guidelines will be translated into tools for practical use by health professionals and used to update health pathways and existing consumer resources. The guidelines will be published in the New Zealand Medical Journal and on the Asthma and Respiratory Foundation of New Zealand (ARFNZ) websites, as well as being disseminated widely via a range of publications, training opportunities, and other communication channels to health professionals, nursing, pharmacy and medical schools, primary health organisations, and district health boards.

Implementation

The implementation of the guidelines by organisations will require communication, education, and training strategies.

Expiry Date

The expiry date for the guidelines is 2025.

COPD in Māori

Māori rights in regard to health, recognised in Te Tiriti o Waitangi and other national and international declarations, promote and require both Māori participation in health-related decision making as well as equity of access and health outcomes for all New Zealanders.

  • The burden of COPD among Māori is one of the most significant health disparities in New Zealand: hospitalisation rates for Māori are 3.5 times higher than non-Māori, non-Pacific, and non-Asian rates, and COPD mortality for Māori is 2.2 times higher.8
  • Māori whānau also have greater exposure to environmental triggers for COPD, such as smoking and poor housing.
  • This burden of COPD translates to large inequities in lost years of healthy life and underscores the urgent need for health service models to address high and growing need for COPD treatment in Māori.
  • Māori should be considered a high-risk group requiring targeted care. This should address risk factors such as poor housing, overcrowding, health literacy, inadequate tailoring of health information, obesity, smoking, and poor access to pulmonary rehabilitation and healthcare services.
  • Māori have much worse lung function for given levels of smoking,9 and the burden of COPD affects Māori 15–20 years younger than non-Māori.10 This makes smoking cessation even more important for Māori, and COPD should be considered at a younger age among Māori smokers.
  • There is a very high incidence of lung cancer among Māori.

Major barriers to good COPD management for Māori include poor access to care, inattention to culturally accepted practices, discontinuous and poor-quality care, and inadequate provision of understandable health information. As Māori place a high value on whakawhanaungatanga (the making of culturally meaningful connections with others), the absence of culturally appropriate practices can hinder attendance in mainstream pulmonary rehabilitation programmes.11 Cultural safety and a pro-equity approach is essential.

It is recommended that:

  • Healthcare providers should undertake clinical audit or other quality-improvement activities to monitor and improve COPD care and outcomes for Māori.
  • A systematic approach to health literacy and COPD education for Māori whānau is required.
  • Healthcare providers should support staff to develop cultural safety skills for engaging Māori with COPD and their whānau.
  • Assess patients using a Māori model of care: https://www.health.govt.nz/our-work/populations/maori-health/maori-health-models.

Māori leadership is required in the development of COPD management programmes, including pulmonary rehabilitation, to improve access to COPD care and facilitate ‘wrap around’ services that address the wider determinants of health (such as housing, financial factors, access to health care and access to pulmonary rehabilitation programmes) for Māori with COPD.

COPD in Pacific people

Similar considerations apply to Pacific people, who also have a disproportionate burden of COPD. Pacific people’s hospitalisation rates are 2.7 times higher than those of other New Zealanders.8

It is recommended that:

Pathogenesis

Most people with COPD will have smoked cigarettes or inhaled noxious particles causing lung inflammation. Airway inflammation is a normal response to smoking but seems to be accentuated in those who go on to develop COPD. Some people develop COPD without smoking or apparent exposures. COPD may also develop in patients with other chronic lung diseases such as asthma.

The inflammatory process in COPD is mostly neutrophil, macrophage, and T-lymphocyte mediated. This inflammation leads to narrowing of peripheral airways and destruction of alveoli, causing airflow obstruction and decreased gas transfer.

Inflammation, fibrosis, and sputum production in small airways causes air trapping during expiration leading to hyperinflation. This reduces inspiratory capacity and causes shortness of breath on exercise.

In patients presenting at a young age (particularly those younger than 40), alpha-1 antitrypsin deficiency should be considered. This genetic defect causes a reduction in the major anti-protease in lung parenchyma, leaving the lung susceptible to the destructive effects of neutrophil elastase and other endogenous proteases, which are released as part of the inflammatory response to smoking.

Diagnosis

A diagnosis of COPD should be considered in anyone who presents with cough, sputum production, wheeze, or shortness of breath, particularly those above the age of 40 years. There is usually a history of cigarette smoking or exposure to smoke other noxious substances.

  • Physical examination and chest x-ray are rarely diagnostic in early COPD, but they may be valuable in excluding other diagnoses and co-morbidities such as lung cancer, pulmonary fibrosis and cardiac failure.
  • Other causes for the patient’s symptoms should always be considered, as common comorbidities such as heart disease and obesity may co-exist with COPD and in some patients will be the dominant cause of breathlessness.
  • The diagnosis of COPD should be confirmed by spirometry (see Spirometry). If this is not available in primary care, patients should be referred for this. There are few contra-indications, but a small proportion of patients cannot do adequate spirometry.
  • Spirometry should be avoided during infections, because of the risk of transmitting infections such as influenza, SARS-CoV-2 (COVID-19), or tuberculosis.
  • Peak flows are not useful for diagnosing or managing COPD.
  • Usually asthma and COPD are easy to differentiate. Asthma is an episodic disease and usually, but not always, presents at a younger age or with a history of being “chesty” as a child. However, a mixed pattern of asthma-COPD overlap (ACO) exists, and it is sometimes difficult to distinguish which is the principal cause of airway limitation (see section Asthma and COPD overlap (ACO)).

Assess severity

  • Spirometry assesses the severity of airflow obstruction. Used in conjunction with the severity of symptoms, this helps to assess the severity of COPD (Table 1). Although Table 1 also shows the typical symptoms, the severity of the symptoms does not necessarily correspond to the severity of airflow obstruction.
  • The effect of breathlessness on daily activities can be quantified using the modified Medical Research Council (mMRC) Dyspnoea Scale (Table 2).
  • The COPD Assessment Test (CAT) is an eight-item questionnaire that can measure the symptomatic impact of COPD and response to treatment (Appendix 2).
  • Functional tests, such as the six-minute walk test, shuttle walk tests and sit-to-stand tests, can help to assess functional limitation, disease progression and response to treatment.

Table 1: Severity classification for COPD. (Adapted from Lung Foundation Australia’s Stepwise Manage-ment of Stable COPD available at https://lungfoundation.com.au/wp-content/uploads/2018/09/Informa-tion-Paper-Stepwise-Management-of-Stable-COPD-Apr2020.pdf.)

FEV1=forced expiratory volume in one second. PaO2=partial pressure of oxygen, arterial. PaCO2=partial pressure of carbon dioxide, arterial.

Table 2: Modified Medical Research Council (mMRC) Dyspnoea Scale for grading the severity of breathlessness during daily activities*

* The mMRC Dyspnoea Scale is very similar to the original MRC Scale, which ranges from 1 to 5 rather than 0 to 4 (ie, MRC grade 3=modified MRC grade 2).

Spirometry

Spirometry is the most useful test of lung function to diagnose and assess the severity of COPD. This may be done both before and after a bronchodilator to assess reversibility, but the diagnosis and severity are determined by post-bronchodilator measurements.

  • Irreversible airflow obstruction is indicated by a post-bronchodilator forced expiry volume in once second to forced vital capacity (FEV1/FVC) ratio<0.70*.
  • The severity of the obstruction is diagnosed using the post-bronchodilator FEV1 as a % of the predicted value (Table 1).
  • It is possible to have airflow obstruction with an FEV1/FVC ratio<0.70* but an FEV1 in the normal range.
  • A restrictive pattern on spirometry is not consistent with a diagnosis of COPD and, if it is not due to technically inadequate spirometry, suggests an alternative cause of symptoms (eg, morbid obesity, neuromuscular weakness, or interstitial lung disease). Patients with a restrictive pattern may benefit from specialist referral for further investigation.
  • Some patients with COPD cannot blow out long enough to do a true FVC. The Forced Expiratory Volume at 6 seconds (FEV6) can be used as an approximation of the FVC.
  • A small subset of patients with normal spirometry have evidence of emphysema on CT scan and impairment of gas exchange. There is limited evidence to guide management in these patients, but if they are symptomatic or having exacerbations, we recommend treatment for COPD according to this guideline.

(*Note: There is disagreement about the criteria for airflow obstruction. The FEV1/FVC ratio naturally declines with age, and defining airflow obstruction by an FEV1/FVC ratio <0.70 may miss mild airflow obstruction in younger patients and over-diagnose it in the elderly. Some guidelines recommend using an age-specific lower limit of normal. But for clinical purposes, the <0.70 cut-point is easy to apply and unlikely to greatly influence management in those with mild airflow obstruction. The grading of severity also varies between guidelines, with the GOLD guidelines using different categories to COPD-X (in Table 1). But this is also unlikely to greatly influence clinical management.)

Reversibility testing

When performing reversibility testing, the first measurements should be done before bronchodilators:

  • Bronchodilators should be withheld for the duration recommended in the consensus ATS/ERS guidelines.4 This ranges from 4–6 hours for a short-acting beta agonist (SABA) to 48 hours for an ultra long-acting beta agonist (LABA).
  • Spirometry is repeated at least 15 minutes after giving a bronchodilator (usually 400mcg salbutamol via spacer).
  • Many patients with COPD will have some improvement after a bronchodilator (“partial reversibility”), but if spirometry becomes normal (FEV1/FVC>0.7* and FEV1>80% predicted), COPD is excluded (by definition).
  • The consensus definition of a significant bronchodilator response is arbitrarily defined as a ≥12% change from baseline with an absolute improvement of ≥200ml, but this does not predict who will benefit from bronchodilator treatment.
  • If the response to bronchodilator is substantial (>400mL improvement in FEV1) then asthma or Asthma-COPD Overlap is likely.

(*Note: There is disagreement about the criteria for airflow obstruction. The FEV1/FVC ratio naturally declines with age, and defining airflow obstruction by an FEV1/FVC ratio <0.70 may miss mild airflow obstruction in younger patients and over-diagnose it in the elderly. Some guidelines recommend using an age-specific lower limit of normal. But for clinical purposes, the <0.70 cut-point is easy to apply and unlikely to greatly influence management in those with mild airflow obstruction. The grading of severity also varies between guidelines, with the GOLD guidelines using different categories to COPD-X (in Table 1). But this is also unlikely to greatly influence clinical management.)

Non-pharmacological management (Box 1)

Smoking cessation

Stopping smoking is the most important treatment for COPD: every person who is still smoking should be offered help to quit. Reducing smoking-related health risks requires complete cessation of all tobacco and other smoked products, including marijuana/cannabis.

  • All forms of nicotine replacement therapy, in association with smoking cessation support, are useful in aiding smoking cessation and increase the rate of quitting.
  • Oral bupropion, varenicline, and nortriptyline have been shown to be effective and should be considered in those patients struggling to give up despite nicotine replacement therapy.
  • Most of these are fully funded in New Zealand and a prescription for this should be discussed with a health professional.
  • Referral to a local smoking cessation support service is recommended.

E-cigarettes and vaping are probably less harmful to health than smoking, but short-term studies suggest that they are not risk free.5 E-cigarettes and vapes that contain nicotine are highly addictive.

  • E-cigarettes used within the context of a supportive smoking cessation programme have been shown to aid in smoking cessation in selected groups of motivated patients.
  • The long-term safety of e-cigarettes and vaping have not been shown. Smokers using e-cigarettes or vaping to quit smoking should be advised to stop using e-cigarettes and vaping as soon as possible after quitting smoking.
  • No e-cigarette or vape is currently approved as a smoking cessation tool.
  • E-cigarettes and vapes should never be used near an oxygen source, as this is a fire risk.

Physical activity

Patients with COPD benefit from physical activity and should be encouraged to:

  • Be active on most, preferably all, days of the week.
  • Do at least 20–30 minutes of exercise per day. More is better.
  • Exercise to an intensity that should cause the patient to “huff and puff” or feel breathless: Getting out of breath will not cause harm.
  • Do muscle strengthening activities on two or more days each week.

Pulmonary rehabilitation

Pulmonary rehabilitation should be offered to all patients with COPD. Although there may be barriers to attending pulmonary rehabilitation classes, there are a variety of ways to deliver pulmonary rehabilitation to patients in different settings depending on local respiratory services and patient preferences.

  • Pulmonary rehabilitation reduces breathlessness, improves quality of life, and reduces depression in patients with COPD.
  • Patients gain significant benefit from rehabilitation regardless of the degree of breathlessness, but the most breathless patients benefit the most.
  • Exacerbations of COPD are an indication for referral to pulmonary rehabilitation and an early return to pulmonary rehabilitation after exacerbation should be encouraged. This has been shown to reduce further hospitalisations and may reduce mortality.
  • Exercise training is the cornerstone of pulmonary rehabilitation, and regular post-rehabilitation exercise is required to sustain the benefits.
  • The benefits of pulmonary rehabilitation decline over time and repeat attendance at pulmonary rehabilitation programmes should be encouraged in patients with functional decline or exacerbations.
  • If someone is unable to access a pulmonary rehabilitation programme, an in-home exercise programme should be considered.

Breathlessness management strategies

In addition to pulmonary rehabilitation, patients may benefit from seeing a respiratory physiotherapist for individualised breathing exercises or breathless management strategies:

  • Diaphragmatic breathing and pursed lips breathing exercises may benefit some patients. These support and correct the breathing pattern disorders caused by COPD and improve exercise capacity, but they have inconsistent effects on dyspnoea or health-related quality of life scores.
  • Constant load threshold inspiratory muscle training improves inspiratory muscle strength, quality of life, dyspnoea, and exercise capacity.
  • Hand-held fan therapy: the airflow and cooling effects of the fan, alongside other breathlessness management strategies, such as relaxation, pacing, and positioning, can reduce dyspnoea.

Other things that may help:

  • Hospital clinical teams working with the primary healthcare team can help enhance quality of life and reduce disability for patients with COPD.
  • Patients may also benefit from local support groups.
  • Consider including a cognitive behavioural component in the self-management plan to assist with reducing anxiety and breathlessness.
  • Consider screening for urinary incontinence related to cough.

Other useful resources are given in Appendix 4 and 5.

Sputum management/sputum clearance techniques

Patients with chronic sputum production may benefit from seeing a physiotherapist (ideally a respiratory physiotherapist) for an individualised chest clearance plan. Airway clearance techniques enhance sputum clearance, reduce hospital admissions, and improve health-related quality of life, and they may also improve exercise tolerance and reduce the need for antibiotics.

  • A wide variety of airway clearance techniques are available. No one technique is superior for all patients.
  • The choice of technique should be based on the clinician’s assessment, resource availability, and patient acceptability.

Nutrition

Both malnutrition and obesity are common and contribute to morbidity and mortality in COPD. Poor eating habits, sedentary lifestyles, smoking, and corticosteroid use further compromise nutritional status.

  • The key goals of nutritional management are to eat a balanced diet, to achieve and maintain a healthy weight, and to avoid unintentional weight loss. Consider referral to a dietician, or high-calorie nutritional supplements, for those who are malnourished.
  • There is evidence that weight loss is beneficial for those who are obese.
  • Unintentional weight loss should be investigated for potential malignancy.

Housing

There is good evidence that a warm, dry, and smoke-free home is associated with better asthma control, and it is likely that the same is true for COPD.

Assisted ventilation

Non‐invasive ventilation (NIV) with bi‐level positive airway pressure reduces mortality and need for intubation in patients admitted to hospital with acute hypercapnic respiratory failure as a result of an exacerbation of COPD (see section Management). In most instances, NIV is not required once the patient has recovered.

  • People who have chronic hypercapnic respiratory failure, despite adequate treatment, and have needed assisted ventilation (invasive or non-invasive) during an exacerbation, or with worsening hypercapnia on long-term oxygen therapy, should be referred to a specialist centre for consideration of long-term NIV.
  • Red flags to consider for need for home NIV:
    – Previously required assisted ventilation
    – Obstructive sleep apnoea
    – Obesity hypoventilation
    – Persistent nocturnal hypoxia
    – Neuromuscular conditions
    – Spinal/chest wall deformities

Interventional approaches to the management of COPD

Thoracic surgery is rarely performed for COPD. The two situations where it may be considered are bullectomy or lung volume reduction surgery. Neither procedure increases life expectancy. Both have significant complication rates and are only performed in specialist centres after careful multi-disciplinary assessment.

Bullectomy

Bullectomy can be considered where there is a very large bulla compressing other lung tissue. Removing the bulla allows the preserved lung tissue to function better.

Lung volume reduction surgery

Lung volume reduction surgery can improve exercise capacity in people with upper-lobe predominant emphysema. The surgery has a significant early mortality, but there is no difference in long-term mortality.

Interventional bronchoscopy

Bronchoscopic lung volume reduction approaches have been developed as alternatives to lung volume reduction surgery. These aim to reduce gas-trapping and improve lung mechanics in advanced emphysema, which can lead to improved lung function, symptoms, and quality of life in carefully selected patients. Endobronchial valve therapy has the most evidence and is available in New Zealand. It is only effective in those with intact fissures and no collateral ventilation as one-way valves are inserted to cause collapse of lung segments. Endobronchial valve therapy does not reduce mortality and has significant complication rates.

Lung transplantation

Consideration for lung transplantation is appropriate in younger patients (usually <65) with very severe obstruction and severe symptoms, or progressive deterioration despite optimised management, including smoking cessation and pulmonary rehabilitation. Referral to the transplant service should be made by a respiratory specialist.

Box 1: Key messages for non-pharmacological management of COPD.

Improving patient understanding

Identify and manage social and cultural issues

Health literacy, cultural context, and the degree of social isolation or support are key factors affecting a person’s understanding of and attitude to COPD. See also sections COPD in Māori and COPD in Pacific people.

  • These factors impact on COPD management, appropriate inhaler technique, adherence to treatment and appropriate use of self-management plans.
  • These factors also have a considerable impact on the success of smoking cessation.
  • Awareness of the social and cultural factors will enhance communication between clinicians and patients and improve health outcomes.
  • There are many practical challenges for people living with COPD, such as completing everyday tasks, holding down a job, and having access to transport. Awareness of these challenges and referral to support services where available can be beneficial.

Optimise knowledge of COPD and adherence to treatment

  • Patient understanding of the disease, appropriate inhaler technique and adherence to treatment are important factors in COPD management.
  • There are many inhalers available to treat COPD, and people can easily get confused about these. Demonstrate the use of the inhalers and ensure that patients can use them correctly.
  • Clinicians should ask about the patient’s understanding of the disease and the rationale for treatment, to clarify misunderstandings, and to work to remove barriers to adherence and good self-management. It is important to provide information to the patient and whānau in a format that they can understand.

Develop an action plan

Personalised action plans (self-management plans) improve quality of life and reduce hospital admissions and should be offered to all people with COPD.

  • Action plans should be personalised and focus on recognising and treating deteriorating symptoms.
  • Patients at risk of exacerbations may be offered antibiotics and prednisone to have at home as part of their action plan. The patient should be advised of a timeframe for clinical review once they have started these medicines for an acute exacerbation of COPD.
  • Action plans should be checked at each COPD review.

The Asthma and Respiratory Foundation of New Zealand’s COPD Action Plan is shown in Appendix 3.

Electronic versions are available at: www.nzrespiratoryguidelines.co.nz.

Develop a breathlessness plan

  • A breathlessness plan can reduce the severity and impact of breathlessness. Interventions and techniques that can improve breathlessness include self-management education, breathing exercises, sitting upright and leaning forwards (‘positioning’), using pursed lip breathing, and a hand-held fan.
  • Oxygen is not an effective treatment for breathlessness in patients who are not hypoxic.
  • Smoking cessation also improves breathlessness.

Asthma and Respiratory Foundation of New Zealand’s ‘Breathlessness Strategies for COPD’ is shown in Appendix 4 and is available at www.nzrespiratoryguidelines.co.nz.

Pharmacological management (Box 2)

The purpose of pharmacological management in COPD is symptom control and prevention of exacerbations, with the aim of improving quality of life.

  • Check inhaler adherence and inhaler technique regularly. Make sure that these are optimal before escalating treatment.
  • Treatment escalation should follow a stepwise approach based on breathlessness and exacerbation frequency. It should take into account patient preferences, regimen complexity, cost, and side effects.
  • Effects of treatment on dyspnoea should be apparent within six weeks.
  • Effects on exacerbation frequency may need to be assessed over 6 to 12 months.

Inhaled medication for COPD

  • Short-acting beta2 agonists (SABA: salbutamol or terbutaline) and the short-acting muscarinic antagonist (SAMA: ipratropium), either individually or in combination, can be taken as-needed to provide short-term relief of breathlessness. Short-term response to SABA or SAMA (reversibility testing) does not predict benefit from long-acting bronchodilator therapy.
  • For patients with ongoing dyspnoea despite as-needed SABA, SAMA, or combination SABA/SAMA, a regular long-acting muscarinic antagonist (LAMA) such as tiotropium, glycopyrronium, or umeclidinium is recommended, unless there is evidence of asthma/COPD overlap (see Asthma and COPD overlap (ACO)). Do not continue to use ipratropium in patients taking a LAMA, except in emergencies.
  • It is not necessary to have a trial of regular short-acting bronchodilators before starting a LAMA if symptoms, exacerbation history or spirometry suggest that a long-acting bronchodilator is desirable.
  • Both LAMAs and LABAs improve lung function, symptoms and quality of life, but LAMAs are recommended as the first-line long-acting medication for COPD because they reduce exacerbation risk and have fewer side effects. If LAMAs are contra-indicated, a long-acting beta agonist (LABA) such as salmeterol, formoterol, or indacaterol is recommended.
  • In patients who remain breathless or who continue to exacerbate despite treatment with a single long-acting bronchodilator, dual LAMA/LABA therapy is recommended (eg, glycopyrronium/indacaterol, umeclidinium/vilanterol, or olodaterol/tiotropium). Combination therapy with a LABA and LAMA improves lung function, reduces symptoms, and reduces exacerbations compared to either drug alone.
  • LABA/LAMA is preferred over inhaled corticosteroid (ICS)/LABA as initial therapy for most patients with frequent exacerbations because ICS increases the risk of pneumonia.
  • These medications may have risks, particularly at higher doses in patients with cardiac disease. If there is no evidence of benefit, consider stopping them.
  • Patients with an eosinophilic pattern of disease may benefit from ICS/LABA instead of LABA/LAMA. Retrospective analyses suggest that blood eosinophil counts predict the benefit of ICS in preventing exacerbations: people with blood eosinophil counts <100cells/µL are least likely to benefit and people with counts ≥300cells/µL are most likely to benefit. A single blood test may not be representative as eosinophil counts can vary over time. Blood eosinophil counts performed when a patient is taking oral steroids will not be informative.
  • An ICS should form part of the regimen for any patient with asthma/COPD overlap. This should usually be prescribed as an ICS/LABA combination inhaler to avoid the risk of LABA monotherapy in patients with poor adherence to a separate ICS inhaler.
  • Prescriptions should be based on drug class. Choice of specific LABAs and LAMAs should be guided by patient preference and their ability to use the inhaler device. A list of inhalers available in New Zealand is available at www.nzrespiratoryguidelines.co.nz. Dry-powder inhalers have a substantially lower impact on greenhouse gases than pressurised metered-dose inhalers.
  • Six weeks is a reasonable timeframe to assess improvement in breathlessness following a medication change.
  • The COPD assessment test is an eight-item questionnaire that can be used to measure the symptomatic impact of COPD and response to therapy (see Assess severity and Appendix 2).

Role of triple therapy (LABA/LAMA/ICS)

  • Escalation to triple LABA/LAMA/ICS therapy should be considered in patients who continue to exacerbate (twice or more a year) despite adherence to dual LAMA/LABA or ICS/LABA therapy and optimal inhaler technique.
  • A subset of patients with persistent breathlessness and exercise limitation, despite LABA/LAMA combination therapy, may benefit from triple therapy with LABA, LAMA, and ICS. However, the increased risk of pneumonia with regular ICS should be considered.
  • Direct escalation to dual or triple therapy, without stepwise up-titration, may be reasonable in the setting of a severe or recurrent exacerbations.

ICS withdrawal

  • The risk of pneumonia in patients with severe COPD is increased with regular ICS. Withdrawing ICS should be considered if:
  • There is no evidence of benefit from ICS in terms of improved symptoms or fewer exacerbations.
  • The patient develops pneumonia or other ICS adverse effects.
  • The patient does not have a history of frequent exacerbations and is stable.
  • If ICS treatment is withdrawn, the patient should be reviewed at 4–6 weeks to ensure that this doesn’t cause a deterioration in symptoms.
  • Withdrawal of ICS may not be appropriate if the blood eosinophil count is elevated. A blood eosinophil count ≥300cells/µL has been shown to be associated with an increased exacerbation risk after ICS withdrawal.
  • ICS should not be withdrawn in patients with a diagnosis of asthma/COPD overlap (see section Asthma and COPD overlap (ACO)).

Table 3: Simplified maintenance inhaler management of COPD.

Additional therapies

  • There is no evidence that routine use of nebulisers is beneficial in patients with COPD.
  • Theophylline has not shown consistent benefits on exacerbation, lung function, symptoms, or quality of life in randomised controlled trials. In view of the narrow therapeutic index and side-effect profile of theophylline, we do not recommend its routine use in the management of COPD.
  • There is no evidence of benefit from long-term oral corticosteroids.
  • Long-term macrolide antibiotics, such azithromycin and erythromycin, can reduce risk of exacerbations over one year in former smokers who have exacerbations despite optimal inhaled treatment. Azithromycin is not currently funded in New Zealand for this indication. Long-term macrolide therapy is associated with significant risks, including bacterial resistance, gastrointestinal and cardiovascular side effects, and hearing impairment. Long-term macrolides should rarely be initiated without specialist advice.
  • Regular treatment with mucolytics (eg, erdosteine, carbocysteine, or N-acetylcysteine) may reduce the risk of exacerbations in some patients. These treatments are not currently funded in New Zealand.
  • In patients with severe and very severe COPD and a history of exacerbations, PDE4 inhibitors (eg, roflumilast) improve lung function, reduce the risk of exacerbations, and have modest benefits for symptoms and quality of life. They have significant gastrointestinal side effects. These treatments are not currently funded in New Zealand
  • Alpha-1 antitrypsin augmentation therapy may slow the progression of emphysema in patients with alpha-1 antitrypsin deficiency. This is not currently funded in New Zealand.

Box 2: Key messages for pharmacological management of COPD.

Oxygen therapy

  • Oxygen is a treatment for hypoxia, not dyspnoea. Oxygen does not reduce the sensation of breathlessness in patients who are not hypoxic. Oxygen may not improve breathlessness even in those who are hypoxic.
  • Oxygen is a drug therapy and should be prescribed.
  • Long-term oxygen therapy has survival benefits for COPD patients with severe hypoxaemia. It must be used for at least 16 hours a day. The survival benefits are not apparent until months or years after starting treatment.
  • Evaluation of the patient and consideration for long-term oxygen therapy supply should be done by a specialist respiratory service (Box 3). The causes of the hypoxia should be explored, and the patient’s pharmacological and non-pharmacological management should be optimised. A target saturation range and oxygen flow rate should be established.
  • Patients should adhere to the amount of oxygen prescribed and be monitored for adverse effects.

Box 3: Criteria for oxygen.

Flying with oxygen

Flying is generally safe for patients with COPD, including those with chronic respiratory failure who are on long-term oxygen therapy.

  • Before flying, patients should ideally be clinically stable.
  • Supplemental oxygen is unlikely to be required if the resting oxygen saturation is ≥95%, and is likely to be required if oxygen saturation is ≤88%. Patients with oxygen saturation values between these levels might require specialist assessment.
  • Those already on long-term oxygen therapy need an increase in flow rate of 1–2L per minute during the flight.
  • Patients receiving oxygen therapy will need to contact the airline prior to flying.

Vaccination

  • Yearly influenza vaccination reduces serious illness and death in patients with COPD and should be actively promoted to patients with COPD.
  • Pneumococcal vaccination probably decreases the incidence of pneumonia and reduces the risk of exacerbations in patients with COPD, but the evidence for this is conflicting and pneumococcal vaccination is not currently funded for this indication in New Zealand.
  • Two types of pneumococcal vaccine are approved for use. If the healthcare professional and patient consider this an appropriate treatment, a suggested schedule is one dose of 13-valent protein conjugate vaccine (PCV13, Prevenar 13®) given first, followed at least eight weeks later by the first dose of 23-valent polysaccharide vaccine (23PPV, Pneumovax 23®). A second dose of 23PPV is given a minimum of five years later and a third dose at age ≥65 years.

Acute exacerbations

COPD exacerbations are characterised by a change in the patient’s baseline dyspnoea, cough, and/or sputum that is beyond normal day-to-day variations, is acute in onset, and may warrant a change in regular medication or hospital admission. Key symptoms of exacerbations include increased shortness of breath, increased sputum purulence and volume, increased cough, and wheeze.

Exacerbations of COPD are associated with an accelerated loss of lung function, particularly in patients with mild disease. Prolonged exacerbations are associated with worse health status and more frequent future exacerbations.

Early diagnosis and prompt management of exacerbations of COPD may prevent functional deterioration and reduce hospital admissions. Education of the patient, carers, other support people, and family may aid in the early detection of exacerbations.

Assessment (Figures 1 and 2)

  • Most exacerbations can be managed at home. Indications for hospitalisation include, but are not limited to, a sudden worsening of symptoms, confusion or drowsiness, signs such as cyanosis and peripheral oedema, failure to respond to medical management, low oxygen saturation by pulse oximetry (SpO2), the presence of serious co-morbidities, including heart failure and newly occurring arrhythmias, and insufficient home support or lack of telephone or transport.
  • A guide to acute severity assessment is shown in Table 4.
  • Several prognostic scores have been proposed. The most validated one is DECAF, but this includes COPD with pneumonia and requires a blood gas, complete blood count (for eosinophils), and chest x-ray, which are unlikely to be available in primary care. An alternative is CURB-65, which was developed for pneumonia but has been found to be equally effective at predicting short term-mortality in COPD in New Zealand studies.6 CRB-65 is a simpler version that does not require any laboratory measures (Table 5).
  • A chest x-ray and electrocardiogram help to identify alternative diagnoses and complications, such as pulmonary oedema, pulmonary embolus, pneumothorax, pneumonia, pleural effusion, arrhythmias, myocardial ischaemia, and others. Biomarkers (troponins, B-natriuretic peptide, D-dimer) can help to identify comorbidities and abnormalities of these are associated with a worse prognosis.

Table 4: Assessment of exacerbation severity.

Table 5: Assessment of short-term (one-month) prognosis.

*Score 1 point for the presence of each factor. #DECAF scores have been validated in patients with COPD and pneumonia, and CURB65 and CRB65 have not.

Management (Box 4, Figures 1 and 2)

Use breathless management strategies (Appendix 4): sit, rest arms on a chair or table, use a fan, and practise breathing control techniques

Bronchodilators

  • Short-acting inhaled beta2 agonists with or without short-acting anti-muscarinics are the initial bronchodilator of choice to treat an acute exacerbation. These can be delivered via pressurised metered dose inhaler and spacer, dry powder inhalers, or nebuliser. We recommend salbutamol via a spacer. One actuation of the inhaler should be used each time and repeated as necessary.
  • Spacer technique is important when using a pressurised metered dose inhaler. In an exacerbation, we recommend one actuation into the spacer followed by 4—6 tidal breaths. Observe and repeat if required.
  • The bronchodilator effect of 8—10 puffs of 100mcg salbutamol via spacer is equivalent to a 5mg salbutamol nebuliser. We recommend that no more than five puffs are used at a time (given individually via spacer).
  • If patients do not respond to multiple doses of inhaled short-acting beta2 agonist, additional bronchodilator treatment such as ipratropium is recommended.
  • Nebulisers may increase the risk for aerosolisation of viruses such as SARS-CoV-2 (COVID-19). There is no evidence that nebulisers are more effective than inhalers via a spacer, and we recommend that nebulisers should be avoided in any patient who could be infected with respiratory viruses. If they are used, appropriate aerosolisation infection precautions should be implemented.
  • If a salbutamol nebuliser is necessary, we recommend a maximum dose of 2.5mg at a time. Patients with COPD often have cardiac co-morbidities. Higher doses are associated with an increased risk of tremors, elevated heart rate, palpitations, and lower blood pressure, without evidence of any additional benefit.
  • If nebulisers are given for acute COPD exacerbations, they should be air driven to reduce the risk of type 2 respiratory failure due to high flow oxygen.
  • Maintenance LABA, LAMA, and ICS should be continued during an exacerbation.
  • We do not recommend the routine use of intravenous (IV) magnesium for COPD exacerbations.
  • We do not recommend adrenaline for COPD exacerbations in the absence of anaphylaxis.

Corticosteroids

• Systemic corticosteroids (eg, prednisone 40mg once daily) can improve lung function, improve oxygenation, and shorten recovery time. They should usually be given for five days. Longer courses should generally be avoided due to the risk of side effects.

• Intravenous steroids should be avoided. There is no evidence of benefit compared with oral corticosteroids for treatment failure, relapse, or mortality. Hyperglycaemia rates are higher with IV corticosteroids.

Antibiotics

  • Respiratory tract infections are the most common precipitants of exacerbations of COPD. These may be viral, bacterial, or mixed. Common bacterial pathogens include Haemophilus influenzae, Streptococcus pneumonia, and Moraxella catarrhalis. Mycoplasma pneumoniae and Chlamydia pneumoniae have also been reported. Pseudomonas aeruginosa and Staphylococcus aureus are uncommon but occur more frequently in severe COPD.
  • Antibiotics, when indicated by the presence of purulent sputum, fever and/or raised inflammatory markers (CRP >40), can shorten recovery time and reduce the risk of relapse and treatment failure, and should be prescribed for 5–7 days.
  • Oral antibiotics such as amoxicillin or doxycycline are recommended. If treatment failure or resistant organisms are suspected, amoxycillin-clavulanate can be prescribed. If pneumonia, Pseudomonas or Staphylococci are suspected, appropriate antibiotics should be used.

Oxygen

  • If indicated, oxygen should be prescribed and titrated via nasal prongs or a controlled flow device to target saturations of 88–92%.
  • Oxygen delivery via a high-flow humidified nasal device can improve ventilation and airway clearance as well as reduce the physiological dead space and work of breathing.

Supported ventilation

  • Non-invasive ventilation (NIV) reduces mortality by about 50%, reduces need for intubation, and shortens length of stay in patients with rising arterial carbon dioxide tension (PaCO2) levels due to COPD. It should be considered in patients who present with hypercapnic respiratory failure (arterial pH <7.35, PaCO2 >6kPa/45mmHg).
  • An arterial blood gas should be considered in every patient with a severe exacerbation, an oxygen saturation less than 90%, or signs of cor pulmonale.
  • A venous blood gas pH ≤7.34 has good sensitivity and specificity for acidaemia (pH ≤7.35) but does not reliably predict arterial PaCO2 and cannot diagnose hypercapnic respiratory failure. An arterial blood gas is necessary to assess the need for NIV.
  • Ward-based NIV can reduce the requirement for HDU/ICU admission but should be conducted in an appropriately monitored setting with trained clinical staff.
  • At the time of initiating NIV, the goals and limits of care should be considered and a clear written escalation plan established.

Airway clearance techniques

  • Patients with excess sputum production benefit from airway clearance techniques during an exacerbation.
  • Airway clearance techniques should be individualised to the patient.

Before discharge

  • Ensure that adequate education is provided regarding COPD management, including smoking cessation, use of inhalers, and the development of an acute management/action plan.
  • Ensure that clear follow-up plans are in place, as the risk for further exacerbations is greatest following an exacerbation.
  • Ensure that there is sufficient support at home for the patient to manage during their recovery. This may require social work, physiotherapy, occupational therapy, and other allied health input.
  • Recommend primary care follow-up within two weeks.
  • Consider follow-up spirometry if this has not been done.
  • Refer to a pulmonary rehabilitation programme unless recently completed or contra-indicated.

After an exacerbation

  • Having an exacerbation is the greatest risk factor for a further exacerbation.
  • Each exacerbation is associated with a faster decline in lung function and increased mortality.
  • Exacerbations should be used as an opportunity to review the pharmacological and non-pharmacological strategies in place and to develop a personalised action plan.
  • Review of inhaler technique and adherence should occur in every patient following an exacerbation (see section Optimise knowledge of COPD and adherence to treatment).
  • All medications should be reviewed following an exacerbation of COPD and adjusted as appropriate.
  • Refer to a pulmonary rehabilitation programme unless recently completed or contra-indicated.

Box 4: Key messages for exacerbation management in COPD.

Figure 1: Pre-hospital management of acute exacerbation of COPD.

Figure 2: Hospital management of exacerbation of COPD.

Comorbidities and treatable traits

Identify and manage comorbidities

  • People with COPD often have other conditions. Lung cancer, bronchiectasis, ischaemic heart disease, congestive heart failure, diabetes, anxiety, depression, gastro-oesophageal reflux, and osteoporosis are all more common among people with COPD than in the general population.
  • These conditions can negatively impact on the management of COPD and, in turn, the presence of COPD can negatively impact on the treatment and prognosis of comorbid conditions.
  • A systematic approach to the assessment and management of comorbidities has been proposed as part of the treatable traits concept. This approach recommends that management is personalised to the individual, with the use of biomarkers where available, and the systematic multidimensional identification and treatment of all comorbidities or disease characteristics, which may contribute to the patient’s presentation and are potentially amenable to treatment (‘treatable traits’). There is preliminary evidence to suggest that this approach improves quality of life.

Lung cancer

  • There is a strong association between COPD and lung cancer, more so than is explained by the shared risk factor of smoking.
  • Haemoptysis is not a symptom of COPD and should be investigated to rule out lung cancer. Unexplained weight loss and a new persistent cough may also be symptoms of lung cancer.
  • Although patients with severe COPD may be unfit for surgery because of poor lung function, they may still be eligible for curative-intent cancer treatment. Newer radiotherapy techniques such as stereotactic ablative radiotherapy can deliver curative-intent treatment with little effect on lung function.
  • A person with lung cancer who has a poor life expectancy due to advanced COPD or other comorbidities may not require any treatment for an early stage, slow-growing and asymptomatic lung cancer.

Cardiac disease

  • People with COPD are at increased risk of ischaemic heart disease and cardiac failure because of the shared risk factors of age and smoking status. Severe COPD is associated with pulmonary hypertension and cor pulmonale. People with COPD should have a cardiovascular risk assessment done.
  • Smoking cessation reduces cardiovascular risk as well as the rate of lung function decline in COPD.
  • If beta-blockers are needed for cardiac disease, then cardioselective beta-blockers such as bisoprolol should be used. Inhaled SABA and LABA therapy can be used alongside cardioselective beta-blocker therapy.
  • Bronchodilators may have pro-arrhythmic effects. There is an acceptable safety profile for long-acting beta agonist and anticholinergic bronchodilators at prescribed doses, but caution should be employed with high doses of short-acting beta2-agonists during a COPD exacerbation or when using theophylline. There may be a risk of developing arrhythmias such as atrial fibrillation in these situations.

Mental health disorders

  • Anxiety and depression are common in COPD. Breathlessness, activity limitation, and loss of social connections are risk factors for the development of anxiety and depression. In turn, anxiety and depression increase the perception of breathlessness and may increase symptom burden, leading to a reduction in social activity and exercise avoidance.
  • Treatment of anxiety and depression should not change in the presence of COPD. Participation in a pulmonary rehabilitation programme reduces anxiety and depression scores.
  • Smoking and therefore COPD are common among people with mental health disorders, and COPD may be underdiagnosed and undertreated in this group.

Other comorbidities

  • The presence of gastro-oesophageal reflux is a risk factor for COPD exacerbations, possibly due to lung injury from aspiration. It is sensible to treat reflux symptoms with proton pump inhibitors, although it has not been proven that this reduces the risk of COPD exacerbations.
  • Allergic rhinitis may increase COPD symptoms.
  • Obstructive sleep apnoea syndrome and obesity-hypoventilation syndrome lead to worse night-time hypoxaemia in people with COPD. Appropriate treatment of these comorbidities with nocturnal continuous positive airways pressure (CPAP) or NIV can improve sleep quality, reduce pulmonary hypertension, and may reduce mortality.
  • Identification of coexisting non-COPD lung disease such as bronchiectasis or interstitial lung disease is an opportunity to use disease-specific treatment to improve respiratory symptoms. (See also section Asthma and COPD overlap (ACO)).

Multiple comorbidities and frailty

  • People with multiple comorbidities are more vulnerable to adverse outcomes including mortality. COPD treatments may impact on control of comorbid conditions. For example, prednisone taken for a COPD exacerbation can adversely affect diabetic glycaemic control.
  • COPD is a risk factor for falls. Hypoxemia, dyspnoea, and fatigue are associated with impaired balance.
  • Cognitive impairment is common in COPD, particularly during exacerbations. This can affect COPD disease education and adherence to medication and self-management plans.
  • Some COPD treatments such as pulmonary rehabilitation or lung transplantation may not be able to be delivered safely due to comorbidities.
  • People with COPD and comorbidities may be taking many medications. COPD medication can add to the problem of polypharmacy and we recommend a regular medicines review.

Asthma and COPD overlap (ACO) (Box 5)

Patients with features of both asthma and COPD appear to have a worse prognosis than those with COPD alone according to many, but not all, studies. Treatment recommendations are based on expert opinion only because asthma and COPD overlap (ACO) patients have largely been excluded from controlled trials.

  • Patients with ACO are broadly characterised by the following:|
    – asthma diagnosed before aged 40 years old, and
    – a smoking history of >10 pack years or comparable aero-pollutant exposure, with
    – highly variable expiratory volumes (FEV1 >400ml) and/or
    – elevated eosinophils (>0.3x106).
  • We recommend inhaled corticosteroids in low or moderate doses to target asthma-like inflammatory pathways in combination with single or dual long-acting bronchodilator.
  • We recommend ICS/LABA as initial therapy followed by the addition of LAMA (ie, triple therapy) if there are persistent symptoms or exacerbations.
  • We recommend using either an asthma or COPD action plan depending on the dominant clinical features.
  • Although recent studies in asthma favour the use of combined budesonide/formoterol reliever inhalers, the role of these inhalers in ACO remains uncertain, as there are no data to support this approach at this time.

Box 5: Principles of management of asthma–COPD overlap.

End-of-life care

Advance care planning

End-of-life care is important in advanced COPD. As the goals of care change, patients and their family/whānau require realistic advice and support to make informed decisions and plan for the future.

  • Discussion about advance care plans and advance directives should be undertaken as part of usual management at a suitable time in the disease course.
  • Advance care plans can be made at any stage of the disease and do not need to wait until the patient is approaching the end of life.
  • Most patients with life-limiting conditions prefer to identify their goals of treatment and discuss preferences for end-of-life care early. Good communication with patients who have a terminal illness is associated with better end-of-life care and fewer medical interventions.
  • A useful strategy when deciding whether end-of-life discussions are appropriate is to consider the question: “Would I be surprised if this patient died in the next 12 months?”
  • The following features should also prompt health practitioners to consider initiating discussions about advance care plans, centred on the patient’s preferences for end-of-life care:
    – Breathless at rest or on minimal exertion or housebound
    – Weight loss or cachexia
    – FEV1<30% of predicted
    – Meets criteria for long-term oxygen therapy
    – Two or more hospitalisations in the previous year for exacerbations
  • An admission with respiratory failure requiring non-invasive ventilation
  • A structured advance care plan will reduce the burden of setting the ceiling of care by unfamiliar staff and family members during an acute admission and allow implementation of a patient’s choice of health care when they are no longer capable of expressing their choice.
  • In general, patients and their family/whānau want an honest conversation that is balanced between realistic information and appropriate hope.
  • Consider involving local hospice and/or palliative care services.

More details and Advance Care Plans are available at: www.advancecareplanning.org.nz.

Palliation of dyspnoea

Morphine

  • Morphine reduces respiratory effort and the sensation of breathlessness.
  • Lower doses are usually required than used for pain (eg, 2.5mg to 5mg every four hours, or as required).
  • Consider lower doses for older patients.
  • Dose can be gradually titrated as for pain. But aim for comfort rather than resolution of dyspnoea.
  • If greater than two doses per day of morphine liquid are regularly being used with effect, convert to low-dose, slow-release morphine capsules (eg, 10 mg twice a day). In this case, it would also be reasonable to make small amount of as-required morphine liquid (2.5mg to 5 mg as required) available to the patient.
  • Oral morphine doses are generally <40 mg per day when used for dyspnoea alone.

Benzodiazepines

  • Evidence for benzodiazepines for breathlessness in COPD is lacking. Benzodiazepines may be harmful and are not recommended as a first-line treatment of breathlessness.
  • Benzodiazepines increase the risk of falls among patients with COPD and may also increase the risk of COPD exacerbations and pneumonia.
  • Benzodiazepines should not be used in patients at risk of hypercapnic respiratory failure.

Appendices

Appendix 1: The four-step COPD consultation.

These steps are likely to need more than one consultation.

Appendix 2: COPD assessment test (CAT): https://assets-global.website-files.com/5e332a62c703f6340a2faf44/602c8a966b39518510d20f2c_4878%20-%20appendix%202.pdf

Appendix 3: COPD action plan: https://assets-global.website-files.com/5e332a62c703f6340a2faf44/602c8a9603e1140b3fac6394_4878%20-%20appendix%203.pdf

Appendix 4: Breathlessness strategies for COPD: https://assets-global.website-files.com/5e332a62c703f6340a2faf44/602c8a9676d8e10447d74284_4878%20-%20appendix%204.pdf

Appendix 5: Breathlessness strategies: quick reference guide: https://assets-global.website-files.com/5e332a62c703f6340a2faf44/602c8a969551dd13aba750f8_4878%20-%20appendix%205.pdf

Appendix 6: Useful documents and resources.

Summary

Abstract

The purpose of the Asthma and Respiratory Foundation of New Zealand’s COPD Guidelines Quick Reference Guide is to provide simple, practical, evidence-based recommendations for the diagnosis, assessment and management of chronic obstructive pulmonary disease (COPD) in clinical practice. The intended users are health professionals responsible for delivering acute and chronic COPD care in community and hospital settings, and those responsible for the training of such health professionals.

Aim

Method

Results

Conclusion

Author Information

Robert J Hancox: Waikato District Health Board, Hamilton; University of Otago, Dunedin. nStuart Jones: Middlemore Hospital, Counties Manukau, Auckland. Christina Baggott: Medical Research Institute of New Zealand. David Chen: Canterbury Clinical Network, Christchurch. Nicola Corna: Middlemore Hospital, Counties Manukau, Auckland. Cheryl Davies: Tu Kotahi Māori Asthma Trust. James Fingleton: Medical Research Institute of New Zealand; Capital & Coast District Health Board, Wellington. Jo Hardy: Medical Research Institute of New Zealand. Syed Hussain: Auckland District Health Board. Betty Poot: Hutt Valley District Health Board, Lower Hutt; School of Nursing, Midwifery and Health Practice, Victoria University of Wellington, Wellington. Jim Reid: University of Otago, Dunedin; Best Practice Advisory Centre (BPAC), Dunedin. Justin Travers: Hutt Valley District Health Board, Lower Hutt. Joanna Turner: Asthma and Respiratory Foundation of New Zealand. Robert Young: Auckland District Health Board.

Acknowledgements

We thank Leanne Te Karu and Teresa Demetriou for their valued contribution towards these guidelines.

Correspondence

Robert Hancox, Department of Preventive & Social Medicine, Dunedin Medical Campus, University of Otago, +3 479 8512 (phone), +3 479 7298 (fax)

Correspondence Email

bob.hancox@otago.ac.nz

Competing Interests

Dr Young reports: I receive honorarium from GSK for giving educational talks on COPD management or attending advisory meetings. However, this did not impact on my contribution to this guideline. Dr Baggott reports personal fees from Astra Zeneca, personal fees from Novartis, outside the submitted work. Nicola Corna reports other from Boehringer Ingelheim, other from Astra Zeneca, other from Astra Zeneca, grants from Adherium, outside the submitted work. Dr Fingleton reports grants, personal fees and non-financial support from AstraZeneca, grants from Genentech, grants, personal fees and non-financial support from GlaxoSmithKline, personal fees and non-financial support from Boheringer lngleheim, outside the submitted work. Dr Hardy reports non-financial support from Astrazeneca, outside the submitted work. Dr Hancox reports grants from Astra Zeneca, grants from GlaxoSmithKline, personal fees from Menarini, other from Boehringer Ingelheim, outside the submitted work.

1. Yang IA, Brown JL, George J, Jenkins S, McDonald CF, McDonald V, et al. The COPD-X Plan: Australian and New Zealand Guidelines for the management of Chronic Obstructive Pulmonary Disease 2020. Report No.: Version 2.61 (February 2020).

2. Global Initiative For Chronic Obstructive Lung Disease. Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease (2020 Report). Global Initiative For Chronic Obstructive Lung Disease; 2020.

3. Asthma COPD and Asthma - COPD Overlap Syndrome (ACOS). Global Strategy for Asthma Management and Prevention and the Global Strategy for the Diagnosis, Management and Prevention of Chronic Obstructive Pulmonary Disease.; 2015.

4. Graham BL, Steenbruggen I, Miller MR, Barjaktarevic IZ, Cooper BG, Hall GL, et al. Standardization of Spirometry 2019 Update. An Official American Thoracic Society and European Respiratory Society Technical Statement. Am J Respir Crit Care Med. 2019;200:e70-e88.

5. McDonald CF, Jones S, Beckert L, Bonevski B, Buchanan T, Bozier J, Carson-Chahhoud K V., Chapman DG, Dobler CC, Foster JM, Hamor P, Hodge S, Holmes PW, Larcombe AN, Marshall HM, McCallum GB, Miller A, Pattemore P, Roseby R, See H V., Stone E, Thompson BR, Ween MP, Peters MJ. Electronic cigarettes: A position statement from the Thoracic Society of Australia and New Zealand*. Respirology 2020;1–8.doi:10.1111/resp.13904.

6. Shafuddin E, Chang CL, Hancox RJ. Comparing severity scores in exacerbations of chronic obstructive pulmonary disease. Clin Respir J. 2018;12(12):2668-75.

7. National Ambulance Sector Clinical Working Group. Clinical Procedures & Guidelines 2019. St John & Wellington Free Ambulance.

8. Telfar Barnard L, Zhang J. The impact of respiratory disease in New Zealand: 2018 update. Asthma and Respiratory Foundation of New Zealand; 2019.

9. Hopkins, RJ, Kendall, C, Gamble, GD and Young, RP. Are New Zealand Maori More Susceptible to Smoking Related Lung Cancer? – A Comparative Case-Case Study. EC Pulmonary and Respiratory Medicine. (2019): 8.1 72-91

10. Loring, B. Literature Review: Respiratory Health for Maori. Asthma and Respiratory Foundation. 2009

11. Levack WM, Jones B, Grainger R, Boland P, Brown M, Ingham TR. Whakawhanaungatanga: the importance of culturally meaningful connections to improve uptake of pulmonary rehabilitation by Māori with COPD - a qualitative study. Int J Chron Obstruct Pulmon Dis. 2016;11:489-501.

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Chronic obstructive pulmonary disease (COPD) encompasses chronic bronchitis, emphysema, and chronic airflow obstruction. It is characterised by persistent respiratory symptoms and airflow limitation that is not fully reversible.

COPD is associated with a range of pathological changes in the lung. The airflow limitation is usually progressive and associated with an inflammatory response to inhaled noxious particles or gases.1,2

Symptoms include cough, sputum production, shortness of breath, and wheeze. At first, these are often ascribed to “a smokers cough”, “getting old” or being “unfit”. Cough and sputum production may precede wheeze by many years. Symptoms may worsen and become severe and chronic, but not all of those with cough and wheeze advance to progressive disease.

Patients with COPD often have exacerbations, when symptoms become much worse and require more intensive treatment. These exacerbations have a significant mortality.

Many patients have extra-pulmonary effects and important co-morbidities that contribute to the severity of the disease. Important co-morbidities include asthma, bronchiectasis, lung cancer and heart disease. COPD can lead to debilitation, polycythaemia, osteoporosis, cachexia, depression and anxiety.

COPD is often confused with asthma. They are separate diseases, although some asthmatics develop irreversible airflow obstruction and some patients with COPD have a mixed inflammatory pattern. Asthma–COPD overlap (ACO) may be present when it can be difficult to distinguish between the diseases, or in patients who have both conditions.3

Guidelines review

The following documents were reviewed to formulate this Quick Reference Guide: COPD-X Australian and New Zealand Guidelines 20201 and the Global Initiative for Chronic Obstructive Lung Disease (GOLD) 2020.2 A systematic review was not performed, although relevant references were reviewed when necessary. Readers are referred to the COPD-X and GOLD documents for the more comprehensive detail and references that they provide. References are only provided when they differ from the COPD-X guidelines.

Grading

No levels of evidence grades are provided, due to the format of the Quick Reference Guide. Readers are referred to the above documents for the level of evidence on which the recommendations in this Quick Reference Guide are based.

Guideline development group

This group included representatives from a range of professions and disciplines relevant to the scope of the guidelines. The group did not include consumer representation.

Robert J Hancox, Stuart Jones, Christina Baggott, James Fingleton, Jo Hardy, Syed Hussain, and Justin Travers are respiratory physicians. Robert Young is a general physician. David Chen is a respiratory physiotherapist. Cheryl Davies is manager of the Tu Kotahi Maori Asthma Trust. Nicola Corna and Betty Poot are respiratory nurse practitioners. Jim Reid is a general practitioner. Joanna Turner is a pharmacist and research and education manager at the Asthma and Respiratory Foundation of New Zealand.

Peer review

The draft guidelines were peer-reviewed by a wide range of respiratory health experts and representatives from key professional organisations, including representatives from Asthma New Zealand, the Australian College of Emergency Medicine, Hutt Valley District Health Board, the Medical Research Institute of New Zealand, the New Zealand Medical Association, the New Zealand Nurses Organisation Te Rūnanga o Aotearoa, the NZNO College of Respiratory Nurses, Physiotherapy New Zealand, the Royal New Zealand College of General Practitioners, the New Zealand branch of the Thoracic Society of Australia and New Zealand, and Wellington Free Ambulance.

Dissemination plan

The guidelines will be translated into tools for practical use by health professionals and used to update health pathways and existing consumer resources. The guidelines will be published in the New Zealand Medical Journal and on the Asthma and Respiratory Foundation of New Zealand (ARFNZ) websites, as well as being disseminated widely via a range of publications, training opportunities, and other communication channels to health professionals, nursing, pharmacy and medical schools, primary health organisations, and district health boards.

Implementation

The implementation of the guidelines by organisations will require communication, education, and training strategies.

Expiry Date

The expiry date for the guidelines is 2025.

COPD in Māori

Māori rights in regard to health, recognised in Te Tiriti o Waitangi and other national and international declarations, promote and require both Māori participation in health-related decision making as well as equity of access and health outcomes for all New Zealanders.

  • The burden of COPD among Māori is one of the most significant health disparities in New Zealand: hospitalisation rates for Māori are 3.5 times higher than non-Māori, non-Pacific, and non-Asian rates, and COPD mortality for Māori is 2.2 times higher.8
  • Māori whānau also have greater exposure to environmental triggers for COPD, such as smoking and poor housing.
  • This burden of COPD translates to large inequities in lost years of healthy life and underscores the urgent need for health service models to address high and growing need for COPD treatment in Māori.
  • Māori should be considered a high-risk group requiring targeted care. This should address risk factors such as poor housing, overcrowding, health literacy, inadequate tailoring of health information, obesity, smoking, and poor access to pulmonary rehabilitation and healthcare services.
  • Māori have much worse lung function for given levels of smoking,9 and the burden of COPD affects Māori 15–20 years younger than non-Māori.10 This makes smoking cessation even more important for Māori, and COPD should be considered at a younger age among Māori smokers.
  • There is a very high incidence of lung cancer among Māori.

Major barriers to good COPD management for Māori include poor access to care, inattention to culturally accepted practices, discontinuous and poor-quality care, and inadequate provision of understandable health information. As Māori place a high value on whakawhanaungatanga (the making of culturally meaningful connections with others), the absence of culturally appropriate practices can hinder attendance in mainstream pulmonary rehabilitation programmes.11 Cultural safety and a pro-equity approach is essential.

It is recommended that:

  • Healthcare providers should undertake clinical audit or other quality-improvement activities to monitor and improve COPD care and outcomes for Māori.
  • A systematic approach to health literacy and COPD education for Māori whānau is required.
  • Healthcare providers should support staff to develop cultural safety skills for engaging Māori with COPD and their whānau.
  • Assess patients using a Māori model of care: https://www.health.govt.nz/our-work/populations/maori-health/maori-health-models.

Māori leadership is required in the development of COPD management programmes, including pulmonary rehabilitation, to improve access to COPD care and facilitate ‘wrap around’ services that address the wider determinants of health (such as housing, financial factors, access to health care and access to pulmonary rehabilitation programmes) for Māori with COPD.

COPD in Pacific people

Similar considerations apply to Pacific people, who also have a disproportionate burden of COPD. Pacific people’s hospitalisation rates are 2.7 times higher than those of other New Zealanders.8

It is recommended that:

Pathogenesis

Most people with COPD will have smoked cigarettes or inhaled noxious particles causing lung inflammation. Airway inflammation is a normal response to smoking but seems to be accentuated in those who go on to develop COPD. Some people develop COPD without smoking or apparent exposures. COPD may also develop in patients with other chronic lung diseases such as asthma.

The inflammatory process in COPD is mostly neutrophil, macrophage, and T-lymphocyte mediated. This inflammation leads to narrowing of peripheral airways and destruction of alveoli, causing airflow obstruction and decreased gas transfer.

Inflammation, fibrosis, and sputum production in small airways causes air trapping during expiration leading to hyperinflation. This reduces inspiratory capacity and causes shortness of breath on exercise.

In patients presenting at a young age (particularly those younger than 40), alpha-1 antitrypsin deficiency should be considered. This genetic defect causes a reduction in the major anti-protease in lung parenchyma, leaving the lung susceptible to the destructive effects of neutrophil elastase and other endogenous proteases, which are released as part of the inflammatory response to smoking.

Diagnosis

A diagnosis of COPD should be considered in anyone who presents with cough, sputum production, wheeze, or shortness of breath, particularly those above the age of 40 years. There is usually a history of cigarette smoking or exposure to smoke other noxious substances.

  • Physical examination and chest x-ray are rarely diagnostic in early COPD, but they may be valuable in excluding other diagnoses and co-morbidities such as lung cancer, pulmonary fibrosis and cardiac failure.
  • Other causes for the patient’s symptoms should always be considered, as common comorbidities such as heart disease and obesity may co-exist with COPD and in some patients will be the dominant cause of breathlessness.
  • The diagnosis of COPD should be confirmed by spirometry (see Spirometry). If this is not available in primary care, patients should be referred for this. There are few contra-indications, but a small proportion of patients cannot do adequate spirometry.
  • Spirometry should be avoided during infections, because of the risk of transmitting infections such as influenza, SARS-CoV-2 (COVID-19), or tuberculosis.
  • Peak flows are not useful for diagnosing or managing COPD.
  • Usually asthma and COPD are easy to differentiate. Asthma is an episodic disease and usually, but not always, presents at a younger age or with a history of being “chesty” as a child. However, a mixed pattern of asthma-COPD overlap (ACO) exists, and it is sometimes difficult to distinguish which is the principal cause of airway limitation (see section Asthma and COPD overlap (ACO)).

Assess severity

  • Spirometry assesses the severity of airflow obstruction. Used in conjunction with the severity of symptoms, this helps to assess the severity of COPD (Table 1). Although Table 1 also shows the typical symptoms, the severity of the symptoms does not necessarily correspond to the severity of airflow obstruction.
  • The effect of breathlessness on daily activities can be quantified using the modified Medical Research Council (mMRC) Dyspnoea Scale (Table 2).
  • The COPD Assessment Test (CAT) is an eight-item questionnaire that can measure the symptomatic impact of COPD and response to treatment (Appendix 2).
  • Functional tests, such as the six-minute walk test, shuttle walk tests and sit-to-stand tests, can help to assess functional limitation, disease progression and response to treatment.

Table 1: Severity classification for COPD. (Adapted from Lung Foundation Australia’s Stepwise Manage-ment of Stable COPD available at https://lungfoundation.com.au/wp-content/uploads/2018/09/Informa-tion-Paper-Stepwise-Management-of-Stable-COPD-Apr2020.pdf.)

FEV1=forced expiratory volume in one second. PaO2=partial pressure of oxygen, arterial. PaCO2=partial pressure of carbon dioxide, arterial.

Table 2: Modified Medical Research Council (mMRC) Dyspnoea Scale for grading the severity of breathlessness during daily activities*

* The mMRC Dyspnoea Scale is very similar to the original MRC Scale, which ranges from 1 to 5 rather than 0 to 4 (ie, MRC grade 3=modified MRC grade 2).

Spirometry

Spirometry is the most useful test of lung function to diagnose and assess the severity of COPD. This may be done both before and after a bronchodilator to assess reversibility, but the diagnosis and severity are determined by post-bronchodilator measurements.

  • Irreversible airflow obstruction is indicated by a post-bronchodilator forced expiry volume in once second to forced vital capacity (FEV1/FVC) ratio<0.70*.
  • The severity of the obstruction is diagnosed using the post-bronchodilator FEV1 as a % of the predicted value (Table 1).
  • It is possible to have airflow obstruction with an FEV1/FVC ratio<0.70* but an FEV1 in the normal range.
  • A restrictive pattern on spirometry is not consistent with a diagnosis of COPD and, if it is not due to technically inadequate spirometry, suggests an alternative cause of symptoms (eg, morbid obesity, neuromuscular weakness, or interstitial lung disease). Patients with a restrictive pattern may benefit from specialist referral for further investigation.
  • Some patients with COPD cannot blow out long enough to do a true FVC. The Forced Expiratory Volume at 6 seconds (FEV6) can be used as an approximation of the FVC.
  • A small subset of patients with normal spirometry have evidence of emphysema on CT scan and impairment of gas exchange. There is limited evidence to guide management in these patients, but if they are symptomatic or having exacerbations, we recommend treatment for COPD according to this guideline.

(*Note: There is disagreement about the criteria for airflow obstruction. The FEV1/FVC ratio naturally declines with age, and defining airflow obstruction by an FEV1/FVC ratio <0.70 may miss mild airflow obstruction in younger patients and over-diagnose it in the elderly. Some guidelines recommend using an age-specific lower limit of normal. But for clinical purposes, the <0.70 cut-point is easy to apply and unlikely to greatly influence management in those with mild airflow obstruction. The grading of severity also varies between guidelines, with the GOLD guidelines using different categories to COPD-X (in Table 1). But this is also unlikely to greatly influence clinical management.)

Reversibility testing

When performing reversibility testing, the first measurements should be done before bronchodilators:

  • Bronchodilators should be withheld for the duration recommended in the consensus ATS/ERS guidelines.4 This ranges from 4–6 hours for a short-acting beta agonist (SABA) to 48 hours for an ultra long-acting beta agonist (LABA).
  • Spirometry is repeated at least 15 minutes after giving a bronchodilator (usually 400mcg salbutamol via spacer).
  • Many patients with COPD will have some improvement after a bronchodilator (“partial reversibility”), but if spirometry becomes normal (FEV1/FVC>0.7* and FEV1>80% predicted), COPD is excluded (by definition).
  • The consensus definition of a significant bronchodilator response is arbitrarily defined as a ≥12% change from baseline with an absolute improvement of ≥200ml, but this does not predict who will benefit from bronchodilator treatment.
  • If the response to bronchodilator is substantial (>400mL improvement in FEV1) then asthma or Asthma-COPD Overlap is likely.

(*Note: There is disagreement about the criteria for airflow obstruction. The FEV1/FVC ratio naturally declines with age, and defining airflow obstruction by an FEV1/FVC ratio <0.70 may miss mild airflow obstruction in younger patients and over-diagnose it in the elderly. Some guidelines recommend using an age-specific lower limit of normal. But for clinical purposes, the <0.70 cut-point is easy to apply and unlikely to greatly influence management in those with mild airflow obstruction. The grading of severity also varies between guidelines, with the GOLD guidelines using different categories to COPD-X (in Table 1). But this is also unlikely to greatly influence clinical management.)

Non-pharmacological management (Box 1)

Smoking cessation

Stopping smoking is the most important treatment for COPD: every person who is still smoking should be offered help to quit. Reducing smoking-related health risks requires complete cessation of all tobacco and other smoked products, including marijuana/cannabis.

  • All forms of nicotine replacement therapy, in association with smoking cessation support, are useful in aiding smoking cessation and increase the rate of quitting.
  • Oral bupropion, varenicline, and nortriptyline have been shown to be effective and should be considered in those patients struggling to give up despite nicotine replacement therapy.
  • Most of these are fully funded in New Zealand and a prescription for this should be discussed with a health professional.
  • Referral to a local smoking cessation support service is recommended.

E-cigarettes and vaping are probably less harmful to health than smoking, but short-term studies suggest that they are not risk free.5 E-cigarettes and vapes that contain nicotine are highly addictive.

  • E-cigarettes used within the context of a supportive smoking cessation programme have been shown to aid in smoking cessation in selected groups of motivated patients.
  • The long-term safety of e-cigarettes and vaping have not been shown. Smokers using e-cigarettes or vaping to quit smoking should be advised to stop using e-cigarettes and vaping as soon as possible after quitting smoking.
  • No e-cigarette or vape is currently approved as a smoking cessation tool.
  • E-cigarettes and vapes should never be used near an oxygen source, as this is a fire risk.

Physical activity

Patients with COPD benefit from physical activity and should be encouraged to:

  • Be active on most, preferably all, days of the week.
  • Do at least 20–30 minutes of exercise per day. More is better.
  • Exercise to an intensity that should cause the patient to “huff and puff” or feel breathless: Getting out of breath will not cause harm.
  • Do muscle strengthening activities on two or more days each week.

Pulmonary rehabilitation

Pulmonary rehabilitation should be offered to all patients with COPD. Although there may be barriers to attending pulmonary rehabilitation classes, there are a variety of ways to deliver pulmonary rehabilitation to patients in different settings depending on local respiratory services and patient preferences.

  • Pulmonary rehabilitation reduces breathlessness, improves quality of life, and reduces depression in patients with COPD.
  • Patients gain significant benefit from rehabilitation regardless of the degree of breathlessness, but the most breathless patients benefit the most.
  • Exacerbations of COPD are an indication for referral to pulmonary rehabilitation and an early return to pulmonary rehabilitation after exacerbation should be encouraged. This has been shown to reduce further hospitalisations and may reduce mortality.
  • Exercise training is the cornerstone of pulmonary rehabilitation, and regular post-rehabilitation exercise is required to sustain the benefits.
  • The benefits of pulmonary rehabilitation decline over time and repeat attendance at pulmonary rehabilitation programmes should be encouraged in patients with functional decline or exacerbations.
  • If someone is unable to access a pulmonary rehabilitation programme, an in-home exercise programme should be considered.

Breathlessness management strategies

In addition to pulmonary rehabilitation, patients may benefit from seeing a respiratory physiotherapist for individualised breathing exercises or breathless management strategies:

  • Diaphragmatic breathing and pursed lips breathing exercises may benefit some patients. These support and correct the breathing pattern disorders caused by COPD and improve exercise capacity, but they have inconsistent effects on dyspnoea or health-related quality of life scores.
  • Constant load threshold inspiratory muscle training improves inspiratory muscle strength, quality of life, dyspnoea, and exercise capacity.
  • Hand-held fan therapy: the airflow and cooling effects of the fan, alongside other breathlessness management strategies, such as relaxation, pacing, and positioning, can reduce dyspnoea.

Other things that may help:

  • Hospital clinical teams working with the primary healthcare team can help enhance quality of life and reduce disability for patients with COPD.
  • Patients may also benefit from local support groups.
  • Consider including a cognitive behavioural component in the self-management plan to assist with reducing anxiety and breathlessness.
  • Consider screening for urinary incontinence related to cough.

Other useful resources are given in Appendix 4 and 5.

Sputum management/sputum clearance techniques

Patients with chronic sputum production may benefit from seeing a physiotherapist (ideally a respiratory physiotherapist) for an individualised chest clearance plan. Airway clearance techniques enhance sputum clearance, reduce hospital admissions, and improve health-related quality of life, and they may also improve exercise tolerance and reduce the need for antibiotics.

  • A wide variety of airway clearance techniques are available. No one technique is superior for all patients.
  • The choice of technique should be based on the clinician’s assessment, resource availability, and patient acceptability.

Nutrition

Both malnutrition and obesity are common and contribute to morbidity and mortality in COPD. Poor eating habits, sedentary lifestyles, smoking, and corticosteroid use further compromise nutritional status.

  • The key goals of nutritional management are to eat a balanced diet, to achieve and maintain a healthy weight, and to avoid unintentional weight loss. Consider referral to a dietician, or high-calorie nutritional supplements, for those who are malnourished.
  • There is evidence that weight loss is beneficial for those who are obese.
  • Unintentional weight loss should be investigated for potential malignancy.

Housing

There is good evidence that a warm, dry, and smoke-free home is associated with better asthma control, and it is likely that the same is true for COPD.

Assisted ventilation

Non‐invasive ventilation (NIV) with bi‐level positive airway pressure reduces mortality and need for intubation in patients admitted to hospital with acute hypercapnic respiratory failure as a result of an exacerbation of COPD (see section Management). In most instances, NIV is not required once the patient has recovered.

  • People who have chronic hypercapnic respiratory failure, despite adequate treatment, and have needed assisted ventilation (invasive or non-invasive) during an exacerbation, or with worsening hypercapnia on long-term oxygen therapy, should be referred to a specialist centre for consideration of long-term NIV.
  • Red flags to consider for need for home NIV:
    – Previously required assisted ventilation
    – Obstructive sleep apnoea
    – Obesity hypoventilation
    – Persistent nocturnal hypoxia
    – Neuromuscular conditions
    – Spinal/chest wall deformities

Interventional approaches to the management of COPD

Thoracic surgery is rarely performed for COPD. The two situations where it may be considered are bullectomy or lung volume reduction surgery. Neither procedure increases life expectancy. Both have significant complication rates and are only performed in specialist centres after careful multi-disciplinary assessment.

Bullectomy

Bullectomy can be considered where there is a very large bulla compressing other lung tissue. Removing the bulla allows the preserved lung tissue to function better.

Lung volume reduction surgery

Lung volume reduction surgery can improve exercise capacity in people with upper-lobe predominant emphysema. The surgery has a significant early mortality, but there is no difference in long-term mortality.

Interventional bronchoscopy

Bronchoscopic lung volume reduction approaches have been developed as alternatives to lung volume reduction surgery. These aim to reduce gas-trapping and improve lung mechanics in advanced emphysema, which can lead to improved lung function, symptoms, and quality of life in carefully selected patients. Endobronchial valve therapy has the most evidence and is available in New Zealand. It is only effective in those with intact fissures and no collateral ventilation as one-way valves are inserted to cause collapse of lung segments. Endobronchial valve therapy does not reduce mortality and has significant complication rates.

Lung transplantation

Consideration for lung transplantation is appropriate in younger patients (usually <65) with very severe obstruction and severe symptoms, or progressive deterioration despite optimised management, including smoking cessation and pulmonary rehabilitation. Referral to the transplant service should be made by a respiratory specialist.

Box 1: Key messages for non-pharmacological management of COPD.

Improving patient understanding

Identify and manage social and cultural issues

Health literacy, cultural context, and the degree of social isolation or support are key factors affecting a person’s understanding of and attitude to COPD. See also sections COPD in Māori and COPD in Pacific people.

  • These factors impact on COPD management, appropriate inhaler technique, adherence to treatment and appropriate use of self-management plans.
  • These factors also have a considerable impact on the success of smoking cessation.
  • Awareness of the social and cultural factors will enhance communication between clinicians and patients and improve health outcomes.
  • There are many practical challenges for people living with COPD, such as completing everyday tasks, holding down a job, and having access to transport. Awareness of these challenges and referral to support services where available can be beneficial.

Optimise knowledge of COPD and adherence to treatment

  • Patient understanding of the disease, appropriate inhaler technique and adherence to treatment are important factors in COPD management.
  • There are many inhalers available to treat COPD, and people can easily get confused about these. Demonstrate the use of the inhalers and ensure that patients can use them correctly.
  • Clinicians should ask about the patient’s understanding of the disease and the rationale for treatment, to clarify misunderstandings, and to work to remove barriers to adherence and good self-management. It is important to provide information to the patient and whānau in a format that they can understand.

Develop an action plan

Personalised action plans (self-management plans) improve quality of life and reduce hospital admissions and should be offered to all people with COPD.

  • Action plans should be personalised and focus on recognising and treating deteriorating symptoms.
  • Patients at risk of exacerbations may be offered antibiotics and prednisone to have at home as part of their action plan. The patient should be advised of a timeframe for clinical review once they have started these medicines for an acute exacerbation of COPD.
  • Action plans should be checked at each COPD review.

The Asthma and Respiratory Foundation of New Zealand’s COPD Action Plan is shown in Appendix 3.

Electronic versions are available at: www.nzrespiratoryguidelines.co.nz.

Develop a breathlessness plan

  • A breathlessness plan can reduce the severity and impact of breathlessness. Interventions and techniques that can improve breathlessness include self-management education, breathing exercises, sitting upright and leaning forwards (‘positioning’), using pursed lip breathing, and a hand-held fan.
  • Oxygen is not an effective treatment for breathlessness in patients who are not hypoxic.
  • Smoking cessation also improves breathlessness.

Asthma and Respiratory Foundation of New Zealand’s ‘Breathlessness Strategies for COPD’ is shown in Appendix 4 and is available at www.nzrespiratoryguidelines.co.nz.

Pharmacological management (Box 2)

The purpose of pharmacological management in COPD is symptom control and prevention of exacerbations, with the aim of improving quality of life.

  • Check inhaler adherence and inhaler technique regularly. Make sure that these are optimal before escalating treatment.
  • Treatment escalation should follow a stepwise approach based on breathlessness and exacerbation frequency. It should take into account patient preferences, regimen complexity, cost, and side effects.
  • Effects of treatment on dyspnoea should be apparent within six weeks.
  • Effects on exacerbation frequency may need to be assessed over 6 to 12 months.

Inhaled medication for COPD

  • Short-acting beta2 agonists (SABA: salbutamol or terbutaline) and the short-acting muscarinic antagonist (SAMA: ipratropium), either individually or in combination, can be taken as-needed to provide short-term relief of breathlessness. Short-term response to SABA or SAMA (reversibility testing) does not predict benefit from long-acting bronchodilator therapy.
  • For patients with ongoing dyspnoea despite as-needed SABA, SAMA, or combination SABA/SAMA, a regular long-acting muscarinic antagonist (LAMA) such as tiotropium, glycopyrronium, or umeclidinium is recommended, unless there is evidence of asthma/COPD overlap (see Asthma and COPD overlap (ACO)). Do not continue to use ipratropium in patients taking a LAMA, except in emergencies.
  • It is not necessary to have a trial of regular short-acting bronchodilators before starting a LAMA if symptoms, exacerbation history or spirometry suggest that a long-acting bronchodilator is desirable.
  • Both LAMAs and LABAs improve lung function, symptoms and quality of life, but LAMAs are recommended as the first-line long-acting medication for COPD because they reduce exacerbation risk and have fewer side effects. If LAMAs are contra-indicated, a long-acting beta agonist (LABA) such as salmeterol, formoterol, or indacaterol is recommended.
  • In patients who remain breathless or who continue to exacerbate despite treatment with a single long-acting bronchodilator, dual LAMA/LABA therapy is recommended (eg, glycopyrronium/indacaterol, umeclidinium/vilanterol, or olodaterol/tiotropium). Combination therapy with a LABA and LAMA improves lung function, reduces symptoms, and reduces exacerbations compared to either drug alone.
  • LABA/LAMA is preferred over inhaled corticosteroid (ICS)/LABA as initial therapy for most patients with frequent exacerbations because ICS increases the risk of pneumonia.
  • These medications may have risks, particularly at higher doses in patients with cardiac disease. If there is no evidence of benefit, consider stopping them.
  • Patients with an eosinophilic pattern of disease may benefit from ICS/LABA instead of LABA/LAMA. Retrospective analyses suggest that blood eosinophil counts predict the benefit of ICS in preventing exacerbations: people with blood eosinophil counts <100cells/µL are least likely to benefit and people with counts ≥300cells/µL are most likely to benefit. A single blood test may not be representative as eosinophil counts can vary over time. Blood eosinophil counts performed when a patient is taking oral steroids will not be informative.
  • An ICS should form part of the regimen for any patient with asthma/COPD overlap. This should usually be prescribed as an ICS/LABA combination inhaler to avoid the risk of LABA monotherapy in patients with poor adherence to a separate ICS inhaler.
  • Prescriptions should be based on drug class. Choice of specific LABAs and LAMAs should be guided by patient preference and their ability to use the inhaler device. A list of inhalers available in New Zealand is available at www.nzrespiratoryguidelines.co.nz. Dry-powder inhalers have a substantially lower impact on greenhouse gases than pressurised metered-dose inhalers.
  • Six weeks is a reasonable timeframe to assess improvement in breathlessness following a medication change.
  • The COPD assessment test is an eight-item questionnaire that can be used to measure the symptomatic impact of COPD and response to therapy (see Assess severity and Appendix 2).

Role of triple therapy (LABA/LAMA/ICS)

  • Escalation to triple LABA/LAMA/ICS therapy should be considered in patients who continue to exacerbate (twice or more a year) despite adherence to dual LAMA/LABA or ICS/LABA therapy and optimal inhaler technique.
  • A subset of patients with persistent breathlessness and exercise limitation, despite LABA/LAMA combination therapy, may benefit from triple therapy with LABA, LAMA, and ICS. However, the increased risk of pneumonia with regular ICS should be considered.
  • Direct escalation to dual or triple therapy, without stepwise up-titration, may be reasonable in the setting of a severe or recurrent exacerbations.

ICS withdrawal

  • The risk of pneumonia in patients with severe COPD is increased with regular ICS. Withdrawing ICS should be considered if:
  • There is no evidence of benefit from ICS in terms of improved symptoms or fewer exacerbations.
  • The patient develops pneumonia or other ICS adverse effects.
  • The patient does not have a history of frequent exacerbations and is stable.
  • If ICS treatment is withdrawn, the patient should be reviewed at 4–6 weeks to ensure that this doesn’t cause a deterioration in symptoms.
  • Withdrawal of ICS may not be appropriate if the blood eosinophil count is elevated. A blood eosinophil count ≥300cells/µL has been shown to be associated with an increased exacerbation risk after ICS withdrawal.
  • ICS should not be withdrawn in patients with a diagnosis of asthma/COPD overlap (see section Asthma and COPD overlap (ACO)).

Table 3: Simplified maintenance inhaler management of COPD.

Additional therapies

  • There is no evidence that routine use of nebulisers is beneficial in patients with COPD.
  • Theophylline has not shown consistent benefits on exacerbation, lung function, symptoms, or quality of life in randomised controlled trials. In view of the narrow therapeutic index and side-effect profile of theophylline, we do not recommend its routine use in the management of COPD.
  • There is no evidence of benefit from long-term oral corticosteroids.
  • Long-term macrolide antibiotics, such azithromycin and erythromycin, can reduce risk of exacerbations over one year in former smokers who have exacerbations despite optimal inhaled treatment. Azithromycin is not currently funded in New Zealand for this indication. Long-term macrolide therapy is associated with significant risks, including bacterial resistance, gastrointestinal and cardiovascular side effects, and hearing impairment. Long-term macrolides should rarely be initiated without specialist advice.
  • Regular treatment with mucolytics (eg, erdosteine, carbocysteine, or N-acetylcysteine) may reduce the risk of exacerbations in some patients. These treatments are not currently funded in New Zealand.
  • In patients with severe and very severe COPD and a history of exacerbations, PDE4 inhibitors (eg, roflumilast) improve lung function, reduce the risk of exacerbations, and have modest benefits for symptoms and quality of life. They have significant gastrointestinal side effects. These treatments are not currently funded in New Zealand
  • Alpha-1 antitrypsin augmentation therapy may slow the progression of emphysema in patients with alpha-1 antitrypsin deficiency. This is not currently funded in New Zealand.

Box 2: Key messages for pharmacological management of COPD.

Oxygen therapy

  • Oxygen is a treatment for hypoxia, not dyspnoea. Oxygen does not reduce the sensation of breathlessness in patients who are not hypoxic. Oxygen may not improve breathlessness even in those who are hypoxic.
  • Oxygen is a drug therapy and should be prescribed.
  • Long-term oxygen therapy has survival benefits for COPD patients with severe hypoxaemia. It must be used for at least 16 hours a day. The survival benefits are not apparent until months or years after starting treatment.
  • Evaluation of the patient and consideration for long-term oxygen therapy supply should be done by a specialist respiratory service (Box 3). The causes of the hypoxia should be explored, and the patient’s pharmacological and non-pharmacological management should be optimised. A target saturation range and oxygen flow rate should be established.
  • Patients should adhere to the amount of oxygen prescribed and be monitored for adverse effects.

Box 3: Criteria for oxygen.

Flying with oxygen

Flying is generally safe for patients with COPD, including those with chronic respiratory failure who are on long-term oxygen therapy.

  • Before flying, patients should ideally be clinically stable.
  • Supplemental oxygen is unlikely to be required if the resting oxygen saturation is ≥95%, and is likely to be required if oxygen saturation is ≤88%. Patients with oxygen saturation values between these levels might require specialist assessment.
  • Those already on long-term oxygen therapy need an increase in flow rate of 1–2L per minute during the flight.
  • Patients receiving oxygen therapy will need to contact the airline prior to flying.

Vaccination

  • Yearly influenza vaccination reduces serious illness and death in patients with COPD and should be actively promoted to patients with COPD.
  • Pneumococcal vaccination probably decreases the incidence of pneumonia and reduces the risk of exacerbations in patients with COPD, but the evidence for this is conflicting and pneumococcal vaccination is not currently funded for this indication in New Zealand.
  • Two types of pneumococcal vaccine are approved for use. If the healthcare professional and patient consider this an appropriate treatment, a suggested schedule is one dose of 13-valent protein conjugate vaccine (PCV13, Prevenar 13®) given first, followed at least eight weeks later by the first dose of 23-valent polysaccharide vaccine (23PPV, Pneumovax 23®). A second dose of 23PPV is given a minimum of five years later and a third dose at age ≥65 years.

Acute exacerbations

COPD exacerbations are characterised by a change in the patient’s baseline dyspnoea, cough, and/or sputum that is beyond normal day-to-day variations, is acute in onset, and may warrant a change in regular medication or hospital admission. Key symptoms of exacerbations include increased shortness of breath, increased sputum purulence and volume, increased cough, and wheeze.

Exacerbations of COPD are associated with an accelerated loss of lung function, particularly in patients with mild disease. Prolonged exacerbations are associated with worse health status and more frequent future exacerbations.

Early diagnosis and prompt management of exacerbations of COPD may prevent functional deterioration and reduce hospital admissions. Education of the patient, carers, other support people, and family may aid in the early detection of exacerbations.

Assessment (Figures 1 and 2)

  • Most exacerbations can be managed at home. Indications for hospitalisation include, but are not limited to, a sudden worsening of symptoms, confusion or drowsiness, signs such as cyanosis and peripheral oedema, failure to respond to medical management, low oxygen saturation by pulse oximetry (SpO2), the presence of serious co-morbidities, including heart failure and newly occurring arrhythmias, and insufficient home support or lack of telephone or transport.
  • A guide to acute severity assessment is shown in Table 4.
  • Several prognostic scores have been proposed. The most validated one is DECAF, but this includes COPD with pneumonia and requires a blood gas, complete blood count (for eosinophils), and chest x-ray, which are unlikely to be available in primary care. An alternative is CURB-65, which was developed for pneumonia but has been found to be equally effective at predicting short term-mortality in COPD in New Zealand studies.6 CRB-65 is a simpler version that does not require any laboratory measures (Table 5).
  • A chest x-ray and electrocardiogram help to identify alternative diagnoses and complications, such as pulmonary oedema, pulmonary embolus, pneumothorax, pneumonia, pleural effusion, arrhythmias, myocardial ischaemia, and others. Biomarkers (troponins, B-natriuretic peptide, D-dimer) can help to identify comorbidities and abnormalities of these are associated with a worse prognosis.

Table 4: Assessment of exacerbation severity.

Table 5: Assessment of short-term (one-month) prognosis.

*Score 1 point for the presence of each factor. #DECAF scores have been validated in patients with COPD and pneumonia, and CURB65 and CRB65 have not.

Management (Box 4, Figures 1 and 2)

Use breathless management strategies (Appendix 4): sit, rest arms on a chair or table, use a fan, and practise breathing control techniques

Bronchodilators

  • Short-acting inhaled beta2 agonists with or without short-acting anti-muscarinics are the initial bronchodilator of choice to treat an acute exacerbation. These can be delivered via pressurised metered dose inhaler and spacer, dry powder inhalers, or nebuliser. We recommend salbutamol via a spacer. One actuation of the inhaler should be used each time and repeated as necessary.
  • Spacer technique is important when using a pressurised metered dose inhaler. In an exacerbation, we recommend one actuation into the spacer followed by 4—6 tidal breaths. Observe and repeat if required.
  • The bronchodilator effect of 8—10 puffs of 100mcg salbutamol via spacer is equivalent to a 5mg salbutamol nebuliser. We recommend that no more than five puffs are used at a time (given individually via spacer).
  • If patients do not respond to multiple doses of inhaled short-acting beta2 agonist, additional bronchodilator treatment such as ipratropium is recommended.
  • Nebulisers may increase the risk for aerosolisation of viruses such as SARS-CoV-2 (COVID-19). There is no evidence that nebulisers are more effective than inhalers via a spacer, and we recommend that nebulisers should be avoided in any patient who could be infected with respiratory viruses. If they are used, appropriate aerosolisation infection precautions should be implemented.
  • If a salbutamol nebuliser is necessary, we recommend a maximum dose of 2.5mg at a time. Patients with COPD often have cardiac co-morbidities. Higher doses are associated with an increased risk of tremors, elevated heart rate, palpitations, and lower blood pressure, without evidence of any additional benefit.
  • If nebulisers are given for acute COPD exacerbations, they should be air driven to reduce the risk of type 2 respiratory failure due to high flow oxygen.
  • Maintenance LABA, LAMA, and ICS should be continued during an exacerbation.
  • We do not recommend the routine use of intravenous (IV) magnesium for COPD exacerbations.
  • We do not recommend adrenaline for COPD exacerbations in the absence of anaphylaxis.

Corticosteroids

• Systemic corticosteroids (eg, prednisone 40mg once daily) can improve lung function, improve oxygenation, and shorten recovery time. They should usually be given for five days. Longer courses should generally be avoided due to the risk of side effects.

• Intravenous steroids should be avoided. There is no evidence of benefit compared with oral corticosteroids for treatment failure, relapse, or mortality. Hyperglycaemia rates are higher with IV corticosteroids.

Antibiotics

  • Respiratory tract infections are the most common precipitants of exacerbations of COPD. These may be viral, bacterial, or mixed. Common bacterial pathogens include Haemophilus influenzae, Streptococcus pneumonia, and Moraxella catarrhalis. Mycoplasma pneumoniae and Chlamydia pneumoniae have also been reported. Pseudomonas aeruginosa and Staphylococcus aureus are uncommon but occur more frequently in severe COPD.
  • Antibiotics, when indicated by the presence of purulent sputum, fever and/or raised inflammatory markers (CRP >40), can shorten recovery time and reduce the risk of relapse and treatment failure, and should be prescribed for 5–7 days.
  • Oral antibiotics such as amoxicillin or doxycycline are recommended. If treatment failure or resistant organisms are suspected, amoxycillin-clavulanate can be prescribed. If pneumonia, Pseudomonas or Staphylococci are suspected, appropriate antibiotics should be used.

Oxygen

  • If indicated, oxygen should be prescribed and titrated via nasal prongs or a controlled flow device to target saturations of 88–92%.
  • Oxygen delivery via a high-flow humidified nasal device can improve ventilation and airway clearance as well as reduce the physiological dead space and work of breathing.

Supported ventilation

  • Non-invasive ventilation (NIV) reduces mortality by about 50%, reduces need for intubation, and shortens length of stay in patients with rising arterial carbon dioxide tension (PaCO2) levels due to COPD. It should be considered in patients who present with hypercapnic respiratory failure (arterial pH <7.35, PaCO2 >6kPa/45mmHg).
  • An arterial blood gas should be considered in every patient with a severe exacerbation, an oxygen saturation less than 90%, or signs of cor pulmonale.
  • A venous blood gas pH ≤7.34 has good sensitivity and specificity for acidaemia (pH ≤7.35) but does not reliably predict arterial PaCO2 and cannot diagnose hypercapnic respiratory failure. An arterial blood gas is necessary to assess the need for NIV.
  • Ward-based NIV can reduce the requirement for HDU/ICU admission but should be conducted in an appropriately monitored setting with trained clinical staff.
  • At the time of initiating NIV, the goals and limits of care should be considered and a clear written escalation plan established.

Airway clearance techniques

  • Patients with excess sputum production benefit from airway clearance techniques during an exacerbation.
  • Airway clearance techniques should be individualised to the patient.

Before discharge

  • Ensure that adequate education is provided regarding COPD management, including smoking cessation, use of inhalers, and the development of an acute management/action plan.
  • Ensure that clear follow-up plans are in place, as the risk for further exacerbations is greatest following an exacerbation.
  • Ensure that there is sufficient support at home for the patient to manage during their recovery. This may require social work, physiotherapy, occupational therapy, and other allied health input.
  • Recommend primary care follow-up within two weeks.
  • Consider follow-up spirometry if this has not been done.
  • Refer to a pulmonary rehabilitation programme unless recently completed or contra-indicated.

After an exacerbation

  • Having an exacerbation is the greatest risk factor for a further exacerbation.
  • Each exacerbation is associated with a faster decline in lung function and increased mortality.
  • Exacerbations should be used as an opportunity to review the pharmacological and non-pharmacological strategies in place and to develop a personalised action plan.
  • Review of inhaler technique and adherence should occur in every patient following an exacerbation (see section Optimise knowledge of COPD and adherence to treatment).
  • All medications should be reviewed following an exacerbation of COPD and adjusted as appropriate.
  • Refer to a pulmonary rehabilitation programme unless recently completed or contra-indicated.

Box 4: Key messages for exacerbation management in COPD.

Figure 1: Pre-hospital management of acute exacerbation of COPD.

Figure 2: Hospital management of exacerbation of COPD.

Comorbidities and treatable traits

Identify and manage comorbidities

  • People with COPD often have other conditions. Lung cancer, bronchiectasis, ischaemic heart disease, congestive heart failure, diabetes, anxiety, depression, gastro-oesophageal reflux, and osteoporosis are all more common among people with COPD than in the general population.
  • These conditions can negatively impact on the management of COPD and, in turn, the presence of COPD can negatively impact on the treatment and prognosis of comorbid conditions.
  • A systematic approach to the assessment and management of comorbidities has been proposed as part of the treatable traits concept. This approach recommends that management is personalised to the individual, with the use of biomarkers where available, and the systematic multidimensional identification and treatment of all comorbidities or disease characteristics, which may contribute to the patient’s presentation and are potentially amenable to treatment (‘treatable traits’). There is preliminary evidence to suggest that this approach improves quality of life.

Lung cancer

  • There is a strong association between COPD and lung cancer, more so than is explained by the shared risk factor of smoking.
  • Haemoptysis is not a symptom of COPD and should be investigated to rule out lung cancer. Unexplained weight loss and a new persistent cough may also be symptoms of lung cancer.
  • Although patients with severe COPD may be unfit for surgery because of poor lung function, they may still be eligible for curative-intent cancer treatment. Newer radiotherapy techniques such as stereotactic ablative radiotherapy can deliver curative-intent treatment with little effect on lung function.
  • A person with lung cancer who has a poor life expectancy due to advanced COPD or other comorbidities may not require any treatment for an early stage, slow-growing and asymptomatic lung cancer.

Cardiac disease

  • People with COPD are at increased risk of ischaemic heart disease and cardiac failure because of the shared risk factors of age and smoking status. Severe COPD is associated with pulmonary hypertension and cor pulmonale. People with COPD should have a cardiovascular risk assessment done.
  • Smoking cessation reduces cardiovascular risk as well as the rate of lung function decline in COPD.
  • If beta-blockers are needed for cardiac disease, then cardioselective beta-blockers such as bisoprolol should be used. Inhaled SABA and LABA therapy can be used alongside cardioselective beta-blocker therapy.
  • Bronchodilators may have pro-arrhythmic effects. There is an acceptable safety profile for long-acting beta agonist and anticholinergic bronchodilators at prescribed doses, but caution should be employed with high doses of short-acting beta2-agonists during a COPD exacerbation or when using theophylline. There may be a risk of developing arrhythmias such as atrial fibrillation in these situations.

Mental health disorders

  • Anxiety and depression are common in COPD. Breathlessness, activity limitation, and loss of social connections are risk factors for the development of anxiety and depression. In turn, anxiety and depression increase the perception of breathlessness and may increase symptom burden, leading to a reduction in social activity and exercise avoidance.
  • Treatment of anxiety and depression should not change in the presence of COPD. Participation in a pulmonary rehabilitation programme reduces anxiety and depression scores.
  • Smoking and therefore COPD are common among people with mental health disorders, and COPD may be underdiagnosed and undertreated in this group.

Other comorbidities

  • The presence of gastro-oesophageal reflux is a risk factor for COPD exacerbations, possibly due to lung injury from aspiration. It is sensible to treat reflux symptoms with proton pump inhibitors, although it has not been proven that this reduces the risk of COPD exacerbations.
  • Allergic rhinitis may increase COPD symptoms.
  • Obstructive sleep apnoea syndrome and obesity-hypoventilation syndrome lead to worse night-time hypoxaemia in people with COPD. Appropriate treatment of these comorbidities with nocturnal continuous positive airways pressure (CPAP) or NIV can improve sleep quality, reduce pulmonary hypertension, and may reduce mortality.
  • Identification of coexisting non-COPD lung disease such as bronchiectasis or interstitial lung disease is an opportunity to use disease-specific treatment to improve respiratory symptoms. (See also section Asthma and COPD overlap (ACO)).

Multiple comorbidities and frailty

  • People with multiple comorbidities are more vulnerable to adverse outcomes including mortality. COPD treatments may impact on control of comorbid conditions. For example, prednisone taken for a COPD exacerbation can adversely affect diabetic glycaemic control.
  • COPD is a risk factor for falls. Hypoxemia, dyspnoea, and fatigue are associated with impaired balance.
  • Cognitive impairment is common in COPD, particularly during exacerbations. This can affect COPD disease education and adherence to medication and self-management plans.
  • Some COPD treatments such as pulmonary rehabilitation or lung transplantation may not be able to be delivered safely due to comorbidities.
  • People with COPD and comorbidities may be taking many medications. COPD medication can add to the problem of polypharmacy and we recommend a regular medicines review.

Asthma and COPD overlap (ACO) (Box 5)

Patients with features of both asthma and COPD appear to have a worse prognosis than those with COPD alone according to many, but not all, studies. Treatment recommendations are based on expert opinion only because asthma and COPD overlap (ACO) patients have largely been excluded from controlled trials.

  • Patients with ACO are broadly characterised by the following:|
    – asthma diagnosed before aged 40 years old, and
    – a smoking history of >10 pack years or comparable aero-pollutant exposure, with
    – highly variable expiratory volumes (FEV1 >400ml) and/or
    – elevated eosinophils (>0.3x106).
  • We recommend inhaled corticosteroids in low or moderate doses to target asthma-like inflammatory pathways in combination with single or dual long-acting bronchodilator.
  • We recommend ICS/LABA as initial therapy followed by the addition of LAMA (ie, triple therapy) if there are persistent symptoms or exacerbations.
  • We recommend using either an asthma or COPD action plan depending on the dominant clinical features.
  • Although recent studies in asthma favour the use of combined budesonide/formoterol reliever inhalers, the role of these inhalers in ACO remains uncertain, as there are no data to support this approach at this time.

Box 5: Principles of management of asthma–COPD overlap.

End-of-life care

Advance care planning

End-of-life care is important in advanced COPD. As the goals of care change, patients and their family/whānau require realistic advice and support to make informed decisions and plan for the future.

  • Discussion about advance care plans and advance directives should be undertaken as part of usual management at a suitable time in the disease course.
  • Advance care plans can be made at any stage of the disease and do not need to wait until the patient is approaching the end of life.
  • Most patients with life-limiting conditions prefer to identify their goals of treatment and discuss preferences for end-of-life care early. Good communication with patients who have a terminal illness is associated with better end-of-life care and fewer medical interventions.
  • A useful strategy when deciding whether end-of-life discussions are appropriate is to consider the question: “Would I be surprised if this patient died in the next 12 months?”
  • The following features should also prompt health practitioners to consider initiating discussions about advance care plans, centred on the patient’s preferences for end-of-life care:
    – Breathless at rest or on minimal exertion or housebound
    – Weight loss or cachexia
    – FEV1<30% of predicted
    – Meets criteria for long-term oxygen therapy
    – Two or more hospitalisations in the previous year for exacerbations
  • An admission with respiratory failure requiring non-invasive ventilation
  • A structured advance care plan will reduce the burden of setting the ceiling of care by unfamiliar staff and family members during an acute admission and allow implementation of a patient’s choice of health care when they are no longer capable of expressing their choice.
  • In general, patients and their family/whānau want an honest conversation that is balanced between realistic information and appropriate hope.
  • Consider involving local hospice and/or palliative care services.

More details and Advance Care Plans are available at: www.advancecareplanning.org.nz.

Palliation of dyspnoea

Morphine

  • Morphine reduces respiratory effort and the sensation of breathlessness.
  • Lower doses are usually required than used for pain (eg, 2.5mg to 5mg every four hours, or as required).
  • Consider lower doses for older patients.
  • Dose can be gradually titrated as for pain. But aim for comfort rather than resolution of dyspnoea.
  • If greater than two doses per day of morphine liquid are regularly being used with effect, convert to low-dose, slow-release morphine capsules (eg, 10 mg twice a day). In this case, it would also be reasonable to make small amount of as-required morphine liquid (2.5mg to 5 mg as required) available to the patient.
  • Oral morphine doses are generally <40 mg per day when used for dyspnoea alone.

Benzodiazepines

  • Evidence for benzodiazepines for breathlessness in COPD is lacking. Benzodiazepines may be harmful and are not recommended as a first-line treatment of breathlessness.
  • Benzodiazepines increase the risk of falls among patients with COPD and may also increase the risk of COPD exacerbations and pneumonia.
  • Benzodiazepines should not be used in patients at risk of hypercapnic respiratory failure.

Appendices

Appendix 1: The four-step COPD consultation.

These steps are likely to need more than one consultation.

Appendix 2: COPD assessment test (CAT): https://assets-global.website-files.com/5e332a62c703f6340a2faf44/602c8a966b39518510d20f2c_4878%20-%20appendix%202.pdf

Appendix 3: COPD action plan: https://assets-global.website-files.com/5e332a62c703f6340a2faf44/602c8a9603e1140b3fac6394_4878%20-%20appendix%203.pdf

Appendix 4: Breathlessness strategies for COPD: https://assets-global.website-files.com/5e332a62c703f6340a2faf44/602c8a9676d8e10447d74284_4878%20-%20appendix%204.pdf

Appendix 5: Breathlessness strategies: quick reference guide: https://assets-global.website-files.com/5e332a62c703f6340a2faf44/602c8a969551dd13aba750f8_4878%20-%20appendix%205.pdf

Appendix 6: Useful documents and resources.

Summary

Abstract

The purpose of the Asthma and Respiratory Foundation of New Zealand’s COPD Guidelines Quick Reference Guide is to provide simple, practical, evidence-based recommendations for the diagnosis, assessment and management of chronic obstructive pulmonary disease (COPD) in clinical practice. The intended users are health professionals responsible for delivering acute and chronic COPD care in community and hospital settings, and those responsible for the training of such health professionals.

Aim

Method

Results

Conclusion

Author Information

Robert J Hancox: Waikato District Health Board, Hamilton; University of Otago, Dunedin. nStuart Jones: Middlemore Hospital, Counties Manukau, Auckland. Christina Baggott: Medical Research Institute of New Zealand. David Chen: Canterbury Clinical Network, Christchurch. Nicola Corna: Middlemore Hospital, Counties Manukau, Auckland. Cheryl Davies: Tu Kotahi Māori Asthma Trust. James Fingleton: Medical Research Institute of New Zealand; Capital & Coast District Health Board, Wellington. Jo Hardy: Medical Research Institute of New Zealand. Syed Hussain: Auckland District Health Board. Betty Poot: Hutt Valley District Health Board, Lower Hutt; School of Nursing, Midwifery and Health Practice, Victoria University of Wellington, Wellington. Jim Reid: University of Otago, Dunedin; Best Practice Advisory Centre (BPAC), Dunedin. Justin Travers: Hutt Valley District Health Board, Lower Hutt. Joanna Turner: Asthma and Respiratory Foundation of New Zealand. Robert Young: Auckland District Health Board.

Acknowledgements

We thank Leanne Te Karu and Teresa Demetriou for their valued contribution towards these guidelines.

Correspondence

Robert Hancox, Department of Preventive & Social Medicine, Dunedin Medical Campus, University of Otago, +3 479 8512 (phone), +3 479 7298 (fax)

Correspondence Email

bob.hancox@otago.ac.nz

Competing Interests

Dr Young reports: I receive honorarium from GSK for giving educational talks on COPD management or attending advisory meetings. However, this did not impact on my contribution to this guideline. Dr Baggott reports personal fees from Astra Zeneca, personal fees from Novartis, outside the submitted work. Nicola Corna reports other from Boehringer Ingelheim, other from Astra Zeneca, other from Astra Zeneca, grants from Adherium, outside the submitted work. Dr Fingleton reports grants, personal fees and non-financial support from AstraZeneca, grants from Genentech, grants, personal fees and non-financial support from GlaxoSmithKline, personal fees and non-financial support from Boheringer lngleheim, outside the submitted work. Dr Hardy reports non-financial support from Astrazeneca, outside the submitted work. Dr Hancox reports grants from Astra Zeneca, grants from GlaxoSmithKline, personal fees from Menarini, other from Boehringer Ingelheim, outside the submitted work.

1. Yang IA, Brown JL, George J, Jenkins S, McDonald CF, McDonald V, et al. The COPD-X Plan: Australian and New Zealand Guidelines for the management of Chronic Obstructive Pulmonary Disease 2020. Report No.: Version 2.61 (February 2020).

2. Global Initiative For Chronic Obstructive Lung Disease. Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease (2020 Report). Global Initiative For Chronic Obstructive Lung Disease; 2020.

3. Asthma COPD and Asthma - COPD Overlap Syndrome (ACOS). Global Strategy for Asthma Management and Prevention and the Global Strategy for the Diagnosis, Management and Prevention of Chronic Obstructive Pulmonary Disease.; 2015.

4. Graham BL, Steenbruggen I, Miller MR, Barjaktarevic IZ, Cooper BG, Hall GL, et al. Standardization of Spirometry 2019 Update. An Official American Thoracic Society and European Respiratory Society Technical Statement. Am J Respir Crit Care Med. 2019;200:e70-e88.

5. McDonald CF, Jones S, Beckert L, Bonevski B, Buchanan T, Bozier J, Carson-Chahhoud K V., Chapman DG, Dobler CC, Foster JM, Hamor P, Hodge S, Holmes PW, Larcombe AN, Marshall HM, McCallum GB, Miller A, Pattemore P, Roseby R, See H V., Stone E, Thompson BR, Ween MP, Peters MJ. Electronic cigarettes: A position statement from the Thoracic Society of Australia and New Zealand*. Respirology 2020;1–8.doi:10.1111/resp.13904.

6. Shafuddin E, Chang CL, Hancox RJ. Comparing severity scores in exacerbations of chronic obstructive pulmonary disease. Clin Respir J. 2018;12(12):2668-75.

7. National Ambulance Sector Clinical Working Group. Clinical Procedures & Guidelines 2019. St John & Wellington Free Ambulance.

8. Telfar Barnard L, Zhang J. The impact of respiratory disease in New Zealand: 2018 update. Asthma and Respiratory Foundation of New Zealand; 2019.

9. Hopkins, RJ, Kendall, C, Gamble, GD and Young, RP. Are New Zealand Maori More Susceptible to Smoking Related Lung Cancer? – A Comparative Case-Case Study. EC Pulmonary and Respiratory Medicine. (2019): 8.1 72-91

10. Loring, B. Literature Review: Respiratory Health for Maori. Asthma and Respiratory Foundation. 2009

11. Levack WM, Jones B, Grainger R, Boland P, Brown M, Ingham TR. Whakawhanaungatanga: the importance of culturally meaningful connections to improve uptake of pulmonary rehabilitation by Māori with COPD - a qualitative study. Int J Chron Obstruct Pulmon Dis. 2016;11:489-501.

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Chronic obstructive pulmonary disease (COPD) encompasses chronic bronchitis, emphysema, and chronic airflow obstruction. It is characterised by persistent respiratory symptoms and airflow limitation that is not fully reversible.

COPD is associated with a range of pathological changes in the lung. The airflow limitation is usually progressive and associated with an inflammatory response to inhaled noxious particles or gases.1,2

Symptoms include cough, sputum production, shortness of breath, and wheeze. At first, these are often ascribed to “a smokers cough”, “getting old” or being “unfit”. Cough and sputum production may precede wheeze by many years. Symptoms may worsen and become severe and chronic, but not all of those with cough and wheeze advance to progressive disease.

Patients with COPD often have exacerbations, when symptoms become much worse and require more intensive treatment. These exacerbations have a significant mortality.

Many patients have extra-pulmonary effects and important co-morbidities that contribute to the severity of the disease. Important co-morbidities include asthma, bronchiectasis, lung cancer and heart disease. COPD can lead to debilitation, polycythaemia, osteoporosis, cachexia, depression and anxiety.

COPD is often confused with asthma. They are separate diseases, although some asthmatics develop irreversible airflow obstruction and some patients with COPD have a mixed inflammatory pattern. Asthma–COPD overlap (ACO) may be present when it can be difficult to distinguish between the diseases, or in patients who have both conditions.3

Guidelines review

The following documents were reviewed to formulate this Quick Reference Guide: COPD-X Australian and New Zealand Guidelines 20201 and the Global Initiative for Chronic Obstructive Lung Disease (GOLD) 2020.2 A systematic review was not performed, although relevant references were reviewed when necessary. Readers are referred to the COPD-X and GOLD documents for the more comprehensive detail and references that they provide. References are only provided when they differ from the COPD-X guidelines.

Grading

No levels of evidence grades are provided, due to the format of the Quick Reference Guide. Readers are referred to the above documents for the level of evidence on which the recommendations in this Quick Reference Guide are based.

Guideline development group

This group included representatives from a range of professions and disciplines relevant to the scope of the guidelines. The group did not include consumer representation.

Robert J Hancox, Stuart Jones, Christina Baggott, James Fingleton, Jo Hardy, Syed Hussain, and Justin Travers are respiratory physicians. Robert Young is a general physician. David Chen is a respiratory physiotherapist. Cheryl Davies is manager of the Tu Kotahi Maori Asthma Trust. Nicola Corna and Betty Poot are respiratory nurse practitioners. Jim Reid is a general practitioner. Joanna Turner is a pharmacist and research and education manager at the Asthma and Respiratory Foundation of New Zealand.

Peer review

The draft guidelines were peer-reviewed by a wide range of respiratory health experts and representatives from key professional organisations, including representatives from Asthma New Zealand, the Australian College of Emergency Medicine, Hutt Valley District Health Board, the Medical Research Institute of New Zealand, the New Zealand Medical Association, the New Zealand Nurses Organisation Te Rūnanga o Aotearoa, the NZNO College of Respiratory Nurses, Physiotherapy New Zealand, the Royal New Zealand College of General Practitioners, the New Zealand branch of the Thoracic Society of Australia and New Zealand, and Wellington Free Ambulance.

Dissemination plan

The guidelines will be translated into tools for practical use by health professionals and used to update health pathways and existing consumer resources. The guidelines will be published in the New Zealand Medical Journal and on the Asthma and Respiratory Foundation of New Zealand (ARFNZ) websites, as well as being disseminated widely via a range of publications, training opportunities, and other communication channels to health professionals, nursing, pharmacy and medical schools, primary health organisations, and district health boards.

Implementation

The implementation of the guidelines by organisations will require communication, education, and training strategies.

Expiry Date

The expiry date for the guidelines is 2025.

COPD in Māori

Māori rights in regard to health, recognised in Te Tiriti o Waitangi and other national and international declarations, promote and require both Māori participation in health-related decision making as well as equity of access and health outcomes for all New Zealanders.

  • The burden of COPD among Māori is one of the most significant health disparities in New Zealand: hospitalisation rates for Māori are 3.5 times higher than non-Māori, non-Pacific, and non-Asian rates, and COPD mortality for Māori is 2.2 times higher.8
  • Māori whānau also have greater exposure to environmental triggers for COPD, such as smoking and poor housing.
  • This burden of COPD translates to large inequities in lost years of healthy life and underscores the urgent need for health service models to address high and growing need for COPD treatment in Māori.
  • Māori should be considered a high-risk group requiring targeted care. This should address risk factors such as poor housing, overcrowding, health literacy, inadequate tailoring of health information, obesity, smoking, and poor access to pulmonary rehabilitation and healthcare services.
  • Māori have much worse lung function for given levels of smoking,9 and the burden of COPD affects Māori 15–20 years younger than non-Māori.10 This makes smoking cessation even more important for Māori, and COPD should be considered at a younger age among Māori smokers.
  • There is a very high incidence of lung cancer among Māori.

Major barriers to good COPD management for Māori include poor access to care, inattention to culturally accepted practices, discontinuous and poor-quality care, and inadequate provision of understandable health information. As Māori place a high value on whakawhanaungatanga (the making of culturally meaningful connections with others), the absence of culturally appropriate practices can hinder attendance in mainstream pulmonary rehabilitation programmes.11 Cultural safety and a pro-equity approach is essential.

It is recommended that:

  • Healthcare providers should undertake clinical audit or other quality-improvement activities to monitor and improve COPD care and outcomes for Māori.
  • A systematic approach to health literacy and COPD education for Māori whānau is required.
  • Healthcare providers should support staff to develop cultural safety skills for engaging Māori with COPD and their whānau.
  • Assess patients using a Māori model of care: https://www.health.govt.nz/our-work/populations/maori-health/maori-health-models.

Māori leadership is required in the development of COPD management programmes, including pulmonary rehabilitation, to improve access to COPD care and facilitate ‘wrap around’ services that address the wider determinants of health (such as housing, financial factors, access to health care and access to pulmonary rehabilitation programmes) for Māori with COPD.

COPD in Pacific people

Similar considerations apply to Pacific people, who also have a disproportionate burden of COPD. Pacific people’s hospitalisation rates are 2.7 times higher than those of other New Zealanders.8

It is recommended that:

Pathogenesis

Most people with COPD will have smoked cigarettes or inhaled noxious particles causing lung inflammation. Airway inflammation is a normal response to smoking but seems to be accentuated in those who go on to develop COPD. Some people develop COPD without smoking or apparent exposures. COPD may also develop in patients with other chronic lung diseases such as asthma.

The inflammatory process in COPD is mostly neutrophil, macrophage, and T-lymphocyte mediated. This inflammation leads to narrowing of peripheral airways and destruction of alveoli, causing airflow obstruction and decreased gas transfer.

Inflammation, fibrosis, and sputum production in small airways causes air trapping during expiration leading to hyperinflation. This reduces inspiratory capacity and causes shortness of breath on exercise.

In patients presenting at a young age (particularly those younger than 40), alpha-1 antitrypsin deficiency should be considered. This genetic defect causes a reduction in the major anti-protease in lung parenchyma, leaving the lung susceptible to the destructive effects of neutrophil elastase and other endogenous proteases, which are released as part of the inflammatory response to smoking.

Diagnosis

A diagnosis of COPD should be considered in anyone who presents with cough, sputum production, wheeze, or shortness of breath, particularly those above the age of 40 years. There is usually a history of cigarette smoking or exposure to smoke other noxious substances.

  • Physical examination and chest x-ray are rarely diagnostic in early COPD, but they may be valuable in excluding other diagnoses and co-morbidities such as lung cancer, pulmonary fibrosis and cardiac failure.
  • Other causes for the patient’s symptoms should always be considered, as common comorbidities such as heart disease and obesity may co-exist with COPD and in some patients will be the dominant cause of breathlessness.
  • The diagnosis of COPD should be confirmed by spirometry (see Spirometry). If this is not available in primary care, patients should be referred for this. There are few contra-indications, but a small proportion of patients cannot do adequate spirometry.
  • Spirometry should be avoided during infections, because of the risk of transmitting infections such as influenza, SARS-CoV-2 (COVID-19), or tuberculosis.
  • Peak flows are not useful for diagnosing or managing COPD.
  • Usually asthma and COPD are easy to differentiate. Asthma is an episodic disease and usually, but not always, presents at a younger age or with a history of being “chesty” as a child. However, a mixed pattern of asthma-COPD overlap (ACO) exists, and it is sometimes difficult to distinguish which is the principal cause of airway limitation (see section Asthma and COPD overlap (ACO)).

Assess severity

  • Spirometry assesses the severity of airflow obstruction. Used in conjunction with the severity of symptoms, this helps to assess the severity of COPD (Table 1). Although Table 1 also shows the typical symptoms, the severity of the symptoms does not necessarily correspond to the severity of airflow obstruction.
  • The effect of breathlessness on daily activities can be quantified using the modified Medical Research Council (mMRC) Dyspnoea Scale (Table 2).
  • The COPD Assessment Test (CAT) is an eight-item questionnaire that can measure the symptomatic impact of COPD and response to treatment (Appendix 2).
  • Functional tests, such as the six-minute walk test, shuttle walk tests and sit-to-stand tests, can help to assess functional limitation, disease progression and response to treatment.

Table 1: Severity classification for COPD. (Adapted from Lung Foundation Australia’s Stepwise Manage-ment of Stable COPD available at https://lungfoundation.com.au/wp-content/uploads/2018/09/Informa-tion-Paper-Stepwise-Management-of-Stable-COPD-Apr2020.pdf.)

FEV1=forced expiratory volume in one second. PaO2=partial pressure of oxygen, arterial. PaCO2=partial pressure of carbon dioxide, arterial.

Table 2: Modified Medical Research Council (mMRC) Dyspnoea Scale for grading the severity of breathlessness during daily activities*

* The mMRC Dyspnoea Scale is very similar to the original MRC Scale, which ranges from 1 to 5 rather than 0 to 4 (ie, MRC grade 3=modified MRC grade 2).

Spirometry

Spirometry is the most useful test of lung function to diagnose and assess the severity of COPD. This may be done both before and after a bronchodilator to assess reversibility, but the diagnosis and severity are determined by post-bronchodilator measurements.

  • Irreversible airflow obstruction is indicated by a post-bronchodilator forced expiry volume in once second to forced vital capacity (FEV1/FVC) ratio<0.70*.
  • The severity of the obstruction is diagnosed using the post-bronchodilator FEV1 as a % of the predicted value (Table 1).
  • It is possible to have airflow obstruction with an FEV1/FVC ratio<0.70* but an FEV1 in the normal range.
  • A restrictive pattern on spirometry is not consistent with a diagnosis of COPD and, if it is not due to technically inadequate spirometry, suggests an alternative cause of symptoms (eg, morbid obesity, neuromuscular weakness, or interstitial lung disease). Patients with a restrictive pattern may benefit from specialist referral for further investigation.
  • Some patients with COPD cannot blow out long enough to do a true FVC. The Forced Expiratory Volume at 6 seconds (FEV6) can be used as an approximation of the FVC.
  • A small subset of patients with normal spirometry have evidence of emphysema on CT scan and impairment of gas exchange. There is limited evidence to guide management in these patients, but if they are symptomatic or having exacerbations, we recommend treatment for COPD according to this guideline.

(*Note: There is disagreement about the criteria for airflow obstruction. The FEV1/FVC ratio naturally declines with age, and defining airflow obstruction by an FEV1/FVC ratio <0.70 may miss mild airflow obstruction in younger patients and over-diagnose it in the elderly. Some guidelines recommend using an age-specific lower limit of normal. But for clinical purposes, the <0.70 cut-point is easy to apply and unlikely to greatly influence management in those with mild airflow obstruction. The grading of severity also varies between guidelines, with the GOLD guidelines using different categories to COPD-X (in Table 1). But this is also unlikely to greatly influence clinical management.)

Reversibility testing

When performing reversibility testing, the first measurements should be done before bronchodilators:

  • Bronchodilators should be withheld for the duration recommended in the consensus ATS/ERS guidelines.4 This ranges from 4–6 hours for a short-acting beta agonist (SABA) to 48 hours for an ultra long-acting beta agonist (LABA).
  • Spirometry is repeated at least 15 minutes after giving a bronchodilator (usually 400mcg salbutamol via spacer).
  • Many patients with COPD will have some improvement after a bronchodilator (“partial reversibility”), but if spirometry becomes normal (FEV1/FVC>0.7* and FEV1>80% predicted), COPD is excluded (by definition).
  • The consensus definition of a significant bronchodilator response is arbitrarily defined as a ≥12% change from baseline with an absolute improvement of ≥200ml, but this does not predict who will benefit from bronchodilator treatment.
  • If the response to bronchodilator is substantial (>400mL improvement in FEV1) then asthma or Asthma-COPD Overlap is likely.

(*Note: There is disagreement about the criteria for airflow obstruction. The FEV1/FVC ratio naturally declines with age, and defining airflow obstruction by an FEV1/FVC ratio <0.70 may miss mild airflow obstruction in younger patients and over-diagnose it in the elderly. Some guidelines recommend using an age-specific lower limit of normal. But for clinical purposes, the <0.70 cut-point is easy to apply and unlikely to greatly influence management in those with mild airflow obstruction. The grading of severity also varies between guidelines, with the GOLD guidelines using different categories to COPD-X (in Table 1). But this is also unlikely to greatly influence clinical management.)

Non-pharmacological management (Box 1)

Smoking cessation

Stopping smoking is the most important treatment for COPD: every person who is still smoking should be offered help to quit. Reducing smoking-related health risks requires complete cessation of all tobacco and other smoked products, including marijuana/cannabis.

  • All forms of nicotine replacement therapy, in association with smoking cessation support, are useful in aiding smoking cessation and increase the rate of quitting.
  • Oral bupropion, varenicline, and nortriptyline have been shown to be effective and should be considered in those patients struggling to give up despite nicotine replacement therapy.
  • Most of these are fully funded in New Zealand and a prescription for this should be discussed with a health professional.
  • Referral to a local smoking cessation support service is recommended.

E-cigarettes and vaping are probably less harmful to health than smoking, but short-term studies suggest that they are not risk free.5 E-cigarettes and vapes that contain nicotine are highly addictive.

  • E-cigarettes used within the context of a supportive smoking cessation programme have been shown to aid in smoking cessation in selected groups of motivated patients.
  • The long-term safety of e-cigarettes and vaping have not been shown. Smokers using e-cigarettes or vaping to quit smoking should be advised to stop using e-cigarettes and vaping as soon as possible after quitting smoking.
  • No e-cigarette or vape is currently approved as a smoking cessation tool.
  • E-cigarettes and vapes should never be used near an oxygen source, as this is a fire risk.

Physical activity

Patients with COPD benefit from physical activity and should be encouraged to:

  • Be active on most, preferably all, days of the week.
  • Do at least 20–30 minutes of exercise per day. More is better.
  • Exercise to an intensity that should cause the patient to “huff and puff” or feel breathless: Getting out of breath will not cause harm.
  • Do muscle strengthening activities on two or more days each week.

Pulmonary rehabilitation

Pulmonary rehabilitation should be offered to all patients with COPD. Although there may be barriers to attending pulmonary rehabilitation classes, there are a variety of ways to deliver pulmonary rehabilitation to patients in different settings depending on local respiratory services and patient preferences.

  • Pulmonary rehabilitation reduces breathlessness, improves quality of life, and reduces depression in patients with COPD.
  • Patients gain significant benefit from rehabilitation regardless of the degree of breathlessness, but the most breathless patients benefit the most.
  • Exacerbations of COPD are an indication for referral to pulmonary rehabilitation and an early return to pulmonary rehabilitation after exacerbation should be encouraged. This has been shown to reduce further hospitalisations and may reduce mortality.
  • Exercise training is the cornerstone of pulmonary rehabilitation, and regular post-rehabilitation exercise is required to sustain the benefits.
  • The benefits of pulmonary rehabilitation decline over time and repeat attendance at pulmonary rehabilitation programmes should be encouraged in patients with functional decline or exacerbations.
  • If someone is unable to access a pulmonary rehabilitation programme, an in-home exercise programme should be considered.

Breathlessness management strategies

In addition to pulmonary rehabilitation, patients may benefit from seeing a respiratory physiotherapist for individualised breathing exercises or breathless management strategies:

  • Diaphragmatic breathing and pursed lips breathing exercises may benefit some patients. These support and correct the breathing pattern disorders caused by COPD and improve exercise capacity, but they have inconsistent effects on dyspnoea or health-related quality of life scores.
  • Constant load threshold inspiratory muscle training improves inspiratory muscle strength, quality of life, dyspnoea, and exercise capacity.
  • Hand-held fan therapy: the airflow and cooling effects of the fan, alongside other breathlessness management strategies, such as relaxation, pacing, and positioning, can reduce dyspnoea.

Other things that may help:

  • Hospital clinical teams working with the primary healthcare team can help enhance quality of life and reduce disability for patients with COPD.
  • Patients may also benefit from local support groups.
  • Consider including a cognitive behavioural component in the self-management plan to assist with reducing anxiety and breathlessness.
  • Consider screening for urinary incontinence related to cough.

Other useful resources are given in Appendix 4 and 5.

Sputum management/sputum clearance techniques

Patients with chronic sputum production may benefit from seeing a physiotherapist (ideally a respiratory physiotherapist) for an individualised chest clearance plan. Airway clearance techniques enhance sputum clearance, reduce hospital admissions, and improve health-related quality of life, and they may also improve exercise tolerance and reduce the need for antibiotics.

  • A wide variety of airway clearance techniques are available. No one technique is superior for all patients.
  • The choice of technique should be based on the clinician’s assessment, resource availability, and patient acceptability.

Nutrition

Both malnutrition and obesity are common and contribute to morbidity and mortality in COPD. Poor eating habits, sedentary lifestyles, smoking, and corticosteroid use further compromise nutritional status.

  • The key goals of nutritional management are to eat a balanced diet, to achieve and maintain a healthy weight, and to avoid unintentional weight loss. Consider referral to a dietician, or high-calorie nutritional supplements, for those who are malnourished.
  • There is evidence that weight loss is beneficial for those who are obese.
  • Unintentional weight loss should be investigated for potential malignancy.

Housing

There is good evidence that a warm, dry, and smoke-free home is associated with better asthma control, and it is likely that the same is true for COPD.

Assisted ventilation

Non‐invasive ventilation (NIV) with bi‐level positive airway pressure reduces mortality and need for intubation in patients admitted to hospital with acute hypercapnic respiratory failure as a result of an exacerbation of COPD (see section Management). In most instances, NIV is not required once the patient has recovered.

  • People who have chronic hypercapnic respiratory failure, despite adequate treatment, and have needed assisted ventilation (invasive or non-invasive) during an exacerbation, or with worsening hypercapnia on long-term oxygen therapy, should be referred to a specialist centre for consideration of long-term NIV.
  • Red flags to consider for need for home NIV:
    – Previously required assisted ventilation
    – Obstructive sleep apnoea
    – Obesity hypoventilation
    – Persistent nocturnal hypoxia
    – Neuromuscular conditions
    – Spinal/chest wall deformities

Interventional approaches to the management of COPD

Thoracic surgery is rarely performed for COPD. The two situations where it may be considered are bullectomy or lung volume reduction surgery. Neither procedure increases life expectancy. Both have significant complication rates and are only performed in specialist centres after careful multi-disciplinary assessment.

Bullectomy

Bullectomy can be considered where there is a very large bulla compressing other lung tissue. Removing the bulla allows the preserved lung tissue to function better.

Lung volume reduction surgery

Lung volume reduction surgery can improve exercise capacity in people with upper-lobe predominant emphysema. The surgery has a significant early mortality, but there is no difference in long-term mortality.

Interventional bronchoscopy

Bronchoscopic lung volume reduction approaches have been developed as alternatives to lung volume reduction surgery. These aim to reduce gas-trapping and improve lung mechanics in advanced emphysema, which can lead to improved lung function, symptoms, and quality of life in carefully selected patients. Endobronchial valve therapy has the most evidence and is available in New Zealand. It is only effective in those with intact fissures and no collateral ventilation as one-way valves are inserted to cause collapse of lung segments. Endobronchial valve therapy does not reduce mortality and has significant complication rates.

Lung transplantation

Consideration for lung transplantation is appropriate in younger patients (usually <65) with very severe obstruction and severe symptoms, or progressive deterioration despite optimised management, including smoking cessation and pulmonary rehabilitation. Referral to the transplant service should be made by a respiratory specialist.

Box 1: Key messages for non-pharmacological management of COPD.

Improving patient understanding

Identify and manage social and cultural issues

Health literacy, cultural context, and the degree of social isolation or support are key factors affecting a person’s understanding of and attitude to COPD. See also sections COPD in Māori and COPD in Pacific people.

  • These factors impact on COPD management, appropriate inhaler technique, adherence to treatment and appropriate use of self-management plans.
  • These factors also have a considerable impact on the success of smoking cessation.
  • Awareness of the social and cultural factors will enhance communication between clinicians and patients and improve health outcomes.
  • There are many practical challenges for people living with COPD, such as completing everyday tasks, holding down a job, and having access to transport. Awareness of these challenges and referral to support services where available can be beneficial.

Optimise knowledge of COPD and adherence to treatment

  • Patient understanding of the disease, appropriate inhaler technique and adherence to treatment are important factors in COPD management.
  • There are many inhalers available to treat COPD, and people can easily get confused about these. Demonstrate the use of the inhalers and ensure that patients can use them correctly.
  • Clinicians should ask about the patient’s understanding of the disease and the rationale for treatment, to clarify misunderstandings, and to work to remove barriers to adherence and good self-management. It is important to provide information to the patient and whānau in a format that they can understand.

Develop an action plan

Personalised action plans (self-management plans) improve quality of life and reduce hospital admissions and should be offered to all people with COPD.

  • Action plans should be personalised and focus on recognising and treating deteriorating symptoms.
  • Patients at risk of exacerbations may be offered antibiotics and prednisone to have at home as part of their action plan. The patient should be advised of a timeframe for clinical review once they have started these medicines for an acute exacerbation of COPD.
  • Action plans should be checked at each COPD review.

The Asthma and Respiratory Foundation of New Zealand’s COPD Action Plan is shown in Appendix 3.

Electronic versions are available at: www.nzrespiratoryguidelines.co.nz.

Develop a breathlessness plan

  • A breathlessness plan can reduce the severity and impact of breathlessness. Interventions and techniques that can improve breathlessness include self-management education, breathing exercises, sitting upright and leaning forwards (‘positioning’), using pursed lip breathing, and a hand-held fan.
  • Oxygen is not an effective treatment for breathlessness in patients who are not hypoxic.
  • Smoking cessation also improves breathlessness.

Asthma and Respiratory Foundation of New Zealand’s ‘Breathlessness Strategies for COPD’ is shown in Appendix 4 and is available at www.nzrespiratoryguidelines.co.nz.

Pharmacological management (Box 2)

The purpose of pharmacological management in COPD is symptom control and prevention of exacerbations, with the aim of improving quality of life.

  • Check inhaler adherence and inhaler technique regularly. Make sure that these are optimal before escalating treatment.
  • Treatment escalation should follow a stepwise approach based on breathlessness and exacerbation frequency. It should take into account patient preferences, regimen complexity, cost, and side effects.
  • Effects of treatment on dyspnoea should be apparent within six weeks.
  • Effects on exacerbation frequency may need to be assessed over 6 to 12 months.

Inhaled medication for COPD

  • Short-acting beta2 agonists (SABA: salbutamol or terbutaline) and the short-acting muscarinic antagonist (SAMA: ipratropium), either individually or in combination, can be taken as-needed to provide short-term relief of breathlessness. Short-term response to SABA or SAMA (reversibility testing) does not predict benefit from long-acting bronchodilator therapy.
  • For patients with ongoing dyspnoea despite as-needed SABA, SAMA, or combination SABA/SAMA, a regular long-acting muscarinic antagonist (LAMA) such as tiotropium, glycopyrronium, or umeclidinium is recommended, unless there is evidence of asthma/COPD overlap (see Asthma and COPD overlap (ACO)). Do not continue to use ipratropium in patients taking a LAMA, except in emergencies.
  • It is not necessary to have a trial of regular short-acting bronchodilators before starting a LAMA if symptoms, exacerbation history or spirometry suggest that a long-acting bronchodilator is desirable.
  • Both LAMAs and LABAs improve lung function, symptoms and quality of life, but LAMAs are recommended as the first-line long-acting medication for COPD because they reduce exacerbation risk and have fewer side effects. If LAMAs are contra-indicated, a long-acting beta agonist (LABA) such as salmeterol, formoterol, or indacaterol is recommended.
  • In patients who remain breathless or who continue to exacerbate despite treatment with a single long-acting bronchodilator, dual LAMA/LABA therapy is recommended (eg, glycopyrronium/indacaterol, umeclidinium/vilanterol, or olodaterol/tiotropium). Combination therapy with a LABA and LAMA improves lung function, reduces symptoms, and reduces exacerbations compared to either drug alone.
  • LABA/LAMA is preferred over inhaled corticosteroid (ICS)/LABA as initial therapy for most patients with frequent exacerbations because ICS increases the risk of pneumonia.
  • These medications may have risks, particularly at higher doses in patients with cardiac disease. If there is no evidence of benefit, consider stopping them.
  • Patients with an eosinophilic pattern of disease may benefit from ICS/LABA instead of LABA/LAMA. Retrospective analyses suggest that blood eosinophil counts predict the benefit of ICS in preventing exacerbations: people with blood eosinophil counts <100cells/µL are least likely to benefit and people with counts ≥300cells/µL are most likely to benefit. A single blood test may not be representative as eosinophil counts can vary over time. Blood eosinophil counts performed when a patient is taking oral steroids will not be informative.
  • An ICS should form part of the regimen for any patient with asthma/COPD overlap. This should usually be prescribed as an ICS/LABA combination inhaler to avoid the risk of LABA monotherapy in patients with poor adherence to a separate ICS inhaler.
  • Prescriptions should be based on drug class. Choice of specific LABAs and LAMAs should be guided by patient preference and their ability to use the inhaler device. A list of inhalers available in New Zealand is available at www.nzrespiratoryguidelines.co.nz. Dry-powder inhalers have a substantially lower impact on greenhouse gases than pressurised metered-dose inhalers.
  • Six weeks is a reasonable timeframe to assess improvement in breathlessness following a medication change.
  • The COPD assessment test is an eight-item questionnaire that can be used to measure the symptomatic impact of COPD and response to therapy (see Assess severity and Appendix 2).

Role of triple therapy (LABA/LAMA/ICS)

  • Escalation to triple LABA/LAMA/ICS therapy should be considered in patients who continue to exacerbate (twice or more a year) despite adherence to dual LAMA/LABA or ICS/LABA therapy and optimal inhaler technique.
  • A subset of patients with persistent breathlessness and exercise limitation, despite LABA/LAMA combination therapy, may benefit from triple therapy with LABA, LAMA, and ICS. However, the increased risk of pneumonia with regular ICS should be considered.
  • Direct escalation to dual or triple therapy, without stepwise up-titration, may be reasonable in the setting of a severe or recurrent exacerbations.

ICS withdrawal

  • The risk of pneumonia in patients with severe COPD is increased with regular ICS. Withdrawing ICS should be considered if:
  • There is no evidence of benefit from ICS in terms of improved symptoms or fewer exacerbations.
  • The patient develops pneumonia or other ICS adverse effects.
  • The patient does not have a history of frequent exacerbations and is stable.
  • If ICS treatment is withdrawn, the patient should be reviewed at 4–6 weeks to ensure that this doesn’t cause a deterioration in symptoms.
  • Withdrawal of ICS may not be appropriate if the blood eosinophil count is elevated. A blood eosinophil count ≥300cells/µL has been shown to be associated with an increased exacerbation risk after ICS withdrawal.
  • ICS should not be withdrawn in patients with a diagnosis of asthma/COPD overlap (see section Asthma and COPD overlap (ACO)).

Table 3: Simplified maintenance inhaler management of COPD.

Additional therapies

  • There is no evidence that routine use of nebulisers is beneficial in patients with COPD.
  • Theophylline has not shown consistent benefits on exacerbation, lung function, symptoms, or quality of life in randomised controlled trials. In view of the narrow therapeutic index and side-effect profile of theophylline, we do not recommend its routine use in the management of COPD.
  • There is no evidence of benefit from long-term oral corticosteroids.
  • Long-term macrolide antibiotics, such azithromycin and erythromycin, can reduce risk of exacerbations over one year in former smokers who have exacerbations despite optimal inhaled treatment. Azithromycin is not currently funded in New Zealand for this indication. Long-term macrolide therapy is associated with significant risks, including bacterial resistance, gastrointestinal and cardiovascular side effects, and hearing impairment. Long-term macrolides should rarely be initiated without specialist advice.
  • Regular treatment with mucolytics (eg, erdosteine, carbocysteine, or N-acetylcysteine) may reduce the risk of exacerbations in some patients. These treatments are not currently funded in New Zealand.
  • In patients with severe and very severe COPD and a history of exacerbations, PDE4 inhibitors (eg, roflumilast) improve lung function, reduce the risk of exacerbations, and have modest benefits for symptoms and quality of life. They have significant gastrointestinal side effects. These treatments are not currently funded in New Zealand
  • Alpha-1 antitrypsin augmentation therapy may slow the progression of emphysema in patients with alpha-1 antitrypsin deficiency. This is not currently funded in New Zealand.

Box 2: Key messages for pharmacological management of COPD.

Oxygen therapy

  • Oxygen is a treatment for hypoxia, not dyspnoea. Oxygen does not reduce the sensation of breathlessness in patients who are not hypoxic. Oxygen may not improve breathlessness even in those who are hypoxic.
  • Oxygen is a drug therapy and should be prescribed.
  • Long-term oxygen therapy has survival benefits for COPD patients with severe hypoxaemia. It must be used for at least 16 hours a day. The survival benefits are not apparent until months or years after starting treatment.
  • Evaluation of the patient and consideration for long-term oxygen therapy supply should be done by a specialist respiratory service (Box 3). The causes of the hypoxia should be explored, and the patient’s pharmacological and non-pharmacological management should be optimised. A target saturation range and oxygen flow rate should be established.
  • Patients should adhere to the amount of oxygen prescribed and be monitored for adverse effects.

Box 3: Criteria for oxygen.

Flying with oxygen

Flying is generally safe for patients with COPD, including those with chronic respiratory failure who are on long-term oxygen therapy.

  • Before flying, patients should ideally be clinically stable.
  • Supplemental oxygen is unlikely to be required if the resting oxygen saturation is ≥95%, and is likely to be required if oxygen saturation is ≤88%. Patients with oxygen saturation values between these levels might require specialist assessment.
  • Those already on long-term oxygen therapy need an increase in flow rate of 1–2L per minute during the flight.
  • Patients receiving oxygen therapy will need to contact the airline prior to flying.

Vaccination

  • Yearly influenza vaccination reduces serious illness and death in patients with COPD and should be actively promoted to patients with COPD.
  • Pneumococcal vaccination probably decreases the incidence of pneumonia and reduces the risk of exacerbations in patients with COPD, but the evidence for this is conflicting and pneumococcal vaccination is not currently funded for this indication in New Zealand.
  • Two types of pneumococcal vaccine are approved for use. If the healthcare professional and patient consider this an appropriate treatment, a suggested schedule is one dose of 13-valent protein conjugate vaccine (PCV13, Prevenar 13®) given first, followed at least eight weeks later by the first dose of 23-valent polysaccharide vaccine (23PPV, Pneumovax 23®). A second dose of 23PPV is given a minimum of five years later and a third dose at age ≥65 years.

Acute exacerbations

COPD exacerbations are characterised by a change in the patient’s baseline dyspnoea, cough, and/or sputum that is beyond normal day-to-day variations, is acute in onset, and may warrant a change in regular medication or hospital admission. Key symptoms of exacerbations include increased shortness of breath, increased sputum purulence and volume, increased cough, and wheeze.

Exacerbations of COPD are associated with an accelerated loss of lung function, particularly in patients with mild disease. Prolonged exacerbations are associated with worse health status and more frequent future exacerbations.

Early diagnosis and prompt management of exacerbations of COPD may prevent functional deterioration and reduce hospital admissions. Education of the patient, carers, other support people, and family may aid in the early detection of exacerbations.

Assessment (Figures 1 and 2)

  • Most exacerbations can be managed at home. Indications for hospitalisation include, but are not limited to, a sudden worsening of symptoms, confusion or drowsiness, signs such as cyanosis and peripheral oedema, failure to respond to medical management, low oxygen saturation by pulse oximetry (SpO2), the presence of serious co-morbidities, including heart failure and newly occurring arrhythmias, and insufficient home support or lack of telephone or transport.
  • A guide to acute severity assessment is shown in Table 4.
  • Several prognostic scores have been proposed. The most validated one is DECAF, but this includes COPD with pneumonia and requires a blood gas, complete blood count (for eosinophils), and chest x-ray, which are unlikely to be available in primary care. An alternative is CURB-65, which was developed for pneumonia but has been found to be equally effective at predicting short term-mortality in COPD in New Zealand studies.6 CRB-65 is a simpler version that does not require any laboratory measures (Table 5).
  • A chest x-ray and electrocardiogram help to identify alternative diagnoses and complications, such as pulmonary oedema, pulmonary embolus, pneumothorax, pneumonia, pleural effusion, arrhythmias, myocardial ischaemia, and others. Biomarkers (troponins, B-natriuretic peptide, D-dimer) can help to identify comorbidities and abnormalities of these are associated with a worse prognosis.

Table 4: Assessment of exacerbation severity.

Table 5: Assessment of short-term (one-month) prognosis.

*Score 1 point for the presence of each factor. #DECAF scores have been validated in patients with COPD and pneumonia, and CURB65 and CRB65 have not.

Management (Box 4, Figures 1 and 2)

Use breathless management strategies (Appendix 4): sit, rest arms on a chair or table, use a fan, and practise breathing control techniques

Bronchodilators

  • Short-acting inhaled beta2 agonists with or without short-acting anti-muscarinics are the initial bronchodilator of choice to treat an acute exacerbation. These can be delivered via pressurised metered dose inhaler and spacer, dry powder inhalers, or nebuliser. We recommend salbutamol via a spacer. One actuation of the inhaler should be used each time and repeated as necessary.
  • Spacer technique is important when using a pressurised metered dose inhaler. In an exacerbation, we recommend one actuation into the spacer followed by 4—6 tidal breaths. Observe and repeat if required.
  • The bronchodilator effect of 8—10 puffs of 100mcg salbutamol via spacer is equivalent to a 5mg salbutamol nebuliser. We recommend that no more than five puffs are used at a time (given individually via spacer).
  • If patients do not respond to multiple doses of inhaled short-acting beta2 agonist, additional bronchodilator treatment such as ipratropium is recommended.
  • Nebulisers may increase the risk for aerosolisation of viruses such as SARS-CoV-2 (COVID-19). There is no evidence that nebulisers are more effective than inhalers via a spacer, and we recommend that nebulisers should be avoided in any patient who could be infected with respiratory viruses. If they are used, appropriate aerosolisation infection precautions should be implemented.
  • If a salbutamol nebuliser is necessary, we recommend a maximum dose of 2.5mg at a time. Patients with COPD often have cardiac co-morbidities. Higher doses are associated with an increased risk of tremors, elevated heart rate, palpitations, and lower blood pressure, without evidence of any additional benefit.
  • If nebulisers are given for acute COPD exacerbations, they should be air driven to reduce the risk of type 2 respiratory failure due to high flow oxygen.
  • Maintenance LABA, LAMA, and ICS should be continued during an exacerbation.
  • We do not recommend the routine use of intravenous (IV) magnesium for COPD exacerbations.
  • We do not recommend adrenaline for COPD exacerbations in the absence of anaphylaxis.

Corticosteroids

• Systemic corticosteroids (eg, prednisone 40mg once daily) can improve lung function, improve oxygenation, and shorten recovery time. They should usually be given for five days. Longer courses should generally be avoided due to the risk of side effects.

• Intravenous steroids should be avoided. There is no evidence of benefit compared with oral corticosteroids for treatment failure, relapse, or mortality. Hyperglycaemia rates are higher with IV corticosteroids.

Antibiotics

  • Respiratory tract infections are the most common precipitants of exacerbations of COPD. These may be viral, bacterial, or mixed. Common bacterial pathogens include Haemophilus influenzae, Streptococcus pneumonia, and Moraxella catarrhalis. Mycoplasma pneumoniae and Chlamydia pneumoniae have also been reported. Pseudomonas aeruginosa and Staphylococcus aureus are uncommon but occur more frequently in severe COPD.
  • Antibiotics, when indicated by the presence of purulent sputum, fever and/or raised inflammatory markers (CRP >40), can shorten recovery time and reduce the risk of relapse and treatment failure, and should be prescribed for 5–7 days.
  • Oral antibiotics such as amoxicillin or doxycycline are recommended. If treatment failure or resistant organisms are suspected, amoxycillin-clavulanate can be prescribed. If pneumonia, Pseudomonas or Staphylococci are suspected, appropriate antibiotics should be used.

Oxygen

  • If indicated, oxygen should be prescribed and titrated via nasal prongs or a controlled flow device to target saturations of 88–92%.
  • Oxygen delivery via a high-flow humidified nasal device can improve ventilation and airway clearance as well as reduce the physiological dead space and work of breathing.

Supported ventilation

  • Non-invasive ventilation (NIV) reduces mortality by about 50%, reduces need for intubation, and shortens length of stay in patients with rising arterial carbon dioxide tension (PaCO2) levels due to COPD. It should be considered in patients who present with hypercapnic respiratory failure (arterial pH <7.35, PaCO2 >6kPa/45mmHg).
  • An arterial blood gas should be considered in every patient with a severe exacerbation, an oxygen saturation less than 90%, or signs of cor pulmonale.
  • A venous blood gas pH ≤7.34 has good sensitivity and specificity for acidaemia (pH ≤7.35) but does not reliably predict arterial PaCO2 and cannot diagnose hypercapnic respiratory failure. An arterial blood gas is necessary to assess the need for NIV.
  • Ward-based NIV can reduce the requirement for HDU/ICU admission but should be conducted in an appropriately monitored setting with trained clinical staff.
  • At the time of initiating NIV, the goals and limits of care should be considered and a clear written escalation plan established.

Airway clearance techniques

  • Patients with excess sputum production benefit from airway clearance techniques during an exacerbation.
  • Airway clearance techniques should be individualised to the patient.

Before discharge

  • Ensure that adequate education is provided regarding COPD management, including smoking cessation, use of inhalers, and the development of an acute management/action plan.
  • Ensure that clear follow-up plans are in place, as the risk for further exacerbations is greatest following an exacerbation.
  • Ensure that there is sufficient support at home for the patient to manage during their recovery. This may require social work, physiotherapy, occupational therapy, and other allied health input.
  • Recommend primary care follow-up within two weeks.
  • Consider follow-up spirometry if this has not been done.
  • Refer to a pulmonary rehabilitation programme unless recently completed or contra-indicated.

After an exacerbation

  • Having an exacerbation is the greatest risk factor for a further exacerbation.
  • Each exacerbation is associated with a faster decline in lung function and increased mortality.
  • Exacerbations should be used as an opportunity to review the pharmacological and non-pharmacological strategies in place and to develop a personalised action plan.
  • Review of inhaler technique and adherence should occur in every patient following an exacerbation (see section Optimise knowledge of COPD and adherence to treatment).
  • All medications should be reviewed following an exacerbation of COPD and adjusted as appropriate.
  • Refer to a pulmonary rehabilitation programme unless recently completed or contra-indicated.

Box 4: Key messages for exacerbation management in COPD.

Figure 1: Pre-hospital management of acute exacerbation of COPD.

Figure 2: Hospital management of exacerbation of COPD.

Comorbidities and treatable traits

Identify and manage comorbidities

  • People with COPD often have other conditions. Lung cancer, bronchiectasis, ischaemic heart disease, congestive heart failure, diabetes, anxiety, depression, gastro-oesophageal reflux, and osteoporosis are all more common among people with COPD than in the general population.
  • These conditions can negatively impact on the management of COPD and, in turn, the presence of COPD can negatively impact on the treatment and prognosis of comorbid conditions.
  • A systematic approach to the assessment and management of comorbidities has been proposed as part of the treatable traits concept. This approach recommends that management is personalised to the individual, with the use of biomarkers where available, and the systematic multidimensional identification and treatment of all comorbidities or disease characteristics, which may contribute to the patient’s presentation and are potentially amenable to treatment (‘treatable traits’). There is preliminary evidence to suggest that this approach improves quality of life.

Lung cancer

  • There is a strong association between COPD and lung cancer, more so than is explained by the shared risk factor of smoking.
  • Haemoptysis is not a symptom of COPD and should be investigated to rule out lung cancer. Unexplained weight loss and a new persistent cough may also be symptoms of lung cancer.
  • Although patients with severe COPD may be unfit for surgery because of poor lung function, they may still be eligible for curative-intent cancer treatment. Newer radiotherapy techniques such as stereotactic ablative radiotherapy can deliver curative-intent treatment with little effect on lung function.
  • A person with lung cancer who has a poor life expectancy due to advanced COPD or other comorbidities may not require any treatment for an early stage, slow-growing and asymptomatic lung cancer.

Cardiac disease

  • People with COPD are at increased risk of ischaemic heart disease and cardiac failure because of the shared risk factors of age and smoking status. Severe COPD is associated with pulmonary hypertension and cor pulmonale. People with COPD should have a cardiovascular risk assessment done.
  • Smoking cessation reduces cardiovascular risk as well as the rate of lung function decline in COPD.
  • If beta-blockers are needed for cardiac disease, then cardioselective beta-blockers such as bisoprolol should be used. Inhaled SABA and LABA therapy can be used alongside cardioselective beta-blocker therapy.
  • Bronchodilators may have pro-arrhythmic effects. There is an acceptable safety profile for long-acting beta agonist and anticholinergic bronchodilators at prescribed doses, but caution should be employed with high doses of short-acting beta2-agonists during a COPD exacerbation or when using theophylline. There may be a risk of developing arrhythmias such as atrial fibrillation in these situations.

Mental health disorders

  • Anxiety and depression are common in COPD. Breathlessness, activity limitation, and loss of social connections are risk factors for the development of anxiety and depression. In turn, anxiety and depression increase the perception of breathlessness and may increase symptom burden, leading to a reduction in social activity and exercise avoidance.
  • Treatment of anxiety and depression should not change in the presence of COPD. Participation in a pulmonary rehabilitation programme reduces anxiety and depression scores.
  • Smoking and therefore COPD are common among people with mental health disorders, and COPD may be underdiagnosed and undertreated in this group.

Other comorbidities

  • The presence of gastro-oesophageal reflux is a risk factor for COPD exacerbations, possibly due to lung injury from aspiration. It is sensible to treat reflux symptoms with proton pump inhibitors, although it has not been proven that this reduces the risk of COPD exacerbations.
  • Allergic rhinitis may increase COPD symptoms.
  • Obstructive sleep apnoea syndrome and obesity-hypoventilation syndrome lead to worse night-time hypoxaemia in people with COPD. Appropriate treatment of these comorbidities with nocturnal continuous positive airways pressure (CPAP) or NIV can improve sleep quality, reduce pulmonary hypertension, and may reduce mortality.
  • Identification of coexisting non-COPD lung disease such as bronchiectasis or interstitial lung disease is an opportunity to use disease-specific treatment to improve respiratory symptoms. (See also section Asthma and COPD overlap (ACO)).

Multiple comorbidities and frailty

  • People with multiple comorbidities are more vulnerable to adverse outcomes including mortality. COPD treatments may impact on control of comorbid conditions. For example, prednisone taken for a COPD exacerbation can adversely affect diabetic glycaemic control.
  • COPD is a risk factor for falls. Hypoxemia, dyspnoea, and fatigue are associated with impaired balance.
  • Cognitive impairment is common in COPD, particularly during exacerbations. This can affect COPD disease education and adherence to medication and self-management plans.
  • Some COPD treatments such as pulmonary rehabilitation or lung transplantation may not be able to be delivered safely due to comorbidities.
  • People with COPD and comorbidities may be taking many medications. COPD medication can add to the problem of polypharmacy and we recommend a regular medicines review.

Asthma and COPD overlap (ACO) (Box 5)

Patients with features of both asthma and COPD appear to have a worse prognosis than those with COPD alone according to many, but not all, studies. Treatment recommendations are based on expert opinion only because asthma and COPD overlap (ACO) patients have largely been excluded from controlled trials.

  • Patients with ACO are broadly characterised by the following:|
    – asthma diagnosed before aged 40 years old, and
    – a smoking history of >10 pack years or comparable aero-pollutant exposure, with
    – highly variable expiratory volumes (FEV1 >400ml) and/or
    – elevated eosinophils (>0.3x106).
  • We recommend inhaled corticosteroids in low or moderate doses to target asthma-like inflammatory pathways in combination with single or dual long-acting bronchodilator.
  • We recommend ICS/LABA as initial therapy followed by the addition of LAMA (ie, triple therapy) if there are persistent symptoms or exacerbations.
  • We recommend using either an asthma or COPD action plan depending on the dominant clinical features.
  • Although recent studies in asthma favour the use of combined budesonide/formoterol reliever inhalers, the role of these inhalers in ACO remains uncertain, as there are no data to support this approach at this time.

Box 5: Principles of management of asthma–COPD overlap.

End-of-life care

Advance care planning

End-of-life care is important in advanced COPD. As the goals of care change, patients and their family/whānau require realistic advice and support to make informed decisions and plan for the future.

  • Discussion about advance care plans and advance directives should be undertaken as part of usual management at a suitable time in the disease course.
  • Advance care plans can be made at any stage of the disease and do not need to wait until the patient is approaching the end of life.
  • Most patients with life-limiting conditions prefer to identify their goals of treatment and discuss preferences for end-of-life care early. Good communication with patients who have a terminal illness is associated with better end-of-life care and fewer medical interventions.
  • A useful strategy when deciding whether end-of-life discussions are appropriate is to consider the question: “Would I be surprised if this patient died in the next 12 months?”
  • The following features should also prompt health practitioners to consider initiating discussions about advance care plans, centred on the patient’s preferences for end-of-life care:
    – Breathless at rest or on minimal exertion or housebound
    – Weight loss or cachexia
    – FEV1<30% of predicted
    – Meets criteria for long-term oxygen therapy
    – Two or more hospitalisations in the previous year for exacerbations
  • An admission with respiratory failure requiring non-invasive ventilation
  • A structured advance care plan will reduce the burden of setting the ceiling of care by unfamiliar staff and family members during an acute admission and allow implementation of a patient’s choice of health care when they are no longer capable of expressing their choice.
  • In general, patients and their family/whānau want an honest conversation that is balanced between realistic information and appropriate hope.
  • Consider involving local hospice and/or palliative care services.

More details and Advance Care Plans are available at: www.advancecareplanning.org.nz.

Palliation of dyspnoea

Morphine

  • Morphine reduces respiratory effort and the sensation of breathlessness.
  • Lower doses are usually required than used for pain (eg, 2.5mg to 5mg every four hours, or as required).
  • Consider lower doses for older patients.
  • Dose can be gradually titrated as for pain. But aim for comfort rather than resolution of dyspnoea.
  • If greater than two doses per day of morphine liquid are regularly being used with effect, convert to low-dose, slow-release morphine capsules (eg, 10 mg twice a day). In this case, it would also be reasonable to make small amount of as-required morphine liquid (2.5mg to 5 mg as required) available to the patient.
  • Oral morphine doses are generally <40 mg per day when used for dyspnoea alone.

Benzodiazepines

  • Evidence for benzodiazepines for breathlessness in COPD is lacking. Benzodiazepines may be harmful and are not recommended as a first-line treatment of breathlessness.
  • Benzodiazepines increase the risk of falls among patients with COPD and may also increase the risk of COPD exacerbations and pneumonia.
  • Benzodiazepines should not be used in patients at risk of hypercapnic respiratory failure.

Appendices

Appendix 1: The four-step COPD consultation.

These steps are likely to need more than one consultation.

Appendix 2: COPD assessment test (CAT): https://assets-global.website-files.com/5e332a62c703f6340a2faf44/602c8a966b39518510d20f2c_4878%20-%20appendix%202.pdf

Appendix 3: COPD action plan: https://assets-global.website-files.com/5e332a62c703f6340a2faf44/602c8a9603e1140b3fac6394_4878%20-%20appendix%203.pdf

Appendix 4: Breathlessness strategies for COPD: https://assets-global.website-files.com/5e332a62c703f6340a2faf44/602c8a9676d8e10447d74284_4878%20-%20appendix%204.pdf

Appendix 5: Breathlessness strategies: quick reference guide: https://assets-global.website-files.com/5e332a62c703f6340a2faf44/602c8a969551dd13aba750f8_4878%20-%20appendix%205.pdf

Appendix 6: Useful documents and resources.

Summary

Abstract

The purpose of the Asthma and Respiratory Foundation of New Zealand’s COPD Guidelines Quick Reference Guide is to provide simple, practical, evidence-based recommendations for the diagnosis, assessment and management of chronic obstructive pulmonary disease (COPD) in clinical practice. The intended users are health professionals responsible for delivering acute and chronic COPD care in community and hospital settings, and those responsible for the training of such health professionals.

Aim

Method

Results

Conclusion

Author Information

Robert J Hancox: Waikato District Health Board, Hamilton; University of Otago, Dunedin. nStuart Jones: Middlemore Hospital, Counties Manukau, Auckland. Christina Baggott: Medical Research Institute of New Zealand. David Chen: Canterbury Clinical Network, Christchurch. Nicola Corna: Middlemore Hospital, Counties Manukau, Auckland. Cheryl Davies: Tu Kotahi Māori Asthma Trust. James Fingleton: Medical Research Institute of New Zealand; Capital & Coast District Health Board, Wellington. Jo Hardy: Medical Research Institute of New Zealand. Syed Hussain: Auckland District Health Board. Betty Poot: Hutt Valley District Health Board, Lower Hutt; School of Nursing, Midwifery and Health Practice, Victoria University of Wellington, Wellington. Jim Reid: University of Otago, Dunedin; Best Practice Advisory Centre (BPAC), Dunedin. Justin Travers: Hutt Valley District Health Board, Lower Hutt. Joanna Turner: Asthma and Respiratory Foundation of New Zealand. Robert Young: Auckland District Health Board.

Acknowledgements

We thank Leanne Te Karu and Teresa Demetriou for their valued contribution towards these guidelines.

Correspondence

Robert Hancox, Department of Preventive & Social Medicine, Dunedin Medical Campus, University of Otago, +3 479 8512 (phone), +3 479 7298 (fax)

Correspondence Email

bob.hancox@otago.ac.nz

Competing Interests

Dr Young reports: I receive honorarium from GSK for giving educational talks on COPD management or attending advisory meetings. However, this did not impact on my contribution to this guideline. Dr Baggott reports personal fees from Astra Zeneca, personal fees from Novartis, outside the submitted work. Nicola Corna reports other from Boehringer Ingelheim, other from Astra Zeneca, other from Astra Zeneca, grants from Adherium, outside the submitted work. Dr Fingleton reports grants, personal fees and non-financial support from AstraZeneca, grants from Genentech, grants, personal fees and non-financial support from GlaxoSmithKline, personal fees and non-financial support from Boheringer lngleheim, outside the submitted work. Dr Hardy reports non-financial support from Astrazeneca, outside the submitted work. Dr Hancox reports grants from Astra Zeneca, grants from GlaxoSmithKline, personal fees from Menarini, other from Boehringer Ingelheim, outside the submitted work.

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