NZ COPD GUIDELINES 2021 - NZ Respiratory Guidelines
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NZ COPD GUIDELINES 2021
NZ COPD GUIDELINES
New Zealand
COPD Guidelines:
Quick Reference Guide
Robert J Hancox, Stuart Jones, Christina Baggott, David Chen,
Nicola Corna, Cheryl Davies, James Fingleton, Jo Hardy, Syed Hussain,
Betty Poot, Jim Reid, Justin Travers, Joanna Turner, Robert Young
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.
C
hronic obstructive pulmonary disease COPD is often confused with asthma.
(COPD) encompasses chronic bronchi- They are separate diseases, although some
tis, emphysema, and chronic airflow asthmatics develop irreversible airflow
obstruction. It is characterised by persistent obstruction and some patients with COPD
respiratory symptoms and airflow limitation have a mixed inflammatory pattern.
that is not fully reversible. Asthma–COPD overlap (ACO) may be present
COPD is associated with a range of patho- when it can be difficult to distinguish
logical changes in the lung. The airflow between the diseases, or in patients who
limitation is usually progressive and asso- have both conditions.3
ciated with an inflammatory response to Guidelines review
inhaled noxious particles or gases.1,2 The following documents were reviewed
Symptoms include cough, sputum to formulate this Quick Reference Guide:
production, shortness of breath, and COPD-X Australian and New Zealand
wheeze. At first, these are often ascribed to Guidelines 20201 and the Global Initiative
“a smokers cough”, “getting old” or being for Chronic Obstructive Lung Disease
“unfit”. Cough and sputum production may (GOLD) 2020.2 A systematic review was
precede wheeze by many years. Symptoms not performed, although relevant refer-
may worsen and become severe and ences were reviewed when necessary.
chronic, but not all of those with cough and Readers are referred to the COPD-X and
wheeze advance to progressive disease. GOLD documents for the more compre-
Patients with COPD often have exacerba- hensive detail and references that they
tions, when symptoms become much worse provide. References are only provided
and require more intensive treatment. These when they differ from the COPD-X
exacerbations have a significant mortality. guidelines.
Many patients have extra-pulmonary effects Grading
and important co-morbidities that contribute No levels of evidence grades are provided,
to the severity of the disease. Important due to the format of the Quick Reference
co-morbidities include asthma, bronchiec- Guide. Readers are referred to the above
tasis, lung cancer and heart disease. COPD can documents for the level of evidence on
lead to debilitation, polycythaemia, osteopo- which the recommendations in this Quick
rosis, cachexia, depression and anxiety. Reference Guide are based.
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Guideline development group Expiry Date
This group included representatives from a The expiry date for the guidelines is 2025.
range of professions and disciplines relevant
to the scope of the guidelines. The group did COPD in Māori
not include consumer representation.
Māori rights in regard to health,
Robert J Hancox, Stuart Jones, Christina recognised in Te Tiriti o Waitangi and other
Baggott, James Fingleton, Jo Hardy, Syed national and international declarations,
Hussain, and Justin Travers are respiratory promote and require both Māori partici-
physicians. Robert Young is a general pation in health-related decision making as
physician. David Chen is a respiratory well as equity of access and health outcomes
physiotherapist. Cheryl Davies is manager for all New Zealanders.
of the Tu Kotahi Maori Asthma Trust.
• The burden of COPD among Māori
Nicola Corna and Betty Poot are respiratory
is one of the most significant health
nurse practitioners. Jim Reid is a general
disparities in New Zealand: hospital-
practitioner. Joanna Turner is a pharmacist
isation rates for Māori are 3.5 times
and research and education manager at
higher than non-Māori, non-Pacific,
the Asthma and Respiratory Foundation of
and non-Asian rates, and COPD
New Zealand.
mortality for Māori is 2.2 times
Peer review higher.8
The draft guidelines were peer-reviewed • Māori whānau also have greater
by a wide range of respiratory health experts exposure to environmental triggers
and representatives from key professional for COPD, such as smoking and poor
organisations, including representatives from housing.
Asthma New Zealand, the Australian College
• This burden of COPD translates to
of Emergency Medicine, Hutt Valley District
large inequities in lost years of healthy
Health Board, the Medical Research Institute
life and underscores the urgent need
of New Zealand, the New Zealand Medical
for health service models to address
Association, the New Zealand Nurses Organ-
high and growing need for COPD
isation Te Rūnanga o Aotearoa, the NZNO
treatment in Māori.
College of Respiratory Nurses, Physiotherapy
New Zealand, the Royal New Zealand College • Māori should be considered a
of General Practitioners, the New Zealand high-risk group requiring targeted
branch of the Thoracic Society of Australia care. This should address risk factors
and New Zealand, and Wellington Free such as poor housing, overcrowding,
Ambulance. health literacy, inadequate tailoring of
health information, obesity, smoking,
Dissemination plan and poor access to pulmonary rehabil-
The guidelines will be translated into tools itation and healthcare services.
for practical use by health professionals
• Māori have much worse lung function
and used to update health pathways and
for given levels of smoking,9 and the
existing consumer resources. The guide-
burden of COPD affects Māori 15–20
lines will be published in the New Zealand
years younger than non-Māori.10 This
Medical Journal and on the Asthma and
makes smoking cessation even more
Respiratory Foundation of New Zealand
important for Māori, and COPD should
(ARFNZ) website, as well as being dissem-
be considered at a younger age among
inated widely via a range of publications,
Māori smokers.
training opportunities, and other commu-
nication channels to health professionals, • There is a very high incidence of lung
nursing, pharmacy and medical schools, cancer among Māori.
primary health organisations, and district Major barriers to good COPD management
health boards. for Māori include poor access to care, inat-
Implementation tention to culturally accepted practices,
The implementation of the guidelines by discontinuous and poor-quality care, and
organisations will require communication, inadequate provision of understandable
education, and training strategies. health information. As Māori place a high
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value on whakawhanaungatanga (the • https://thehub.swa.govt.nz/
making of culturally meaningful connec- resources/pacific-mental-
tions with others), the absence of culturally health-services-and-workforce-
appropriate practices can hinder attendance moving-on-the-blueprint/
in mainstream pulmonary rehabilitation • https://whanauoraresearch.
programmes.11 Cultural safety and a co.nz/wp-content/uploads/
pro-equity approach is essential. formidable/Fonofalemodelex-
It is recommended that: planation1-Copy.pdf
• Healthcare providers should
undertake clinical audit or other qual- Pathogenesis
ity-improvement activities to monitor Most people with COPD will have smoked
and improve COPD care and outcomes cigarettes or inhaled noxious particles
for Māori. causing lung inflammation. Airway inflam-
• A systematic approach to health mation is a normal response to smoking but
literacy and COPD education for Māori seems to be accentuated in those who go on
whānau is required. to develop COPD. Some people develop COPD
• Healthcare providers should support without smoking or apparent exposures.
staff to develop cultural safety skills COPD may also develop in patients with other
for engaging Māori with COPD and chronic lung diseases such as asthma.
their whānau. The inflammatory process in COPD is
• Assess patients using a Māori model mostly neutrophil, macrophage, and T-lym-
of care: https://www.health.govt.nz/ phocyte mediated. This inflammation
our-work/populations/maori-health/ leads to narrowing of peripheral airways
maori-health-models. and destruction of alveoli, causing airflow
obstruction and decreased gas transfer.
Māori leadership is required in the devel-
opment of COPD management programmes, Inflammation, fibrosis, and sputum
including pulmonary rehabilitation, to production in small airways causes air
improve access to COPD care and facil- trapping during expiration leading to hyper-
itate ‘wrap around’ services that address inflation. This reduces inspiratory capacity
the wider determinants of health (such as and causes shortness of breath on exercise.
housing, financial factors, access to health In patients presenting at a young age
care and access to pulmonary rehabilitation (particularly those younger than 40), alpha-1
programmes) for Māori with COPD. antitrypsin deficiency should be considered.
This genetic defect causes a reduction in
COPD in Pacific people the major anti-protease in lung paren-
chyma, leaving the lung susceptible to the
Similar considerations apply to Pacific
destructive effects of neutrophil elastase
people, who also have a disproportionate
and other endogenous proteases, which
burden of COPD. Pacific people’s hospital-
are released as part of the inflammatory
isation rates are 2.7 times higher than those
response to smoking.
of other New Zealanders.8
It is recommended that:
• Pacific people should also be
Diagnosis
A diagnosis of COPD should be considered
considered a high-risk group
in anyone who presents with cough, sputum
requiring targeted care.
production, wheeze, or shortness of breath,
• The approach should include particularly those above the age of 40
addressing risk factors such as years. There is usually a history of ciga-
poor housing, overcrowding, health rette smoking or exposure to smoke other
literacy, obesity, smoking and poor noxious substances.
access to pulmonary rehabilitation
• Physical examination and chest x-ray
and healthcare services.
are rarely diagnostic in early COPD,
• Healthcare providers should consider but they may be valuable in excluding
using a Pacific model of care, such as a other diagnoses and co-morbidities
Fonofale model:
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such as lung cancer, pulmonary limitation, disease progression and response
fibrosis and cardiac failure. to treatment.
• Other causes for the patient’s Spirometry
symptoms should always be Spirometry is the most useful test of
considered, as common comorbid- lung function to diagnose and assess the
ities such as heart disease and obesity severity of COPD. This may be done both
may co-exist with COPD and in some before and after a bronchodilator to assess
patients will be the dominant cause of reversibility, but the diagnosis and severity
breathlessness. are determined by post-bronchodilator
• The diagnosis of COPD should measurements.
be confirmed by spirometry (see • Irreversible airflow obstruction is
Spirometry). If this is not available indicated by a post-bronchodilator
in primary care, patients should forced expiry volume in once second
be referred for this. There are few to forced vital capacity (FEV1/FVC)
contra-indications, but a small ratio
NZ COPD GUIDELINES
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.)
Classification of severity of chronic obstructive pulmonary disease (COPD)
Mild Moderate Severe
Typical Few symptoms Breathless walking on Breathless on minimal
symptoms level ground exertion
Breathless on moder- Increasing limitation Daily activities severely
ate exertion of daily activities curtailed
Little or no effect on Recurrent chest infec- Exacerbations of in-
daily activities tions creasing frequency and
severity
Cough and sputum Exacerbations requir-
production ing oral corticosteroids
and/or antibiotics
Lung function FEV1≈60–80% predicted FEV1≈40–59% predicted FEV1
NZ COPD GUIDELINES
consensus ATS/ERS guidelines.4 This • Oral bupropion, varenicline, and
ranges from 4–6 hours for a short- nortriptyline have been shown to be
acting beta agonist (SABA) to 48 hours effective and should be considered in
for an ultra long-acting beta agonist those patients struggling to give up
(LABA). despite nicotine replacement therapy.
• Spirometry is repeated at least 15 • Most of these are fully funded in New
minutes after giving a bronchodi- Zealand and a prescription for this
lator (usually 400mcg salbutamol via should be discussed with a health
spacer). professional.
• Many patients with COPD will have • Referral to a local smoking cessation
some improvement after a broncho- support service is recommended.
dilator (“partial reversibility”), but if E-cigarettes and vaping are probably
spirometry becomes normal (FEV1/ less harmful to health than smoking, but
FVC>0.7* and FEV1>80% predicted), short-term studies suggest that they are
COPD is excluded (by definition). not risk free.5 E-cigarettes and vapes that
• The consensus definition of a signif- contain nicotine are highly addictive.
icant bronchodilator response is • E-cigarettes used within the context
arbitrarily defined as a ≥12% change of a supportive smoking cessation
from baseline with an absolute programme have been shown to aid in
improvement of ≥200ml, but this does smoking cessation in selected groups
not predict who will benefit from of motivated patients.
bronchodilator treatment.
• The long-term safety of e-cigarettes
• If the response to bronchodilator is and vaping have not been shown.
substantial (>400mL improvement in Smokers using e-cigarettes or vaping
FEV1) then asthma or Asthma-COPD to quit smoking should be advised
Overlap is likely. to stop using e-cigarettes and vaping
as soon as possible after quitting
Non-pharmacological smoking.
management (Box 1) • No e-cigarette or vape is currently
approved as a smoking cessation tool.
Smoking cessation
• E-cigarettes and vapes should never
Stopping smoking is the most important
be used near an oxygen source, as this
treatment for COPD: every person who
is a fire risk.
is still smoking should be offered help to
quit. Reducing smoking-related health risks Physical activity
requires complete cessation of all tobacco Patients with COPD benefit from physical
and other smoked products, including activity and should be encouraged to:
marijuana/cannabis. • Be active on most, preferably all, days
• All forms of nicotine replacement of the week.
therapy, in association with smoking • Do at least 20–30 minutes of exercise
cessation support, are useful in aiding per day. More is better.
smoking cessation and increase the
• Exercise to an intensity that should
rate of quitting.
cause the patient to “huff and puff” or
*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
NZ COPD GUIDELINES
feel breathless: Getting out of breath disorders caused by COPD and
will not cause harm. improve exercise capacity, but they
• Do muscle strengthening activities on have inconsistent effects on dyspnoea
two or more days each week. or health-related quality of life scores.
• Constant load threshold inspiratory
Pulmonary rehabilitation
muscle training improves inspi-
Pulmonary rehabilitation should be
ratory muscle strength, quality of life,
offered to all patients with COPD. Although
dyspnoea, and exercise capacity.
there may be barriers to attending
pulmonary rehabilitation classes, there are • Hand-held fan therapy: the airflow
a variety of ways to deliver pulmonary reha- and cooling effects of the fan,
bilitation to patients in different settings alongside other breathlessness
depending on local respiratory services and management strategies, such as relax-
patient preferences. ation, pacing, and positioning, can
reduce dyspnoea.
• Pulmonary rehabilitation reduces
breathlessness, improves quality Other things that may help:
of life, and reduces depression in • Hospital clinical teams working with
patients with COPD. the primary healthcare team can help
• Patients gain significant benefit enhance quality of life and reduce
from rehabilitation regardless of the disability for patients with COPD.
degree of breathlessness, but the most • Patients may also benefit from local
breathless patients benefit the most. support groups.
• Exacerbations of COPD are an indi- • Consider including a cognitive
cation for referral to pulmonary behavioural component in the
rehabilitation and an early return to self-management plan to assist with
pulmonary rehabilitation after exacer- reducing anxiety and breathlessness.
bation should be encouraged. This has • Consider screening for urinary incon-
been shown to reduce further hospi- tinence related to cough.
talisations and may reduce mortality.
Other useful resources are given in
• Exercise training is the cornerstone Appendix 4 and 5.
of pulmonary rehabilitation, and
regular post-rehabilitation exercise is Sputum management/sputum
required to sustain the benefits. clearance techniques
• The benefits of pulmonary rehabili- Patients with chronic sputum production
tation decline over time and repeat may benefit from seeing a physiotherapist
attendance at pulmonary reha- (ideally a respiratory physiotherapist) for an
bilitation programmes should be individualised chest clearance plan. Airway
encouraged in patients with func- clearance techniques enhance sputum
tional decline or exacerbations. clearance, reduce hospital admissions, and
improve health-related quality of life, and
• If someone is unable to access a
they may also improve exercise tolerance
pulmonary rehabilitation programme,
and reduce the need for antibiotics.
an in-home exercise programme
should be considered. • A wide variety of airway clearance
techniques are available. No one tech-
Breathlessness management nique is superior for all patients.
strategies • The choice of technique should be
In addition to pulmonary rehabili- based on the clinician’s assessment,
tation, patients may benefit from seeing resource availability, and patient
a respiratory physiotherapist for individ- acceptability.
ualised breathing exercises or breathless
management strategies: Nutrition
Both malnutrition and obesity are
• Diaphragmatic breathing and
common and contribute to morbidity and
pursed lips breathing exercises may
mortality in COPD. Poor eating habits,
benefit some patients. These support
sedentary lifestyles, smoking, and cortico-
and correct the breathing pattern
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steroid use further compromise nutritional reduction surgery. Neither procedure
status. increases life expectancy. Both have signif-
• The key goals of nutritional icant complication rates and are only
management are to eat a balanced performed in specialist centres after careful
diet, to achieve and maintain a multi-disciplinary assessment.
healthy weight, and to avoid uninten- Bullectomy
tional weight loss. Consider referral Bullectomy can be considered where there
to a dietician, or high-calorie nutri- is a very large bulla compressing other
tional supplements, for those who are lung tissue. Removing the bulla allows the
malnourished. preserved lung tissue to function better.
• There is evidence that weight loss is
beneficial for those who are obese. Lung volume reduction surgery
Lung volume reduction surgery can
• Unintentional weight loss should be
improve exercise capacity in people with
investigated for potential malignancy.
upper-lobe predominant emphysema. The
Housing surgery has a significant early mortality, but
There is good evidence that a warm, dry, there is no difference in long-term mortality.
and smoke-free home is associated with
better asthma control, and it is likely that
Interventional bronchoscopy
Bronchoscopic lung volume reduction
the same is true for COPD.
approaches have been developed as alter-
Assisted ventilation natives to lung volume reduction surgery.
Non-invasive ventilation (NIV) with These aim to reduce gas-trapping and
bi-level positive airway pressure reduces improve lung mechanics in advanced
mortality and need for intubation in patients emphysema, which can lead to improved
admitted to hospital with acute hypercapnic lung function, symptoms, and quality of life
respiratory failure as a result of an exacer- in carefully selected patients. Endobronchial
bation of COPD (see section Management). In valve therapy has the most evidence and is
most instances, NIV is not required once the available in New Zealand. It is only effective
patient has recovered. in those with intact fissures and no collateral
• People who have chronic hypercapnic ventilation as one-way valves are inserted
respiratory failure, despite adequate to cause collapse of lung segments. Endo-
treatment, and have needed assisted bronchial valve therapy does not reduce
ventilation (invasive or non-invasive) mortality and has significant complication
during an exacerbation, or with rates.
worsening hypercapnia on long-term Lung transplantation
oxygen therapy, should be referred to Consideration for lung transplantation
a specialist centre for consideration of is appropriate in younger patients (usually
long-term NIV.
NZ COPD GUIDELINES
Box 1: Key messages for non-pharmacological management of COPD.
A four-step consultation plan for COPD is shown in Appendix 1.
Recommendations:
• Smoking cessation is the most important component of management, and every
patient who is still smoking should be offered help to quit.
• Offer pulmonary rehabilitation to all patients with COPD.
• Promote regular exercise (20–30 minutes per day).
• Address obesity and under-nutrition.
• Some patients will benefit from review by a respiratory physiotherapist and
breathing exercises.
• Individual breathlessness plans, including handheld fan therapy, can help manage
symptoms.
• A subset of carefully selected patients may benefit from thoracic surgery, endo-
bronchial valve therapy or referral for transplantation. These options should be
considered as part of respiratory specialist review in secondary care.
• These factors impact on COPD and the rationale for treatment, to
management, appropriate inhaler clarify misunderstandings, and to
technique, adherence to treatment work to remove barriers to adherence
and appropriate use of self-man- and good self-management. It is
agement plans. important to provide information to
• These factors also have a considerable the patient and whānau in a format
impact on the success of smoking that they can understand.
cessation. Develop an action plan
• Awareness of the social and cultural Personalised action plans (self-man-
factors will enhance communication agement plans) improve quality of life and
between clinicians and patients and reduce hospital admissions and should be
improve health outcomes. offered to all people with COPD.
• There are many practical challenges • Action plans should be personalised
for people living with COPD, such as and focus on recognising and treating
completing everyday tasks, holding deteriorating symptoms.
down a job, and having access to • Patients at risk of exacerbations may
transport. Awareness of these chal- be offered antibiotics and prednisone
lenges and referral to support services to have at home as part of their action
where available can be beneficial. plan. The patient should be advised of
Optimise knowledge of COPD and a timeframe for clinical review once
they have started these medicines for
adherence to treatment
an acute exacerbation of COPD.
• Patient understanding of the disease,
appropriate inhaler technique and • Action plans should be checked at
adherence to treatment are important each COPD review.
factors in COPD management. The Asthma and Respiratory Foundation
• There are many inhalers available to of New Zealand’s COPD Action Plan is shown
treat COPD, and people can easily get in Appendix 3.
confused about these. Demonstrate Electronic versions are available at: www.
the use of the inhalers and ensure that nzrespiratoryguidelines.co.nz.
patients can use them correctly.
Develop a breathlessness plan
• Clinicians should ask about the • A breathlessness plan can reduce the
patient’s understanding of the disease severity and impact of breathlessness.
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Interventions and techniques that long-acting muscarinic antag-
can improve breathlessness include onist (LAMA) such as tiotropium,
self-management education, breathing glycopyrronium, or umeclidinium
exercises, sitting upright and leaning is recommended, unless there is
forwards (‘positioning’), using pursed evidence of asthma/COPD overlap
lip breathing, and a hand-held fan. (see Asthma and COPD overlap (ACO)).
• Oxygen is not an effective treatment Do not continue to use ipratropium
for breathlessness in patients who are in patients taking a LAMA, except in
not hypoxic. emergencies.
• Smoking cessation also improves • It is not necessary to have a trial of
breathlessness. regular short-acting bronchodilators
before starting a LAMA if symptoms,
Asthma and Respiratory Foundation of
exacerbation history or spirometry
New Zealand’s ‘Breathlessness Strategies
suggest that a long-acting bronchodi-
for COPD’ is shown in Appendix 4 and is
lator is desirable.
available at www.nzrespiratoryguidelines.
co.nz. • Both LAMAs and LABAs improve lung
function, symptoms and quality of
Pharmacological life, but LAMAs are recommended as
the first-line long-acting medication
management (Box 2) for COPD because they reduce exac-
The purpose of pharmacological erbation risk and have fewer side
management in COPD is symptom control effects. If LAMAs are contra-indicated,
and prevention of exacerbations, with the a long-acting beta agonist (LABA) such
aim of improving quality of life. as salmeterol, formoterol, or inda-
caterol is recommended.
• Check inhaler adherence and inhaler
technique regularly. Make sure that • In patients who remain breathless or
these are optimal before escalating who continue to exacerbate despite
treatment. treatment with a single long-acting
bronchodilator, dual LAMA/LABA
• Treatment escalation should follow a
therapy is recommended (eg, glycopy-
stepwise approach based on breath-
rronium/indacaterol, umeclidinium/
lessness and exacerbation frequency.
vilanterol, or olodaterol/tiotropium).
It should take into account patient
Combination therapy with a LABA and
preferences, regimen complexity, cost,
LAMA improves lung function, reduces
and side effects.
symptoms, and reduces exacerbations
• Effects of treatment on dyspnoea compared to either drug alone.
should be apparent within six weeks.
• LABA/LAMA is preferred over
• Effects on exacerbation frequency inhaled corticosteroid (ICS)/LABA as
may need to be assessed over 6 to 12 initial therapy for most patients with
months. frequent exacerbations because ICS
Inhaled medication for COPD increases the risk of pneumonia.
• Short-acting beta2 agonists (SABA: • These medications may have risks,
salbutamol or terbutaline) and the particularly at higher doses in patients
short-acting muscarinic antagonist with cardiac disease. If there is no
(SAMA: ipratropium), either individ- evidence of benefit, consider stopping
ually or in combination, can be taken them.
as-needed to provide short-term relief
• Patients with an eosinophilic pattern
of breathlessness. Short-term response
of disease may benefit from ICS/LABA
to SABA or SAMA (reversibility testing)
instead of LABA/LAMA. Retrospective
does not predict benefit from long-
analyses suggest that blood eosinophil
acting bronchodilator therapy.
counts predict the benefit of ICS in
• For patients with ongoing dyspnoea preventing exacerbations: people with
despite as-needed SABA, SAMA, or blood eosinophil countsNZ COPD GUIDELINES
Box 2: Key messages for pharmacological management of COPD.
A suggested four-step consultation plan for COPD is shown in Appendix 1.
Recommendations:
• Inhaler technique, device suitability, and adherence to treatment should be
reviewed regularly and before any medication changes.
• SABAs and SAMAs can be used for symptom relief.
• We suggest a LAMA as the first-line long-acting bronchodilator, both for breath-
lessness and reduction of exacerbation risk.
• Escalate to LABA/LAMA if LAMA does not control breathlessness/exacerbations.
• The main role for ICS is to prevent exacerbations in patients with frequent
exacerbations.
• Higher blood eosinophils are associated with a greater response to ICS and may
identify patients who should receive ICS/LABA in preference to LABA/LAMA.
• Patients with Asthma/COPD overlap should receive ICS irrespective of blood eosin-
ophils, lung function, and exacerbation frequency: preferably as combination ICS/
LABA
• Within each drug class, choice of treatment should be guided by a patient’s pref-
erence for inhaler device.
• Treatment may be escalated more quickly for patients with severe COPD or frequent
exacerbations.
• Provide all patients with a written/electronic personalised COPD action plan (see
appendix)
Do not*:
• Do not routinely prescribe a SAMA to patients on a LAMA.
• Do not prescribe long-term oral corticosteroids as maintenance therapy for COPD.
• Do not routinely prescribe theophylline.
• Do not use short-term response to bronchodilator (eg, reversibility testing) to predict
benefit from long-term bronchodilator therapy.
• Do not routinely prescribe nebulised therapy in patients with stable COPD.
• Do not withdraw ICS in patients with asthma/COPD overlap or raised blood
eosinophils.
*Do not recommendations are intended as guidance to highlight prescribing practices that
are rarely appropriate. Clinicians must consider the circumstances of individual patients to
decide whether they apply in a specific case.
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with counts ≥300cells/µL are most adherence to dual LAMA/LABA or ICS/
likely to benefit. A single blood test LABA therapy and optimal inhaler
may not be representative as eosin- technique.
ophil counts can vary over time. Blood • A subset of patients with persistent
eosinophil counts performed when a breathlessness and exercise
patient is taking oral steroids will not limitation, despite LABA/LAMA combi-
be informative. nation therapy, may benefit from
• An ICS should form part of the triple therapy with LABA, LAMA, and
regimen for any patient with asthma/ ICS. However, the increased risk of
COPD overlap. This should usually pneumonia with regular ICS should be
be prescribed as an ICS/LABA combi- considered.
nation inhaler to avoid the risk of • Direct escalation to dual or triple
LABA monotherapy in patients with therapy, without stepwise up-titration,
poor adherence to a separate ICS may be reasonable in the setting of a
inhaler. severe or recurrent exacerbations.
• Prescriptions should be based on drug
ICS withdrawal
class. Choice of specific LABAs and
• The risk of pneumonia in patients
LAMAs should be guided by patient
with severe COPD is increased with
preference and their ability to use
regular ICS. Withdrawing ICS should
the inhaler device. A list of inhalers
be considered if:
available in New Zealand is available
at www.nzrespiratoryguidelines. • There is no evidence of
co.nz. Dry-powder inhalers have benefit from ICS in terms of
a substantially lower impact on improved symptoms or fewer
greenhouse gases than pressurised exacerbations.
metered-dose inhalers. • The patient develops pneu-
• Six weeks is a reasonable timeframe to monia or other ICS adverse
assess improvement in breathlessness effects.
following a medication change. • The patient does not have a
• The COPD assessment test is an history of frequent exacerba-
eight-item questionnaire that can be tions and is stable.
used to measure the symptomatic • If ICS treatment is withdrawn, the
impact of COPD and response to patient should be reviewed at 4–6
therapy (see Assess severity and weeks to ensure that this doesn’t
Appendix 2). cause a deterioration in symptoms.
Role of triple therapy (LABA/LAMA/ • Withdrawal of ICS may not be appro-
ICS) priate if the blood eosinophil count
• Escalation to triple LABA/LAMA/ is elevated. A blood eosinophil count
ICS therapy should be considered ≥300cells/µL has been shown to be
in patients who continue to exac- associated with an increased exacer-
erbate (twice or more a year) despite bation risk after ICS withdrawal.
Table 3: Simplified maintenance inhaler management of COPD.
When treating Start with If needed, move on to
COPD without frequent LAMA LABA/LAMA
exacerbations
COPD with frequent LAMA LABA/LAMA (consider ICS/LABA
exacerbations if eosinophilia), then
LABA/LAMA/ICS
Asthma/COPD overlap ICS/LABA ICS/LABA plus LAMA
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• ICS should not be withdrawn in Oxygen therapy
patients with a diagnosis of asthma/ • Oxygen is a treatment for hypoxia, not
COPD overlap (see section Asthma and dyspnoea. Oxygen does not reduce the
COPD overlap (ACO)). sensation of breathlessness in patients
Additional therapies who are not hypoxic. Oxygen may not
• There is no evidence that routine use improve breathlessness even in those
of nebulisers is beneficial in patients who are hypoxic.
with COPD. • Oxygen is a drug therapy and should
• Theophylline has not shown be prescribed.
consistent benefits on exacerbation, • Long-term oxygen therapy has survival
lung function, symptoms, or quality of benefits for COPD patients with severe
life in randomised controlled trials. In hypoxaemia. It must be used for at
view of the narrow therapeutic index least 16 hours a day. The survival
and side-effect profile of theophylline, benefits are not apparent until months
we do not recommend its routine use or years after starting treatment.
in the management of COPD. • Evaluation of the patient and consid-
• There is no evidence of benefit from eration for long-term oxygen therapy
long-term oral corticosteroids. supply should be done by a specialist
• Long-term macrolide antibiotics, such respiratory service (Box 3). The causes
azithromycin and erythromycin, can of the hypoxia should be explored,
reduce risk of exacerbations over and the patient’s pharmacological and
one year in former smokers who non-pharmacological management
have exacerbations despite optimal should be optimised. A target satu-
inhaled treatment. Azithromycin is ration range and oxygen flow rate
not currently funded in New Zealand should be established.
for this indication. Long-term • Patients should adhere to the amount
macrolide therapy is associated of oxygen prescribed and be moni-
with significant risks, including tored for adverse effects.
bacterial resistance, gastrointestinal
and cardiovascular side effects, and
Flying with oxygen
Flying is generally safe for patients with
hearing impairment. Long-term
COPD, including those with chronic respi-
macrolides should rarely be initiated
ratory failure who are on long-term oxygen
without specialist advice.
therapy.
• Regular treatment with mucolytics
• Before flying, patients should ideally
(eg, erdosteine, carbocysteine, or
be clinically stable.
N-acetylcysteine) may reduce the risk
of exacerbations in some patients. • Supplemental oxygen is unlikely to
These treatments are not currently be required if the resting oxygen
funded in New Zealand. saturation is ≥95%, and is likely to be
required if oxygen saturation is ≤88%.
• In patients with severe and very
Patients with oxygen saturation values
severe COPD and a history of exac-
between these levels might require
erbations, PDE4 inhibitors (eg,
specialist assessment.
roflumilast) improve lung function,
reduce the risk of exacerbations, and • Those already on long-term oxygen
have modest benefits for symptoms therapy need an increase in flow rate
and quality of life. They have signif- of 1–2L per minute during the flight.
icant gastrointestinal side effects. • Patients receiving oxygen therapy will
These treatments are not currently need to contact the airline prior to
funded in New Zealand flying.
• Alpha-1 antitrypsin augmentation Vaccination
therapy may slow the progression of • Yearly influenza vaccination reduces
emphysema in patients with alpha-1 serious illness and death in patients
antitrypsin deficiency. This is not with COPD and should be actively
currently funded in New Zealand. promoted to patients with COPD.
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Box 3: Criteria for oxygen.
Criteria for supply of long-term oxygen therapy (LTOT):
• Assess when the patient’s respiratory condition is stable—at least six weeks after
hospital discharge or an acute respiratory illness.
• Arterial oxygen tension (PaO2) (measured by arterial blood gas) less than 7.3kPa
(55mmHg) indicates the need for long-term oxygen (oxygen saturation usuallyNZ COPD GUIDELINES
of serious co-morbidities, including Management (Box 4, Figures 1
heart failure and newly occurring
and 2)
arrhythmias, and insufficient home
Use breathless management strategies
support or lack of telephone or
(Appendix 4): sit, rest arms on a chair or
transport.
table, use a fan, and practise breathing
• A guide to acute severity assessment is control techniques
shown in Table 4.
Bronchodilators
• Several prognostic scores have been
• Short-acting inhaled beta2 agonists
proposed. The most validated one is
with or without short-acting anti-mus-
DECAF, but this includes COPD with
carinics are the initial bronchodilator
pneumonia and requires a blood
of choice to treat an acute exacer-
gas, complete blood count (for eosin-
bation. These can be delivered via
ophils), and chest x-ray, which are
pressurised metered dose inhaler
unlikely to be available in primary
and spacer, dry powder inhalers, or
care. An alternative is CURB-65, which
nebuliser. We recommend salbutamol
was developed for pneumonia but
via a spacer. One actuation of the
has been found to be equally effective
inhaler should be used each time and
at predicting short term-mortality
repeated as necessary.
in COPD in New Zealand studies.6
CRB-65 is a simpler version that does • Spacer technique is important when
not require any laboratory measures using a pressurised metered dose
(Table 5). inhaler. In an exacerbation, we
recommend one actuation into the
• A chest x-ray and electrocardiogram
spacer followed by 4—6 tidal breaths.
help to identify alternative diag-
Observe and repeat if required.
noses and complications, such as
pulmonary oedema, pulmonary • The bronchodilator effect of 8—10
embolus, pneumothorax, pneu- puffs of 100mcg salbutamol via spacer
monia, pleural effusion, arrhythmias, is equivalent to a 5mg salbutamol
myocardial ischaemia, and others. nebuliser. We recommend that no
Biomarkers (troponins, B-natriuretic more than five puffs are used at a time
peptide, D-dimer) can help to identify (given individually via spacer).
comorbidities and abnormalities of • If patients do not respond to multiple
these are associated with a worse doses of inhaled short-acting beta2
prognosis. agonist, additional bronchodilator
Box 4: Key messages for exacerbation management in COPD.
Recommendations:
• Early diagnosis and prompt management of exacerbations of COPD may prevent
functional deterioration and reduce hospital admissions.
• Most mild to moderate exacerbations can be managed at home.
• Short-acting inhaled beta2 agonists with or without short-acting anti-muscarinics are
the initial bronchodilators of choice to treat an acute exacerbation.
• Give short course oral corticosteroids (eg, prednisone 40mg once daily for five days).
• Give short-course antibiotics for purulent sputum and/or other evidence of
infection.
• Titrate oxygen to target saturations of 88–92%
• Non-invasive ventilation (NIV) reduces mortality in patients with hypercapnic respi-
ratory failure due to an acute exacerbation of COPD.
• Careful discharge planning and referral to pulmonary rehabilitation may reduce the
risk of future exacerbations and admissions.
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Table 4: Assessment of exacerbation severity. (Adapted from the National NZ Ambulance Guidelines
2019.7 Not all patients will have all of these features.)
Mild to moderate Severe Life-threatening /
imminent respiratory arrest
More short of breath than usual Very short of breath Extremely short of breath
Able to speak in sentences Only a few words per breath Unable to speak
Usually have wheeze May not have a wheeze
Some chest/neck indrawing Severe neck/chest indrawing May be no chest/neck indrawing
Tripod positioning
SpO2 near usual level SpO2 well below their usual SpO2 rapidly falling
level
Normal level of consciousness May be agitated Severe agitation and/or falling
level of consciousness
Table 5: Assessment of short-term (one-month) prognosis.
CURB65* CRB65* DECAF*#
C – Confusion C – Confusion D – Dyspnoea: unable to leave
house = 1 point; unable to
wash/dress = 2 points
U – Urea >7mmol/L E – EosinophilsNZ COPD GUIDELINES
PRE-HOSPITAL MANAGEMENT
Figure 1: Pre-hospital OF ofACUTE
management of acute exacerbation COPD. EXACERBATION OF COPD
Assess severity
Moderate OR Severe Life-threatening OR
Imminent respiratory arrest
• More short of breath than usual • Very short of breath • Extremely short of breath
• Able to speak in sentences • Only a few words per breath • Unable to speak
• Usually have wheeze • Severe chest/neck indrawing • May not have a wheeze
• Some chest/neck indrawing • Tripod positioning • May be no chest/neck indrawing
• SpO2 near usual level • SpO2 well below their usual level • SpO2 rapidly falling
• Normal level of consciousness • May be agitated • Severe agitation and/or falling level of consciousness
Initial Management Initial Management
• Salbutamol via inhaler & spacer, up to 5 individual puffs • Air‐driven nebuliser: Salbutamol 2.5mg AND Ipratropium 500mcg
• Controlled oxygen, if needed, aiming for SpO2 88‐92% • Controlled oxygen, aiming for SpO2 88‐92%
• Oral prednisone 40mg • Oral prednisone 40mg
• Oral antibiotics if change in sputum or evidence of infection • Oral antibiotics if change in sputum or evidence of infection
Add Nebuliser
Responding? NO • Air‐driven nebuliser:
Salbutamol 2.5mg AND
Ipratropium 500mcg
YES
Continue Treatment Continue Treatment
Repeat salbutamol via inhaler and spacer as needed • Repeat salbutamol nebuliser 2.5mg as needed
Assess appropriateness of hospital transfer
Assess need for hospital
• Patient and whānau preferences (advance care plan)
• Severity of symptoms
• Confusion
• Inability to manage/lack of support at home
• Lack of response to treatment
• Other medical conditions Is Hospital
• Patient and whānau preferences (advance care plan) Transfer
• Document resuscitation status and consider ceiling of Appropriate?
care for all patients
YES NO
Is Hospital
Required?
YES
NO Community/Hospice
Transfer to Hospital based care
Ongoing Management
• Complete 5 days of prednisone
• Complete 5 to 7 days of antibiotics, if indicated
• Salbutamol as‐needed via inhaler & spacer
• Continue regular inhalers unless contraindicated
• Arrange primary care follow‐up within 2 weeks and
update COPD action plan
• Refer to pulmonary rehabilitation unless completed
recently or contra‐indicated
Outpatient Management
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HOSPITAL MANAGEMENT
Figure 2: Hospital management of exacerbation of OF
COPD. ACUTE EXACERBATION OF COPD
Assess severity
Moderate OR Severe Life-threatening OR
Imminent respiratory arrest
• More short of breath than usual • Very short of breath • Extremely short of breath
• Able to speak in sentences • Only a few words per breath • Unable to speak
• Usually have wheeze • Severe chest/neck indrawing • May not have a wheeze
• Some chest/neck indrawing • Tripod positioning • May be no chest/neck indrawing
• SpO2 near usual level • SpO2 well below their usual level • SpO2 rapidly falling
• Normal level of consciousness • May be agitated • Severe agitation and/or falling level of consciousness
Initial Management Initial Management
• Salbutamol via inhaler & spacer, up to 5 individual puffs • Air‐driven nebuliser: Salbutamol 2.5mg AND Ipratropium 500mcg
• Controlled oxygen, if needed, aiming for SpO2 88‐92% • Controlled oxygen, aiming for SpO2 88‐92%
• Oral prednisone 40mg • Oral prednisone 40mg
• Oral antibiotics if change in sputum or evidence of infection • Oral antibiotics if change in sputum or evidence of infection
Add Nebuliser
Reassess after 15 - 30 minutes
• Air‐driven nebuliser:
• Good response to initial management? Salbutamol 2.5mg AND Ipratropium 500mcg
General Considerations
In patients not responding to treatment, consider alternative diagno-
ses (heart failure, acute coronary disease, pneumonia, pneumothorax,
pulmonary embolus). Suggested investigations:
Responding? NO • Chest X Ray and ECG
• Biomarkers (troponin, BNP, +/- d-dimer where appropriate)
YES Consider NIV
In all patients with life-threatening exacerbation or who are requiring
Continue treatment and reasses after 2 hours supplementary oxygen:
• Obtain arterial blood gas and assess for hypercapnic respiratory failure
• Good response to initial management? • Consider any advance care plan, and patient/whānau preferences
• Not breathless or tachycardic at rest?
• Able to manage/ adequate support at home?
Is NIV
YES: Patient deteriorating
indicated?
Is admission
required YES
NO: Patient responding and
discharge appropriate
YES: Patient responding, but discharge
not currently appropriate
NO Start NIV
• Start NIV if pH
6 kPa /45mmHg
• Ensure escalation plan and goals
Continue treatment
At Discharge of care are documented in all
• Repeat Salbutamol 2.5mg nebuliser patients at point of starting NIV
• Provide education and updated COPD action plan as needed
• Ensure clear follow-up plans are in place • Step down to SABA via inhaler &
• Primary care follow-up within 2 weeks spacer once stabilised
• Ensure that there is sufficient support at home
• Refer to pulmonary rehabilitation unless completed
recently or contra-indicated
• Prescribe prednisone and antibiotics if indicated, to Document resuscitation status and consider
complete course. ceiling of care for all patients
Ongoing management:
• Complete 5 days of prednisone
• Complete 5 to 7 days of antibiotics, if indicated
• Salbutamol as‐needed via inhaler & spacer
• Continue regular inhalers unless contraindicated
Consider:
• Sputum clearance
Discharge Patient • Early Mobilisation
Admit Patient
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treatment such as ipratropium is bations of COPD. These may be viral,
recommended. bacterial, or mixed. Common bacterial
• Nebulisers may increase the risk pathogens include Haemophilus
for aerosolisation of viruses such as influenzae, Streptococcus pneumonia,
SARS-CoV-2 (COVID-19). There is no and Moraxella catarrhalis. Myco-
evidence that nebulisers are more plasma pneumoniae and Chlamydia
effective than inhalers via a spacer, pneumoniae have also been reported.
and we recommend that nebulisers Pseudomonas aeruginosa and Staph-
should be avoided in any patient who ylococcus aureus are uncommon but
could be infected with respiratory occur more frequently in severe COPD.
viruses. If they are used, appropriate • Antibiotics, when indicated by the
aerosolisation infection precautions presence of purulent sputum, fever
should be implemented. and/or raised inflammatory markers
• If a salbutamol nebuliser is necessary, (CRP >40), can shorten recovery time
we recommend a maximum dose of and reduce the risk of relapse and
2.5mg at a time. Patients with COPD treatment failure, and should be
often have cardiac co-morbidities. prescribed for 5–7 days.
Higher doses are associated with an • Oral antibiotics such as amoxicillin
increased risk of tremors, elevated or doxycycline are recommended.
heart rate, palpitations, and lower If treatment failure or resistant
blood pressure, without evidence of organisms are suspected, amoxycil-
any additional benefit. lin-clavulanate can be prescribed. If
• If nebulisers are given for acute COPD pneumonia, Pseudomonas or Staph-
exacerbations, they should be air ylococci are suspected, appropriate
driven to reduce the risk of type 2 antibiotics should be used.
respiratory failure due to high flow Oxygen
oxygen. • If indicated, oxygen should be
• Maintenance LABA, LAMA, and prescribed and titrated via nasal
ICS should be continued during an prongs or a controlled flow device to
exacerbation. target saturations of 88–92%.
• We do not recommend the routine use • Oxygen delivery via a high-flow
of intravenous (IV) magnesium for humidified nasal device can improve
COPD exacerbations. ventilation and airway clearance as
• We do not recommend adrenaline for well as reduce the physiological dead
COPD exacerbations in the absence of space and work of breathing.
anaphylaxis.
Supported ventilation
Corticosteroids • Non-invasive ventilation (NIV) reduces
• Systemic corticosteroids (eg, pred- mortality by about 50%, reduces need
nisone 40mg once daily) can improve for intubation, and shortens length
lung function, improve oxygenation, of stay in patients with rising arterial
and shorten recovery time. They carbon dioxide tension (PaCO2) levels
should usually be given for five days. due to COPD. It should be considered
Longer courses should generally be in patients who present with hyper-
avoided due to the risk of side effects. capnic respiratory failure (arterial pH
6kPa/45mmHg).
• Intravenous steroids should be
avoided. There is no evidence of • An arterial blood gas should be
benefit compared with oral corticoste- considered in every patient with a
roids for treatment failure, relapse, or severe exacerbation, an oxygen satu-
mortality. Hyperglycaemia rates are ration less than 90%, or signs of cor
higher with IV corticosteroids. pulmonale.
• A venous blood gas pH ≤7.34 has
Antibiotics
good sensitivity and specificity for
• Respiratory tract infections are the
acidaemia (pH ≤7.35) but does not
most common precipitants of exacer-
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reliably predict arterial PaCO2 and cological and non-pharmacological
cannot diagnose hypercapnic respi- strategies in place and to develop a
ratory failure. An arterial blood gas is personalised action plan.
necessary to assess the need for NIV. • Review of inhaler technique and
• Ward-based NIV can reduce the adherence should occur in every
requirement for HDU/ICU admission patient following an exacerbation (see
but should be conducted in an appro- section Optimise knowledge of COPD
priately monitored setting with and adherence to treatment).
trained clinical staff. • All medications should be reviewed
• At the time of initiating NIV, the following an exacerbation of COPD
goals and limits of care should be and adjusted as appropriate.
considered and a clear written esca- • Refer to a pulmonary rehabilitation
lation plan established. programme unless recently completed
Airway clearance techniques or contra-indicated.
• Patients with excess sputum
production benefit from airway Comorbidities and
clearance techniques during an
exacerbation.
treatable traits
• Airway clearance techniques should
Identify and manage comorbidities
• People with COPD often have other
be individualised to the patient.
conditions. Lung cancer, bronchi-
Before discharge ectasis, ischaemic heart disease,
• Ensure that adequate education congestive heart failure, diabetes,
is provided regarding COPD anxiety, depression, gastro-oesoph-
management, including smoking ageal reflux, and osteoporosis are all
cessation, use of inhalers, and more common among people with
the development of an acute COPD than in the general population.
management/action plan. • These conditions can negatively
• Ensure that clear follow-up plans impact on the management of COPD
are in place, as the risk for further and, in turn, the presence of COPD can
exacerbations is greatest following an negatively impact on the treatment
exacerbation. and prognosis of comorbid conditions.
• Ensure that there is sufficient support • A systematic approach to the
at home for the patient to manage assessment and management of
during their recovery. This may comorbidities has been proposed as
require social work, physiotherapy, part of the treatable traits concept.
occupational therapy, and other allied This approach recommends that
health input. management is personalised to
• Recommend primary care follow-up the individual, with the use of
within two weeks. biomarkers where available, and
the systematic multidimensional
• Consider follow-up spirometry if this
identification and treatment of all
has not been done.
comorbidities or disease charac-
• Refer to a pulmonary rehabilitation teristics, which may contribute to
programme unless recently completed the patient’s presentation and are
or contra-indicated. potentially amenable to treatment
After an exacerbation (‘treatable traits’). There is prelim-
• Having an exacerbation is the greatest inary evidence to suggest that this
risk factor for a further exacerbation. approach improves quality of life.
• Each exacerbation is associated with Lung cancer
a faster decline in lung function and • There is a strong association between
increased mortality. COPD and lung cancer, more so than is
• Exacerbations should be used as an explained by the shared risk factor of
opportunity to review the pharma- smoking.
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