Beyond breathlessness: Diagnosis and management of patients with COPD

COPD is a significant cause of morbidity and mortality

Chronic obstructive pulmonary disease (COPD) is defined as a heterogeneous lung condition characterised by chronic respiratory symptoms due to abnormalities of the airways and alveoli that cause persistent and often progressive airflow obstruction.¹ Previous definitions of COPD emphasised the strong association with tobacco smoking and exposure to other noxious particles or gases.² However, fewer than half of heavy smokers develop COPD, suggesting individual susceptibility to the effects of tobacco smoke varies greatly.¹ Globally, up to one-third of people who develop COPD have never smoked (although some may have been passively exposed).^{2, 3} COPD is generally considered a preventable disease with many of the major risk factors for its development being modifiable (Table 1).¹

---

Table 1. Potential risk factors for the development of COPD.^{1, 4, 5}

Noxious exposures

Individual and social factors

Any smoking exposure (including tobacco, second-hand smoke, cannabis smoking and e-cigarettes/vaping) Household air pollution and biomass exposure, e.g. heating and cooking with wood and coal in poorly ventilated areas Air pollution Occupational exposures to dust, chemical agents and fumes, e.g. agriculture, mining, manufacturing

Genetic predisposition, e.g. alpha-1 antitrypsin deficiency (especially in people of Northern European ancestry) Recurrent respiratory tract infections Anatomical and physiological respiratory dysfunction, e.g. childhood asthma, bronchial hyper-responsiveness Ageing – prevalence increases from 1.5% in people aged 45 – 64 years to 6.9% in people aged 75 years and over6 Lower socioeconomic status Prenatal exposure to tobacco smoke, e.g. maternal smoking or second-hand smoke exposure during pregnancy may affect lung development in utero

Forming a diagnosis of COPD

A formal diagnosis of COPD is based upon spirometry results in a patient with relevant symptoms and signs.⁴ Ideally, spirometry is available and performed in primary care, however, not all clinicians will have the appropriate training and access to equipment. Therefore, some patients will need to be referred to a respiratory service, which can delay the diagnosis for them (see: “Spirometry is essential to establish a diagnosis of COPD”). A comprehensive history, physical examination and laboratory investigations, e.g. full blood count, BNP, also support clinical suspicion and help to rule out other potential causes. This assessment process may require several consultations in primary care, and can also take place while awaiting spirometry results.⁴

Consider COPD in any patient aged over 40 years who presents with a significant history of cigarette smoke exposure, occupational exposure, i.e. dust, fumes or gas, or recurrent respiratory infections and any typical symptoms, e.g. persistent dyspnoea that worsens with exercise, chronic cough and sputum production.^{1, 4} Symptoms such as chest tightness, wheezing and fatigue are also common.¹ Those with more severe disease at first presentation may also report non-respiratory symptoms, e.g. weight loss, reduction in muscle mass, anorexia, anxiety and depression.¹

For more details on the COPD consultation process, see: Appendix 2 of the New Zealand COPD Guidelines: 2025 Update.

Use patient history to identify risk factors

Many patients will be aware that they have increasing breathlessness, increasing frequency or duration of upper respiratory infections and reduction in their physical ability. However, they have attributed these symptoms to normal ageing, a lack of fitness or merely “a smoker’s cough” and medical attention has only been sought now because of the increasing impact on their quality of life, or a specific acute exacerbation.^{1, 4} Some patients (with undiagnosed COPD) can describe periods of significantly worse symptoms without recognising these as exacerbations, e.g. they attributed their symptoms to frequent or persistent lower respiratory tract infections.

Take a history to identify risk factors and symptoms in any patient suspected of having COPD. This should include asking about:¹

• Noxious exposures, i.e. cigarette smoke, occupational or environmental chemicals, dusts
• Previous respiratory conditions including asthma, allergies, sinusitis, nasal polyps, respiratory infections and other relevant medical history, e.g. maternal smoking history during pregnancy
• Family history of chronic respiratory conditions, including COPD; these patients potentially experience more severe COPD symptoms and could be at higher risk of future deterioration¹¹
• Symptom onset pattern, e.g. age at onset, gradual vs acute onset, symptom triggers
• History of prior hospitalisations for respiratory symptoms (or unrecognised exacerbations)
• Co-morbidities such as cardiovascular disease, osteoporosis and musculoskeletal disorders which may further limit the patient’s ability to remain active
• Impact of symptoms on their life, e.g. physical activity, ability to work or fulfil family duties, depression or anxiety, sexual activity
• Family and social support available
• Opportunities to reduce exposure to risk factors or triggers, e.g. smoking cessation

Quantify symptom impact using validated assessment tools

The Modified Medical Research Council (mMRC) Dyspnea Scale (Table 2) is a simple quantitative assessment tool that enables patients to rapidly communicate their level of breathlessness to healthcare professionals on a standardised scale. Initiation of treatment should be considered in patients with COPD and a mMRC score ≥ 2.¹

---

Table 2. Modified Medical Research Council (mMRC) Dyspnea Scale.⁴

Grade
0	“I only get breathless with strenuous exercise”
1	“I get short of breath when hurrying on the level or walking up a slight hill”
2	“I walk slower than people of the same age on the level because of breathlessness” or “I have to stop for breath when walking at my own pace on the level”
3	“I stop for breath after walking 100 metres or after a few minutes on the level”
4	“I am too breathless to leave the house” or “I am breathless when dressing or undressing”

The COPD Assessment Test (CAT) should also be performed to further evaluate the impact of COPD on the patient’s health (Table 3).⁴ The mMRC only measures breathlessness, does not account for patients making lifestyle adjustments around their symptoms and is less sensitive at detecting change in clinical condition.^{1, 12} The CAT measures health status with eight questions, giving a score out of 40; initiation of treatment should be considered in patients with a CAT score ≥ 10.¹

---

Table 3. COPD Assessment Test (CAT).⁴

			Score
I never cough		I cough all the time
I have no phlegm (mucus) in my chest at all		My chest is completely full of phlegm (mucus)
My chest does not feel tight at all		My chest feels very tight
When I walk up a hill or one flight of stairs I am not breathless		When I walk up a hill or one flight of stairs I am very breathless
I am not limited doing any activities at home		I am very limited doing activities at home
I am confident leaving my home despite my lung condition		I am not at all confident leaving my home because of my lung condition
I sleep soundly		I don’t sleep soundly because of my lung condition
I have lots of energy		I have no energy at all
		Total score:

Best Practice Tip: Paper copies of the CAT can be provided in the waiting room for patients to fill out before their consultation or take home and discuss with family/whānau and bring back at the next appointment.

Physical examination can support clinical suspicion

Overt clinical signs of airway obstruction are unlikely to be present in patients with early COPD, e.g. hyperinflation of the chest, hyperresonance to chest percussion, reduced chest expansion, soft breath sounds on auscultation, prolonged expiratory phase.^{1, 5} Physical examination is, however, useful to inform clinical suspicion, identify co-morbidities or alternative causes of symptoms, e.g. the presence of digital clubbing warrants investigation of other respiratory conditions including lung cancer.¹³ Symptoms and signs can be more obvious during an acute COPD exacerbation, e.g. tachypnoea and tachycardia, accessory muscle use and cyanosis.⁵

Spirometry is essential to establish a diagnosis of COPD

COPD cannot be diagnosed based on the presence of symptoms and signs alone. Spirometry is fundamental to a COPD diagnosis.¹ Ideally, reliable spirometry is performed early in the assessment process in a general practice setting. Patients with suspected COPD should be referred to a respiratory service if reliable spirometry is unable to be performed in primary care, or there is uncertainty surrounding a test result.⁴ In this situation, laboratory investigations and imaging may take place before spirometry and a formal diagnosis is often delayed.

Spirometry terminology

• Forced vital capacity (FVC) is the total volume of air exhaled forcefully after a maximal inspiration and is indicative of overall lung capacity.¹⁴ N.B. A single exhalation typically lasts five to six seconds in healthy adults, but may take much longer in people with COPD.¹⁵
• Forced expiratory volume in one second (FEV₁) is the volume of air exhaled during the first second of the forced expiratory manoeuvre.¹⁴ FEV₁ demonstrates mechanical properties of medium to large airways.
• FEV₁/FVC is the ratio of forced expiratory volume in one second to forced vital capacity and is expressed as a fraction or percentage. It can be used to indicate the presence of airflow obstruction, i.e. the person’s airways have narrowed and their ability to exhale is compromised.¹⁴

Spirometry evaluates airflow obstruction

---

Table 4. New Zealand COPD Guidelines: 2025 Update severity assessment tool.⁴

	FEV1	Z-score	Typical symptoms
Mild	60 – 80% predicted value	–1.65 — –2.50	Few symptoms Breathless on moderate exertion Little or no effect on daily activities Cough and sputum production
Moderate	40 – 59% predicted value	–2.51 — –4.00	Breathless walking on level ground Increasing limitation on daily activities Recurrent chest infections Exacerbations requiring oral corticosteroids and/or antibiotics
Severe	< 40% predicted value	< –4.00	Breathless on minimal exertion Daily activities severely curtailed Frequent chest infections Exacerbations of increasing frequency and severity

 

Interpreting Z-score grading for spirometry results

Do not use spirometry results to predict the patient’s treatment response.⁴ Patients with COPD may experience symptomatic and functional benefits from the use of bronchodilators, without any change in spirometry, e.g. increase in exercise capacity, subjective improvement in quality of life or dyspnoea.⁵ Furthermore, an acute response to a bronchodilator dose should not be considered predictive of subsequent treatment response with bronchodilators or inhaled corticosteroids.^{1, 4}

Spirometry is not currently recommended to “screen” for COPD. It should generally be reserved for symptomatic patients or those who are suspected of having COPD due to risk factors, e.g. smoking history, occupational exposures.¹ There is no strong evidence that spirometry screening improves management or outcomes in patients with COPD before they develop significant symptoms.¹

Ruling out other potential causes of symptoms

Arrange relevant laboratory investigations and imaging

Laboratory investigations and imaging are not necessary for COPD diagnosis, but are recommended as part of the initial assessment when COPD is suspected. They can be useful to exclude conditions that may mimic COPD symptoms or identify co-morbidities (see: “The differential diagnosis of COPD”), depending on the clinical situation.

Recommended investigations include:

• Full blood count
  • Establish a baseline blood eosinophil level.¹ During future escalation of treatment, a level > 0.3 × 10⁹/L suggests the patient is more likely to benefit from an inhaled corticosteroid.⁴
  • Elevated haemoglobin and haematocrit indicate secondary polycythaemia and are suggestive of chronic hypoxia.⁵ This could be caused by COPD but may prompt further investigations for other causes, e.g. sleep apnoea.
• Pulse oximetry
  • Establish a baseline oxygen blood saturation level for comparison during COPD exacerbations^{1, 4}
• Brain natriuretic peptide (BNP)^*
  • Request BNP for any patient with a pattern of symptoms and signs indicating possible heart failure⁵
• Electrocardiogram (ECG)^*
  • A baseline ECG is appropriate if COPD is suspected.^{5, 17} Cardiovascular disease is a frequent co-morbidity and cause of death in people with COPD.⁵ The patient’s ECG results (and BNP results) in conjunction with symptoms and signs may indicate further testing is required, e.g. echocardiogram.¹⁷
• Chest X-ray
  • Not routinely required for COPD diagnosis, but can identify non-specific features of COPD, e.g. hyperinflated lungs, flattened diaphragm, hyperlucency of the lungs, and identify (or exclude) other conditions, e.g. lung cancer, pulmonary fibrosis, bronchiectasis, pleural diseases^{1, 5}

For Community Referred Radiology National Clinical Criteria, click here

* Not specifically recommended in the New Zealand COPD Guidelines: 2025 Update, but reasonable investigations to include as part of clinical work up in a primary care setting

Consider requesting alpha-1 antitrypsin serology in younger patients

The differential diagnosis of COPD

Symptoms of COPD overlap with several other conditions, making an initial diagnosis challenging in some cases (Table 5).

Asthma

Heart failure

Bronchiectasis

Additional diagnoses to consider in patients presenting with dyspnoea and other relevant symptoms include: respiratory infection, pulmonary embolism (particularly small recurrent emboli), interstitial lung disease, lung cancer and tuberculosis.^{1, 23}

---

Table 5. Common differential diagnoses of COPD.^{1, 17, 19} N.B. This is not an exhaustive list.

Diagnosis	Characteristics
COPD	Age of onset is usually older, e.g. aged > 40 years History of exposure to noxious particles or gases, e.g. cigarette smoke Symptoms are often continuous and progressive
Asthma	Onset often during childhood but can be at any age Personal or family history of atopy, allergies or asthma Symptoms may vary from day-to-day or over long periods, between seasons Often triggered by exercise, emotions (e.g. laughter), dust or allergies
Heart failure	Older age of onset History of cardiovascular disease Symptoms slowly progressive Presence of pulmonary oedema or ankle swelling Night-time symptoms (orthopnoea) Pulmonary function test suggests volume restriction (not airflow limitation) Diagnosis supported by elevated BNP and echocardiogram
Bronchiectasis	Limited or no smoking history Frequent exacerbations Co-morbid autoimmune conditions may be present Often associated with bacterial infection Bronchial dilation/wall thickening on chest X-ray Chest computed tomography (CT) scan typically required for diagnosis

Non-pharmacological interventions underpin COPD management

Non-pharmacological interventions improve symptom control and quality of life and modify disease progression in people with COPD, regardless of what pharmacological treatments are ultimately required. Interventions include:⁴

Stepwise pharmacological treatment

The pharmacological treatment of COPD has two aims: (1) provide symptom control and (2) reduce the risk of exacerbations as they are associated with increased mortality.⁴ There is limited evidence that medicines modify the long-term decline of lung function associated with COPD.¹ The relationship between symptom severity, airflow limitation and exacerbation frequency varies between patients, necessitating individualised treatment plans.¹ Table 6 lists the current funded medicines/inhalers for COPD treatment in New Zealand.

Introduce medicines in a stepwise approach according to the severity and progression of the patient’s condition, i.e. dyspnoea and exacerbation frequency; this can incorporate results of mMRC, CAT and spirometry (Figure 1).⁴ It can take up to six weeks for improvement in dyspnoea to become apparent, while changes in exacerbation frequency should be assessed over 6 – 12 months.⁴ Consider patient preferences, available devices, complexity of the treatment regimen and potential adverse effects when escalating treatment.⁴

For commentary on different inhaler devices and considerations when choosing the most appropriate medicine delivery system, see: “Paper of the Week: Different inhalers for different folks”, Best Practice Bulletin 112, Nov, 2024.

Best Practice Tip: Check treatment adherence and inhaler technique at each consultation, and especially before escalating the patient’s treatment regimen. This can also be done by community pharmacists; add a note to the prescription.

---

Table 6. Inhaled medicines funded in New Zealand for the management of COPD.²⁴

Class	Medicine	Brand name	Inhaler type	Comments
Short-acting bronchodilators
Short-acting muscarinic antagonist (SAMA)	Ipratropium	Atrovent	Pressurised metered dose inhaler
Short-acting beta2-agonist (SABA)	Salbutamol	SalAir, Ventolin*	Pressurised metered dose inhaler
	Terbutaline	Bricanyl	Turbuhaler
SABA + SAMA combination	Salbutamol + ipratropium	Duolin HFA	Pressurised metered dose inhaler
Long-acting bronchodilators
Long-acting muscarinic antagonist (LAMA)	Glycopyrronium†	Seebri Breezhaler	Dry powder for inhalation	Funded with endorsement for patients diagnosed with COPD (using spirometry, if possible). N.B. Patients who were dispensed tiotropium with Special Authority approval before 1st October, 2018, are also considered endorsed. Only one type of LAMA inhaler is funded at one time
	Tiotropium†	Spiriva, Spiriva Respimat	Dry powder for inhalation, Fine mist inhaler
	Umeclidinium†	Incruse Ellipta	Dry powder for inhalation
Long-acting beta2-agonist (LABA)	Formoterol	Oxis*	Turbuhaler
	Indacaterol	Onbrez Breezhaler	Dry powder for inhalation
	Salmeterol	Serevent	Pressurised metered dose inhaler, Accuhaler
LABA + LAMA combination	Indacaterol + glycopyrronium	Ultibro Breezhaler	Dry powder for inhalation	Special Authority approval requires that patients are first stabilised on a LAMA and are likely to receive additional benefit from a combination inhaler Special Authority renewal requirements for LABA + LAMA combination inhalers were removed from 1st December, 2025 LABA + LAMA combination inhalers are not funded if a patient is also prescribed an ICS + LABA combination inhaler
	Olodaterol + tiotropium	Spiolto Respimat	Fine mist inhaler
	Vilanterol + umeclidinium	Anoro Ellipta	Dry powder for inhalation
Inhaled corticosteroids (ICS)
Inhaled corticosteroid (ICS)	Beclometasone diproprionate	Beclazone, Qvar (ultrafine particle)	Pressurised metered dose inhaler	ICS inhalers should be prescribed alongside a LABA + LAMA in patients with COPD. N.B. COPD is an unapproved indication for any of the single ICS inhalers. Beclazone and Qvar brands of beclometasone dipropionate inhaler are not dose equivalent and cannot be used interchangeably
	Budesonide	Pulmicort	Turbuhaler
	Fluticasone propionate	Flixotide	Pressurised metered dose inhaler, Accuhaler
ICS + LABA combination	Budesonide + formoterol	Symbicort, DuoResp Spiromax, Vannair	Turbuhaler, dry powder for inhalation, pressurised metered dose inhaler	Generally, not recommended as ICS + LABA is associated with inferior clinical outcomes compared with triple treatment (i.e. LABA + LAMA and an ICS inhaler or a single ICS + LAMA + LABA inhaler).1, 4 These inhalers could be considered if prescribed for a concurrent diagnosis such as asthma.
	Fluticasone furoate + vilanterol	Breo Ellipta	Dry powder for inhalation
	Fluticasone propionate + salmeterol	Seretide	Pressurised metered dose inhaler, Accuhaler
ICS + LABA + LAMA combination	Budesonide + glycopyrronium + formoterol‡	Breztri Aerosphere	Pressurised metered dose inhaler	Special Authority approval requires patients to be currently receiving ICS + LABA or LABA + LAMA combination treatment or multiple inhaler triple treatment (i.e. ICS + LAMA + LABA). Patients must also meet at least one of the following clinical criteria: CAT score > 10, ≥ 2 exacerbations or one exacerbation requiring hospitalisation in the previous 12 months, or an eosinophil count ≥ 0.3 × 109/L in the previous 12 months.
	Fluticasone furoate + umeclidinium + vilanterol‡	Trelegy Ellipta	Dry powder for inhalation

* Partly funded

† Funded with endorsement

‡ Funded with Special Authority approval

---

Figure 1. Suggested stepwise treatment for patients with COPD.⁴

Red pathway indicates prompt treatment escalation (recommended)

* SAMA and a LAMA should not be used concurrently

† A LABA + LAMA (single inhaler combination) is preferred, however, current Special Authority criteria for a LABA + LAMA single inhaler requires patients to be stabilised on LAMA treatment first

‡ A LABA + LAMA + ICS (single inhaler combination) is preferred — Special Authority criteria for a LABA + LAMA + ICS single inhaler requires patients to be on ICS + LABA or LABA + LAMA combination treatment, or multiple inhaler triple treatment (i.e. ICS + LAMA + LABA) first

CAT = COPD Assessment Test; COPD = chronic obstructive pulmonary disease, ICS = inhaled corticosteroid; LABA = long-acting beta₂-agonist; LAMA = long-acting muscarinic antagonist; mMRC = Modified Medical Research Council Dyspnea Scale; SABA = short-acting beta₂-agonist; SAMA = short-acting muscarinic antagonist.

---

All patients with symptomatic COPD require a bronchodilator

Short-acting bronchodilator treatment for acute dyspnoea

Almost all patients with symptomatic COPD will require a short-acting bronchodilator inhaler for acute symptom relief. However, prescribing a short-acting bronchodilator alone (i.e. without a long-acting medicine) for COPD is rarely indicated.⁴ This approach should only be considered in patients who report “very occasional” symptoms.⁴ If only a short-acting bronchodilator is appropriate, a combination short-acting beta₂-agonist (SABA) + short-acting muscarinic antagonist (SAMA), e.g. salbutamol + ipratropium produces greater improvements in lung function and symptoms compared with either a SABA or SAMA alone.¹ Escalation to a LAMA (with withdrawal of the SAMA; see below) is recommended if a patient reports regular use of a short-acting bronchodilator.⁴

Long-acting bronchodilator treatment for frequent symptoms

In most cases, a short-acting bronchodilator will not be sufficient to manage the patient’s symptoms. Patients with COPD who use their short-acting bronchodilator inhaler more than occasionally, i.e. on most days, should be prescribed a long-acting bronchodilator as well. New Zealand guidelines recommend prescribing a long-acting muscarinic antagonist (LAMA), e.g. glycopyrronium, tiotropium, or umeclidinium, first-line because of reduced exacerbation risk (compared to a long-acting beta₂-agonist; LABA). A LABA should be selected only if a LAMA is contraindicated, not tolerated or the patient has features of both COPD and asthma (in combination with an ICS).⁴ Choosing a LAMA first-line is also practical, given prompt escalation is recommended in most patients and Special Authority criteria for a LAMA + LABA single inhaler requires patients to have trialled LAMA monotherapy.⁴

Be aware, a LAMA and a SAMA should not be used concurrently.⁴ For patients prescribed a LAMA, prescribe a SABA, e.g. salbutamol, terbutaline.⁴ For patients prescribed a LABA, prescribe either a SABA or a SAMA, e.g. ipratropium.⁴

Best Practice Tip: Frequent use of short-acting bronchodilators for acute symptom relief should prompt review of the patient’s treatment regimen, e.g. check inhaler technique and medicine adherence, consider escalation of treatment.

Prompt treatment escalation is recommended in most patients with COPD via two pathways

Persistent breathlessness add a second long-acting bronchodilator⁴

Escalate to dual combination treatment with a LAMA + LABA for patients with persistent symptoms, despite regular and correct use of a single bronchodilator medicine.⁴ Ideally, a single inhaler should be used to optimise adherence, however, patients initiated on a LABA will need to also trial a LAMA before meeting Special Authority criteria for a funded LAMA + LABA inhaler (Table 6).

Frequent or severe exacerbations add a second long-acting bronchodilator and consider ICS⁴

Consider adding an ICS to a LAMA + LABA dual combination inhaler treatment regimen in patients who have persistent symptoms and experience ongoing exacerbations or require hospitalisation.⁴ Patients with an eosinophilic pattern of COPD, i.e. blood eosinophil level > 0.3 × 10⁹/L, may be more likely to benefit from triple treatment, compared with dual LABA + LAMA treatment (see: “The role of eosinophils in COPD pathophysiology and management”).⁴ An ICS + LABA + LAMA single inhaler is preferred in patients who meet Special Authority criteria (Table 6), as this optimises treatment adherence.⁴

Triple treatment could also be considered for patients who use LAMA + LABA dual combination treatment but continue to report severe symptoms, e.g. persistent dyspnoea, exercise limitations, CAT score > 10 or have a blood eosinophil count ≥ 0.1 × 10⁹/L but ≤ 0.3 × 10⁹/L.^{1, 4}

Options for patients in whom ICS is not recommended

ICS + LABA treatment no longer routinely recommended

Reserve ICS + LABA inhalers for patients with features of both COPD and asthma.⁴ This shift is based on evidence that triple treatment, i.e. ICS + LABA + LAMA, is superior to ICS + LABA, if an inhaled corticosteroid is required.¹ Patients with features of both COPD and asthma who continue to experience symptoms with correct use of their ICS + LABA should trial an ICS + LABA + LAMA single inhaler if they meet Special Authority criteria.⁴

Patients with COPD (but without clinical features of asthma or exacerbations) who are currently stabilised on ICS + LABA treatment can continue treatment.¹ However, consider a switch to LABA + LAMA treatment if the patient’s symptoms worsen; further exacerbations indicate that escalation to triple treatment is required.¹

Weigh potential benefits of long-term ICS treatment against the risk of adverse effects

ICS are potent anti-inflammatory medicines, and when used in combination with dual bronchodilator treatment, can reduce exacerbations by approximately 25% in some patients with COPD.²⁵ However, their non-specific mechanism of action can also comprise the patient’s immune system, increasing the risk of respiratory infection and other adverse effects.²⁵ The use of an ICS in patients with COPD is consistently associated with an increased risk of developing pneumonia; analysis of 19 randomised controlled trials found the risk of developing pneumonia increased by 41% with ICS use for one year or longer.^{25, 29} This is of particular concern in patients with other risk factors for pneumonia, e.g. current smoker, prior history of pneumonia, BMI < 25 kg/m², severe airflow limitation.¹

Discontinuation of ICS treatment in patients with COPD rapidly attenuates the elevated risk of pneumonia.⁵ A large, nested cohort study of more than 100,000 people with COPD treated with an ICS found a 37% decrease in the rate of serious pneumonia following ICS discontinuation.³⁰

Other potential adverse effects associated with ICS include skin bruising, hoarseness and oral candidiasis; using a spacer with a metered dose inhaler and oral rinsing following actuation can help to reduce the risk of local fungal infection.^{1, 24} There is less robust evidence that ICS treatment is also associated with decreased bone density and increased fracture risk, increased risk of diabetes and reduced glycaemic control in people with diabetes, cataracts and mycobacterial infection, including tuberculosis.¹ This increased risk of adverse effects is substantially lower than that associated with oral corticosteroids.¹

Potential benefits of ICS likely outweigh the risks in patients with COPD and a blood eosinophil count ≥ 0.3 × 10⁹/L, however, the decision is less clear and needs to be individually weighed up in patients with lower blood eosinophil counts.²⁵

When to consider withdrawal of ICS treatment

Consider withdrawal of ICS treatment if the patient:⁴

• Shows no evidence of benefit, i.e. no improvement in symptoms or fewer exacerbations
• Develops pneumonia or other ICS-related adverse effects
• Is clinically stable for 12 months and has had no exacerbations in that time

Check the patient’s blood eosinophil level prior to ICS withdrawal. A blood eosinophil count ≥ 0.3 × 10⁹/L increases the patient’s risk of exacerbations after stopping ICS and withdrawal may not be appropriate.⁴

Arrange follow-up four-to-six weeks after the patient stops ICS treatment to assess for worsening of symptoms or CAT score.⁴

Regular follow-up is crucial to optimise treatment

Once stabilised, review patients with COPD regularly to identify disease progression, developing co-morbidities and any opportunities to improve management.¹ Follow-up frequency is determined by the patient’s clinical condition; annual review is appropriate for patients with stable COPD whereas more regular review may be needed for those with more severe disease or co-morbidities.¹⁷

At every follow-up, discuss:^{4, 17}

• Treatment adherence
• Symptom control (e.g. CAT score)
• Exacerbations – frequency and severity
• Smoking cessation support (if applicable)
• Vaccinations – check if due for influenza, pneumococcal or COVID-19

Depending on the clinical situation, additional investigations may also be required at some follow-up appointments:^{1, 4}

• Measure oxygen saturation if appropriate, e.g. the patient has had a recent exacerbation or reports severe symptoms; this will support referral for long-term oxygen therapy in patients with advanced COPD
• Repeat spirometry if the patient has had a recent exacerbation or their clinical condition has deteriorated
• Consider arranging a chest X-ray and referral for non-acute respiratory assessment and chest CT if there has been a substantial deterioration in the patient’s clinical condition since their last review

The findings of this review may suggest escalation or reduction in the patient’s inhaled medicine regimen is required. However, check adherence to inhaler technique and non-pharmacological interventions before adjusting treatment.⁴ If the treatment regimen is modified, arrange a follow-up to evaluate the response after six weeks, using the CAT score and comparison to previous results to quantify benefit.⁴

Review any previously diagnosed co-morbid conditions.⁴ Regular follow-up also provides opportunities to assess the patient for developing conditions that adversely affect COPD, e.g. lung cancer, cardiovascular disease, anxiety, depression. When identified, a “treatable traits” approach is recommended.⁴ This strategy favours individualised disease management by addressing specific characteristics of respiratory disease and co-morbid conditions that contribute to the patient’s clinical status with the overall goal of improving their quality of life.³³

A template for a four-step COPD consultation is available in Appendix 2 of the New Zealand COPD Guidelines: 2025 Update.

When to discuss advance care planning for people with COPD

COPD is a progressive disease. Early discussions regarding changing treatment goals and advance care plans can be useful to open communication with patients and their family/whānau, with the goal of reducing decision burden and facilitating dignified end-of-life care. Clinical features that may prompt these discussions include patients with a FEV₁ < 30% of predicted, those experiencing dyspnoea at rest, multiple exacerbations within 12 months, weight loss or cachexia or meeting criteria for oxygen therapy.⁴ A discussion about palliative care may also be appropriate in patients with severe symptoms and poor quality of life.⁴