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The latest approaches to diagnosing and managing COPD

By Dr Eleanor & Cronin Prof Breda Cushen - 17th Apr 2026

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Reference: April 2026 | Issue 4 | Vol 12 | Page 18

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The Global Initiative for Chronic Obstructive Lung Disease (GOLD) defines COPD as a “heterogenous lung condition characterised by chronic respiratory symptoms (dyspnoea, cough, sputum production and/or exacerbations) due to abnormalities of the airways (bronchitis/bronchiolitis) and/or alveoli (emphysema), that cause persistent, often progressive airflow obstruction”.¹

Despite COPD being the most prevalent chronic respiratory disease in adults, it is an underdiagnosed condition. This in part relates to the fact the signs and symptoms of COPD often go unnoticed until 30-40 per cent of lung function is lost.²

Historically, COPD was more common in men, however in recent years it has become increasingly prevalent in women, likely due to changes in smoking habits. Studies have suggested that women are more susceptible to developing COPD and more likely to develop severe disease compared to men.³

In Ireland, patients with COPD are now eligible for enrolment in the GP-delivered HSE Chronic Disease Management (CDM) programme, which provides for a dedicated six-monthly review incorporating disease optimisation. According to the latest HSE CDM report, 12 per cent of adults enrolled in the programme have COPD.⁴

Pathophysiology and risk factors

The hallmark of COPD is chronic airway inflammation, leading to irreversible structural changes, airflow limitation, and impaired gas exchange. These inflammatory and structural changes persist even after smoking cessation. COPD is also associated with systemic inflammation, which contributes to cardiovascular, skeletal, and metabolic comorbidities.⁵

Tobacco smoking is the most significant risk factor for developing COPD; however, up to 25 per cent of individuals with COPD are non-smokers. Several environmental and host factors play a role in the pathogenesis of the disease.

Environmental risk factors include household and air pollution from burning biomass fuels (eg, coal, wood, and crop residues) and heavy exposure to occupational dusts.

The best documented genetic risk factor for COPD is α1-antitrypsin deficiency. It is also increasingly recognised that COPD can result from reduced peak lung function in early adulthood and/or accelerated lung function decline in later life.⁶

Co-existent asthma

Separating asthma from COPD can be clinically difficult. Typically, the onset of asthma is earlier in life, symptoms are episodic in nature, and airflow obstruction is reversible. However, adults with long-standing asthma may develop fixed airflow obstruction.

The term ‘asthma-COPD overlap syndrome’ (ACOS) was proposed to identify patients who have features of both asthma and COPD, however, this term is controversial and since 2021 GOLD has not recommended its use, instead preferring to delineate COPD and asthma as distinct conditions while recognising that they may share common traits and clinical features.¹

Comorbidities

Comorbidity is common in COPD and associated with a poorer prognosis. COPD is an independent risk factor for cardiovascular morbidity and mortality. Even after adjustments for confounding shared risk factors, patients with COPD have a two- to three-fold increased risk of cardiovascular events, including death.

Heart failure is more common in patients with COPD, and comorbid COPD often delays heart failure diagnosis due to overlapping symptoms and shared mechanisms.⁷

COPD has several extrapulmonary manifestations, including low BMI, malnutrition, and skeletal muscle dysfunction, all of which worsen exercise intolerance. Importantly,
muscle dysfunction is a treatable cause of exercise intolerance through pulmonary rehabilitation.

Osteoporosis and related fractures significantly impact morbidity and mortality in COPD. Although corticosteroids are important in managing COPD exacerbations, they are a leading iatrogenic cause of osteoporosis. Physicians should be mindful of this and limit unnecessary steroid use.⁸

The presence of COPD does not significantly alter the management strategies of common comorbid diseases. However, the diagnosis of comorbid disease in the presence of COPD can be challenging. It is essential that clinicians have a high index of suspicion to ensure early diagnosis and management.

COPD and lung cancer

COPD is an important risk factor for the development of lung cancer, with the greatest risk in patients with emphysema independent of the presence of airflow obstruction or smoking.⁹

Lung cancers that develop in association with COPD are generally more aggressive and carry a poorer prognosis.¹⁰ Two large trials have demonstrated that screening smokers age 50 to 80 years for lung cancer reduces mortality by detecting lung cancer at an earlier stage.¹¹ Screening has not been rolled out nationally in Ireland and is currently in the pilot phase.

Signs and symptoms

The three main symptoms of COPD are chronic cough, dyspnoea, and daily sputum production. Dyspnoea is a cardinal symptom of COPD and highly prevalent across all stages of airflow obstruction. Other symptoms of COPD include wheeze, chest tightness, fatigue, weight loss, and recurrent lower respiratory tract infections.

Although symptoms are often related to the degree of lung function impairment, COPD presents heterogeneously, and even mild airflow obstruction can result in a significant symptom burden.

Symptom scores in COPD are used to assess the severity and impact of symptoms on a patient’s daily life. Common tools include the COPD Assessment test (CAT) and Modified Medical Research Council (mMRC) Dyspnoea Scale.¹

Physical exam findings with COPD vary with disease severity. Typical findings in severe disease include signs of hyperinflation, reduced chest expansion, hyperresonance to percussion, wheeze, and a prolonged expiratory phase.

Diagnosis

Spirometry is required to establish a diagnosis of COPD. Spirometry is a non-invasive, cheap, easily reproducible, and readily available test. Current recommendations suggest that adults who report dyspnoea, chronic cough or chronic sputum production should have spirometry performed, particularly if they have a risk factor for COPD.¹

The most important values obtained by spirometry are the Forced Vital Capacity (FVC) and the Forced Expiratory Volume in one second (FEV1). Airflow obstruction is defined as a postbronchodilator FEV1/FVC ratio of <0.7.

It is important to note that the use of the fixed FEV1/FVC ratio to define COPD may result in over-diagnosis of COPD in the elderly and under-diagnosis in young adults. The Global Lung Initiative has proposed an alternative approach, which utilises z scores and may better account for age-related changes in the lung.

Spirometry is also used to assess disease severity, based on the decrement of FEV1. Table 1 outlines the GOLD grades and severity of airflow obstruction

GOLD GRADES AND SEVERITY OF AIRFLOW OBSTRUCTION IN COPD
GOLD 1	Mild	FEV1 ≥80% predicted
GOLD 2	Moderate	FEV1 50-80% predicted
GOLD 3	Severe	FEV1 30-50% predicted
GOLD 4	Very Severe	FEV1 <30% predicted

TABLE 1: GOLD stages of airflow obstruction

TABLE 2: Additional investigations in COPD

In Ireland, GPs can now refer patients directly for spirometry at specialist respiratory integrated care hubs.

ADDITIONAL INVESTIGATIONS

While spirometry is the only test required for a diagnosis of COPD, additional tests may guide treatment and rule out alternative diagnoses. See Table 2 which details the additional investigations that can be considered in those with COPD.

Management

COPD is a complex and heterogenous disease. There is increasing recognition that adopting a more individualised treatment strategy for patients with COPD is beneficial in terms of improving clinical outcomes and minimising side-effects associated with treatments.

Studies have suggested adopting the ‘treatable traits’ strategy, which involves identifying a set of treatable problems specific to the patients and subsequently developing a personalised treatment plan based on the patient’s ‘phenotype’ or ‘endotype’.¹²

GENERAL MEASURES

1. Vaccinations
People with COPD should receive all recommended vaccinations including the yearly influenza and Covid-19 vaccines. The pneumococcal vaccine is recommended every five years up to the age of 65 years and once after 65 years. The US CDC now also recommends RSV vaccination for individuals >60yrs with chronic lung disease.

2. Smoking cessation
Of all the interventions available for COPD, smoking cessation has the greatest impact on the progression and prognosis of the disease. Evidence suggests that a combination of counselling and pharmacotherapy is the most effective smoking cessation treatment.

When possible, patients should be referred to a comprehensive smoking cessation programme. Nicotine replacement should be prescribed to all without a contraindication. Other pharmacotherapies available include varenicline and bupropion.

Quit.ie is Ireland’s national smoking cessation website, offering free support, personalised quit plans and access to nicotine replacement therapy.¹³

3. Pulmonary rehabilitation
Pulmonary rehabilitation is a multidisciplinary programme that includes skeletal muscle training, respiratory muscle training, psychological support, and nutritional counselling. Optimal benefits are achieved from a programme lasting six to eight weeks.

Pulmonary rehabilitation has been demonstrated to be the most effective treatment for relieving COPD-related shortness of breath. It also reduces hospitalisations following recent exacerbations and improves symptoms of depression and anxiety.

In Ireland, since the introduction of the integrated care respiratory programme, pulmonary rehabilitation is now available to patients nationwide. COPD Support Ireland also offers free exercise classes to which patients can self-refer or be referred by a healthcare professional.¹⁴

Pharmacological therapy

1. BRONCHODILATORS
GOLD recommends a tailored approach based on the level of symptoms and risk of exacerbations. GOLD recommends the ‘ABE’ assessment tool that uses an individual’s symptoms (CAT Score or mMRC Dyspnoea Scale) and exacerbation history to guide pharmacotherapy. See Figure 2.

There are two classes of inhaled bronchodilators, β2-agonists and muscarinic antagonists. Long-acting β2-agonists (LABA) and long-acting muscarinic antagonists (LAMA) are superior for controlling symptoms and are recommended first-line in all symptomatic patients.

Poor adherence is common in COPD and is associated with higher mortality and higher admission rates. There are many factors that impact inhaler adherence in COPD, these include inhaler technique, dosing regimens and patient-related factors such as cognitive impairment.¹⁵

2. INHALED CORTICOSTEROIDS
Studies have demonstrated that blood eosinophils are a potential biomarker to direct inhaled corticosteroids (ICS) treatment and identify patients in whom an ICS will reduce their exacerbation risk. Studies suggest that blood eosinophils <100 cells/µL predicts a poor response to ICS, whereas patients with blood eosinophils >300 cells/µL have the greatest response to ICS.¹⁶

There is evidence that the use of ICS results in a small increased risk of pneumonia, as well as higher rates of oral candidiasis, voice change, and skin bruising.¹⁷ Currently, guidelines recommend the use of ICS in patients with:

1. A history of exacerbations (≥2 moderate exacerbations or ≥1 leading to hospitalisation)
2. Blood eosinophil count >300 cells/µL 
3. Coexistent asthma.

3. BIOLOGICS
Monoclonal antibody (biologic) therapies, which modulate specific inflammatory pathways (eg, IL-5, IL-4/IL-13) are emerging as targeted treatments for select patients with COPD, particularly those with eosinophilic inflammation and frequent exacerbations.

4. AZITHROMYCIN
Studies have shown that azithromycin (250mg or 500mg three times per week) reduced the risk of exacerbations compared to usual care. Azithromycin can be considered in patients with recurrent exacerbations.

There is a lesser benefit in current smokers and prescribers should be aware of side effects including QT prolongation and hearing loss.¹⁸ It is recommended that azithromycin prophylaxis be initiated by a consultant in respiratory medicine and that an ongoing review of azithromycin prophylaxis be carried out every six to 12 months.¹⁹ 

5. THEOPHYLLINE

There is evidence that theophylline, a methylxanthine, has a small bronchodilator effect in COPD, leading to modest improvement in symptoms. However, methylxanthines have several side effects and toxicities, which mean they are not used as first-line agents in COPD.

Non-drug therapies

1. OXYGEN THERAPY AND VENTILATORY SUPPORT
Long-term oxygen therapy (worn >15hrs/day) has been shown to improve survival in selected patients with severe resting hypoxaemia (defined as room air PaO2 <7.3kPa or room air PaO2 <8kPa in the presence of other signs of pulmonary hypertension).²⁰

In patients with moderate hypoxaemia or who desaturate with exercise, current evidence suggests that ambulatory oxygen does not improve survival, breathlessness or hospitalisation rates.²¹ Ambulatory oxygen may be prescribed in patients undergoing rehab or who derive both a symptomatic and functional benefit from its use.

In patients with COPD and persistent stable state hypercapnia, domiciliary non-invasive ventilation has been shown to improve survival, health-related quality of life, exercise tolerance, and exacerbation frequency.²²

2. SURGICAL INTERVENTIONS
In selected COPD patients with severe emphysema and persistent disabling breathlessness, lung volume reduction procedures can be considered. These include surgical lung volume reduction surgery and the less invasive bronchoscopic placement of endobronchial valves or coils.

3. LUNG TRANSPLANT
Patients with COPD should be referred for consideration of lung transplantation when they have progressive disease despite maximal medical therapy. Lung transplantation in those with COPD has been predominantly associated with an improvement in quality of life and not an increase in survival (except in patients with severe α1-antitrypsin deficiency).²³

Exacerbations

An exacerbation of COPD is defined as an episode of worsening dyspnoea and/or cough and sputum that deteriorates over two weeks.¹

Exacerbations should be considered significant events for patients with COPD as they have a significant negative impact on health status and contribute to disease.

One study demonstrated that 20 per cent of patients died within one year following their first COPD exacerbation requiring hospitalisation.²⁴

There is also mounting evidence that COPD exacerbations are associated with a period of increased cardiovascular risk, with one study observing a four-fold increased risk of a major adverse cardiac event in the period following an exacerbation.²⁵

The main triggers for exacerbations are respiratory viral infections, although bacterial infections and environmental factors such as air pollution also play a role.

Clinicians can refer to the HSE Clinical Practice Guideline for the Management of COPD.²⁶

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