Approach

For updates on diagnosis and management of coexisting conditions during the pandemic, see our topic 'Management of coexisting conditions in the context of COVID-19'.

The ultimate goals of treatment of COPD are to prevent and control symptoms, to reduce the severity and number of exacerbations, to improve respiratory capacity for increased exercise tolerance, and to reduce mortality.[1]

There is a stepwise approach to therapy and treatment should be individualised for general health status and comorbid conditions.

The therapeutic approach involves reducing risk factor exposure, appropriate assessment of disease, patient education, pharmacological and non-pharmacological management of stable COPD, and prevention and treatment of acute COPD exacerbations.

Continuous assessment and monitoring of disease

Ongoing monitoring and assessment in COPD ensures that the goals of treatment are being met. Quality of life and patients' sense of well-being will improve, and hospital admissions will be significantly decreased in cases where self- or professional monitoring of disease is being utilised.[41] Such assessment of the medical history should include:

Exposure to risk factors and preventative measures:

  • Tobacco smoke

  • Occupational exposures (fumes, dust, etc.)

  • Influenza and pneumococcal vaccination.

Disease progression and development of complications:

  • Decline in exercise tolerance

  • Increased symptoms

  • Worsened sleep quality

  • Missed work or other activities.

Pharmacotherapy and other medical treatment:

  • How often rescue inhaler is used

  • Any new medicines

  • Compliance with medical regimen

  • Ability to use inhalers properly

  • Adverse effects.

Exacerbation history

  • Urgent care or emergency department visits

  • Recent oral corticosteroid bursts

  • Frequency, severity, and likely causes of exacerbations should be evaluated.

Comorbidities:

  • Assessment of co-existing medical problems (e.g., heart failure).

In addition, objective assessment of lung function should be obtained yearly, or more frequently if there is a substantial increase in symptoms.

Integrated disease management (IDM), in which several healthcare providers (physiotherapist, respiratory physician, nurse, etc.) work together with patients, has been shown to improve quality of life and decrease hospital admissions.[42] [ Cochrane Clinical Answers logo ]

Acute exacerbations

An exacerbation of COPD is defined as an event characterised by a change in the patient's baseline dyspnoea, cough, and/or sputum that is beyond normal day-to-day variations and is acute in onset. See our topic on Acute exacerbation of chronic obstructive pulmonary disease for further information.

Chronic management: stepwise therapy according to GOLD group

The Global Initiative for Chronic Obstructive Lung Disease (GOLD) guidelines recommend that initial treatment is determined by the patient’s GOLD group at diagnosis:[1]

  • Rescue short-acting bronchodilators should be prescribed to all patients for immediate symptom relief. Failure to respond to short-acting bronchodilator may signify an acute exacerbation.

  • For group A patients (few symptoms and low risk of exacerbations), a short-acting or a long-acting bronchodilator is offered first-line. Long-acting beta-2 agonists (LABAs) and long-acting muscarinic antagonists (LAMAs) are preferred over short-acting bronchodilators, except for patients with only occasional dyspnoea.[1] LABAs and LAMAs both significantly improve lung function, dyspnoea, and health status and reduce exacerbation rates. [ Cochrane Clinical Answers logo ] LAMAs have a greater effect on exacerbation reduction than LABAs.[1][43][44] The effect of the bronchodilator should be evaluated. Depending on the response, it should either be continued or stopped or another class of bronchodilator should be tried.[1]

  • For group B patients (more symptoms and low risk of exacerbations), a long-acting bronchodilator should be offered first-line. Either a LAMA or a LABA may be prescribed. There is no evidence to recommend one class of long-acting bronchodilator over another in this group of patients. The choice should depend on the patient's perception of symptom relief. For patients with severe breathlessness, initial treatment with two bronchodilators of different classes may be warranted.

  • For group C patients (few symptoms but higher risk of exacerbations), first-line treatment should be a LAMA. [ Cochrane Clinical Answers logo ]

  • For group D patients (more symptoms and high risk of exacerbations), GOLD recommends starting therapy with a LAMA, a LABA/LAMA combination, or an inhaled corticosteroid (ICS)/LABA combination. A LAMA is the first choice for most patients. A LABA/LAMA combination should be considered if the patient is highly symptomatic (COPD assessment test [CAT] score >20) and an ICS/LABA combination should be considered if the patient’s blood eosinophil count is ≥300 cells/microlitre or the patient has a history of asthma. ICS increases the risk of developing pneumonia in some patients, so should only be used as initial therapy after the possible clinical risks and benefits have been evaluated. [ Cochrane Clinical Answers logo ]

com.bmj.content.model.Caption@3fc3b88d[Figure caption and citation for the preceding image starts]: Initial pharmacologic management of COPDGlobal Initiative for Chronic Obstructive Lung Disease (GOLD). Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease (2020 report); used with permission [Citation ends].

Further treatment is determined by the patient’s dyspnoea/exercise limitation symptom burden and frequency of exacerbations after review and is independent of the patient’s GOLD group at diagnosis.[1] GOLD recommends different treatment pathways depending on whether the primary treatment goal is relieving dyspnoea/exercise limitation symptoms or reducing exacerbations. If treatment is required for both purposes, clinicians should follow the exacerbation pathway. Patients should be reviewed and their inhaler technique and treatment adherence assessed after each adjustment in treatment.[1]

Recommended escalation therapy for patients with persistent dyspnoea/exercise limitation after initial therapy is:[1]

  • Patients taking long-acting bronchodilator monotherapy should start a second long-acting bronchodilator from a different class. If symptoms do not improve, the second long-acting bronchodilator should be stopped. Changing inhaler device or molecules may be considered.

  • For patients taking LABA/ICS therapy, LAMA may be added (triple therapy). Alternatively, LABA/ICS may be switched to LABA/LAMA if the original indication for LABA/ICS was not appropriate, if the patient has not responded to ICS treatment, or if there are significant ICS adverse effects.

  • Dyspnoea due to other causes should be considered, investigated, and treated.

Recommended escalation therapy for patients with persistent exacerbations after initial therapy is:[1]

  • Patients taking long-acting bronchodilator monotherapy should increase therapy to either LABA/LAMA or LABA/ICS. Blood eosinophil counts can identify patients who are more likely to respond to ICS.[45] LABA/ICS may be considered in patients with two or more exacerbations per year and an eosinophil count ≥100 cells/microlitre, or if the history/clinical findings are suggestive of asthma.[1] Patients who have one exacerbation per year are more likely to respond to LABA/ICS if their peripheral eosinophil count is ≥300 cells/microlitre.[46] Patients who take a LABA or LAMA who have blood eosinophils <100 cells/microlitre or who have contraindications to ICS should commence a LABA/LAMA.

  • Patients who take LABA/LAMA and whose blood eosinophils are ≥100 cells/microlitre should escalate to triple therapy with LABA/LAMA/ICS. Multiple studies support triple therapy with LABA/LAMA/ICS as being superior to single- or double-agent therapy with LABA/LAMA or LABA/ICS regarding rate of moderate to severe COPD exacerbations and rate of hospitalisation.[47][48][49][50][51][52] American Thoracic Society guidelines recommend the use of triple therapy in patients who have had one or more exacerbations requiring oral corticosteroids, antibiotics, or hospitalisation in the past year and who have symptoms of dyspnoea or reduced exercise tolerance despite LABA/LAMA dual therapy.[53] UK guidelines recommend the use of triple therapy in patients who have an exacerbation requiring hospitalisation, or two moderate exacerbations within a year, despite dual therapy with LABA/LAMA.[2]

  • Patients who take a LABA/LAMA and whose blood eosinophils are <100 cells/microlitre should add roflumilast or azithromycin.

  • Patients who take LABA/ICS should escalate to triple therapy by adding a LAMA. If ICS is ineffective or causing significant adverse effects, patients may switch to LABA/LAMA.

  • Patients who take LABA/LAMA/ICS may add roflumilast or azithromycin. Roflumilast may be considered in patients with FEV1 <50% predicted and chronic bronchitis, particularly if they have had at least one hospitalisation for an exacerbation in the last year. The risk of developing antibiotic-resistant organisms should be considered when prescribing azithromycin. ICS can be discontinued if it is ineffective or causing adverse effects. Patients with blood eosinophils ≥300 cells/microlitre are at greatest risk of exacerbations after withdrawing ICS.[54]

All patients are candidates for education, vaccination, and smoking cessation interventions.

com.bmj.content.model.Caption@fac9752[Figure caption and citation for the preceding image starts]: Escalation therapy for patients with COPDGlobal Initiative for Chronic Obstructive Lung Disease (GOLD). Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease (2020 report). Reproduced with permission. [Citation ends].

Bronchodilators

Beta-2 agonists are widely used in the treatment of COPD. They increase intracellular cAMP, leading to respiratory smooth muscle relaxation and reduced airway resistance. Muscarinic antagonists (anticholinergics) act as bronchodilators by blocking the cholinergic receptors on the respiratory smooth muscle. This causes muscle relaxation and reduces airflow limitation. Both are available as short-acting and long-acting preparations.

Short-acting beta-2 agonists (e.g., salbutamol) and short-acting muscarinic antagonists (e.g., ipratropium) improve lung function and breathlessness and quality of life. Ipratropium may have a small benefit over short-acting beta-2 agonists in improving health-related quality of life.[55] These agents can be used as rescue therapy when the patient is using long-acting bronchodilator therapy and may be used as initial treatment for patients in GOLD group A if patients only have occasional dyspnoea.[1][56] However, regular use of short-acting bronchodilators is not generally recommended.

Tiotropium, a LAMA, has been shown to reduce risk of exacerbation versus placebo or other maintenance treatments.[57] [ Cochrane Clinical Answers logo ] Newer LAMAs, such as aclidinium, glycopyrronium, and umeclidinium, have at least comparable efficacy to tiotropium, in terms of change from baseline in trough forced expiratory volume in 1 second (FEV1), transitional dyspnoea index focal score, St George's Respiratory Questionnaire score, and rescue medication use.[58] Revefenacin is a nebulised LAMA approved for the maintenance treatment of moderate to severe COPD. There is a suggestion of increased cardiovascular-related mortality in some studies of patients taking short-acting muscarinic antagonists and in some studies of patients taking LAMAs.[59][60] One study concluded that aclidinium was not associated with an increase in major adverse cardiovascular events, compared with placebo.[61] A population-based cohort study found that older men with COPD newly started on LAMAs are at increased risk of urinary tract infections.[62]

Beta agonists and muscarinic antagonists, therefore, provide bronchodilator effects through different pathways. LABAs and LAMAs both significantly improve lung function, dyspnoea, and health status and reduce exacerbation rates. [ Cochrane Clinical Answers logo ] In cases of stable COPD, if the decision is made to use single-agent therapy, LAMA may be superior to LABA agents.[63] LAMAs have a greater effect on exacerbation reduction than LABAs in patients with moderate to very severe COPD.[1][43][44] The long-term safety of LAMA was demonstrated in the UPLIFT trial.[64]

A LABA/LAMA combination may provide a better therapeutic effect without increasing the adverse effects of each class.[65][66][67][68] Combination therapy with a LABA/LAMA reduces exacerbation rate compared with monotherapy. Once-daily LABA/LAMA delivered via a combination inhaler is more associated with a clinically significant improvement in lung function and health-related quality of life in patients with mild/moderate COPD, compared with placebo.[69] Compared to LABA/ICS, a LABA/LAMA combination has fewer exacerbations, a larger improvement of FEV1, a lower risk of pneumonia, and more frequent improvement in quality of life.[70] A systematic review and network meta-analysis found that all LABA/LAMA fixed-dose combinations had a similar efficacy and safety.[71]

Umeclidinium/vilanterol, glycopyrronium/formoterol, indacaterol/glycopyrronium, tiotropium/olodaterol, and aclidinium/formoterol are LABA/LAMA combinations approved for use in COPD. Indacaterol/glycopyrronium showed superior efficacy compared with glycopyrronium or tiotropium in patients with moderate to severe COPD, and compared with salmeterol/fluticasone in preventing COPD exacerbation.[72][73] Umeclidinium/vilanterol decreases the risk of exacerbations in patients with mild/moderate COPD.[69]

As outlined above, GOLD makes recommendations on the initial agent based on the patient’s risk group (A, B, C, or D).[1] American Thoracic Society guidelines recommend initiating LABA/LAMA dual therapy in preference to monotherapy in patients with COPD who have dyspnoea or exercise intolerance.[53] UK guidelines recommend initiating dual therapy with a LABA/LAMA or LABA/ICS if a patient has symptoms or exacerbations despite non-pharmacological treatment and using a short-acting bronchodilator as needed.[2]

Inhaled corticosteroids

Inhaled corticosteroids are indicated in some patients with COPD who suffer from frequent exacerbations.[1][74] They should always be prescribed in combination with long-acting bronchodilators. Inhaled corticosteroids are believed to be effective because of their anti-inflammatory effects. Long-term inhaled corticosteroid use reduces the need to use rescue therapy and reduces exacerbations, and may also decrease mortality.[75][76][77] [ Cochrane Clinical Answers logo ]

The effect of treatment regimens containing ICS is higher in patients at higher risk of exacerbations (two or more exacerbations and/or one hospitalisation in the previous year).[49][51][73] Blood eosinophil count may predict the effectiveness of adding inhaled corticosteroids to regular long-acting bronchodilator treatment to prevent exacerbations.[78] Little or no effect is seen at eosinophil counts of <100 cells/microlitre, while maximal effect is seen at blood eosinophil counts of >300 cells/microlitre.[45][79] These thresholds indicate approximate cut-off values which may help clinicians predict the likelihood of a treatment benefit.[1] Former smokers are more corticosteroid-responsive than current smokers at any eosinophil count.[78]

Several studies have pointed to an increased risk of pneumonia in patients with COPD taking inhaled corticosteroids.[80] This risk is slightly higher for fluticasone in comparison with budesonide.[81] A systematic review and meta-analysis found that, despite a significant increase in unadjusted risk of pneumonia associated with use of inhaled corticosteroids, pneumonia fatality and overall mortality were not increased in randomised controlled trials and were decreased in observational studies.[82] Therefore, an individualised treatment approach that assesses a patient's risk of pneumonia versus the benefit of decreased exacerbations should be implemented.[80][83][84] Concern is also raised with regards to increased risk of tuberculosis and influenza in adult patients with COPD who are on inhaled corticosteroid therapy.[85] ICS may also cause oropharyngeal candidiasis and hoarseness.[80]

Clinicians should weigh the potential benefits and risks of prescribing ICS and discuss these with the patient.[2] GOLD advise that a history of hospitalisation for an exacerbation of COPD, two or more moderate exacerbations per year despite regular long-acting bronchodilators, blood eosinophils of ≥300 cells/microlitre, and/or previous or concomitant asthma all strongly favour initiating ICS. Repeated episodes of pneumonia, blood eosinophils <100 cells/microlitre, and/or history of mycobacterial infection are all factors against the use of ICS. Use of ICS can be considered in patients with one moderate exacerbation of COPD per year despite regular long-acting bronchodilator therapy and/or peripheral eosinophils 100-300 cells/microlitre.[1]

Long-term use of oral corticosteroids in COPD is not recommended.[53] Some patients with severe disease are unable to completely stop treatment after starting corticosteroids for an acute exacerbation. In this case, the dose should be kept as low as possible and consideration given to osteoporosis prophylaxis.[2]

Combined bronchodilator and corticosteroid preparations

A combination preparation of a long-acting bronchodilator and an inhaled corticosteroid may be used for patients who require both these agents. [ Cochrane Clinical Answers logo ] This is convenient and may help with compliance in some patients. The choice of therapy in this class is based on availability and individual response and preference.[86] Combination therapy with an inhaled corticosteroid and a LABA is superior to use of either agent alone.[87][88] [ Cochrane Clinical Answers logo ] The combination may be provided in separate inhalers or a combination inhaler.

Multiple studies support triple therapy with LABA/LAMA/ICS as being superior to single- or double-agent therapy with LABA/LAMA or LABA/ICS regarding rate of moderate to severe COPD exacerbations and rate of hospitalisation.[47][48][49][50][51][52][89][79][90] Use of ICS also slows the rate of decline in lung function following an exacerbation in patients with mild to moderate COPD and elevated blood eosinophils.[91] One randomised controlled trial has reported a reduction in all-cause mortality in patients with FEV1 <50% and at least one exacerbation in the past year who take fluticasone furoate/umeclidinium/vilanterol, compared with patients taking umeclidinium/vilanterol. Patients with mild COPD and at least two moderate or one severe exacerbations in the last year also had reduced all-cause mortality when taking fluticasone furoate/umeclidinium/vilanterol, compared with umeclidinium/vilanterol.[92] Increasing the dose of budesonide in triple therapy does not decrease the rate of exacerbations, compared with standard dose triple therapy.[90] Before prescribing triple therapy, clinicians should assess whether another physical or mental condition could be causing the patient’s symptoms. UK guidelines advise clinicians to review patients taking triple therapy for relief of daily symptoms after 3 months. Treatment should be changed to LABA/LAMA if the patient’s symptoms have not improved.[2] The ICS may be withdrawn if the patient has had no exacerbations in the past year.[53]

Phosphodiesterase-4 inhibitors

Roflumilast is an oral phosphodiesterase-4 inhibitor which inhibits the breakdown of cAMP. It is an option for patients who have persistent exacerbations despite therapy with long-acting bronchodilators and corticosteroids, or for whom addition of ICS to long-acting bronchodilators is not appropriate.[1] Roflumilast offers benefit in improving lung function and reducing the likelihood of exacerbations. However, it has little impact on quality of life or symptoms.[93]

Antibiotics

Prophylactic antibiotics, such as macrolides, may be considered for reducing the risk of acute exacerbation, particularly in patients who have frequent exacerbations and are refractory to standard therapy.[94][95][96] Use of prophylactic macrolide antibiotics decreases the frequency of exacerbations in patients with COPD but long-term azithromycin use is associated with clinically significant hearing loss, which in many cases was reversible.[97] [ Cochrane Clinical Answers logo ] There are no data showing the efficacy or safety of chronic azithromycin treatment beyond 1 year of treatment.

Azithromycin therapy is believed to be most effective in preventing acute exacerbation, with greater efficacy seen in older patients and milder GOLD stages. Little evidence of treatment benefit is seen in current smokers.[98] Azithromycin increases the risk of colonisation with macrolide-resistant organisms and should not be prescribed for patients with hearing impairment, resting tachycardia, or apparent risk of QTc prolongation.[99]

UK guidelines advise that prophylactic azithromycin could be considered for patients who have more than three acute exacerbations requiring corticosteroid therapy and at least one exacerbation requiring hospitalisation per year.[100] Before starting prophylactic antibiotics, baseline ECG and liver function tests should be performed, a sputum sample obtained for culture and sensitivity (including tuberculosis testing), the patient’s sputum clearance technique should be optimised, and bronchiectasis should be excluding with a CT scan.[2][100] ECG and liver tests should be repeated after 1 month of treatment. A head-to-head comparison of fluoroquinolones, tetracyclines, and macrolides given for 12 to 13 weeks to people with COPD did not identify a difference in efficacy or safety between antibiotic classes, but the sample sizes of included studies were small and the studies were of short duration; further research is required in this area.[101]

Prophylactic antibiotic therapy should be reviewed at 6 and 12 months to determine whether there is a benefit in terms of exacerbation rates.[100] If antibiotic therapy is not effective it should be stopped.

Methylxanthines

Theophylline (a methylxanthine agent) is a bronchodilator that acts by increasing cAMP and subsequent respiratory smooth muscle relaxation. It is not commonly used because of limited potency, narrow therapeutic window, high risk profile, and frequent drug-drug interactions. Theophylline is indicated for persistent symptoms if inhaled therapy is insufficient to relieve airflow obstruction. Theophylline has modest effects on lung function in moderate to severe COPD.[102] GOLD advise that theophylline should only be used if other long-term bronchodilator treatments are unavailable or unaffordable.[1] Experts may prescribe theophylline after a patient has exhausted all options for inhaled therapies.

Patient education and self-management

All patients should be well educated about the disease course and symptoms of exacerbation or decompensation. Their expectation of the disease, treatment, and prognosis should be realistic. It is important to remember that no medicine has been shown to modify the long-term decline in lung function, and the primary goal of pharmacotherapy is to control symptoms and prevent complications.

One Cochrane review found that self-management interventions that include an action plan for acute exacerbations of COPD are associated with improvements in health-related quality of life and fewer admissions to hospital for respiratory problems. An exploratory analysis found a small, but significantly higher, respiratory-related mortality rate for self-management compared to usual care, although no excess risk of all-cause mortality was seen.[103] Self-management plans should include personalised advice on: breathlessness and stress management techniques, energy conservation, avoiding aggravating factors, how to monitor symptoms, how to manage worsening symptoms, and contact information to use in the event of an exacerbation.[1]

Helping patients to self-manage should ideally address psychosocial concerns and patients’ personal beliefs about COPD and its management. Many patients report losses and limitations on their lifestyle and social interaction after a diagnosis of COPD. Symptoms of anxiety, depression, and frustration are common.[104] A systematic review found a small beneficial effect of cognitive behavioural therapy-based psychological treatment and symptoms of depression, compared with education or no intervention, although the evidence was limited by heterogeneity between trials and inability to blind participants and researchers to the intervention.[105]

One randomised controlled trial found that a telephone health coaching intervention to promote behaviour change in patients with mild COPD in primary care led to improvements in self-management activities, but did not improve health-related quality of life.[106] A meta-analysis found that health coaching that included goal setting, motivational interviewing, and COPD-related health education significantly improved health-related quality of life and reduced hospital admissions for an exacerbation of COPD, but did not decrease all-cause hospital admissions.[107]

Patients who use inhaled therapies should receive training on inhaler device technique. The majority of patients make at least one error in using their inhaler and incorrect inhaler use is associated with worse disease control.[108][109] Poor technique is more likely when patients are using multiple devices or have never received inhaler technique training.[110] Demonstration of inhaler use by a clinician, device selection, and reviewing technique at subsequent appointments can improve inhaler technique.[111] Demonstration using a placebo device may be most effective for teaching inhaler technique to adults aged ≥65 years.[112] Patients should be asked to bring their inhalers to clinic to facilitate a review of inhaler use.[1]

Physical activity is recommended for all patients with COPD.[1] One systematic review and meta-analysis of randomised controlled trials found that exercise training on its own can improve physical activity in COPD, and greater improvements can be made with the addition of physical activity counselling.[113] Another systematic review and meta-analysis found that a combination of aerobic exercise and strength training was more effective than strength training or endurance training alone in increasing the 6-minute walking distance.[114] A Cochrane review found limited evidence for improvement in physical activity with physical activity counselling, exercise training, and pharmacological management of COPD. The authors commented that assessment of quality had been limited by lack of methodological detail and the diverse range of interventions had primarily been assessed in single studies.[115] The optimal timing, components, duration, and models for improving physical activity remain unclear. Meta-analyses suggest that yoga and Qigong can improve exercise capacity and pulmonary function in patients with COPD.[116][117]

Smoking cessation and vaccination

Smoking cessation should be encouraged in all patients, in addition to guidance on avoiding occupational or environmental tobacco smoke exposures.[1][2] Smoking cessation significantly reduces the rate of progression of COPD and risk of malignancies. It also reduces the risk of coronary and cerebrovascular diseases. Among different therapeutic modalities in COPD, the only two factors that improve survival are smoking cessation and oxygen supplementation.

Usual smoking-cessation programmes include counselling, group meetings, and drug therapy.[118] Some patients may need frequent referrals to achieve success. Smoking cessation that includes pharmacotherapy and intensive counselling has a higher success rate and is cost effective in COPD, with low costs per quality-adjusted life year.[119][120][121]

Patients should be vaccinated against influenza virus and Streptococcus pneumoniae.[1][122] Vaccination against influenza is associated with fewer exacerbations of COPD.[122][123] [ Cochrane Clinical Answers logo ] Guidance from the US Centers for Disease Control and Prevention (CDC) advises a single dose of 23-valent pneumococcal polysaccharide vaccination for all patients with COPD who have not previously received the recommended pneumococcal vaccine.[124]

Mucolytics

Patients with the chronic bronchitis phenotype of COPD often produce thick sputum on a frequent basis. Mucolytic agents are not associated with an increase in adverse effects and may be beneficial during exacerbations of COPD. [ Cochrane Clinical Answers logo ] They result in a small reduction in the frequency of acute exacerbations and in days of disability per month, but do not improve lung function or quality of life.[125] One meta-analysis comparing erdosteine, carbocisteine, and acetylcysteine concluded that erdosteine had the most favourable safety and efficacy profile. Erdosteine reduced the risk of hospitalisation due to an acute exacerbation, and erdosteine and acetylcysteine reduced the duration of an acute exacerbation.[126] Erdosteine and carbocisteine are not available in the US and some other countries. Mucolytic agents may be most beneficial for patients not on inhaled corticosteroids.[1]

Pulmonary rehabilitation

Pulmonary rehabilitation compromises aerobic exercise, strength training, and education. It should be initiated for patients who remain symptomatic despite bronchodilator therapy and is recommended to start early in the course of the disease, when they start feeling shortness of breath with regular activity and walking on a level surface. GOLD guidelines recommend pulmonary rehabilitation for patient groups B to D.[1]

Pulmonary rehabilitation relieves dyspnoea and fatigue, improves emotional function, and enhances a sense of control to a moderately large and clinically significant extent.[127] Extensive pulmonary rehabilitation following hospital admission with an acute exacerbation of COPD decreases the risk of readmission, improves health-related quality of life, and reduces mortality. [ Cochrane Clinical Answers logo ] It also decreases the depression and anxiety related to this disease, and reduces hospitalisation in patients with COPD.[128] The benefit appears to subside after termination of the course unless patients follow a home exercise schedule.[129] Benefits of home- or community-based pulmonary rehabilitation on respiratory symptoms and quality of life in patients with COPD could match those of the hospital-based rehabilitation programmes.[130][131] Early progressive exercise rehabilitation beyond current standard physiotherapy practice during hospital admission for COPD is not recommended and could be associated with a higher 12-month mortality.[132] There is evidence to support starting pulmonary rehabilitation within 1 month of an acute exacerbation.[133][134]

Oxygen therapy

GOLD guidelines recommend long-term oxygen therapy in stable patients who have:[1]

  • PaO₂ ≤7.3 kPa (55 mmHg) or SaO₂ ≤88%, with or without hypercapnia confirmed twice over a 3-week period; or

  • PaO₂ between 7.3 kPa (55 mmHg) and 8.0 kPa (60 mmHg), or SaO₂ of 88%, if there is evidence of pulmonary hypertension, peripheral oedema suggesting congestive cardiac failure, or polycythaemia (haematocrit > 55%).

Supplemental oxygen should be titrated to achieve SaO₂ ≥90%. The patient should be reassessed after 60 to 90 days to determine whether oxygen is still indicated and is therapeutic.[1] Among different therapeutic modalities in COPD, the only two factors that improve survival are smoking cessation and oxygen supplementation.

Oxygen therapy helps to minimise pulmonary hypertension by decreasing pulmonary artery pressure, and improves exercise tolerance and quality of life. It has been shown to improve survival.[1][31]

There is some evidence that oxygen can relieve breathlessness when given during exercise to mildly hypoxaemic and non-hypoxaemic people with COPD who do not otherwise qualify for home oxygen therapy.[135]

Air travel is safe for most patients receiving long-term oxygen therapy.[1] Patients with SaO₂ >95% at sea level and SaO₂ ≥84% after a 6-minute walk test may travel by air without further assessment. Supplemental oxygen is recommended for patients with SaO₂ 92% to 95% at sea level and SaO₂ <84% after a 6-minute walk test, and for patients with SaO₂ <92% at sea level. Hypoxia-altitude simulation testing should be performed for other patients.[136]

Surgery

Surgical interventions (bullectomy, lung volume reduction surgery,[137][138] [ Cochrane Clinical Answers logo ] and lung transplant) are the last step in the management of COPD. They are used to improve lung dynamics, exercise adherence, and quality of life.[138] Lung volume reduction surgery is indicated in patients with very severe airflow limitation, and especially in patients with localised upper lobe disease and lower than normal exercise capacity.[137] [ Cochrane Clinical Answers logo ] Bullectomy is an option in COPD patients with dyspnoea in whom CT reveals huge bullae occupying at least 30% of the hemithorax. Severely poor functional status and severe decrease in FEV1 (<500 mL) make these options less favourable. Endobronchial valve insertion can produce clinically meaningful improvements in appropriately selected patients with COPD.[139]

Criteria for referral for lung transplantation include:[140]

  • Progressive disease, despite maximal treatment including medication, pulmonary rehabilitation, and oxygen therapy.

  • Patient is not a candidate for endoscopic or surgical lung volume reduction surgery (LVRS). Simultaneous referral of patients with COPD for both lung transplant and LVRS evaluation is appropriate.

  • Body mass index, airflow Obstruction, Dyspnoea, and Exercise (BODE) index of 5 to 6.

  • PaCO₂ >50 mmHg or 6.6 kPa and/or PaO₂ <60 mmHg or 8 kPa.

  • FEV1 <25% predicted.

[ BODE Index for COPD Survival Prediction ]

Lung transplantation has been shown to improve quality of life and functional capacity.[138] However, lung transplantation does not appear to confer a survival benefit.[141]

Palliative care

Palliative therapies to improve symptoms of dyspnoea, offer nutritional support, address anxiety and depression, and reduce fatigue may benefit patients with COPD who experience these despite optimal medical therapy.[1] End-of-life care and hospice admission should be considered for patients with very advanced disease. Patient and family should be well educated about the process, and it is suggested that discussions should be held early in the course of the disease before acute respiratory failure develops.[142] Opioid analgesics, fans, neuromuscular electrical stimulation, and chest wall vibration can relieve dyspnoea.[1] Long-acting oral and parenteral opioids may be considered for treating dyspnoea in patients with severe COPD.[1] One study has suggested that low doses of an opioid analgesic and a benzodiazepine are safe and are not associated with increased hospital admissions or mortality.[143]

One Cochrane review concluded that there is no evidence for or against benzodiazepines for the relief of breathlessness in people with advanced cancer and COPD.[144]

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