11 Liverpool University Hospitals NHS Foundation Trust, UK / National Heart and Lung Institute, Imperial College, London, UK / School of Clinical Medicine, College of Health Sciences, University of Kwazulu-Natal, South Africa;
Find articles by Kevin Mortimer12 University of Ferrara, Ferrara, Italy;
Find articles by Alberto Papi13 Respiratory Medicine Unit and Oxford Respiratory NIHR Biomedical Research Centre, Nuffield Department of Medicine, University of Oxford, UK;
Find articles by Ian Pavord14 Pneumologie, Hôpital Cochin AP-HP.Centre, Université Paris, France;
Find articles by Nicolas Roche15 Pulmocare Research and Education (PURE) Foundation, Pune, India;
Find articles by Sundeep Salvi16 St. Paul’s Hospital University of British Columbia, Vancouver, Canada;
Find articles by Don D. Sin17 University of Manchester, Manchester, UK;
Find articles by Dave Singh18 University Hospital, Birmingham, UK;
Find articles by Robert Stockley19 Universidad de la República Hospital Maciel Montevideo, Uruguay; and
Find articles by M. Victorina López Varela20 Department of Medicine, Pulmonary and Critical Care Medicine, University Medical Center Giessen and Marburg, Philipps-University, German Center for Lung Research (DZL), Marburg, Germany
Find articles by Claus F. Vogelmeier 1 Univ. Barcelona, Hospital Clinic, IDIBAPS and CIBERES, Spain; 2 Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts, USA; 3 Lewis Katz School of Medicine at Temple University, Philadelphia, Pennsylvania, USA;4 University of Exeter Medical School College of Medicine and Health, University of Exeter, Exeter, Devon, UK;
5 South Texas Veterans Health Care System, University of Texas Health, San Antonio, Texas, USA; 6 National Heart & Lung Institute, Imperial College London, United Kingdom; 7 McGill University Health Centre, McGill University, Montreal, Canada; 8 University of Michigan, Ann Arbor, Michigan, USA; 9 Weill Cornell Medical Center/ New York-Presbyterian Hospital, New York, New York, USA;10 Hospital Universitario de Caracas Universidad Central de Venezuela Centro Médico de Caracas, Caracas, Venezuela;
11 Liverpool University Hospitals NHS Foundation Trust, UK / National Heart and Lung Institute, Imperial College, London, UK / School of Clinical Medicine, College of Health Sciences, University of Kwazulu-Natal, South Africa;
12 University of Ferrara, Ferrara, Italy;13 Respiratory Medicine Unit and Oxford Respiratory NIHR Biomedical Research Centre, Nuffield Department of Medicine, University of Oxford, UK;
14 Pneumologie, Hôpital Cochin AP-HP.Centre, Université Paris, France; 15 Pulmocare Research and Education (PURE) Foundation, Pune, India; 16 St. Paul’s Hospital University of British Columbia, Vancouver, Canada; 17 University of Manchester, Manchester, UK; 18 University Hospital, Birmingham, UK; 19 Universidad de la República Hospital Maciel Montevideo, Uruguay; and20 Department of Medicine, Pulmonary and Critical Care Medicine, University Medical Center Giessen and Marburg, Philipps-University, German Center for Lung Research (DZL), Marburg, Germany
Corresponding author.Correspondence and requests for reprints should be addressed to Dr. Alvar Agustí, Institut Respiratori, Clinic Barcelona, C/Villarroel 170, 08036 Barcelona, Spain. E-mail: tac.cinilc@itsugaa.
* Co–first authors. Received 2023 Jan 17; Accepted 2023 Feb 28. Copyright © 2023 by the American Thoracic SocietyThis article is open access and distributed under the terms of the Creative Commons Attribution Non-Commercial No Derivatives License 4.0. For commercial usage and reprints, please e-mail Diane Gern (gro.cicaroht@nregd).
The Global Initiative for Chronic Obstructive Lung Disease (GOLD) has published the complete 2023 GOLD report, which can be freely downloaded from its web page (www.goldcopd.org) together with a “pocket guide” and a “teaching slide set” (1). It contains important changes compared to earlier versions, and incorporates 387 new references (1). Here, we present an executive summary of this GOLD 2023 report (1) that (1) summarizes aspects that are relevant from a clinician’s perspective and (2) updates evidence published since the prior executive summary in 2017.
The definition of a disease should only include the characteristics that distinguish it from other diseases (2). Accordingly, GOLD 2023 proposes a new definition of COPD that, at variance with previous documents (3), focuses exclusively on these characteristics, separately from its epidemiology, causes, risk factors, and diagnostic criteria that are discussed on their own.
GOLD 2023 defines COPD as a heterogeneous lung condition characterized by chronic respiratory symptoms (dyspnea, cough, expectoration, and/or exacerbations) due to abnormalities of the airways (bronchitis, bronchiolitis) and/or alveoli (emphysema) that cause persistent, often progressive, airflow obstruction.
COPD results from dynamic, cumulative, and repeated gene (G) - environment (E) interactions over the lifetime (T) that damage the lungs and/or alter their normal development/aging processes (GETomics) (4).
Cigarette smoking is a key environmental risk factor for COPD. Cigarette smokers have a higher prevalence of respiratory symptoms and lung function abnormalities, a greater annual rate of FEV1 decline, and a greater COPD mortality rate than nonsmokers (5); yet fewer than 50% of heavy smokers develop COPD (6). Passive exposure to cigarette smoke, other types of tobacco smoke (e.g., pipe, cigar, water pipe) (7–9), and marijuana (10) are also risk factors for COPD (11). Smoking during pregnancy poses a risk for the fetus, by altering lung growth and development in utero, and possibly priming the immune system for abnormal/enhanced responses in the future (4, 12).
In low- and middle-income countries (LMICs), COPD in nonsmokers may be responsible for up to 60–70% of cases (13). Because the LMICs contribute to over 85% of all COPD cases, non-smoking risk factors account for over 50% of the global burden of COPD (13). Wood, animal dung, crop residues, and coal (i.e., biomass), typically burned in poorly functioning stoves, may lead to very high levels of household air pollution (14), which is associated with increased COPD risk, although the extent to which household air pollution versus other poverty-related exposures explains the association is unclear (15, 16). Compared to COPD in smokers, COPD in nonsmokers is more common in females, of younger age, and exhibits similar (or milder) respiratory symptoms and quality-of-life impairment. They have similar spirometric indices but greater small airway obstruction, less emphysema, and a lesser rate of lung function decline. Finally, they show lower neutrophil count, higher eosinophil numbers in the sputum (13), and a similar defect in macrophage phagocytosis of pathogenic bacteria (17). Research is needed to understand how interventions aimed at decreasing household air pollution can reduce the risk of COPD as well as what is the most appropriate pharmacotherapy for this type of COPD (13).
Occupational exposures, including organic and inorganic dusts, chemical agents, and fumes, are an underappreciated environmental risk factor for COPD (18, 19). The US National Health and Nutrition Examination Survey III estimated the fraction of COPD attributable to workplace exposures was 19.2% overall, and 31.1% among never-smokers (20).
Air pollution, which typically consists of particulate matter (PM), ozone, oxides of nitrogen or sulfur, heavy metals, and other greenhouse gases, is a major worldwide cause of COPD, responsible for ∼50% of the attributable risk for COPD in LMICs (1). The risk of air pollution to individuals is dose-dependent, with no apparent “safe” threshold. Even in countries with relatively low ambient air pollution, chronic exposure to PM
The most relevant genetic risk factor for COPD identified are mutations in SERPINA1, leading to α-1 antitrypsin deficiency, a major circulating inhibitor of serine proteases (24). The PiZZ genotype affects 0.12% of COPD patients, and its prevalence ranges from 1 in 408 in Northern Europe to 1 in 1,274 in Eastern Europe (25). There is no increased COPD risk in heterozygotes (MZ and SZ) in the absence of smoking (26).
Other genetic variants have also been associated with reduced lung function and risk of COPD; their individual effect size is small, although their co-occurrence may increase disease susceptibility (27).
At birth, the lungs are not fully developed. They grow and mature until about 20–25 years of age (earlier in females), when lung function reaches its peak (5). This is followed by a relatively short plateau and a final phase of mild lung function decline due to physiological lung aging. This normal lung function trajectory can be altered by processes occurring during gestation, birth, childhood, and adolescence that affect lung growth (hence, peak lung function) and/or processes shortening the plateau phase and/or accelerating the aging phase (28). Indeed, in the general population, there is a range of lung function trajectories through the lifetime (28). Trajectories below the normal range are associated with a higher prevalence and earlier incidence of multimorbidity and premature death (29), whereas those above the normal range are associated with healthier aging and fewer cardiovascular and respiratory events, as well as with a survival benefit (30, 31).
Factors in early life termed “childhood disadvantage factors,” including prematurity, low birth weight, maternal smoking during pregnancy, repeated respiratory infections, and poor nutrition, among others, are key determinants of peak lung function attained in early adulthood (32–39). Reduced peak lung function in early adulthood increases the risk of COPD later in life (32, 40, 41). In fact, approximately 50% of patients develop COPD due to accelerated decline in FEV1 over time, while the other 50% develop it due to abnormal lung growth and development (with normal lung function decline over time) (42).
The prevalence of COPD in developed countries is now almost equal in males and females (43). Women report more dyspnea and worse health status scores and have a higher incidence of exacerbations compared with men at similar severity of airflow limitation (44).
Poverty and lower socioeconomic status are consistently associated with airflow obstruction (45) and increased risk of COPD (46). It is likely that this reflects exposures to household and outdoor air pollutants, crowding, poor nutrition, infections, or other factors related to low socioeconomic status.
Many different studies have reported that asthma and atopy in infancy may be significant risk factors for COPD in adulthood (47, 48). However, it is important to remember that abnormal lung development in childhood and adolescence can cause asthma-like symptoms. Given that poor lung development is associated with COPD in adulthood (see above), some of these infants and adolescents may have been mislabeled as “asthma.”
Severe respiratory infections in childhood have been associated with reduced lung function and increased respiratory symptoms in adulthood (47, 49). In adults, chronic bronchial infection, particularly with Pseudomonas aeruginosa, is associated with accelerated FEV1 decline (50). In many parts of the world, tuberculosis (51) and HIV infection (52) are also important risk factors for COPD.
A diagnosis of COPD should be considered in any patient who complains of dyspnea, chronic cough or sputum production, a history of recurrent lower respiratory tract infections, and/or a history of exposure to risk factors for the disease (see above), but forced vital capacity maneuver during spirometry showing the presence of a post-bronchodilator FEV1/FVC ratio 0.7 is needed to establish the diagnosis of COPD. The FEV1 also serves to determine the severity of airflow obstruction (GOLD grades 1, 2, 3, 4 or mild, moderate, severe, and very severe). Yet, several important aspects related to forced spirometry need to be considered here.
First, airflow obstruction that is not fully reversible is not specific for COPD. For instance, it may also be found in patients with asthma and other diseases, so the clinical context and risk factors (see above) must also be considered when establishing a diagnosis of COPD.
Second, if the post-bronchodilator FEV1/FVC ratio is between 0.60 and 0.80 on a single spirometric measurement, this should be confirmed by repeat spirometry on a separate occasion, as in some cases the ratio may change as a result of biological variation when measured at a later interval (53, 54). When the initial post-bronchodilator FEV1/FVC ratio is
Third, there is a long-standing debate on whether it is better to use a fixed FEV1/FVC ratio of lower limit of normal (LLN) for the diagnosis of COPD. GOLD favors the use of the former because it is simple and independent of reference values, since it relates to variables measured in the same individual and has been used in all the clinical trials that form the evidence base on which treatment recommendations are drawn. GOLD 2023 acknowledges that use of a fixed FEV1/FVC ratio 1/FVC. LLN values are based on the normal distribution and classify the bottom 5% of the healthy population as abnormal. Thus, LLN values are highly dependent on the choice of reference equations as well as race/ethnicity, and there are no longitudinal studies available validating the use of the LLN. Further, using the fixed ratio is not inferior to LLN regarding prognosis (57). Finally, the risk of misdiagnosis and overtreatment of individual patients using the fixed ratio as a diagnostic criterion is limited, as spirometry is only one biological measurement to establish the clinical diagnosis of COPD in the appropriate clinical context (symptoms and risk factors). Diagnostic simplicity and consistency are crucial for the busy clinician.
Fourth, while post-bronchodilator spirometry is required for the diagnosis and assessment of COPD, assessing the degree of reversibility of airflow obstruction to inform therapeutic decisions is no longer recommended (58). The degree of reversibility in a single patient varies over time and has not been shown to differentiate COPD from asthma (except when airflow limitation disappears following bronchodilators, which is incompatible with COPD), or to predict the response to long-term treatment with bronchodilators or corticosteroids (59). Accordingly, it is not necessary nor advised (1) to stop inhaled medication before obtaining spirometry measurements during follow-up of patients.
Finally, the role of screening spirometry in the general population for the diagnosis of COPD is also controversial. In asymptomatic individuals without any significant exposure to tobacco or other risk factors, screening spirometry is probably not indicated. By contrast, in those with symptoms and/or risk factors (e.g., >20 pack-years of smoking, recurrent chest infections, prematurity, or other significant early-life events), the diagnostic yield for COPD is relatively high, and spirometry should be considered as a method for case finding (1).
As mentioned above, it is now well established that a range of lung function trajectories exist through life (28, 60) and that COPD can develop by both abnormal lung development and/or accelerated lung aging (42). This has generated some terminological confusion, so GOLD proposes the use of the following terminology (1).
The word “early” means “near the beginning of a process.” Because COPD can start early in life and take a long time to manifest clinically, identifying “early” COPD is difficult. Further, a biological “early” related to the initial mechanisms that eventually lead to COPD should be differentiated from a clinical “early,” which reflects the initial perception of symptoms, functional limitation, and/or structural abnormalities noted. Thus, GOLD proposes to use the term “early COPD” only to discuss the “biological” first steps of the disease in an experimental setting.
Some studies have used “mild” airflow obstruction as a surrogate for “early” disease (61). This assumption is incorrect because not all patients started their journey from a normal peak lung function in early adulthood, so some of them may never suffer “mild” disease in terms of “severity” of airflow obstruction (28). Further, “mild” disease can occur at any age and may progress, or not, over time (60). Accordingly, GOLD proposes that “mild” should be used only to describe the severity of airflow obstruction measured spirometrically.
The term “young COPD” is seemingly straightforward because it directly relates to the “chronological” age of the patient (62). Given that lung function peaks at around 20 years (5) and starts to decline around 40–50 years, GOLD proposes to operationally consider “young COPD” in patients aged 20–50 years (63), whether from having never achieved normal peak lung function in early adulthood and/or from shorter plateau and/or early lung function decline (64, 65). COPD in “young” people may be associated with significant structural and functional lung abnormalities with substantial impact on health (65, 66). A family history of respiratory diseases and/or early-life events (including hospitalizations before the age of 5 years) is reported by a significant proportion of young patients with COPD (65).
This term has been proposed to identify individuals of any age, with respiratory symptoms and/or other detectable structural (e.g., emphysema) and/or functional abnormalities (e.g., hyperinflation, reduced lung diffusing capacity, rapid FEV1 decline), in the absence of airflow obstruction on post-bronchodilator spirometry (i.e., FEV1/FVC > 0.7) (67). These patients may (or may not) develop persistent airflow obstruction (i.e., COPD) over time (67). Yet, people with pre-COPD so defined should already be considered “patients” because they suffer symptoms and/or have functional and/or structural abnormalities. Currently, there is no evidence on what the best treatment is for these patients (68). There urgently is a need for RCTs, both in patients with “pre-COPD” and in young people with COPD (69). Research in this area would benefit from pediatric-to-adult cohorts and more active case-finding strategies.
Based on the different causes (or etiotypes) that can contribute to COPD (see above), GOLD 2023 proposes a new taxonomic classification of COPD ( Figure 1 ) that reflects two recent proposals (2, 72). It aims to raise awareness about non–smoking-related COPD and to stimulate research on the mechanisms and corresponding diagnostic, preventive, or therapeutic approaches for these other etiotypes of COPD which are highly prevalent around the globe (13).
Proposed taxonomy (etiotypes) for COPD. COPD = chronic obstructive pulmonary disease. Reprinted with permission of www.goldcopd.org from Reference 1.
Patients with COPD may complain of dyspnea, wheezing, chest tightness, fatigue, activity limitation, and/or cough with or without sputum production and may experience acute respiratory events characterized by acute worsening of respiratory symptoms called exacerbations that require specific preventive and therapeutic measures. Patients with COPD frequently harbor other comorbid diseases (multimorbidity) that influence their clinical condition and prognosis (73), independently of the severity of airflow obstruction due to COPD (73), and require specific treatment (see below).
Once the diagnosis of COPD has been confirmed by spirometry, the goals of the initial assessment of COPD to guide therapy are to determine (1) the severity of airflow limitation (GOLD spirometric grades); (2) the nature and magnitude of current symptoms; (3) the previous history of moderate and severe exacerbations (the best estimate of the risk of future exacerbations); and (4) the presence and type of multimorbidity.
GOLD 2023 modifies the ABCD assessment tool of previous editions (74) to recognize the clinical impact of exacerbations independently of the level of symptoms of the patient (75) ( Figure 2 ). The thresholds proposed for symptoms (x-axis) and history of exacerbations in the previous year (y-axis) are unchanged from previous GOLD documents, so the A and B groups remain unchanged, while the former C and D groups are now merged into a single group termed “E” (for “Exacerbations”). This has implications for the initial pharmacological treatment recommendations, as discussed below. The practical value of this proposal needs to be validated by appropriate clinical research.
GOLD ABE assessment tool. Exacerbation history refers to exacerbations experienced the previous year. CAT = COPD Assessment Test; GOLD = Global Initiative for Chronic Obstructive Lung Disease; mMRC = modified Medical Research Dyspnea Questionnaire. Reprinted with permission of www.goldcopd.org from Reference 1.
A chest X-ray cannot confirm a diagnosis of COPD. However, radiological changes associated with COPD may include signs of lung hyperinflation (flattened diaphragm and increased retrosternal air space), lung hyperlucency, and rapid tapering of the vascular markings. On the other hand, a chest X-ray can help exclude alternative diagnoses and establish the presence of significant comorbidities such as concomitant pulmonary fibrosis, bronchiectasis, pleural diseases, kyphoscoliosis, and cardiomegaly.
CT of the chest can provide information of potential clinical relevance, including: (1) presence, severity, and distribution of emphysema. This has implications for potential surgical or endoscopic lung volume reduction and is associated with faster FEV1 decline, higher mortality, and increased risk of lung cancer (76); (2) about 30% of COPD patients have bronchiectasis visible on CT, which is associated with increased exacerbation frequency and mortality (77); (3) most COPD patients fulfill the inclusion/exclusion criteria for lung cancer screening in the general population (78, 79), so they should be offered a similar strategy (1); (4) quantification of airway abnormalities, although these methods are less well standardized than those used for emphysema quantification (80–82); and (5) a CT offers information about COPD comorbidities, including coronary artery calcifications, pulmonary artery enlargement, bone density, and muscle mass, some of which are associated with all-cause mortality independently of the severity of airflow obstruction (83). Thus, GOLD 2023 recommends chest CT in COPD patients with persistent exacerbations, symptoms out of proportion to airflow limitation severity, severe airflow obstruction with significant hyperinflation and gas trapping, or for those who meet criteria for lung cancer screening.
Pharmacological therapy must always be associated with nonpharmacological measures described later, starting with smoking cessation when needed.
Because inhaled therapy is the cornerstone of COPD treatment, the appropriate use of these devices is crucial to optimize the benefit-risk ratio of any inhaled therapy. Achieving this goal requires educating and training the providers and the patients in the correct use of the device. Regular assessment at follow-up is necessary to maintain their effective use. Details on the choice of device can be found in the complete GOLD 2023 document and include availability, patient preferences, and ability to perform the correct inhalation maneuver (84).
Figure 3 shows the 2023 GOLD recommendation for initiation of pharmacological therapy. The treatment of patients in Group A has not changed. In contrast, for patients in Group B, a dual long-acting bronchodilator combination (β2 adrenergic [LABA] + anti-muscarinic [LAMA] bronchodilators) is now recommended since dual therapy is more effective than monotherapy, with similar side effects (85–87). For patients in Group E, LAMA + LABA is also the recommended initial therapy, except for those patients with blood eosinophils ≥300 cells/μl, in whom starting triple therapy (LABA + LAMA + ICS) can be considered. This is a practical recommendation; direct evidence is not available to guide therapy in naïve individuals. The role of the blood eosinophil count for the reduction of the exacerbation risk with ICS is explicitly discussed below. The use of LABA + ICS in COPD is no longer encouraged. If there is an indication for an ICS, then LABA + LAMA + ICS has been shown to be superior to LABA + ICS and is therefore the preferred choice (88, 89). If patients with COPD have concomitant asthma, they should be treated as if they have asthma (90).
Initial pharmacological treatment. CAT = COPD Assessment Test; eos = eosinophils; ICS = inhaled corticosteroid; LABA = long-acting β2 adrenergic receptor agonist; LAMA = long-acting antimuscarinic agonist; mMRC = modified Medical Research Dyspnea Questionnaire. Reprinted with permission of www.goldcopd.org from Reference 1.
Following initial therapy, patients should be reassessed guided by the principles of first review and assess, then adjust if needed.
GOLD 2023 continues to recommend that follow-up treatment be based on two key treatable traits (TTs) (91): dyspnea and occurrence of exacerbations ( Figure 4 ). TTs can be identified based on clinical recognition (phenotypes) and/or on deep understanding of critical causal pathways (endotypes) through validated biomarkers (e.g., circulating eosinophils to guide treatment with inhaled corticosteroids (ICS) in COPD patients with evidence of T2 inflammation) (91). Importantly, TTs can coexist in the same patient (92) and change with time (spontaneously or because of treatment). GOLD 2023 recommendations for follow-up treatment for both TTs (dyspnea and exacerbations) broadly follow previous recommendations but no longer include LABA + ICS for the reasons stated above (see I nitial P harmacological T reatment ).
Follow-up pharmacological treatment. For definition of abbreviations, see Figure 3 . Reprinted with permission of www.goldcopd.org from Reference 1.
For patients with persistent dyspnea or exercise limitation on bronchodilator monotherapy, a step up to LABA + LAMA is recommended. If this does not improve symptoms, clinicians should consider switching inhaler device or molecules, as well as investigating and treating other causes of dyspnea.
For patients continuing to have exacerbations (with or without dyspnea) on bronchodilator monotherapy, escalation to LABA + LAMA is recommended, except for patients with blood eosinophils ≥300 cells/μl, who may be escalated to LABA + LAMA + ICS. For patients with persistent exacerbations on LABA + LAMA, escalation to LABA + LAMA + ICS is recommended if they have blood eosinophils ≥100 cells/μl. For patients continuing to exacerbate despite therapy with LABA + LAMA + ICS or those who have an eosinophil count of 1 < 50% predicted) (93–95) or a macrolide (particularly in patients who are not current smokers) may be considered (96, 97).
Patients whose pharmacological treatment is modified should be closely monitored. Treatment escalation has not been systematically tested, and trials of de-escalation are limited to withdrawing ICS (98). As indicated in Figure 4 , ICS de-escalation can be considered if pneumonia or other considerable side effects develop. In case of a blood eosinophil count ≥300 cells/μl, ICS de-escalation is more likely to be associated with development of exacerbations. Finally, if a patient with COPD and no features of asthma has already been treated—for whatever reason—with LABA + ICS and is well controlled in terms of symptoms and exacerbations, then LABA + ICS could be continued. However, if they remain dyspneic, switching to LABA + LAMA should be considered, and if they have further exacerbations, treatment should be escalated to LABA + LAMA + ICS.
Factors to consider when adding treatment with inhaled corticosteroids (ICSs) to long-acting bronchodilators (note that the scenario is different when considering ICS withdrawal). COPD = chronic obstructive pulmonary disease. Reprinted with permission of www.goldcopd.org from Reference 1.
Chronic bronchitis (CB) has been traditionally defined by “cough and sputum production for at least 3 months per year for 2 consecutive years” (in the absence of another cause that can explain this, a caveat that is often forgotten). The prevalence of CB in COPD patients ranges from 27–35%, being higher in males, younger age, greater pack-years of smoking, more severe airflow obstruction, rural location, and increased occupational exposures. CB is associated with accelerated lung function decline, exacerbations, and mortality in COPD patients. Treatment of CB is unresolved but can include smoking cessation, long-acting muscarinic antagonists, oral mucolytics, and antioxidants or oscillating positive expiratory pressure therapy; the use of inhaled mucolytics or recombinant human DNase has not shown promise (1). Liquid nitrogen metered cryospray, rheoplasty, and targeted lung denervation are currently undergoing evaluation for CB treatment.
In LMICs, there is limited availability and affordability of essential inhaled therapies for people with COPD, and this global inequity must be addressed urgently as part of efforts to achieve Universal Health Coverage and Sustainable Development Goal 3 (107). On the other hand, even in developed countries, most inhaled medicines are still branded.
Pharmacotherapy has the potential to reduce the rate of lung function decline, but further studies are needed to know what patients can benefit most since not all patients exhibit accelerated lung function decline (1). On the other hand, a number of pharmacological and nonpharmacological interventions ( Figure 6 ) reduce mortality in selected patients with COPD. This emphasizes the need to implement targeted case-finding strategies, apply adequate patient characterization, and provide appropriate individualized therapy.
Evidence supporting a reduction in mortality with pharmacotherapy and nonpharmacotherapy in patients with COPD. Superscript numerals are reference citations as follows: 1 (89, 192), 2 (193), 3 (156, 157, 194), 4 (195, 196), 5 (197), and 6 (198). CI = confidence interval; COPD = chronic obstructive pulmonary disease; ETHOS = Efficacy and Safety of Triple Therapy in Obstructive Lung Disease; HR = hazard ratio; IMPACT = Informing the Pathway of Chronic Obstructive Pulmonary Disease Treatment; MRC = Medical Research Council; NOTT = Nocturnal Oxygen Therapy Trial; RCT = randomized clinical trial; RR = risk ratio. Reprinted with permission of www.goldcopd.org from Reference 1.
Nonpharmacological treatment is a key part of the comprehensive management of COPD.
All patients should receive basic information about COPD and its treatment (respiratory medications and inhalation devices), strategies to minimize dyspnea, and advice about when to seek help.
Approximately 40% of people with COPD continue to smoke despite knowing that they have the disease, and this behavior has a negative impact on prognosis and progression of the disease (108). All patients who continue to smoke should be offered help and treatment to quit.
Depending on local guidelines, patients should be offered vaccination against influenza, pneumococcus, COVID-19, pertussis, and herpes zoster, if they have not already received these (1).
Physical activity is decreased in COPD patients (109), so all patients with COPD should be encouraged to keep active. The challenge is promoting and maintaining physical activity (110, 111). Technology-based interventions have the potential to provide convenient and accessible means to enhance exercise self-efficacy, and to educate and motivate patients to make healthy lifestyle changes (112).
Pulmonary rehabilitation (PR), including community and home-based, is beneficial (1). Accordingly, patients with high symptom burden and risk of exacerbations (GOLD groups B and E) should be recommended to take part in a formal PR program designed and delivered in a structured manner, considering the individual’s COPD characteristics and comorbidities (113–116).
Tele-rehabilitation has been proposed as an alternative to the traditional approaches. This has become even more relevant in the COVID-19 pandemic era, when in-person PR has not been feasible. However, it is important to distinguish between evidence-based tele-rehabilitation models and pandemic-adapted models. Multiple trials performed in groups and individuals with a large variety of tele-rehabilitation delivery platforms (videoconferencing, telephone only, website with telephone support, mobile application with feedback, centralized “hub” for people to come together) suggest that tele-rehabilitation is safe and has similar benefits to those of center-based PR across a range of outcomes (117). However, the optimal forms of delivery, content, and duration are not yet established (118, 119).
The criteria for prescribing long-term oxygen therapy and ventilator support remain unchanged and are described in detail in the GOLD 2023 report (1).
In selected patients with symptomatic heterogeneous or homogeneous emphysema and significant hyperinflation refractory to optimized medical care, surgical or bronchoscopic modes of lung volume reduction may be considered ( Figure 7 ). In patients with a large bulla, surgical bullectomy is an option, and in selected patients with very severe COPD and without relevant contraindications, lung transplantation may be considered.
