Global Strategy for the Diagnosis, Management and Prevention of Chronic Obstructive Lung Disease 2017 Report - GOLD Executive Summary

CLINICAL PRACTICE GUIDELINES
Global Strategy for the Diagnosis, Management and Prevention
of Chronic Obstructive Lung Disease 2017 Report
GOLD Executive Summary
CLAUS F. VOGELMEIER,1* G ERARD J. CRINER, 2* F ERNANDO J. MARTINEZ,3* A NTONIO ANZUETO, 4,5
P ETER J. BARNES, 6 JEAN BOURBEAU, 7 B ARTOLOME R. CELLI, 8 RONGCHANG CHEN, 9 MARC DECRAMER, 10
LEONARDO M. FABBRI,11 P ETER FRITH, 12 D AVID M.G. HALPIN, 13 M. V ICTORINA LÓPEZ VARELA, 14
MASAHARU NISHIMURA, 15 N ICOLAS ROCHE, 16 ROBERTO RODRIGUEZ-ROISIN,17 D ON D. SIN, 18
D AVE SINGH, 19 R OBERT STOCKLEY, 20 J ØRGEN VESTBO, 19 J ADWIGA A. WEDZICHA 6 AND A LVAR AGUSTI21
1University of Marburg, Member of the German Center for Lung Research (DZL), Marburg, Germany; 2Lewis Katz School of
Medicine at Temple University, Philadelphia, Pennsylvania; 3New York-Presbyterian Hospital, Weill Cornell Medical Center,
New York, New York; 4University of Texas Health Science Center, San Antonio, Texas; 5South Texas Veterans Health Care
System, San Antonio, Texas; 6National Heart and Lung Institute, Imperial College, London, United Kingdom; 7McGill University
Health Centre, McGill University, Montreal, Quebec, Canada; 8Brigham and Women’s Hospital, Boston, Massachusetts; 9State
Key Lab for Respiratory Disease, Guangzhou Institute of Respiratory Disease, First Affiliated Hospital of Guangzhou Medical
University, Guangzhou, China; 10University of Leuven, Leuven, Belgium; 11University of Modena and Reggio Emilia, Modena,
Italy; 12Faculty of Medicine, Flinders University, Bedford Park, South Australia, Australia; 13Royal Devon and Exeter Hospital,
Exeter, United Kingdom; 14Universidad de la República, Hospital Maciel, Montevideo, Uruguay; 15Hokkaido University School
of Medicine, Sapporo, Japan; 16Hôpital Cochin (Assistance Publique–Hôpitaux de Paris), University Paris Descartes, Paris,
France; 17Thorax Institute, Hospital Clinic Universitat de Barcelona, Barcelona, Spain; 18St. Paul’s Hospital, University of British
Columbia, Vancouver, British Columbia, Canada; 19University of Manchester, Manchester, United Kingdom; 20University
Hospital, Birmingham, United Kingdom; and 21Hospital Clínic, Universitat de Barcelona, Centro de Investigación Biomédica en
Red de Enfermedade Respiratorias, Barcelona, Spain
ABSTRACT
This Executive Summary of the Global Strategy for the
Diagnosis, Management and Prevention of COPD, Global
Initiative for Chronic Obstructive Lung Disease (GOLD)
2017 Report focuses primarily on the revised and novel
parts of the document. The most significant changes
include: (i) the assessment of chronic obstructive pulmo-
nary disease has been refined to separate the spirometric
assessment from symptom evaluation. ABCD groups are
now proposed to be derived exclusively from patient
symptoms and their history of exacerbations; (ii) for each
of the groups A to D, escalation strategies for pharmaco-
logical treatments are proposed; (iii) the concept of de-
escalation of therapy is introduced in the treatment
assessment scheme; (iv)non-pharmacological therapies
are comprehensively presented and (v) the importance of
co-morbid conditions in managing COPD is reviewed.
Key words: chronic obstructive pulmonary disease, COPD
diagnosis, COPD management, COPD prevention.
CONTENTS
Introduction
Definition and Factors that Influence Chronic Obstruc-
tive Pulmonary Disease Development and Progression
Key points
Definition and pathogenesis
Factors that influence disease development and
progression
Diagnosis and Initial Assessment
Key points
Diagnosis
Symptoms
Medical history
Assessment
Assessment of symptoms
Choice of thresholds
Assessment of exacerbation risk
Assessment of concomitant chronic diseases (co-
morbidities)
Revised combined COPD assessment
Alpha-1 antitrypsin deficiency
Additional investigations
Prevention and Maintenance Therapy
Key points
Smoking cessation
Correspondence: Claus F. Vogelmeier, Department of
Medicine, Pulmonary and Critical Care Medicine, University of
Marburg, Baldingerstrasse 1, Marburg 35043, Germany.
Email: [e-mail]
*These authors contributed equally to this article.
This document is a joint publication by Respirology, the
American Journal of Respiratory and Critical Care Medicine,
European Respiratory Journal and Archivos de
Bronconeumologia. The document was peer reviewed by the
Global Initiative for Chronic Obstructive Lung Disease (GOLD)
prior to journal submission.
Received 30 January 2017; accepted 30 January 2017.
© 2017 The American Thoracic Society. Published with permission from the American Thoracic Society Respirology (2017) 22, 575–601
doi: 10.1111/resp.13012

Vaccinations
Pharmacologic therapy for stable COPD
Rehabilitation, Education and Self-Management
Pulmonary rehabilitation
Education, self-management and integrative care
Supportive, Palliative, End-of-Life and Hospice Care
Symptom control and palliative care
End-of-life and hospice care
Other Treatments
Oxygen therapy and ventilatory support
Interventional Therapy
Surgical interventions
Bronchoscopic interventions to reduce hyperinflation
in severe emphysema
Management of Stable COPD
Key points
Identify and reduce exposure to risk factors
Treatment of Stable COPD
Pharmacologic treatment
Non-pharmacologic treatment
Monitoring and Follow-Up
Key points
Management of exacerbations
Treatment Options
Treatment setting
Pharmacologic treatment
Respiratory support
Hospital discharge and follow-up
Prevention of exacerbations
COPD and Co-Morbidities
Key points
Cardiovascular disease
Hypertension
Osteoporosis
Anxiety and depression
COPD and lung cancer
Metabolic syndrome and diabetes
Gastroesophageal reflux
Bronchiectasis
Obstructive sleep apnoea
INTRODUCTION
This Executive Summary of the Global Strategy for the
Diagnosis, Management and Prevention of Chronic
Obstructive Pulmonary Disease (COPD) Global Initiative
for Chronic Obstructive Lung Disease (GOLD) 2017
Report is based on peer-reviewed publications to
October 2016. Levels of evidence are assigned to
evidence-based recommendations where appropriate.
Categories used to grade the levels of evidence are pro-
vided in Table S1 (Supplementary Information).
DEFINITION AND FACTORS THAT
INFLUENCE CHRONIC OBSTRUCTIVE
PULMONARY DISEASE
DEVELOPMENT AND PROGRESSION
K EY P O I NT S
• Chronic obstructive pulmonary disease (COPD) is
a common, preventable and treatable disease that
is characterized by persistent respiratory symp-
toms and airflow limitation due to airway and/or
alveolar abnormalities usually caused by signifi-
cant exposure to noxious particles or gases.
• Dyspnoea, cough and/or sputum production are
the most frequent symptoms; symptoms are com-
monly under-reported by patients.
• Tobacco smoking is the main risk exposure for
COPD, but environmental exposures such as bio-
mass fuel exposure and air pollution may contrib-
ute. Besides exposures, host factors (genetic
abnormalities, abnormal lung development and
accelerated ageing) predispose individuals to
develop COPD.
• COPD may be punctuated by acute worsening of
respiratory symptoms, called exacerbations.
• In most patients, COPD is associated with signifi-
cant concomitant chronic diseases, which
increase morbidity and mortality.
Definition and pathogenesis
Chronic obstructive pulmonary disease (COPD) is a
common, preventable and treatable disease character-
ized by persistent respiratory symptoms and airflow
limitation that is due to airway and/or alveolar
abnormalities usually caused by significant exposure to
noxious particles or gases.
The chronic airflow limitation that characterizes COPD
is caused by a mixture of small airway disease
(e.g. obstructive bronchiolitis) and parenchymal destruc-
tion (emphysema), the relative contributions of which vary
from person to person. Chronic inflammation causes
structural changes, small airway narrowing and destruction
of lung parenchyma. A loss of small airways may contrib-
ute to airflow limitation and mucociliary dysfunction, a
characteristic feature of the disease.
Chronic respiratory symptoms may precede the
development of airflow limitation and be associated
with acute respiratory events. 1 Chronic respiratory
symptoms may exist in individuals with normal spi-
rometry 1,2 and a significant number of smokers without
airflow limitation have structural evidence of lung dis-
ease manifested by the presence of emphysema, airway
wall thickening and gas trapping. 1,2
Factors that influence disease development
and progression
Although cigarette smoking is the most well-studied COPD
risk factor, epidemiological studies demonstrate that non-
smokers may also develop chronic airflow limitation.3
Compared to smokers with COPD, never-smokers with
chronic airflow limitation have fewer symptoms, milder
disease and a lower burden of systemic inflammation.4
Never-smokers with chronic airflow limitation do not have
an increased risk of lung cancer or cardiovascular co-mor-
bidities; however, they have an increased risk of pneumo-
nia and mortality from respiratory failure.4
Processes occurring during gestation, birth and expo-
sures during childhood and adolescence affect lung
growth.5,6 Reduced maximal attained lung function
(as measured by spirometry) may identify individuals at
increased risk for COPD.2,7 Factors in early life termed
© 2017 The American Thoracic Society. Published with permission from the American Thoracic Society Respirology (2017) 22, 575–601
576 CF Vogelmeier et al.

‘childhood disadvantage factors’ are as important as heavy
smoking in predicting lung function in adult life.8 An exam-
ination of three different longitudinal cohorts found that
approximately 50% of patients developed COPD owing to
an accelerated decline in forced expiratory volume in 1 s
(FEV1); the other 50% developed COPD owing to abnormal
lung growth and development.
Cigarette smokers have a higher prevalence of respira-
tory symptoms and lung function abnormalities, a greater
annual rate of decline in FEV1 and a greater COPD mor-
tality rate than non-smokers.9 Other types of tobacco
(e.g. pipe, cigar, water pipe)10–12 and marijuana13 are also
risk factors for COPD. Passive exposure to cigarette
smoke, also known as environmental tobacco smoke,
may also contribute to respiratory symptoms and COPD14
by increasing the lung’s total burden of inhaled particles
and gases. Smoking during pregnancy may pose a risk for
the foetus, by affecting in utero lung growth and develop-
ment, and possibly priming the immune system.15
Occupational exposures, including organic and inor-
ganic dusts, chemical agents and fumes, are under-
appreciated risk factors for COPD development.16,17
Wood, animal dung, crop residues and coal, typically
burned in open fires or poorly functioning stoves, may
lead to indoor air pollution. 18 Indoor pollution from
biomass cooking and heating in poorly ventilated
dwellings is a risk for COPD. 19–21
Asthma may be a risk for the development of chronic
airflow limitation and COPD.22
Airway hyper-responsiveness can exist without a
clinical diagnosis of asthma and is an independent pre-
dictor of COPD and respiratory mortality in population
studies. 23,24 It may indicate a risk for excessive lung
function decline in mild COPD. 25
A history of severe childhood respiratory infection is
associated with reduced lung function and increased respi-
ratory symptoms in adulthood.26 HIV infection accelerates
the onset of smoking-related emphysema and COPD;27
tuberculosis has also been identified as a risk factor for
COPD as well as a potential co-morbidity.28–30
DIAGNOSIS AND INITIAL
ASSESSMENT
KEY P OI NTS
• COPD should be considered in any patient with
dyspnoea, chronic cough or sputum production,
and/or a history of exposure to risk factors.
• Spirometry is required to make the diagnosis; a
post-bronchodilator FEV1/forced vital capacity
(FVC) less than 0.70 confirms the presence of per-
sistent airflow limitation.
• The goals of COPD assessment are to determine
the level of airflow limitation, the impact of dis-
ease on the patient’s health status and the risk of
future events (such as exacerbations, hospital
admissions or death) to guide therapy.
• Concomitant chronic diseases occur frequently in
patients with COPD and should be treated
because they can independently affect mortality
and hospitalizations.
Diagnosis
COPD should be considered in any patient with dys-
pnoea, chronic cough or sputum production and/or a
history of exposure to risk factors for the disease
(Fig. 1, Table 1). Spirometry is required to make the
diagnosis in this clinical context; 31 a post-
bronchodilator FEV 1 /FVC less than 0.70 confirms the
presence of persistent airflow limitation and identifies
the presence of COPD in patients with appropriate
symptoms and predisposing risks.
Symptoms
Chronic and progressive dyspnoea is the most charac-
teristic symptom of COPD.
Dyspnoea. Dyspnoea is a major cause of the disabil-
ity and anxiety in COPD. 32 The terms used to describe
dyspnoea vary individually and culturally. 33
Cough. Chronic cough is often the first symptom of
COPD and frequently discounted by the patient as a con-
sequence of smoking and/or environmental exposures.
Sputum production. Regular sputum production ≥
3 months in two consecutive years is the classical defi-
nition of chronic bronchitis 34 ; an arbitrary definition
that does not reflect the range of sputum production
reported in COPD. Patients producing large volumes of
sputum may have underlying bronchiectasis.
Wheezing and chest tightness. Wheezing and chest
tightness may vary between days, and throughout a
single day.
Additional features in severe disease. Fatigue,
weight loss and anorexia are common in patients with
more severe forms of COPD. 35,36
Medical history
A detailed medical history of any patient who is known,
or suspected, to have COPD should include:
• Exposure to risk factors, such as smoking and occu-
pational or environmental exposures.
• Past medical history, including asthma, allergy, sinusi-
tis, or nasal polyps; respiratory infections in childhood;
other chronic respiratory and non-respiratory diseases.
• Family history of COPD or other chronic respiratory
diseases.
Figure 1 Pathways to the diagnosis of chronic obstructive
pulmonary disease.
Respirology (2017) 22, 575–601 © 2017 The American Thoracic Society. Published with permission from the American Thoracic Society
GOLD executive summary 577

• Pattern of symptom development: age of onset, type
of symptom, more frequent or prolonged ‘winter
colds’, and social restriction.
• History of exacerbations or previous hospitalizations
for a respiratory disorder.
• Presence of co-morbidities, such as heart disease, oste-
oporosis, musculoskeletal disorders, and malignancies.
• Impact of disease on patient’s life, including limita-
tion of activity, missed work and economic impact,
and feelings of depression or anxiety.
• Social and family support available to the patient.
• Possibilities for reducing risk factors, especially
smoking cessation.
Physical examination. Although important for gen-
eral health, a physical examination is rarely diagnostic
in COPD. Physical signs of airflow limitation/hyperin-
flation are usually not identifiable until significantly
impaired lung function is present. 37,38
Spirometry. Spirometry is the most reproducible
and objective measurement of airflow limitation. It is a
noninvasive and readily available test. Good quality
spirometry is possible in any healthcare setting; all
healthcare workers who care for patients with COPD
should have access to spirometry.
A post-bronchodilator fixed ratio of FEV 1 /FVC less
than 0.70 is the spirometric criterion for airflow limita-
tion. This criterion is simple and independent of refer-
ence values and has been used in numerous clinical
trials. However, it may result in more frequent diagno-
sis of COPD in the elderly, 39,40 and less frequent diag-
nosis in adults younger than 45 years, 40 especially in
mild disease, compared with a cut-off based on the
lower limit of normal (LLN) values for FEV 1 /FVC. Sev-
eral limitations occur with using LLN as the diagnostic
criterion for spirometric obstruction: (i) LLN values are
dependent on the choice of reference equations that
use post-bronchodilator FEV 1 , (ii) there are no longitu-
dinal studies that validate using the LLN and
(iii) studies using LLN in populations where smoking is
not the major cause of COPD are lacking.
Normal spirometry may be defined by a new approach
from the Global Lung Initiative (GLI).41,42 Using GLI
equations, z-scores were calculated for FEV1, FVC and
FEV1/FVC and compared to fixed ratio data. The findings
suggest that among adults with GLI-defined normal spi-
rometry, the use of a fixed ratio may misclassify indivi-
duals as having respiratory impairment. These findings
await additional study in other cohorts.
The risk of misdiagnosis and over-treatment using
the fixed ratio as a diagnostic criterion is limited
because spirometry is only one parameter used to
establish the clinical diagnosis of COPD. GOLD favours
using the fixed ratio over LLN because diagnostic sim-
plicity and consistency are crucial for the busy clinician.
Assessing the degree of reversibility of airflow limita-
tion (e.g. measuring FEV 1 before and after bronchodila-
tor or corticosteroids) to make therapeutic decisions is
not recommended43 because it does not aid the diag-
nosis of COPD, differentiate COPD from asthma, or
predict the long-term response to treatment.44
In asymptomatic individuals without exposures to
tobacco or other noxious stimuli, screening spirometry is
not indicated. However, in those with symptoms and/or
risk factors (e.g. >20 pack-years of smoking or recurrent
chest infections), the diagnostic yield for COPD is rela-
tively high and spirometry should be considered.45,46
GOLD advocates active case finding45,47 (i.e. performing
spirometry in patients with symptoms and/or risk fac-
tors) but not routine screening spirometry in asympto-
matic individuals without COPD risk factors.
Assessment
The goals of COPD assessment to guide therapy are
(i) to determine the level of airflow limitation; (ii) to
define its impact on the patient’s health status, and
(iii) to identify the risk of future events (such as exacer-
bations, hospital admissions or death).
To achieve these goals, COPD assessment must con-
sider separately the following aspects of the disease:
• Presence and severity of the spirometric abnormality
• Current nature and magnitude of symptoms
• History/future risk of exacerbations
• Presence of co-morbidities
Table 1 Key indicators for considering a diagnosis of chronic obstructive pulmonary disease (COPD)
Consider COPD, and perform spirometry, if any of these indicators are present in an individual older than age 40 years.
These indicators are not diagnostic themselves, but the presence of multiple key indicators increases the probability of
a diagnosis of COPD. Spirometry is required to establish a diagnosis of COPD.
Dyspnoea that is Progressive over time
Characteristically worse with exercise
Persistent
Chronic cough May be intermittent and may be unproductive
Recurrent wheeze
Chronic sputum production With any pattern
Recurrent lower respiratory tract infections
History of risk factors Host factors (such as genetic factors, congenital/developmental
abnormalities etc.)
Tobacco smoke
Smoke from home cooking and heating fuels
Occupational dusts, vapours, fumes, gases and other chemicals
Family history of COPD and/or childhood factors For example, low birthweight, childhood respiratory infections
© 2017 The American Thoracic Society. Published with permission from the American Thoracic Society Respirology (2017) 22, 575–601
578 CF Vogelmeier et al.

Classification of severity of airflow limitation.
Spirometry should be performed after administration
of an adequate dose of at least one short-acting inhaled
bronchodilator in order to minimize variability.
The role of spirometry for the diagnosis, assessment
and follow-up of COPD is summarized in Table 2.
Assessment of symptoms
COPD was previously viewed as a disease largely charac-
terized by breathlessness. A simple measure of breath-
lessness such as the modified British Medical Research
Council (mMRC) Questionnaire 48 was considered ade-
quate for the assessment of symptoms.49–51 However,
COPD impacts patients well beyond dyspnoea.52 For this
reason, a comprehensive assessment of symptoms is
recommended. The most comprehensive disease-
specific health status questionnaires include the Chronic
Respiratory Questionnaire53 and St George’s Respiratory
Questionnaire (SGRQ).54 These are too complex to use in
clinical practice, but shorter measures, such as the COPD
Assessment Test (CAT™), are suitable.
Choice of thresholds
SGRQ scores less than 25 are uncommon in COPD
patients 55 and scores greater than or equal to 25 are
very uncommon in healthy persons. 56,57 The equivalent
cut-off point for the CAT is 10. 58 An mMRC threshold of
greater than or equal to 2 is used to separate ‘less
breathlessness’ from ‘more breathlessness’.
Assessment of exacerbation risk
The best predictor of frequent exacerbations (defined
as two or more exacerbations per year) is a history of
earlier treated events. 59 Hospitalization for a COPD
exacerbation has a poor prognosis and an increased
risk of death. 60
Blood eosinophil count. Post hoc analysis of two
clinical trials in patients with COPD with an exacerba-
tion history showed that higher blood eosinophil
counts may predict increased exacerbation rates in
patients treated with long-acting β-agonists (LABAs)
(without inhaled corticosteroid, ICS).61,62 The treatment
effect of ICS/LABA versus LABA on exacerbations was
greater in patients with higher blood eosinophil counts.
These findings suggest that blood eosinophil counts
(i) are a biomarker of exacerbation risk in patients with
a history of exacerbations, and (ii) can predict the
effects of ICSs on exacerbation prevention. Prospective
trials are required to validate the use of blood eosino-
phil counts to predict ICS effects, to determine a cut-off
threshold for blood eosinophils that predicts exacerba-
tion risk and to clarify blood eosinophil cut-off values
that could be used in clinical practice.
Assessment of concomitant chronic diseases
(co-morbidities)
Patients with COPD often have important concomitant
chronic illnesses as COPD represents an important com-
ponent of multimorbidity particularly in the elderly.60,63–65
Revised combined COPD assessment
The ‘ABCD’ assessment tool of the 2011 GOLD Report
was a major step forward from the simple spirometric
grading system of earlier GOLD reports because it incor-
porated patient-reported outcomes and highlighted the
importance of exacerbation prevention in COPD man-
agement. However, there were important limitations.
ABCD assessment performed no better than spirometric
grades for mortality prediction or other important health
outcomes.66–68 Moreover, group D outcomes were modi-
fied by two parameters: lung function and/or exacerba-
tion history, which caused confusion.69 To address these
concerns, the 2017 GOLD Report provides a refinement
of the ABCD assessment that separates spirometric
grades from ABCD groupings. For some therapy recom-
mendations, especially pharmacologic treatments, ABCD
groups are derived exclusively from patient symptoms
and their exacerbation history. However, spirometry, in
conjunction with patient symptoms and exacerbation
history, remains vital for the diagnosis, prognostication
and consideration of other important therapeutic
approaches, especially non-pharmacologic therapies.
This new approach to assessment is illustrated in
Figure 2.
In the refined assessment scheme, patients should
undergo spirometry to determine the severity of airflow
limitation (i.e. spirometric grade). They should also
undergo assessment of either dyspnoea using mMRC
or symptoms using CAT. Finally, their history of exacer-
bations (including prior hospitalizations) should be
recorded.
The number provides information regarding severity
of airflow limitation (spirometric grades 1–4), whereas
the letter (groups A–D) provides information regarding
symptom burden and risk of exacerbation. FEV 1 is a
very important parameter at the population level in the
Table 2 Role of spirometry
• Diagnosis
• Assessment of severity of airflow obstruction (for prognosis)
• Follow-up assessment
 Therapeutic decisions
• Pharmacologic in selected circumstances (e.g. discrepancy between spirometry and level of symptoms)
• Consider alternative diagnoses when symptoms are disproportionate to degree of airflow obstruction
• Non-pharmacologic (e.g. interventional procedures)
 Identification of rapid decline
Respirology (2017) 22, 575–601 © 2017 The American Thoracic Society. Published with permission from the American Thoracic Society
GOLD executive summary 579

prediction of important clinical outcomes, such as mor-
tality and hospitalizations, or prompting consideration
for non-pharmacologic therapies, such as lung reduc-
tion or lung transplantation. However, at the individual
patient level, FEV1 loses precision and thus cannot be
used alone to determine all therapeutic options. Fur-
thermore, in some circumstances, such as during hos-
pitalization or urgent presentation to the clinic or
emergency room, the ability to assess patients based
on symptoms and exacerbation history, independent of
the spirometric value, allows clinicians to initiate a
treatment plan based on the revised ABCD scheme.
This approach acknowledges the limitations of FEV 1 in
making treatment decisions for individualized patient
care and highlights the importance of patient symp-
toms and exacerbation risks in guiding therapies in
COPD. The separation of airflow limitation from clini-
cal parameters makes it clearer what is being evaluated
and ranked. This should facilitate more precise treat-
ment recommendations based on parameters that are
driving the patient’s symptoms at any given time.
Example. Consider two patients—both patients with
FEV 1 less than 30% predicted, CAT scores of 18, one
with no exacerbations in the past year and the other
with three exacerbations in the past year. Both would
have been labelled GOLD D in the prior classification
scheme. However, with the new proposed scheme, the
subject with three exacerbations in the past year would
be labelled GOLD grade 4, group D. Individual deci-
sions on pharmacotherapeutic approaches would use
the recommendations based on the ABCD assessment
to treat the patient’s major problem at this time (i.e.
persistent exacerbations). The other patient, who has
had no exacerbations, would be classified as GOLD
grade 4, group B. In such patients—besides pharmaco-
therapy and rehabilitation—lung reduction, lung trans-
plantation or bullectomy may be important therapeutic
considerations, given their symptom burden and level
of spirometric limitation.
Alpha-1 antitrypsin deficiency
The World Health Organization recommends that all
patients with a diagnosis of COPD be screened once
for alpha-1 antitrypsin deficiency. 70 A low concentra-
tion (<20% normal) is suggestive of homozygous defi-
ciency. Family members should be screened and
together with the patient referred to specialist centres
for advice and management.
Additional investigations
In order to rule out other concomitant disease contri-
buting to respiratory symptoms, or in cases where
patients do not respond to the treatment plan as
expected, additional testing may be required. Thoracic
imaging (chest X-ray, chest computed tomography
(CT)), assessment of lung volumes and/or diffusion
capacity, oximetry and arterial blood gas measurement,
and exercise testing and assessment of physical activity
should be considered.
Composite scores. The BODE (Body mass index,
Obstruction, Dyspnoea and Exercise) method gives a
composite score that is a better predictor of subse-
quent survival than any single component.71 Simpler
alternatives that do not include exercise testing need
validation to confirm suitability for routine clinical
use. 72,73
Differential diagnoses. In some patients, features of
asthma and COPD may coexist. The terms asthma–
COPD overlap syndrome (ACOS) or asthma–COPD
overlap (ACO) acknowledge the overlap of these two
common disorders causing chronic airflow limitation
rather than a distinct syndrome. Most other potential
differential diagnoses are easier to distinguish
from COPD.
Other considerations. Some patients without evi-
dence of airflow limitation have evidence of structural
lung disease on chest imaging (emphysema, gas trap-
ping, airway wall thickening). Such patients may
report exacerbations of respiratory symptoms or even
require treatment with respiratory medications on a
chronic basis. Whether these patients have acute or
chronic bronchitis, a persistent form of asthma, or an
earlier presentation of what will become COPD as it is
currently defined is unclear and requires further
study.
Figure 2 The refined ABCD
assessment tool. CAT, COPD
Assessment Test; COPD, chronic
obstructive pulmonary disease;
GOLD, Global Initiative for Chronic
Obstructive Lung Disease; mMRC,
modified British Medical Research
Council questionnaire.
© 2017 The American Thoracic Society. Published with permission from the American Thoracic Society Respirology (2017) 22, 575–601
580 CF Vogelmeier et al.