Chronic obstructive pulmonary disease: Diagnosis and

staging
Authors: MeiLan King Han, MD, MS, Mark T Dransfield, MD, Fernando J Martinez, MD, MS
Section Editor: James K Stoller, MD, MS
Deputy Editor: Paul Dieffenbach, MD

Contributor Disclosures

All topics are updated as new evidence becomes available and our peer review process is complete.

Literature review current through: Apr 2024. | This topic last updated: Nov 28, 2023.

INTRODUCTION

Chronic obstructive pulmonary disease (COPD) is a common respiratory condition

characterized by cough, dyspnea, and airflow limitation [1]. Approximately 10 percent of
individuals aged 40 years or older have COPD, although the prevalence varies between
countries and increases with age [1-4]. COPD is consistently ranked among the top causes of
death in the United States, killing more than 120,000 individuals each year [5,6]; prior to the
COVID-19 (coronavirus disease 2019) pandemic, it was the third leading cause worldwide [7].
As a consequence of its high prevalence and chronicity, COPD causes high resource
utilization with frequent clinician office visits, multiple hospitalizations due to acute
exacerbations, and the need for chronic therapy [8].

Establishing a correct diagnosis of COPD is important because appropriate management can

decrease symptoms (especially dyspnea), reduce the frequency and severity of
exacerbations, improve health status, improve exercise capacity, and prolong survival [9].
Many health conditions in older adults can result in dyspnea or cough, so respiratory
symptoms should not be attributed to COPD without appropriate evaluation and diagnosis.

The definition, clinical manifestations, diagnostic evaluation, and staging of COPD are
discussed here. The risk factors, natural history, prognosis, and treatment of COPD are
discussed separately.
● (See "Chronic obstructive pulmonary disease: Risk factors and risk reduction".)
● (See "Chronic obstructive pulmonary disease: Prognostic factors and comorbid
conditions".)
● (See "Stable COPD: Overview of management".)
● (See "COPD exacerbations: Clinical manifestations and evaluation".)
● (See "COPD exacerbations: Management".)
DEFINITIONS

COPD should be understood in the context of other closely related common respiratory
conditions (emphysema, chronic bronchitis, and chronic obstructive asthma) that represent
an overlapping spectrum of airway diseases.

COPD — The Global Initiative for Chronic Obstructive Lung Disease (GOLD), a project
initiated by the National Heart, Lung, and Blood Institute (NHLBI) and the World Health
Organization (WHO), defines COPD as a "heterogeneous lung condition characterized by
chronic respiratory symptoms (dyspnea, cough, expectoration, exacerbations) due to
abnormalities of the airway (bronchitis, bronchiolitis) and/or alveoli (emphysema) that cause
persistent, often progressive, airflow obstruction" [1,10].

In practice, the diagnosis of COPD requires all of the following (see 'Diagnosis' below):
● The presence of pulmonary symptoms (dyspnea, cough, or sputum production)
● The appropriate clinical context (most notably but not exclusively tobacco exposure)
( table 1)
● Evidence of airflow limitation

Chronic bronchitis — Chronic bronchitis is defined as a chronic productive cough over a

defined period, classically for at least three months in each of two successive years, in a
patient in whom other causes of chronic cough (eg, bronchiectasis) have been excluded [1].
It may precede or follow development of airflow limitation [1,11,12]. This definition has been
used in many studies, despite the arbitrarily selected symptom duration. By age 35 to 40
years, cigarette smokers may develop chronic bronchitis and start to have intermittent
exacerbations of their symptoms even in the absence of airflow obstruction [13].

Emphysema — Emphysema describes enlargement of the airspaces distal to the terminal

bronchioles that is accompanied by destruction of the airspace walls, a pathologic finding
frequently seen in patients with COPD [14]. This finding manifests clinically with decreased
breath sounds and evidence of hyperinflation of the lungs on examination or imaging; it is
frequently associated with dyspnea. Emphysema is classically not accompanied by
macroscopic fibrosis. While emphysema can exist in individuals who do not have airflow
limitation, it is more common among patients who have moderate or severe airflow
obstruction [1,15-17].

The various subtypes of emphysema (eg, proximal acinar, panacinar, distal acinar) are
described below. (See 'Pathology' below.)

Airflow limitation — Airflow limitation is physiologically defined as an abnormally reduced

ability to exhale efficiently. The severity and presence of airflow limitation are determined by
evaluating the forced expiratory volume in one second (FEV1) and the ratio of the FEV1 to the
total forced expiratory volume (aka, forced vital capacity [FVC]). (See 'Spirometry' below and
"Office spirometry", section on 'Interpretation'.)

Airflow limitation may be fixed or may change in response to exogenous factors (eg,
environmental exposure, temperature, and medications). Asthma is defined by significant
variability in airflow obstruction, whereas COPD is characterized by obstruction that is not
fully reversible with medication.

Asthma — The Global Initiative for Asthma (GINA) gives the following definition of asthma:
"Asthma is a chronic inflammatory disorder of the airways that leads to recurrent episodes of
wheezing, breathlessness, chest tightness, and coughing. These episodes are associated
with widespread, but variable, airflow obstruction that is often reversible either
spontaneously or with treatment" [1]. The episodic nature of the symptoms and reversibility
of airflow obstruction are clinical features that help distinguish asthma from COPD. However,
adults with longstanding asthma may develop persistent airflow limitation. Distinguishing
these patients from those with COPD is difficult, particularly in the context of additional
COPD risk factors ( table 1).

Interrelationships among these conditions — Chronic bronchitis and emphysema were

previously incorporated into the definition of COPD [18,19], and their clinical features overlap
those of patients with asthma and COPD. This has caused considerable confusion regarding
appropriate classification of patients with respiratory symptoms and COPD risk factors.
Important points about these interrelationships include:
● COPD – Patients with emphysema or chronic bronchitis and persistent
postbronchodilator airflow limitation meet the definition of COPD. Chronic bronchitis,
emphysema, and postbronchodilator airflow limitation commonly occur together [20].
● Asthma – Patients with asthma who only have inducible airway obstruction or whose
airflow limitation is completely reversible with bronchodilator therapy are not
considered to have COPD.
● Asthma and COPD – Patients with asthma whose airflow limitation does not remit
completely and who have other appropriate clinical risk factors (eg, older age, exposure
history) are considered to have both asthma and COPD. The etiology and pathogenesis
of COPD in such patients may be different from that of other COPD patients ( table 2).
While descriptors "asthma and COPD overlap (ACO)" and "COPD-A" have been proposed
to identify patients with airway disease who have features of both asthma and COPD,
the topic remains controversial. No single, universally accepted definition has emerged.
Central to most of the proposed definitions are age >40 years, history of asthma at a
younger age, persistent postbronchodilator airflow obstruction, and evidence of partial
bronchodilator reversibility. (See "Asthma and COPD overlap (ACO)".)
 Further study of this relationship will be needed to determine with certainty how
treatment algorithms should be tailored to these patients [21,22]. An evolving literature
suggests differential responses to inhaled glucocorticoids in patients with or without
increased circulating eosinophils [23,24]. Peripheral eosinophilia is recommended by
GOLD and our authors for use clinically to guide pharmacotherapy in all patients with
COPD. (See "Stable COPD: Follow-up pharmacologic management", section on 'Blood
eosinophils, inhaled corticosteroids, and exacerbations'.)

Subgroups of COPD patients with eosinophilia may experience clinical improvement with
biologic medications shown to have benefit in asthma. (See "Stable COPD: Follow-up
pharmacologic management", section on 'Future directions' and "Management of
refractory chronic obstructive pulmonary disease", section on 'Frequent exacerbations
despite azithromycin or roflumilast'.)
● Pre-COPD – Patients with chronic bronchitis or emphysema without irreversible airway
obstruction do not have COPD but are at high risk for developing the disease [25,26].
The term "pre-COPD" is used to identify such individuals who have either respiratory
symptoms, radiographic abnormalities consistent with COPD, or early lung function
changes in the context of COPD risk factors but do not have airway obstruction as
defined by FEV1/FVC <0.7. There is not full consensus on the defining features of pre-
COPD, but diagnostic criteria have been proposed ( table 3) [1,27,28].

Epidemiologic studies suggest that nearly 50 percent of current and former smokers
without airway obstruction have respiratory symptoms, which correlate with reduced
exercise capacity, radiographic emphysema and wall thickening, and lung function at the
lower end of the normal range [16,17]. Those with borderline airway obstruction
(FEV1/FVC <0.75), greater smoking history, and chronic bronchitis have an increased
likelihood of subsequent COPD diagnosis [29].

While many of these "pre-COPD" patients are treated off-label with bronchodilators or
inhaled glucocorticoids, one large trial failed to show improvement in respiratory
symptoms or quality of life with dual long-acting bronchodilator therapy (indacaterol-
glycopyrrolate) versus placebo in this population [30]. Hence, existing evidence does not
support inhaled bronchodilator therapies for symptomatic patients without airway
limitation. Additional study is needed to determine appropriate preventative and
maintenance therapies for this population.
● Other airway diseases – Patients with airflow limitation due to diseases that have a
known etiology or a specific pathology (eg, cystic fibrosis, bronchiectasis, obliterative
bronchiolitis) are not considered to have COPD. However, these exclusions are loosely
defined [31].
PATHOLOGY

Histology is not obtained from patients with COPD as part of the diagnostic work-up. The
predominant pathologic changes of COPD are found in the airways, but changes are also
seen in the lung parenchyma and pulmonary vasculature. In a given individual, the pattern
of pathologic changes depends on features of the underlying disease (eg, chronic bronchitis,
emphysema, alpha-1 antitrypsin deficiency), genetic susceptibility, and disease severity [1].
While radiographic methods do not have the resolution of histology, high-resolution
computed tomography (HRCT) can assess lung parenchyma [32], airways [33], and
pulmonary vasculature [34]. (See 'Additional testing' below.)

Pathologic features of COPD (by compartment) include:

● Airways – In the airways, COPD results in chronic inflammation, increased numbers of
goblet cells, mucus gland hyperplasia, fibrosis, as well as narrowing in and loss of small
airways. In addition, airway collapse frequently occurs due to the loss of tethering
caused by emphysematous destruction of alveolar walls [15]. Among patients with
chronic bronchitis who have mucus hypersecretion, an increased number of goblet cells
and enlarged submucosal glands are typically seen.

Chronic airway inflammation in chronic bronchitis and emphysema is frequently

characterized by the presence of CD8+ T-lymphocytes, neutrophils, and CD68+
monocytes/macrophages ( picture 1) [35-39]. In comparison, the bronchial
inflammation of asthma is more often characterized by the presence of CD4+ T-
lymphocytes, eosinophils, and increased interleukin (IL)-4 and IL-5 [40-42]. These
findings are not diagnostic, however, as there can be significant overlap between these
inflammatory airway phenotypes in individual patients.
● Lung parenchyma – Emphysema affects the structures distal to the terminal bronchiole,
consisting of the respiratory bronchiole, alveolar ducts, alveolar sacs, and alveoli, known
collectively as the acinus. These structures in combination with their associated
capillaries and interstitium form the lung parenchyma. The part of the acinus that is
affected by permanent dilation or destruction determines the subtype of emphysema.

• Proximal acinar (also known as centrilobular) emphysema refers to abnormal dilation

or destruction of the respiratory bronchiole, the central portion of the acinus. It is
commonly associated with cigarette smoking and is the most common emphysema
subtype seen in patients with COPD. Centrilobular emphysema is also seen in coal
workers’ pneumoconiosis.

• Panacinar emphysema refers to enlargement or destruction of all parts of the acinus.

Diffuse panacinar emphysema is a characteristic of alpha-1 antitrypsin deficiency,
 although it can be seen in combination with proximal acinar emphysema in other
patients with COPD. (See "Clinical manifestations, diagnosis, and natural history of
alpha-1 antitrypsin deficiency".)

• In distal acinar (also known as paraseptal) emphysema, the alveolar ducts are
predominantly affected. Distal acinar emphysema may occur alone or in combination
with proximal acinar and panacinar emphysema. When it occurs alone, extensive
subpleural paraseptal emphysema may be associated with spontaneous
pneumothorax, but it is otherwise of little clinical significance. (See "Pneumothorax in
adults: Epidemiology and etiology".)
● Pulmonary vasculature – Changes in the pulmonary vasculature in COPD include
intimal hyperplasia and smooth muscle hypertrophy/hyperplasia, which are thought to
be due to chronic hypoxic vasoconstriction of the small pulmonary arteries [43].

CLINICAL PRESENTATION

Symptoms and pattern of onset — The three cardinal symptoms of COPD are dyspnea,
chronic cough, and sputum production; the most common early symptom is exertional
dyspnea. Less common symptoms include wheezing and chest tightness ( table 4A).
However, any of these symptoms may develop independently and with variable intensity.

There are various ways in which patients with COPD present [44]:
● Patients who have an extremely sedentary lifestyle but few complaints – These
patients require careful questioning to elicit a history that is suggestive of COPD. Some
patients unknowingly avoid exertional dyspnea by shifting their expectations and
limiting their activity. They may be unaware of the extent of their limitations or that their
limitations are due to respiratory symptoms, although they may complain of fatigue.
● Patients who present with progressive dyspnea and chronic cough – For these
patients, dyspnea may initially be noticed only during exertion. However, it eventually
becomes noticeable with progressively less exertion or even at rest. The chronic cough is
characterized by the insidious onset of sputum production, which occurs in the morning
initially but may progress to occur throughout the day. The daily sputum volume rarely
exceeds 60 milliliters. The sputum is usually mucoid but becomes more purulent during
exacerbations.
● Patients who present with intermittent pulmonary symptoms and signs – These
patients have minimal symptoms at baseline but episodically develop some of the
following: cough, purulent sputum, wheezing, fatigue, and dyspnea. Typically, the
interval between exacerbations decreases as the severity of the COPD increases. This
 symptom complex can be a diagnostic challenge due to overlap with other common
chronic diseases. For example, the combination of intermittent wheezing and dyspnea
may lead to an incorrect diagnosis of asthma. Conversely, other illnesses with similar
episodic manifestations (eg, heart failure, bronchiectasis, bronchiolitis) are often
incorrectly diagnosed as a COPD exacerbation ( table 5). (See "COPD exacerbations:
Management".)

Approximately 62 percent of patients with moderate to severe COPD report variability in

symptoms (eg, dyspnea, cough, sputum, wheezing, or chest tightness) over the course of the
day or week to week; morning is typically the worst time of day [45].

Patients with COPD may experience weight gain (due to activity limitations), weight loss
(possibly due to dyspnea while eating or increased metabolic work of breathing), limitation
of activity (including sexual), cough, syncope, or feelings of depression or anxiety. Weight
loss generally reflects more advanced disease and is associated with a worse prognosis.

Comorbid diseases that may accompany COPD include lung cancer, bronchiectasis,
cardiovascular disease, osteoporosis, metabolic syndrome, skeletal muscle weakness,
anxiety, depression, and cognitive dysfunction. Patients may also report a family history of
COPD or other chronic respiratory illness [1,46-51].

Risk factors, including smoking and inhalational exposures — For patients presenting
with respiratory symptoms, it is critical to assess for the genetic, developmental, and
environmental risk factors that can predispose to the development of COPD ( table 4A)
[1,27,52]. The increasing recognition of these varying risk factors beyond smoking alone
have led to a proposed taxonomy of COPD "etiotypes" ( table 2). Understanding the
predominant etiology of disease in a given patient may allow for more targeted risk
reduction. A more complete discussion of COPD risk factors and risk reduction can be found
elsewhere. (See "Chronic obstructive pulmonary disease: Risk factors and risk reduction".)

The most common risk factor for COPD is cigarette smoking. Other exposures including
passive smoke and biomass fuel use also play significant roles worldwide [1,53,54].
● Smoking history – The amount and duration of smoking contribute to disease severity
[1,55-57]. Thus, a key step in the evaluation of patients with suspected COPD is to
ascertain the number of pack-years smoked (packs of cigarettes per day multiplied by
the number of years). A smoking history should include the age of starting and the age
of quitting, as patients may underestimate the number of years they smoked. With
enough smoking, almost all smokers will develop measurably reduced lung function [9].
While studies have shown an overall "dose-response curve" for smoking and lung
function, some individuals develop severe disease with fewer pack-years and others
have minimal to no symptoms despite many pack-years [9].
 The exact threshold for the duration/intensity of cigarette smoking that will result in
COPD varies from one individual to another. In the absence of an additional
genetic/environmental/occupational predisposition, smoking less than 10 to 15 pack-
years of cigarettes is unlikely to result in COPD.
● History of fume and dust exposure – The environmental/occupational history may
disclose other important risk factors for COPD, such as exposure to fumes or organic or
inorganic dusts, including household biomass smoke. These exposures help to explain
the significant minority of patients with COPD who never smoked [55,58,59].
● Other risk factors – Certain pulmonary and systemic infections are known to cause
permanent structural changes in the lung that predispose to COPD. In particular,
childhood pneumonias, tuberculosis infection, and human immunodeficiency virus (HIV)
are associated with high risk for later development of COPD [52]. Similarly, premature
birth and early-life asthma may affect the development of the lung and increase the risk
of COPD. A history of asthma is also important to elicit because poorly controlled asthma
in adulthood may progress to fixed airflow limitation and COPD [58,60]. A strong family
history of COPD or other chronic respiratory illnesses, particularly early in life, may
suggest a genetic predisposition to COPD.

Physical examination — The findings on physical examination of the chest vary with COPD
severity ( table 4A and table 4B). (See 'Assessment of severity and staging' below.)
● Mild disease – In mild disease, the physical examination may be normal. Subtle clues
include prolonged expiratory time and faint end-expiratory wheezes on forced
exhalation.
● Moderate to severe disease – As the severity of the airway obstruction increases,
physical examination may reveal hyperinflation (eg, increased resonance to percussion),
decreased breath sounds, wheezes, crackles at the lung bases, and/or distant heart
sounds [61]. Features of severe disease include an increased anteroposterior diameter
of the chest ("barrel-shaped" chest) and a depressed diaphragm with limited movement
based on chest percussion.
● End-stage disease and chronic respiratory failure – Patients with end-stage COPD
may adopt positions that relieve dyspnea, such as leaning forward with arms
outstretched and weight supported on the palms or elbows. This posture may be
evident during the examination or may be suggested by the presence of callouses or
swollen bursae on the extensor surfaces of forearms. Other physical examination
findings include use of the accessory respiratory muscles of the neck and shoulder
girdle, expiration through pursed lips, paradoxical retraction of the lower interspaces
during inspiration (ie, Hoover sign) [62,63], cyanosis, asterixis due to severe hypercapnia,
 and an enlarged, tender liver due to right heart failure. Neck vein distention may also be
observed because of increased intrathoracic pressure, especially during expiration.
● Adjunctive signs – Yellow stains on the fingers due to nicotine and tar from burning
tobacco are a clue to ongoing and heavy cigarette smoking [64]. Clubbing of the digits is
not typical in COPD (even with associated hypoxemia). Its presence suggests
comorbidities such as lung cancer, interstitial lung disease, or bronchiectasis.

DIAGNOSTIC EVALUATION

Whom to evaluate — Further diagnostic evaluation for COPD is appropriate in adults who
report dyspnea, chronic cough, or chronic sputum production, or who have had a gradual
decline in activity level, particularly if they have risk factors for COPD (eg, cigarette smoking,
indoor biomass smoke) ( table 4A) [1,56]. Adults without any symptoms should not
undergo further testing for COPD. (Related Pathway(s): Chronic obstructive pulmonary
disease: Initial diagnosis.)

Some patients with significant symptomatic COPD fail to report these symptoms to
physicians. We agree with the Global Initiative for Chronic Obstructive Lung Disease (GOLD)
in advocating for active case finding among at risk individuals [1]. The CAPTURE
questionnaire (Chronic obstructive pulmonary disease Assessment in Primary care To
identify Undiagnosed Respiratory disease and Exacerbation risk) is a well-validated tool that
can help identify occultly symptomatic patients who would likely benefit from therapy for
COPD and would therefore be candidates for diagnostic evaluation using spirometry
( table 6) [65,66]. Notably, in one large trial of its use as a screening tool for clinically
significant COPD in a primary care population, the CAPTURE questionnaire exhibited a
sensitivity 48 percent, specificity 89 percent, positive predictive value 10 percent, and
number needed to screen of 82 [67].

Based both on the post hoc analysis of results from the CAPTURE screening trial [67] and the
increased emphasis on symptoms rather than airflow limitation as a driver of therapeutic
strategies [1], use of CAPTURE without peak flow measurements may identify patients
appropriate for further evaluation and therapy. Patients with a questionnaire score of 0 to 2
are at lower risk, whereas those with scores 3 to 6 should undergo spirometric evaluation.

Current guidelines do not support population-based screening of asymptomatic adults for

COPD with spirometry [68,69], as asymptomatic mild airflow obstruction does not require
treatment [56,69]. Asymptomatic and nonsmoking individuals with mild airflow obstruction
but no history of asthma do not have the same progressive decline in lung function that is
observed among individuals who have a similar degree of airflow obstruction and are
symptomatic or continue to smoke [70].
How to evaluate — Patients at risk for COPD should be evaluated with spirometry; we also
typically obtain laboratory testing for dyspnea (eg, complete blood count, thyroid-
stimulating hormone, N-terminal pro hormone brain natriuretic peptide [BNP]) and a chest
radiograph to assess for other cardiac and pulmonary conditions.

Spirometry — Spirometry is required to establish the diagnosis of COPD. When evaluating a

patient for possible COPD, we typically perform spirometry before and after bronchodilator
administration to determine whether airflow limitation is present and whether it is partially
or fully reversible. Airflow limitation that is irreversible or only partially reversible with
bronchodilator treatment is a defining physiologic feature of COPD. Patients without airflow
limitation on prebronchodilator spirometry are highly unlikely to have COPD. (See "Office
spirometry", section on 'Post-bronchodilator spirometry'.)

The most important values measured during spirometry are the forced expiratory volume in
one second (FEV1) and the forced vital capacity (FVC). The postbronchodilator ratio of
FEV1/FVC determines whether nonreversible airflow limitation is present [1]; the
postbronchodilator percent predicted value for FEV1 determines the severity of airflow
limitation ( algorithm 1). The ratio of FEV1/FVC is not used to determine severity of airflow
limitation because FVC often decreases with increasing obstruction due to air trapping or
premature termination of exhalation.

An abnormal postbronchodilator FEV1/FVC ratio has traditionally been thought to be more

reliable than prebronchodilator measurements. However, several cohort studies have
demonstrated that prebronchodilator values are reproducible [71], and that obstruction only
found on postbronchodilator measurements (due to a preferential FVC response to
bronchodilator) is less common [72]. We agree with GOLD that prebronchodilator FEV1/FVC
alone may acceptably be used as an initial test to determine the presence of airflow
limitation [1]. Those without airflow limitation on prebronchodilator testing are unlikely to
have COPD and do not require bronchodilator administration to further exclude the
diagnosis. In contrast, those with prebronchodilator airflow limitation should undergo
postbronchodilator testing to establish the diagnosis of COPD.

Patients with significant smoking exposure and abnormal prebronchodilator FEV1/FVC, but
normal postbronchodilator FEV1/FVC, do not meet diagnostic criteria for COPD; however,
they are at high risk for developing COPD. Such patients comprised 6 percent of former or
current heavy smokers in one cohort [73]. Compared with smokers without
prebronchodilator obstruction, these patients had a higher likelihood of progression to
COPD (hazard ratio [HR] 6.2, 95% CI 4.6-8.3), with 61 percent (versus 14 percent) progressing
to COPD within five years [73]. We reassess this group of patients with repeat spirometry
after one year, or earlier if they have worsening symptoms.
● Threshold for airflow limitation – The ideal threshold for establishing airflow limitation
in the diagnosis of COPD has not been empirically determined. We agree with the GOLD
recommendations, which support the simple and well-established use of
postbronchodilator FEV1/FVC <0.7 as the threshold for nonreversible airflow limitation
[1].

However, the FEV1/FVC ratio decreases with age, so use of the fifth percentile lower limit
of normal (LLN) of the FEV1/FVC ratio (or, equivalently, a z-score of -1.645) rather than the
absolute value of <0.7 has been advocated by some as a dividing point for the diagnosis
of COPD and other obstructive lung diseases [74-79]. In practice, the adverse
consequences of overdiagnosis of COPD in the elderly by use of a fixed ratio are
somewhat mitigated by checking spirometry only in patients with symptoms and risk
factors for COPD, but underdiagnosis of younger persons with abnormal airflow for age
remains a concern. (See "Office spirometry", section on 'Ratio of FEV1/FVC' and
"Selecting reference values for pulmonary function tests", section on 'Spirometry'.)

One large study pooling data from nearly 25,000 adults in population-based cohorts
found that a fixed threshold of 0.7 was nearly optimal for determining persons at
increased risk for COPD hospitalization or death, performing slightly better than LLN
[80]. However, an analysis of current and former smokers with airflow limitation based
on GOLD criteria but normal lung function based on LLN found that these patients had
normal measures of multiple other respiratory-related phenotypes, including CT-
measured emphysema and gas trapping [81].

Evidence from one United States cohort of middle-aged ever-smokers demonstrated

that Black participants without airway obstruction had disproportionately lower FVCs
(and hence higher FEV1/FVC ratios) than age- and sex-matched White participants
without airway obstruction, a finding which correlated with more significant symptoms
despite the absence of spirometrically defined COPD [82].
● Alternatives to FEV1/FVC – The forced expiratory volume in six seconds (FEV6), obtained
by stopping the expiratory effort after six seconds rather than at cessation of airflow, is
an acceptable surrogate for the FVC [83-87]. The advantages of the FEV1/FEV6 include
less frustration by the patient and technician trying to achieve an end-of-test plateau,
less chance of syncope, shorter testing time, and better repeatability, without loss of
sensitivity or specificity. If used, the LLN for FEV1/FEV6 from the Third National Health
and Nutrition Examination Survey (NHANES III) is a reasonable threshold to diagnose
airflow limitation. Global Lung Function Initiative (GLI) spirometry equations do not
include FEV6 reference values, so this method cannot be used with spirometry software
that relies on these equations. (See "Office spirometry", section on 'Forced expiratory
volume in six seconds' and "Office spirometry", section on 'Ratio of FEV1/FVC'.)
Additional testing — In the setting of chronic respiratory symptoms and appropriate risk
factors, spirometry is the only testing required for the diagnosis of COPD. Additional testing
is directed at ruling out alternative diagnoses.
● Laboratory studies – For patients with dyspnea, we obtain laboratory studies as part of
a broad evaluation for potential etiologies. This often includes a complete blood count
for assessment of anemia, an assessment of electrolytes and kidney function, a thyroid-
stimulating hormone level, and a plasma BNP or N-terminal pro-BNP (NT-proBNP)
concentration as a component of the evaluation of suspected heart failure (HF). (See
"Approach to the patient with dyspnea", section on 'Initial testing in chronic dyspnea'.)
● Chest radiograph – For patients with suspected COPD, we typically obtain a chest
radiograph to evaluate for alternative parenchymal processes and assess pulmonary
comorbidities. Plain chest radiographs have a poor sensitivity for detecting COPD. As an
example, only about half of patients with COPD of moderate severity are identified as
having COPD by a plain chest radiograph (ie, sensitivity of 50 percent).

Radiographic features suggestive of COPD (usually seen in advanced disease) include:

• Rapidly tapering vascular shadows, increased radiolucency of the lung, a flat

diaphragm, and a long, narrow heart shadow on a frontal radiograph ( image 1).

• A flat diaphragmatic contour and an increased retrosternal airspace on a lateral

radiograph ( image 2). These findings are due to hyperinflation.

• Bullae, defined as radiolucent areas larger than one centimeter in diameter and
surrounded by arcuate hairline shadows. They are due to locally severe disease and
may or may not be accompanied by widespread emphysema ( image 3).

• When advanced COPD leads to pulmonary hypertension and cor pulmonale,

prominent hilar vascular shadows and encroachment of the heart shadow on the
retrosternal space may be seen [88,89]. The cardiac enlargement may become evident
only by comparison with previous chest radiographs. (See "Treatment and prognosis
of pulmonary arterial hypertension in adults (group 1)".)
● Computed tomography, for alternative diagnoses or if spirometry is not available –
There are settings where thoracic CT is routinely available and accessible, whereas
spirometric testing can be challenging to obtain. CT has greater sensitivity and
specificity than standard chest radiography for the detection of emphysema. This is
particularly true with high-resolution computed tomography (HRCT; ie, collimation of 1
to 2 mm) [90-94]. Expiratory scans, particularly when used in conjunction with the
inspiratory scans, can help to assess nonemphysematous air trapping as a surrogate
measure for small airway abnormalities [95] (see "High resolution computed
tomography of the lungs").
In the absence of other findings, CT-detected emphysema, air trapping, and airway
remodelling involving a significant portion of the lungs is highly suggestive of COPD,
and some have advocated for these findings as an alternative diagnostic pathway [52].
Because spirometry has a larger role in disease staging, is more cost-effective, and
avoids unnecessary radiation exposure, we do not favor this approach unless spirometry
cannot be obtained.

CT scanning may also be performed when symptoms or the physical examination

suggest a potential complication of COPD (eg, pneumonia, pneumothorax, giant bullae),
an alternate diagnosis (eg, thromboembolic disease) is suspected, or lung cancer
screening is indicated [1]. (See "Evaluation and medical management of giant bullae",
section on 'Evaluation' and "Clinical presentation, evaluation, and diagnosis of the
nonpregnant adult with suspected acute pulmonary embolism" and "Screening for lung
cancer", section on 'Low-dose chest CT'.)

Certain CT scan features can anatomically characterize the emphysema as centriacinar

(centrilobular), panacinar, or paraseptal, although this is usually not necessary for
clinical management [93,96]:

• Centriacinar emphysema occurs preferentially in the upper lobes and produces holes
in the center of secondary pulmonary lobules. The walls of emphysematous spaces
are usually imperceptible, but central vessels may be visible ( image 4). In contrast,
the walls of cysts in pulmonary Langerhans histiocytosis, another cystic lung disease
of cigarette smokers, are thicker ( image 5). (See 'Pathology' above.)

• Panacinar emphysema more commonly involves the lung bases and involves the
entire secondary pulmonary lobule ( image 6). Panacinar emphysema can cause a
generalized paucity of vascular structures. Among patients with alpha-1 antitrypsin
deficiency, panacinar emphysema is the more common pattern. (See "Clinical
manifestations, diagnosis, and natural history of alpha-1 antitrypsin deficiency",
section on 'Clinical manifestations'.)

• Paraseptal (distal acinar) emphysema produces small, subpleural collections of gas

located in the periphery of the secondary pulmonary lobule ( image 7). It is
considered to be the precursor of bullae ( image 8). (See 'Pathology' above.)

Newer CT scanners with higher resolution and new analytical methods can resolve
airway dimensions, although the clinical significance of these measures is undefined
[93,97-99]. Similarly, high-resolution scans can detect pruning of the distal vascular tree,
which arises from destruction of alveoli and their associated capillary beds due to
emphysema [34]. Quantitative parameters based on lung density, airway wall
thickening, airway dilation, and vascular pruning have all been established to gauge
 severity of emphysema, airway disease, and pulmonary vascular pathology, respectively,
but they have been used primarily as research tools and are not yet widely available.

DIAGNOSIS

The presence of symptoms compatible with COPD (eg, dyspnea at rest or on exertion, cough
with or without sputum production, progressive limitation of activity) is suggestive of the
diagnosis, especially if there is a history of exposure to triggers of COPD (eg, tobacco smoke,
occupational dust, indoor biomass smoke), a family history of chronic lung disease, or
presence of associated comorbidities ( table 1). (Related Pathway(s): Chronic obstructive
pulmonary disease: Initial diagnosis.)

The diagnosis of COPD is confirmed by the following [1,100]:

● Spirometry demonstrating airflow limitation (ie, a forced expiratory volume in one
second/forced vital capacity [FEV1/FVC] ratio less than 0.7 or below the lower limit of
normal [LLN]) that is incompletely reversible after the administration of an inhaled
bronchodilator ( table 4A-B). (See 'Spirometry' above.)
● Absence of an alternative explanation for the symptoms and airflow limitation
( table 5) [1]. The differential diagnosis of COPD is discussed below. (See 'Differential
diagnosis' below and "Approach to the patient with dyspnea".)

DIFFERENTIAL DIAGNOSIS

Among patients who present in mid or later life with dyspnea, cough, and sputum
production, the differential diagnosis is broad (eg, heart failure, COPD, interstitial lung
disease, thromboembolic disease) ( table 5). Typically, persistent airflow limitation on
pulmonary function testing and absence of radiographic features of heart failure or
interstitial lung disease direct the clinician to a narrower differential, which includes COPD,
chronic obstructive asthma, bronchiectasis, tuberculosis, constrictive bronchiolitis, and
diffuse panbronchiolitis [1]. Importantly, these conditions are not mutually exclusive and
commonly occur together. For example, patients with asthma may develop COPD, and
patients with COPD may have concurrent bronchiectasis.
● Chronic obstructive asthma – Older patients with a lifetime history of asthma may
develop chronic airway remodeling including fixed airway obstruction. For patients
without risk factors for COPD, chronic obstructive asthma is the presumed diagnosis in
these cases. In patients with risk factors for COPD, however, a clear distinction between
chronic obstructive asthma and COPD is not possible. As an example, a patient who has
suffered from atopic asthma since childhood and smoked cigarettes for 15 years in their
 twenties and thirties could present in their fifties with a combination of asthma and
COPD. Recognizing the coexistence of these diseases is essential in devising a treatment
plan that reflects both underlying disease processes. (See 'Interrelationships among
these conditions' above and "Asthma in adolescents and adults: Evaluation and
diagnosis" and "Asthma and COPD overlap (ACO)".)
● Chronic bronchitis with normal spirometry – A small portion of cigarette smokers
have a chronic productive cough for three months in each of two successive years but
do not have airflow limitation on pulmonary function tests. They are not considered to
have COPD, although they may develop COPD if they continue to smoke. (See
'Interrelationships among these conditions' above.)
● Central airway obstruction – Central airway obstruction can be caused by numerous
benign and malignant processes and can mimic COPD with a slowly progressive dyspnea
on exertion followed by dyspnea with minimal activity ( table 7). Monophonic wheezing
or stridor may be present. Symptoms are minimally improved by inhaled bronchodilator,
if at all. A high index of suspicion is needed as conventional chest radiographs are rarely
diagnostic. Though insensitive, flow-volume loops can show the characteristic changes
of central airway obstruction, frequently before abnormalities in the spirometric
volumes are noted ( figure 1 and figure 2) [101]. A high-resolution computed
tomography (HRCT) scan with three-dimensional reconstruction can be helpful. The gold
standard for diagnosis is direct visualization. (See "Clinical presentation, diagnostic
evaluation, and management of malignant central airway obstruction in adults", section
on 'Diagnostic evaluation and initial management' and "Presentation and diagnostic
evaluation of non-life-threatening and nonmalignant subglottic and tracheal stenosis in
adults", section on 'Initial diagnostic testing'.)
● Bronchiectasis – Bronchiectasis, a condition of abnormal widening of the bronchi that is
associated with chronic or recurrent infection, shares many clinical features with COPD,
including inflamed and easily collapsible airways, obstruction to airflow, and
exacerbations characterized by increased dyspnea and sputum production.
Bronchiectasis is suspected on the basis of prominent symptoms of cough and daily
mucopurulent sputum production. The diagnosis is usually established clinically based
on the characteristic cough and sputum production and the presence of bronchial wall
thickening and luminal dilatation on chest CT scans. (See "Clinical manifestations and
diagnosis of bronchiectasis in adults".)
● Heart failure – Heart failure is a common cause of dyspnea among middle-aged and
older patients and some patients experience chest tightness and wheezing with fluid
overload due to heart failure. Occasionally, airflow limitation is noted, although a
restrictive pattern is more common. Heart failure is usually differentiated by the
 presence of fine basilar crackles, radiographic evidence of an increased heart size, and
pulmonary edema. The brain natriuretic peptide (BNP) is typically increased in heart
failure but can also be increased during right heart strain from cor pulmonale. (See
"Heart failure: Clinical manifestations and diagnosis in adults".)
● Tuberculosis – In an area endemic for tuberculosis, the overall prevalence of airflow
obstruction was 31 percent among those with a past history of tuberculosis compared
with 14 percent among those without [102,103]. This association was unchanged after
adjustment for respiratory disease in childhood, smoking, and exposure to dust and
smoke. Thus, tuberculosis is both a risk factor for COPD and a potential comorbidity [1].
(See "Pulmonary tuberculosis: Clinical manifestations and complications".)
● Constrictive bronchiolitis – Constrictive bronchiolitis, also known as bronchiolitis
obliterans, is characterized by submucosal and peribronchiolar fibrosis that causes
concentric narrowing of the bronchiolar lumen. Constrictive bronchiolitis is most
commonly seen following inhalation injury, transplantation (eg, bone marrow, lung), or
in the context of rheumatoid lung or inflammatory bowel disease ( table 8). Symptoms
include progressive onset of cough and dyspnea associated with hypoxemia at rest or
with exercise. Crackles may be present. Pulmonary function tests show a progressive
and irreversible airflow limitation. Findings on inspiratory CT scan include centrilobular
bronchial wall thickening, bronchiolar dilation, tree-in-bud pattern, and a mosaic
ground-glass attenuation pattern. (See "Overview of bronchiolar disorders in adults",
section on 'Bronchiolitis obliterans'.)
● Diffuse panbronchiolitis – Diffuse panbronchiolitis is predominantly seen in male
nonsmokers of East Asian descent. Almost all have chronic sinusitis. On pulmonary
function testing, an obstructive defect is common, although a mixed obstructive-
restrictive pattern may also be seen. Chest radiographs and HRCT scans show diffuse
centrilobular nodular and linear opacities corresponding to thickened and dilated
bronchiolar walls with intraluminal mucous plugs. (See "Diffuse panbronchiolitis",
section on 'Diagnosis'.)
● Lymphangioleiomyomatosis – Lymphangioleiomyomatosis (LAM) is seen primarily in
young females of childbearing age. Pulmonary function testing frequently reveals mild
airflow obstruction, although a mixed obstructive-restrictive pattern may be seen. CT
scans typically demonstrate small, thin-walled cysts that can at times be confused with
emphysema. However, the airspaces in emphysema are not actually cysts but are caused
by the destruction of alveolar walls and permanent enlargement of distal airspaces, so
the "walls" are typically inapparent. (See 'Diagnosis' above and "Sporadic
lymphangioleiomyomatosis: Epidemiology and pathogenesis" and "Diagnostic approach
to the adult with cystic lung disease".)
POST-DIAGNOSTIC WORK-UP

Following a diagnosis of COPD, additional testing may be appropriate to assess disease

severity and guide optimal initial therapeutic management.

Etiologic evaluation, including alpha-1 antitrypsin testing — If not performed prior to

establishing the diagnosis, a new diagnosis of COPD should prompt a search for underlying
etiologic factors. For many patients, the etiology is long-term cigarette smoking. However, it
is important to review with the patient whether underlying asthma, workplace exposures,
indoor use of biomass fuel, a prior history of tuberculosis, or familial predisposition is
contributory because mitigation of ongoing exposures may reduce disease progression
( table 2). (See 'Risk factors, including smoking and inhalational exposures' above and
"Chronic obstructive pulmonary disease: Risk factors and risk reduction".)

It is appropriate to test all patients with COPD for alpha-1 antitrypsin (AAT) deficiency by
obtaining an AAT serum level and AAT genotyping ( algorithm 2) [1,104,105]. (See "Clinical
manifestations, diagnosis, and natural history of alpha-1 antitrypsin deficiency", section on
'Evaluation and diagnosis'.)

Exercise capacity — Objectively measured exercise impairment is a strong signal of overall

health status and a predictor of prognosis in COPD [106,107]. For patients with COPD, we
perform a formal six-minute walk test with ambulatory oximetry measurement. This allows
for assessment of exercise capacity as well as a determination of gas exchange during
exercise. Patients with exertional hypoxemia should have further assessment of their gas
exchange. (See 'Assessing gas exchange, in select patients' below.)

Timed walking tests can assess pulmonary disability and may uncover previously
unrecognized severe disease in patients with reduced dyspnea perception or sedentarism.
Exercise testing is also standard part of preprogram evaluation for pulmonary rehabilitation,
which is recommended for COPD patients with dyspnea or a history of exacerbations. (See
"Evaluation of pulmonary disability", section on 'Exercise tests' and "Pulmonary
rehabilitation", section on 'Preprogram evaluation'.)

Lung volumes, for those with impaired vital capacity — When a reduced forced vital
capacity (FVC) is present on postbronchodilator spirometry, we perform lung volume
measurement by body plethysmography to determine whether the reduction in FVC is due to
air trapping, hyperinflation, or a concomitant restrictive ventilatory defect. Body
plethysmography is strongly preferred for lung volume measurement when available
because gas dilution methods may be insensitive for the detection of air trapping. Decreased
inspiratory capacity (IC) and vital capacity, accompanied by an increased total lung capacity
(TLC), functional residual capacity (FRC), and residual volume (RV), are indicative of
hyperinflation. An increased FRC or RV with a normal TLC is indicative of air trapping without
hyperinflation. Restrictive deficits will present with a reduced TLC, and restrictive interstitial
lung diseases will demonstrate reductions in TLC, FRC, and RV. (See "Overview of pulmonary
function testing in adults", section on 'Lung volumes' and "Dynamic hyperinflation in
patients with COPD".)

Assessing gas exchange, in select patients — We perform additional assessment of gas

exchange in patients with COPD with moderate to severe airflow limitation (forced expiratory
volume in one second [FEV1] ≤50 percent predicted or z-score ≤-2.5), marginal resting oxygen
saturation [O2Sat] (O2Sat ≤92 percent), exertional hypoxemia (O2Sat <90 percent), or severe
dyspnea (modified Medical Research Council [mMRC] score ≥2) (calculator 1).
● Diffusing capacity for carbon monoxide (DLCO) – Although DLCO decreases in
proportion to the severity of emphysema in most patients with COPD, it cannot be used
to detect mild emphysema because it is neither a sensitive nor a specific test. However,
reductions in DLCO are associated with increased symptoms, worsened health status,
and increased risk of death independently of airflow obstruction and other clinical
findings [108-110]. DLCO reductions out of proportion to airflow limitation may suggest
concomitant restrictive lung disease or pulmonary hypertension, which require further
work-up. (See "Clinical features and diagnosis of pulmonary hypertension of unclear
etiology in adults".)
● Arterial blood gas – A resting arterial blood gas demonstrating arterial oxygen tension
(PaO2) ≤55 mmHg (7.33 kPa) is an indication for continuous supplemental oxygen.
Similarly, the presence of chronic respiratory acidosis ( figure 3 and figure 4) should
lead to evaluation for sleep-disordered breathing and possible nocturnal noninvasive
ventilation. (See "Long-term supplemental oxygen therapy" and "Nocturnal ventilatory
support in COPD".)
● CT imaging – While chest CT imaging is not recommended for all patients, we agree
with the global initiative for obstructive lung disease recommendations, which suggest
CT imaging in the following circumstances: patients with persistent exacerbations;
symptoms out of proportion to disease severity on lung function testing; FEV1 less than
45 percent predicted with significant hyperinflation (as consideration for endobronchial
valve placement); those meeting criteria for lung volume reduction surgery; and patients
meeting criteria for lung cancer screening [1].

ASSESSMENT OF SEVERITY AND STAGING

Several different strategies have been devised to categorize patients for the purposes of
disease management and prognosis. While historical approaches generally weighed
spirometric values more strongly, it has been increasingly recognized that other aspects of
disease, such as the severity of symptoms, risk of exacerbations, and the presence of
comorbidities, are important to the patient's experience and to disease prognosis [1,111].

GOLD classification systems — While the Global Initiative for Chronic Obstructive Lung
Disease (GOLD) strategy recommends COPD diagnosis using symptoms accompanied by a
forced expiratory volume in one second (FEV1)/ forced vital capacity (FVC) ratio <0.7, the
severity of obstruction is determined by the FEV1 percent predicted. The GOLD system uses
four grades:
● GOLD 1 (mild disease): FEV1 ≥80 percent predicted
● GOLD 2 (moderate disease): FEV1 between 50 and 80 percent predicted
● GOLD 3 (severe disease): FEV1 between 30 and 50 percent predicted
● GOLD 4 (very severe disease): FEV1 <30 percent predicted

This spirometric severity grading system is important due to its simplicity and subsequent
use in many clinical trials and observational studies; however, its prognostic capacity for
mortality is modest [112].

Other groups have suggested potential spirometry-derived alternatives to the GOLD Grade
system. For example, the STaging of Airflow obstruction by Ratio (STAR) severity classification
scheme was derived using approximately the 25th, 50th, and 75th percentile of the FEV1/FVC
ratios from the COPDGene cohort study and validated using COPDGene and a second
independent cohort [113]. Like GOLD, this classification divides patients with COPD into 4
stages: STAR stage 1 is defined by an FEV1/FVC ratio between 0.6 and 0.7; STAR stage 2 by an
FEV1/FVC ratio between 0.5 and 0.6; STAR stage 3 by an FEV1/FVC ratio between 0.4 and 0.5;
and STAR stage 4 by an FEV1/FVC ratio <0.4.

The GOLD and STAR systems provided similar discrimination for mortality and successfully
separated patients in the studied observational cohorts by dyspnea, respiratory quality of
life, and imaging assessments of disease [113]. A potential advantage of the STAR system is
that it does not rely on predicted lung size based on age, height, or race/ethnicity. It does,
however, depend on obtaining good-quality spirometry (eg, expiratory plateau in the last
second of expiration or expiratory time ≥15 seconds) [114]. STAR requires further validation
in population-based cohorts before it can be widely adopted.

While GOLD grade relates to spirometric severity of disease, GOLD recommends a different
system, the ABE assessment tool, for use in determining initial therapy. The GOLD ABE
assessment tool uses an individual’s symptoms (ie, modified Medical Research Council
[mMRC] dyspnea scale (calculator 1) or COPD Assessment Test (calculator 2)) and
exacerbation history to guide pharmacotherapy ( algorithm 3) [1]. The multidimensional
GOLD "ABE" evaluation is discussed in more detail separately in the context of initial
management of COPD. (See "Stable COPD: Initial pharmacologic management".) (Related
Pathway(s): Chronic obstructive pulmonary disease: Severity assessment and selection of
initial therapy in adults.)

We agree with the GOLD strategy to monitor postbronchodilator spirometry yearly to track
decline in FEV1, which may identify patients whose disease is progressing more quickly than
usual. Follow-up spirometric assessment may also be helpful in therapeutic decision making
when considering multiple potential causes of worsening dyspnea. Finally, spirometric values
remain an essential component of decision making for lung volume reduction and lung
transplantation. (See "Management of refractory chronic obstructive pulmonary disease",
section on 'Lung Volume Reduction, in select patients with dyspnea' and "Management of
refractory chronic obstructive pulmonary disease", section on 'Lung transplantation'.)

BODE index — The BODE index is another system for assessment of COPD severity and
prognosis. It is calculated based on weight (body mass index [BMI]), airflow limitation (FEV1),
dyspnea (mMRC dyspnea score) (calculator 1), and exercise capacity (six-minute walk
distance) (calculator 3), and it has been used to assess an individual’s risk of death. This index
provides better prognostic information than the FEV1 alone and can be used to assess
therapeutic response to medications, pulmonary rehabilitation therapy, and other
interventions [106,107,113,115]. (See "Chronic obstructive pulmonary disease: Prognostic
factors and comorbid conditions", section on 'BODE index'.)

COPD Foundation system — The COPD Foundation has introduced a system that includes
seven severity domains, each of which has therapeutic implications ( figure 5) [56,100].
These domains are based upon assessment of spirometry, regular symptoms, number of
exacerbations in the past year, oxygenation, emphysema on CT scan or air trapping on lung
volumes, presence of chronic bronchitis, and comorbidities. Within the spirometry domain,
the COPD Foundation uses five grades:
● SG 0: Normal spirometry
● SG 1: Mild, postbronchodilator FEV1/forced vital capacity (FVC) ratio <0.7, FEV1 ≥60
percent predicted
● SG 2: Moderate, postbronchodilator FEV1/FVC ratio <0.7, FEV1 between 30 and 60 percent
predicted
● SG 3: Severe, postbronchodilator FEV1/FVC ratio <0.7, FEV1 <30 percent predicted
● SG U: Undefined, postbronchodilator FEV1/FVC ratio >0.7, FEV1 <80 percent predicted

An advantage of this staging system is that it simplifies the interpretation of spirometry; any
spirometric finding results in a classification, which is not the case in the GOLD system.

While FEV1 is used to gauge severity, the FEV1/FVC ratio is not used for this purpose because
measurement of FVC becomes less reliable as the disease progresses (the long exhalations
are difficult for the patients), thus making the ratio less accurate unless high-quality
spirometry is ensured ( algorithm 1). (See "Chronic obstructive pulmonary disease:
Prognostic factors and comorbid conditions", section on 'Forced expiratory volume in one
second' and "Office spirometry", section on 'Interpretation'.)

SOCIETY GUIDELINE LINKS

Links to society and government-sponsored guidelines from selected countries and regions
around the world are provided separately. (See "Society guideline links: Chronic obstructive
pulmonary disease".)

INFORMATION FOR PATIENTS

UpToDate offers two types of patient education materials, “The Basics” and “Beyond the
Basics.” The Basics patient education pieces are written in plain language, at the 5th to 6th
grade reading level, and they answer the four or five key questions a patient might have
about a given condition. These articles are best for patients who want a general overview
and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are
longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th
grade reading level and are best for patients who want in-depth information and are
comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to
print or e-mail these topics to your patients. (You can also locate patient education articles
on a variety of subjects by searching on “patient info” and the keyword(s) of interest.)
● Basics topics (see "Patient education: Chronic obstructive pulmonary disease (COPD)
(The Basics)" and "Patient education: Chronic bronchitis (The Basics)" and "Patient
education: Medicines for COPD (The Basics)")
● Beyond the Basics topics (see "Patient education: Chronic obstructive pulmonary disease
(COPD) (Beyond the Basics)")

SUMMARY AND RECOMMENDATIONS

● Definitions – The Global Initiative for Chronic Obstructive Lung Disease (GOLD) defines
COPD as follows: "COPD is a heterogeneous lung condition characterized by chronic
respiratory symptoms due to abnormalities of the airway and/or alveoli that cause
persistent, often progressive, airflow obstruction." (See 'Definitions' above.)

Substantial overlap exists between COPD and the other disorders that may cause airflow
limitation (eg, emphysema, chronic bronchitis, asthma, bronchiectasis, bronchiolitis).
(See 'Interrelationships among these conditions' above.)
● Clinical features – Common presentations of COPD include patients with few
complaints but an extremely sedentary lifestyle; patients with chronic, daily respiratory
symptoms (eg, dyspnea on exertion, cough); and patients with recurrent acute
exacerbations (eg, wheezing, cough, dyspnea, fatigue). Patients should be asked about
current smoking and the number of pack-years smoked (packs of cigarettes per day
multiplied by the number of years); other inhalational exposures; tuberculosis, HIV, and
childhood pulmonary infections; a history of asthma; and a family history of lung
diseases. The physical examination of the chest varies with the severity of the COPD but
is often normal in mild disease ( table 4A-B). (See 'Clinical Presentation' above.)
● Diagnostic evaluation – The diagnosis of COPD should be considered and spirometry
performed pre- and postbronchodilator administration in all patients who report any
combination of dyspnea, chronic cough, or chronic sputum production, especially if
there is a history of exposure to triggers of COPD (eg, tobacco smoke, occupational dust,
indoor biomass smoke), a family history of chronic lung disease, or presence of
associated comorbidities ( table 1). For individuals with risk factors, use of the
CAPTURE (Chronic obstructive pulmonary disease Assessment in Primary care To
identify Undiagnosed Respiratory disease and Exacerbation risk) questionnaire and peak
flow measurement to assess unreported symptoms and potential air flow limitation may
identify additional symptomatic patients appropriate for further evaluation. (Related
Pathway(s): Chronic obstructive pulmonary disease: Initial diagnosis.)

• Spirometry pre- and postbronchodilator – COPD is confirmed when a patient with

compatible symptoms is found to have irreversible airflow limitation (ie, a
postbronchodilator forced expiratory volume in one second [FEV1]/forced vital
capacity [FVC] ratio less than 0.7 [or below the lower limit of normal (LLN)]) and no
alternative explanation for the symptoms and airflow obstruction. (See 'Spirometry'
above and 'Diagnosis' above.)

• Additional testing – In the evaluation of patients with COPD, laboratory studies and
chest radiography are typically performed to exclude alternative diagnoses, evaluate
for comorbidities, or assess a change in symptoms that suggests a complication of
COPD. Chest CT is performed to evaluate abnormalities seen on the conventional
chest radiograph, to exclude certain complications of COPD (eg, thromboembolic
disease, lung cancer), or when a patient is being considered for lung volume
reduction surgery, endobronchial valves, or lung transplantation. (See 'Additional
testing' above.)
● Differential diagnosis – Among patients who present in mid- or later-life with dyspnea,
cough, and sputum production, the differential diagnosis is broad (eg, heart failure,
 COPD, interstitial lung disease, thromboembolic disease) ( table 5). (See 'Differential
diagnosis' above.)
● Post-diagnostic work-up – Following a diagnosis of COPD, additional testing may be
appropriate to assess disease severity and guide optimal initial therapeutic
management.

• Etiologic evaluation, including alpha-1 antitrypsin testing – If not performed prior

to establishing the diagnosis, a new diagnosis of COPD should prompt a search for
underlying etiologic factors ( table 2). It is appropriate to test all patients with COPD
for alpha-1 antitrypsin (AAT) deficiency by obtaining an AAT serum level and AAT
genotyping ( algorithm 2).

• Exercise capacity – For patients with COPD, we perform a formal six-minute walk test
with ambulatory oximetry measurement. This allows for assessment of exercise
capacity as well as a determination of gas exchange during exercise.

• Other studies – Assessment of lung volumes and gas exchange are appropriate for
patients with evidence of more severe disease. (See 'Lung volumes, for those with
impaired vital capacity' above and 'Assessing gas exchange, in select patients' above.)
● Assessment of severity and staging

• The original GOLD staging system was based solely on postbronchodilator FEV1.
Although well-recognized and commonly used, it has been criticized for
underestimating the importance of the severity of symptoms, risk of exacerbations,
and presence of comorbidities in predicting outcome. (See 'Assessment of severity
and staging' above.)

• The revised GOLD "ABE" strategy uses a combination of an individual's symptoms and
history of exacerbations and hospitalizations due to exacerbations to stratify
symptoms and exacerbation risk and guide therapy ( algorithm 3). (See 'GOLD
classification systems' above.)

• Other multidimensional staging systems include the BODE index (calculator 3) and
the COPD Foundation system ( figure 5). (See 'BODE index' above and 'COPD
Foundation system' above.)

ACKNOWLEDGMENT

The editorial staff at UpToDate acknowledge Stephen Rennard, MD, who contributed to
earlier versions of this topic review.

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