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Chronic obstructive pulmonary disease: Definition, clinical manifestations, diagnosis, and staging
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Chronic obstructive pulmonary disease: Definition, clinical manifestations, diagnosis, and staging
Disclosures:
MeiLan King Han, MD, MS
Nothing to disclose.
Mark T Dransfield, MD
Grant/Research/Clinical Trial Support: Boehringer Ingelheim [COPD (Tiotropium bromide)]; GlaxoSmithKline [COPD (Fluticasone/salmeterol, mepolizumab, fluticasone furoate/vilanterol, umeclidinium/vilanterol)]; Novartis [COPD]; AstraZeneca [COPD]. Consultant/Advisory Boards: GlaxoSmithKline [COPD (Fluticasone/salmeterol, mepolizumab, fluticasone furoate/vilanterol, umeclidinium/vilanterol)].
Fernando J Martinez, MD, MS
Grant/Research/Clinical Trial Support: Forest [COPD (Roflumilast)]; GSK [COPD (Fluticasone, Vilanterol, Umecladinium and novel agents)]; Janssens [COPD (novel inhaled agents)]; Nycomed/Takeda [COPD (Roflumilast)]. Consultant/Advisory Boards: BI [COPD (Tiotropium and Olodaterol)]; CSA Medical [COPD (novel approach)]; Forest [COPD (Roflumilast)]; Genentech [COPD (novel agents)]; GSK [COPD (Fluticasone, Vilanterol, Umecladinium and novel agents)]; Ikaria [COPD (novel compounds)]; Pearl [COPD (novel compounds)]; Pfizer [COPD (novel compounds)]; Roche [COPD (novel compounds)].
James K Stoller, MD, MS
Consultant/Advisory Boards:
CSL Behring [Alpha-1 antitrypsin deficiency (Augmentation therapy (IV alpha-1 antiprotease))]; Kamada [Alpha-1 antitrypsin deficiency (Augmentation therapy (IV alpha-1 antiprotease))]; Baxter [Alpha-1 antitrypsin deficiency (Augmentation therapy (IV alpha-1 antiprotease))]; Grifols [Alpha-1 antitrypsin deficiency (Augmentation therapy (IV alpha-1 antiprotease))]; Boehringer Ingelheim [COPD (Bronchodilators (various))]; Arrowhead Research [Alpha-1 antitrypsin deficiency].
Helen Hollingsworth, MD
Nothing to disclose.
All topics are updated as new evidence becomes available and our
is complete.
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 []. As current and former smokers are also at risk for a number of other medical problems for which treatment is very different, 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 in this topic review. The risk factors, natural history, prognosis, and treatment of COPD are discussed separately. (See
and .)Several features of COPD patients identify individuals with different prognoses and/or responses to treatment. Whether these features identify separate &phenotypes& of COPD or reflect disease severity remains unclear []. However, evaluation of these features can help guide clinical management, and their use in classification of patients is now recommended []. (See
below.)&Chronic obstructive pulmonary disease (COPD), a common preventable and treatable disease, is characterized by airflow limitation that is usually progressive and associated with an enhanced chronic inflammatory response in the airways and the lung to noxious particles or gases. Exacerbations and comorbidities contribute to the overall severity in individual patients.&The various subtypes of emphysema (eg, proximal acinar, panacinar, distal acinar) are described below. (See
below.)●Patients with asthma whose airflow obstruction is completely reversible are not considered to have COPD (subset nine in the figure).●Patients with asthma whose airflow obstruction does not remit completely are considered to have COPD (subsets six, seven, and eight in the figure). The etiology and pathogenesis of the COPD in such patients may be different from that of patients with chronic bronchitis or emphysema.●Chronic bronchitis and emphysema with airflow obstruction commonly occur together (subset five in the figure) []. Some of these patients may also have asthma (subset eight in the figure).●Individuals with asthma may develop a chronic productive cough, either spontaneously or due to exposure (eg, cigarette smoke, allergen). Such patients are often referred to as having asthmatic bronchitis, although this terminology has not been officially endorsed in clinical practice guidelines (subset six in the figure).●Persons with chronic bronchitis, emphysema, or both are not considered to have COPD unless they have airflow obstruction (subsets one, two, and eleven in the figure) [].●Patients with airflow obstruction due to diseases that have a known etiology or a specific pathology (eg, cystic fibrosis, bronchiectasis, obliterative bronchiolitis) are not considered to have COPD (subset 10 in the figure). However, these exclusions are loosely defined [].●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, but can also be seen in coal workers& pneumoconiosis.●Panacinar emphysema refers to enlargement or destruction of all parts of the acinus. Diffuse panacinar emphysema is most commonly associated with alpha-1 antitrypsin deficiency, although it can be seen in combination with proximal emphysema in smokers. (See .)●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, the usual association is spontaneous pneumothorax in a young adult. (See .)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 a genetic/environmental/occupational predisposition, smoking less than 10 to 15 pack years of cigarettes is unlikely to result in COPD. On the other hand, the single best variable for predicting which adults will have airflow obstruction on spirometry is a history of more than 40 pack years of smoking (positive likelihood ratio [LR], 12 [95% CI, 2.7-50]) []. The chronologically taken environmental/occupational history may disclose other important risk factors for COPD, such as exposure to fumes or organic or inorganic dusts. These exposures help to explain the 20 percent of patients with COPD (defined by lung function alone) and the 20 percent of patients who die from COPD who never smoked []. A history of asthma should also be sought, as COPD is often misdiagnosed as asthma. In addition, asthma may progress to fixed airflow limitation and COPD []. (See .)There are three typical ways in which patients with COPD present []: ●Patients who have an extremely sedentary lifestyle but few complaints 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 respiratory symptoms generally complain of dyspnea and chronic cough. The 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 volume rarely exceeds 60 mL. The sputum is usually mucoid, but becomes purulent during exacerbations.●Patients who present with episodes of increased cough, purulent sputum, wheezing, fatigue, and dyspnea that occur intermittently, with or without fever. Diagnosis can be problematic in such patients. The combination of wheezing plus dyspnea may lead to an incorrect diagnosis of asthma. Conversely, other illnesses with similar manifestations are often incorrectly diagnosed as a COPD exacerbation (eg, heart failure, bronchiectasis, bronchiolitis) (). The interval between exacerbations decreases as the severity of the COPD increases. (See .)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- morning is typically the worst time of day [].Patients with COPD may experience weight gain (due to activity limitations), weight loss (possibly due to dyspnea while eating), 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. However, the majority of COPD patients are overweight or obese.Comorbid diseases that may accompany COPD include lung cancer, coronary heart disease, osteoporosis, metabolic syndrome, skeletal muscle weakness, depression, and cognitive dysfunction. Patients may also report a family history of COPD or other chronic respiratory illness []. ●Early in the disease, the physical examination may be normal, or may show only prolonged expiration or wheezes on forced exhalation.●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 []. 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. ●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's sign) [], 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.●Yellow stains on the fingers due to nicotine and tar from burning tobacco are a clue to ongoing and heavy cigarette smoking []. Clubbing of the digits is not typical in COPD (even with associated hypoxemia) and suggests comorbidities such as lung cancer, interstitial lung disease, or bronchiectasis.●Assessment for anemia is an important step in the evaluation of dyspnea. Measurement of plasma brain natriuretic peptide (BNP) or N-terminal pro-BNP (NT-proBNP) concentrations is useful as a component of the evaluation of suspected heart failure (HF). Blood glucose, urea nitrogen, creatinine, electrolytes, calcium, phosphorus, and thyroid stimulating hormone may be appropriate depending on the degree of clinical suspicion for an alternate diagnosis. (See .)●Among stable COPD patients with normal kidney function, an elevated serum bicarbonate may indirectly identify chronic hypercapnia. In the presence of chronic hypercapnia, the serum bicarbonate is typically increased due to a compensatory metabolic alkalosis (). Abnormal results must be confirmed with arterial blood gas measurement. (See .)●Testing for alpha-1 antitrypsin (AAT) deficiency should be obtained in all symptomatic adults with persistent airflow obstruction on spirometry. Especially suggestive subsets include the presence of emphysema in a young individual (eg, age &45 years), emphysema in a nonsmoker or minimal smoker, emphysema characterized by predominantly basilar changes on the chest radiograph, or a family history of emphysema []. However, AAT deficiency may be present in a patient with otherwise &typical& COPD. A serum level of AAT below 11 micromol/L (~57 mg/dL by nephelometry) in combination with a severe deficient genotype is diagnostic. (See .)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 airflow l the postbronchodilator percent predicted value for FEV1 determines the severity of airflow limitation as shown in the table (). The indications for measuring ABGs (eg, arterial oxygen tension [PaO2], carbon dioxide tension [PaCO2], and acidity [pH]), which must be considered in the clinical context, include the following:●Low FEV1 (eg, &50 percent predicted)●Low oxygen saturation by pulse oximetry (eg, &92 percent)●Depressed level of consciousness●Acute exacerbation of COPD●Assessment for hypercapnia in at risk patients 30 to 60 minutes after initiation of supplemental oxygen (see )In patients with mild to moderate COPD, arterial blood gases usually reveal mild or moderate hypoxemia without hypercapnia. As the disease progresses, the hypoxemia becomes more severe and hypercapnia may develop. Hypercapnia becomes progressively more likely when the FEV1 approaches or falls below one liter. Blood gas abnormalities worsen during acute exacerbations and may also worsen during exercise and sleep. The compensatory responses to acute and chronic respiratory acidosis are shown in the figure and discussed separately (). (See .)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 ().●A flat diaphragmatic contour and an increased retrosternal airspace on a lateral radiograph (). 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 ().●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 []. The cardiac enlargement may become evident only by comparison with previous chest radiographs. (See .)Certain CT scan features can determine whether the emphysema is centriacinar (centrilobular), panacinar, or paraseptal, although this is usually not necessary for clinical management []. ●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 (). In contrast, the walls of cysts in pulmonary Langerhans histiocytosis, another cystic lung disease of cigarette smokers, are thicker (). (See
above.)●Panacinar emphysema more commonly involves the lung bases and involves the entire secondary pulmonary lobule (). 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 .)●Paraseptal (distal acinar) emphysema produces small, subpleural collections of gas located in the periphery of the secondary pulmonary lobule (). It is considered to be the precursor of bullae (). (See
above.)Newer CT scanners with higher resolution and new analytical methods can resolve airway dimensions, although the clinical significance of these measures is undefined []. Quantitative parameters based on lung density, as measured by CT scan, have been established to gauge emphysema, but are currently used primarily as research tools.●Spirometry demonstrating airflow limitation (ie, a forced expiratory volume in one second/forced vital capacity [FEV1/FVC] ratio less than 0.7 or less than the lower limit of normal [LLN] PLUS an FEV1 less than 80 percent of predicted) that is incompletely reversible after the administration of an inhaled bronchodilator (). (See
above.)●Absence of an alternative explanation for the symptoms and airflow limitation () []. The differential diagnosis of COPD is discussed below. (See
below and .)After confirming the presence of COPD, the next step is to consider the cause. For the majority of 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. In areas of high prevalence of alpha-1 antitrypsin (AAT) deficiency, it is appropriate to screen all patients with COPD by obtaining an AAT serum level []. (See
above and .)●Chronic obstructive asthma & In some patients with chronic asthma, a clear distinction from COPD is not possible. As an example, a patient, who has had 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. The importance of recognizing the coexistence of these diseases is in devising a treatment plan that is adapted to reflect both underlying disease processes. (See
above and .) ●Chronic bronchitis with normal spirometry & A small portion of cigarette smokers have a chronic productive cough for three months in 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. Some treatments for COPD may improve their cough. (See
above.)●Central airway stenosis & Central airway stenosis 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. 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 ( and ) []. A high resolution CT scan with three-dimensional reconstruction can be helpful. The gold standard for diagnosis is direct visualization. (See .)●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 computed tomographic (CT) scans. (See .)●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 is typically increased in heart failure, but can also be increased during right heart strain from cor pulmonale. (See .)●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. 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 []. (See .)●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 (). 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 .)●Diffuse panbronchiolitis & Diffuse panbronchiolitis is predominantly seen in male nonsmokers of 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 high resolution CT scans show diffuse centrilobular nodular and linear opacities corresponding to thickened and dilated bronchiolar walls with intraluminal mucous plugs. (See .)●Lymphangioleiomyomatosis & Lymphangioleiomyomatosis (LAM) is seen primarily in young women 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
above and .)On the other hand, waiting for patients to report symptoms may miss a large number of patients who have COPD, as 20 percent of individuals with severe airway obstruction due to smoking or asthma will not report symptoms. Decrements in forced expiratory volume in one second (FEV1), even within the normal range, are associated with increased risk of acute cardiac events independent of age, gender, and smoking history []. Thus, performance of spirometry seems reasonable whenever COPD is a diagnostic consideration. The diagnosis of COPD may alter management of concurrent conditions and may affect the approach to exercise. Exclusion of COPD can often contribute to clinical management as much as its diagnosis by leading to alternative diagnoses. Several tools for evaluating symptom severity have been proposed. The GOLD guidelines suggest using instruments such as the modified Medical Research Council (mMRC) dyspnea scale (), the Clinical COPD Questionnaire (), or the COPD Assessment Tool (CAT) []. The most widely used tool, the St. George's Respiratory Questionnaire (SGRQ), is a 76 item questionnaire that includes three component scores (ie, symptoms, activity, and impact on daily life) and a total score. While valuable for research purposes in patients with COPD, asthma, and bronchiectasis, it is too long and complicated for use in routine clinical practice [].●Group A: Low risk, less symptoms: Typically GOLD 1 or GOLD 2 (mild or moderate airflow limitation) and/or 0 to 1 exacerbation per year and mMRC grade 0 to 1 or CAT score &10.●Group B: Low risk, more symptoms: Typically GOLD 1 or GOLD 2 (mild or moderate airflow limitation) and/or 0 to 1 exacerbation per year and mMRC grade &2 or CAT score &10.●Group C: High risk, less symptoms: Typically GOLD 3 or GOLD 4 (severe or very severe airflow limitation) and/or &2 exacerbations per year and mMRC grade 0 to 1 or CAT score &10.●Group D: High risk, more symptoms: Typically GOLD 3 or GOLD 4 (severe or very severe airflow limitation) and/or &2 exacerbations per year and mMRC grade &2 or CAT score &10.Other systems for assessing disease severity in the COPD patient have been proposed. The BODE index, which is calculated based on weight (BMI), airway obstruction (FEV1), dyspnea (mMRC dyspnea score), and exercise capacity (six-minute walk distance) (), 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 []. (See .)●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, 30 percent &FEV1 &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 predictedAn advantage of this staging system is that it simplifies the interpre any spirometric finding results in a classification, which is not the case in GOLD.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. (See .)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
and )●Beyond the Basics topics (see )●The Global Initiative for Chronic Obstructive Lung Disease (GOLD) defines COPD as follows: &Chronic obstructive pulmonary disease (COPD), a common preventable and treatable disease, is characterized by airflow limitation that is usually progressive and associated with an enhanced chronic inflammatory response in the airways and the lung to noxious particles or gases. Exacerbations and comorbidities contribute to the overall severity in individual patients.& (See
above.)●Substantial overlap exists between COPD and the other disorders that cause airflow limitation (eg, emphysema, chronic bronchitis, asthma, bronchiectasis, bronchiolitis) as illustrated in the figure (). (See
above.)●Common presentations of COPD include patients with few complaints, but an extremely patients with chronic, daily respiratory symptoms (eg, dyspnea on exertion, cough); and patients with recurrent acute exacerbations (eg, wheezing, cough, dyspnea, fatigue). The physical examination of the chest varies with the severity of the COPD, but is often normal in mild disease (). (See
above.)●The diagnosis of COPD should be considered and spirometry performed 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 (). (See
above.)●COPD is confirmed when a patient with compatible symptoms is found to have irreversible airflow limitation (ie, a post bronchodilator forced expiratory volume in one second [FEV1]/forced vital capacity [FVC] ratio less than 0.7 [or less than the lower limit of normal] and an FEV1 &80 percent predicted) and no alternative explanation for the symptoms and airflow obstruction. (See
above.)●In areas of high prevalence of alpha-1 antitrypsin (AAT) deficiency, all symptomatic adults with fixed airflow obstruction on spirometry should be tested for AAT deficiency with an AAT serum level. (See
above and .)●In the evaluation of patients with COPD, chest radiography is typically performed to exclude alternative diagnoses, evaluate for comorbidities, or assess a change in symptoms that suggests a complication of COPD. Chest computed tomography is performed to evaluate abnormalities seen on the conventional chest radiograph, to exclude certain complications of COPD (eg, thromboembolic disease), or when a patient is being considered for lung volume reduction surgery. (See
above.)●The original FEV1-based GOLD staging system is shown in the table (). Although well recognized and commonly used, the GOLD staging system has been criticized for underestimating the importance of the extrapulmonary manifestations of COPD in predicting outcome. Other multidimensional staging systems (eg, GOLD combined assessment tool, BODE index) address this criticism (). (See
above.)●The management of COPD and strategies for smoking cessation are discussed separately. (See
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