Pulmonary Medicine

COPD: Clinical Manifestations and Management (include pulmonary rehabilitation)

What every physician needs to know:

COPD is a common heterogeneous disorder, affecting nearly 15.7 million Americans (6.4%) and is currently the third leading cause of death in the US. The actual prevalence of COPD is likely even higher, as >50% of adults with low pulmonary function were unaware that they had COPD.

COPD is defined as chronic expiratory airflow limitation that is not fully reversible and encompasses several pathological processes. To varying degrees, some or all of these processes may be present in individual patients, resulting in considerable clinical, physiologic, and pathologic heterogeneity. Clinical features of COPD are nonspecific, and individuals may incorrectly be labeled as having COPD. Alternatively, symptoms may be subtle and discounted by patients, resulting in substantial under diagnosis. Spirometry is necessary to make the diagnosis, and should be considered in patients with dyspnea, chronic cough or sputum production, and a history of exposure to risk factors.

The most important risk factor for COPD in industrialized nations is chronic exposure to cigarette smoke. The incidence of COPD amongst current/former smokers is commonly cited as 15%, although more recent studies suggest that the incidence is likely higher, perhaps closer to 25%. The variability in disease susceptibility reflects the complex interaction between host and environmental factors. Additionally, while not all smokers develop COPD as defined by spirometry, clinically meaningful respiratory disease may develop in about half of smokers with a substantial smoking history (>10-20 pack-years).

COPD is generally regarded as a progressive disease. In the classic description of longitudinal lung function in COPD, Fletcher et al., showed that lung function declines in everyone with age, but suggested that patients with COPD have accelerated lung function decline compared to those without COPD. However, recent studies have demonstrated that this accelerated lung function decline describes approximately half of patients with COPD, as the other half of patients with COPD have reduced lung function earlier in life. In parallel with the natural decline in lung function that occurs with aging, COPD has been regarded as a disease of the elderly. However, mild disease, which may limit physical activity and have prognostic implications, may be diagnosed in the fourth or fifth decades of life.

COPD is a systemic disorder that is associated with extra-pulmonary diseases (Table 1), many of which have a higher incidence in smokers than in non-smokers. However, the co-occurrence of COPD and these conditions is higher than would be expected based simply on their frequency. Whether this co-occurrence reflects shared risk factors or a pathogenetic process whereby lung disease leads to extra-pulmonary manifestations is unknown. For the clinician, careful assessment and management of conditions associated with COPD is required in the management of COPD, and consideration of co-morbidities in COPD is important in patients with associated conditions. Ultimately, patients with COPD requires an integrated approach that combines pharmacotherapy, non-pharmacologic approaches, and in selected cases, surgery.

Table I.

Risk factors for COPD

Classification:

COPD has long been recognized as a clinically heterogeneous disorder. One classic description classified COPD patients as "pink puffers" or "blue bloaters”. The term "pink puffer" is used to describe a patient with emphysema whose gas exchange and arterial oxygen saturation are relatively well maintained. The term "blue bloater" refers to a patient with chronic bronchitis who has hypoxia due to ventilation-perfusion abnormalities with pulmonary hypertension and right heart failure. This classification does not capture the full heterogeneity of COPD and thus has fallen out of favor with COPD now classified according to pathophysiologic hallmarks.

  • Findings in emphysema include destruction of alveolar walls and airflow limitation resulting from the loss of lung elastic recoil and lack of tethering of small airways. This causes small airway collapse, particularly with forced exhalation, which contributes to expiratory airflow limitation. Anatomic forms of emphysema include centrilobular emphysema, the common form in cigarette smokers, and panlobular emphysema, a disorder classically associated with emphysema in non-smoking, alpha-1 antitrypsin-deficient patients. In centrilobular disease, the central lobular region is destroyed, while peripheral lobular alveoli may be relatively intact, while in panlobular emphysema, the entire lobule is affected uniformly. Often, centrilobular emphysema is most prominent in the upper lobes and superior segments of the lower lobes, while panlobular emphysema may be most prominent in the lower lobes. Additional subtypes of emphysema have been described, although their clinical significance remains unclear.

  • Findings in chronic bronchitis include the presence of cough and sputum; the most common definition requires symptoms on most days for ≥3 months in 2 consecutive years, although this definition is arbitrary. Another pathophysiologic hallmark is mucus hypersecretion due to enlargement of the mucus glands and goblet cell metaplasia. The increased airway secretions may contribute to airflow limitation, but they are not usually the major reason for expiratory airflow limitation.

  • Small airway bronchiolitis is a major cause of expiratory airflow limitation in COPD patients, especially those who predominantly have chronic bronchitis. Inflammation in the small airways is an early site of pathology in relatively healthy smokers and progress and lead to narrowing and airway fibrosis. Disease of the small airways may be present without prominent cough and sputum, resulting in airflow limitation without clear symptoms that meet the definition of chronic bronchitis. Conversely, subjects with marked cough and sputum may have relatively normal airflow.

  • COPD is also a disease of the pulmonary vasculature. Patients with emphysema demonstrate a reduction in the number and luminal diameter of pulmonary vessels. This is thought to contribute to ventilation-perfusion abnormalities and the development of pulmonary hypertension in patients with COPD. Disease of the capillary bed may also contribute to the development of emphysema as well as cardiovascular disease commonly associated with COPD. The cause for pulmonary vascular disease in COPD is likely multifactorial, including cellular death and dysfunction as a consequence of oxidative stress and chronic inflammation.

Are you sure your patient has COPD? What should you expect to find?

The most common symptoms of COPD include cough, sputum production, and dyspnea, particularly dyspnea on exertion. These symptoms may arise from a variety of diverse etiologies, and therefore the diagnosis of COPD requires confirmation with spirometry.

COPD develops slowly over many years and clinical features may be subtle. Since patients develop exertional dyspnea, many limit their level of activity or adjust their expectations to a lower level of functioning and thus have no complaints. The clinician must inquire not only about dyspnea but also about habitual levels of exertional activity to determine which levels precipitate dyspnea. The same is true for non-smokers with COPD. COPD should be suspected in all individuals with reduced exertional activity, particularly if it is associated with dyspnea.

Cough and sputum production may be the defining features of chronic bronchitis, although airflow limitation can result from small airways in the absence of cough and sputum. Therefore, a clinical diagnosis cannot distinguish emphysema from airways disease with much reliability. Signs that may be present in late disease include prolongation of expiratory airflow, signs related to hyperinflation of the chest, and if airways disease is present, adventitial lung sounds, including rhonchi and wheezes. However, these findings are neither sensitive nor reliable, and definitive diagnosis requires spirometry. While COPD is defined by expiratory airflow limitation (of which there are several causes), not all expiratory airflow limitation is due to COPD.

Which individuals are at greatest risk of developing COPD?

COPD is a complex disease that results from gene-environment interactions. Cigarette smoking accounts for about half of the attributable risk, and both active and passive smokers are at risk. However, not all smokers develop COPD and lung function decline among smokers is highly variable. Familial aggregation of COPD has been recognized and genetic studies have suggested inheritable risks. Recent genome-wide association studies have identified regions of genetic variability associated with COPD susceptibility, but the related gene identified only represents a small amount of the inheritability. Alpha-1 antitrypsin deficiency has been established as a risk gene and the only COPD related gene for which genetic testing is routinely performed.

A family history of COPD, a smoking history, exposure to passive smoke, living in an environment with indoor or outdoor air pollution, a history of asthma, or an occupational history associated with a significant exposure to dusts or fumes should prompt an order for spirometry. Other important risk factors include age ≥ 65, gender, race, and lower economic and educational status. If available, a history of childhood infections or low birth weight should prompt spirometry as well (Table 2).

Table II.

Extrapulmonary Diseases Associated with COPD

What laboratory studies should you order to help make the diagnosis, and how should you interpret the results?

  • Measurement of Alpha-1 Antitrypsin (AAT) Level

The one genetic disorder unequivocally associated with COPD is alpha-1 antitrypsin (AAT) deficiency. AAT levels can be quantified in the blood and the AAT protein can be phenotyped. The diagnosis of AAT deficiency is usually made by first determining the level and then the phenotype.

AAT has many genetic variants. The most common is the M form; an individual with two copies of the M form has normal levels of AAT. The most common deficient form is the Z form. Individuals who are heterozygous (MZ) have intermediate levels of AAT and are not thought to be at increased risk for emphysema, while those who are homozygous for the Z form (ZZ) have severe deficiency of AAT and are at risk for emphysema. Those with rarer forms of deficiency, such as SZ or null, are also at risk.

AAT testing is generally recommended for individuals with COPD who are relatively young (<50 years), who have basilar-predominant disease, who have a family history of emphysema, or who have a limited smoking history. However, patients with COPD and AAT deficiency may present with none of these features. Since replacement therapy is available for AAT deficiency, routine testing of all newly diagnosed patients with COPD is advocated by some experts.

  • Blood Gases and Pulse Oximetry

As COPD progresses, compromised gas exchange may lead to arterial hypoxemia and CO2 retention. CO2 retention is best diagnosed with an arterial blood gas. For patients with a PaO2 <55 mm Hg, mortality is reduced with oxygen therapy. Blood gas testing is the most definitive method of assessment for hypoxemia, but this information is commonly obtained via pulse oximetry.

  • Sputum testing

Routine sputum analysis is not recommended for the evaluation of suspected COPD unless the patient presents with an exacerbation of their symptoms.

What imaging studies will be helpful in making or excluding the diagnosis of COPD?

Routine CXR is often used in the diagnosis of COPD. However CXR findings do not establish a diagnosis of COPD. Findings which may be present with severe disease include flattening of the diaphragm, increased substernal airspace, attenuation of vascular markings, and thickening of airways, but the findings are insensitive. CXR may be helpful in excluding other conditions.

Chest CT scanning may be more useful than routine CXR in the evaluation of COPD. While CT cannot establish a diagnosis of COPD (spirometry is required), it may be useful in determining the severity of emphysema and in documenting the presence of other pulmonary disease, including bronchiectasis, interstitial lung disease, and lung cancer.

What non-invasive pulmonary diagnostic studies will be helpful in making or excluding the diagnosis of COPD?

  • Spirometry

The diagnosis of COPD requires spirometry, which also permits staging of the severity of airflow limitation. Spirometry is a simple non-invasive test readily performed in an office setting. Despite our understanding of risk factors for COPD, the US Preventative Task Force did not find evidence that screening for COPD in asymptomatic persons improves health-related quality of life, morbidity, or mortality.

The Global Initiative for Chronic Obstructive Lung Disease (GOLD) guidelines for diagnosis are based on the ratio of the forced expiratory volume of air in one second (FEV1) to the total volume exhaled (the forced vital capacity, FVC). When post-bronchodilator FEV1/FVC is <0.7, the diagnosis of COPD is established. However, FEV1, FVC, and the FEV1/FVC all decline with age. Thus use of the "fixed ratio" of 0.7 results in overdiagnosis of COPD among the elderly and underdiagnosis among younger patients. While this cut-off remains the most widely recommended practice, some experts advocate an interpretation scheme based on the lower limit of normal or z-scores to improve the accuracy for the spirometric diagnosis of COPD.

Once the diagnosis of COPD is established, the FEV1 expressed as a percentage of predicted normal, is used to grade the severity of airflow limitation. While treatment is based in part on the severity of airflow limitation, it is also driven by other clinically features that may not closely correlate with FEV1. Earlier version of the GOLD criteria was based sole on the severity of airflow obstruction. However, relevant features that incorporate assessments of COPD exacerbations and dyspnea severity into the characterization of COPD were recently incorporated. (Table 4)

  • Lung Volumes and Diffusion Capacity

Additional pulmonary function testing, such as lung volumes and diffusion capacity, may be helpful in supporting a diagnosis of emphysema. Increased lung volumes with air-trapping are a feature of emphysema as is a loss of diffusion capacity.

  • Electrocardiogram, (ECG), echocardiography, and cardiac stress testing are useful in patients with exertional dyspnea, especially if it is associated with other symptoms of ischemia, such as chest pain. Cardiovascular disease is a leading cause of death in COPD patients, and both coronary disease and left ventricular dysfunction are common in these patients. The clinician should thus have a low threshold to consider a cardiac work-up for symptoms related to COPD. In addition, echocardiography can assess for the presence of pulmonary hypertension secondary to lung disease, which can contribute to dyspnea.

  • A sleep study may be helpful for patients with COPD who often complain of increased wakefulness and decreased quality of sleep. Studies have demonstrated an increased risk for pulmonary hypertension and right ventricular remodeling in COPD patients with concomitant obstructive sleep apnea (termed overlap syndrome). In addition, if patients have resting daytime hypercarbia (PaCO2 > 52), non-invasive positive pressure ventilation may improve quality of life and reduce COPD exacerbations.

  • A cardiopulmonary exercise test (CPET) measures oxygen uptake and carbon dioxide production during graded exercise. CPET may be used to establish work performed during exercise, to measure the anaerobic threshold, and to determine maximum oxygen uptake, maximum ventilation, and maximum "oxygen pulse." If blood gases are obtained, CPET may be used to determine dead space ventilation. These parameters may be helpful in determining whether a respiratory or cardiac cause is responsible for dyspnea or exercise limitation. In addition, CPET can be used to establish parameters that are useful for optimizing a treatment prescription for pulmonary rehabilitation.

What diagnostic procedures will be helpful in making or excluding the diagnosis of COPD?

Please see section on non-invasive pulmonary diagnostic studies.

What pathology/cytology/genetic studies will be helpful in making or excluding the diagnosis of COPD?

The histologic findings of COPD are readily recognizable. Lung tissue with alveolar wall destruction may be used to establish a diagnosis of emphysema. Similarly, hypertrophy of airway mucus glands, with or without metaplasia of airway epithelium, infiltration of the airway wall with inflammatory cells, and accumulation of myofibroblasts and extracellular matrix proteins may establish the presence of airway disease. However, the diagnosis is generally made without the need for lung biopsy and lung biopsies are not recommended for this purpose.

Beware there are other diseases that can mimic COPD.

A number of pulmonary conditions may result in expiratory airflow limitation (Table 3), although most can be readily diagnosed by tests including chest imaging or lung biopsy. In the absence of definitive testing, the differential diagnosis of obstructive lung diseases may be difficult, and the clinician should consider alternative diagnoses as well.

Table III.

Pulmonary Disorders Associated with Expiratory Airflow Limitation

Asthma is an important diagnostic consideration in the evaluation of COPD. Classically, asthma tends to be diagnosed earlier in life, have a wide range of symptoms, and be associated with atopy, but this is not necessary. Asthma and COPD may coexist in the same patient. Amongst smokers, asthma is an independent risk factor for the development of COPD, and even in never smokers, asthma may progress to fixed airflow limitation, which is clinically indistinguishable from COPD. Fixed airway obstruction occurs in up to 15% of asthmatics, and asthma accounts for a large proportion of COPD in non-smokers. Whether these findings result from a process distinct from what occurs in the small airways of smokers is debated. A patient with asthma may have abnormal airflow; however, if airway function reverts to normal spontaneously or in response to treatment, COPD is excluded. If abnormal airflow is always present in a subject who meets criteria for asthma, according to current practice, both asthma and COPD should be diagnosed. Whether the coexistence of asthma and COPD represents a distinct clinical entity remains unclear; however recognizing that asthma and COPD are present concurrently is important clinically as treatment for both conditions is required. One useful finding is that COPD is associated with a concomitant decrease in DLCO, unlike asthma.

Cigarette smoke exposure is also a risk factor for coronary disease and congestive heart failure, and these cardiac diseases commonly coexist in COPD patients. Similarly, cigarette smoke exposure is a risk factor for lung cancer. The US Preventative Task Force recommends low-dose CT scan screening for patients aged 55-80 years who have smoked in the past 15 years, have a ≥ 30 pack year smoking history, and who are capable and willing to undergo curative lung surgery. Mild bronchiectasis is common in COPD patients and can be frequently identified on CXR or chest CT. Whether individuals with bronchiectasis represent a specific subset of patients with COPD is unclear, although they typically have more severe cough and more frequent and severe exacerbations of lung disease than do those without bronchiectasis. Hypercapnia can occur in patients with COPD, but can also occur in conditions such as obesity hypoventilation syndrome and neuromuscular disease.

If you decide the patient has COPD, how should the patient be managed?

The most important risk factor for COPD is cigarette smoking. Smoking cessation is a key goal for all of these individuals. Smoking cessation slows the rate at which disease progresses, and the benefits are greater the earlier cessation is achieved. Mortality from associated diseases, particularly heart disease, is also improved following smoking cessation. The same smoking cessation strategies that are used in other smokers should be used in COPD patients. Nicotine replacement, bupropion, and varencicline have been tested in COPD patients and have been found effective in this population. Except for smoking cessation, no specific therapy has been demonstrated to alter loss of lung function to a degree considered clinically important.

Pharmacologic management

Current pharmacologic strategies to treat COPD can improve symptoms and are associated with a modest reduction in the rate of lung function decline. Pharmacotherapy can also reduce COPD exacerbations, in which symptoms of dyspnea, cough, and sputum production are increased substantially above baseline. COPD exacerbations are associated with accelerated lung function decline and mortality, and therefore strategies that limit exacerbations may reduce lung function decline. No study has ever demonstrated that any particular pharmacotherapy improves mortality and the clinical importance for pharmacotherapy to slow disease progression remains to be determined.

(1) Bronchodilators

The key to improving performance in COPD is bronchodilator therapy. By improving expiratory airflow, all bronchodilators reduce lung inflation, particularly the dynamic hyperinflation that occurs with exercise. As a result, these agents may improve dyspnea with exertion and bronchodilators are a first-line therapy for patients with COPD.

Three classes of bronchodilators are available: ß-adrenergic agonists, anti-muscarinics, and theophylline. Inhaled medications are generally preferred over oral agents because their therapeutic ratio is better. Inhaled medications are available as metered-dose inhalers, dry powder inhalers, and nebulized solutions. All deliver medication effectively, but each requires education in proper use. Inhaler technique should be monitored regularly as many patients incorrectly use their devices. The number of devices available for inhaled therapies has increased significantly in the past decade, including soft-mist inhalers which may provide better drug delivery in a subset of patients. Selection of an inhaler type and specific device can be highly individual; many find dry powder inhalers to be most convenient, while nebulized solutions are often preferred by patients with severe disease.

Rapid-acting ß-agonists and anti-muscarinic agents may be appropriate for patients who are seldom symptomatic or for acute episodes of dyspnea. Combination short-acting ß-agonists and anti-muscarinic are more effective than monotherapy for symptoms and FEV1 improvement. Long-acting ß-agonist bronchodilators and long-acting anti-muscarinics that can be taken once or twice daily are also available. Since patients with COPD are always physiologically limited, most with regular symptoms or significant activity limitation should be treated with regular doses of long-acting bronchodilators. The efficacy of tiotropium, a long-acting anti-muscarinic, in reducing dyspnea, exacerbations, and quality of life scores, has been demonstrated in a large clinical trial. Similar to short acting therapy, combined use of long-acting ß-agonist bronchodilators and long-acting anti-muscarinics significantly improves airflow compared to use of a single agent. Long-acting anti-muscarinic therapy is generally well tolerated but dry mouth is common. Inhaled long-acting ß-agonists are also well tolerated, but may produce tachycardia and precipitate cardiac arrhythmias in susceptible individuals.

(2) Corticosteroid therapy

COPD is associated with systemic and airway inflammation. Corticosteroids may provide symptomatic benefit for a select group of COPD patients, particularly those with frequent exacerbations. However, the use of corticosteroids is not without considerable risks.

Short courses of oral steroids can be utilized for COPD exacerbations to acutely improve oxygenation, dyspnea, and duration of symptoms. These courses should be no longer than 5-7 days and while higher dosages of corticosteroids have been used, 40 mg of prednisone or its equivalent dose is likely sufficient. Long term monotherapy with either oral steroids or inhaled steroids is not recommended. The use of combination long-acting ß-agonist and inhaled steroid has been shown to be beneficial in reducing exacerbations and improving symptoms compared to long-acting ß-agonist alone. However, the use of inhaled steroids in COPD may be associated with an increased risk of pneumonia. This increased risk is modest but nontrivial given that patients with COPD already have an increased risk of pneumonia. Inhaled steroids are also associated with an increased risk for oral candidiasis and a small increased risk for fracture, particularly at higher doses.

Current GOLD guidelines reserve combination long acting ß-agonist/inhaled steroid or long acting anti-muscarinic/inhaled steroid for patients with a history of at least two exacerbations or one exacerbation requiring hospitalization. Certain factors may be associated with a response to inhaled steroids, including a history of asthma or atopy, sputum eosinophilia, and peripheral eosinophilia. There are few comparative studies of combination long-acting ß-agonist/long-acting anti-muscarinic therapy vs. combination long acting ß-agonist/inhaled steroid. However, a recent study showed long-acting ß-agonist/long-acting anti-muscarinic therapy to be superior in regards to symptom control, FEV1 improvement, and exacerbation reduction.

(3) Theophylline

Theophylline has a modest bronchodilator effect and may improve symptoms further when added to bronchodilators. However the clinical significance of the modest improvement in airflow is unclear, and routine use of theophylline, which has a narrow therapeutic index, is not recommended. Some patients respond to one class of drugs and not to another, and the response may vary with time. As a result, empiric therapy with one or more bronchodilators in each patient is key. A general therapeutic guideline is shown in (Table 4).

Table IV.

Severity of Obstructive Lung Disease

(4) PDE4 inhibitors and macrolides

In patients with severe disease associated with multiple exacerbations who fail maximal inhaler therapy, the oral PDE4 inhibitor, roflumilast can be considered to reduce exacerbations. The most common side effect of roflumilast is diarrhea, which frequently improves with ongoing use. In a similar patient population, azithromycin can be considered as it has been shown to reduce exacerbations, likely due to the anti-inflammatory properties of macrolides. However, chronic use of azithromycin is associated with hearing loss and resistant mycobacteria, and the long-term consequences of macrolide therapy on changes in the resistance pattern of the airway microbiota remains unclear. Lastly, this therapy may be only beneficial in former smokers.

Non-pharmacologic management

(1) Pulmonary rehabilitation

Patients with COPD experience dyspnea with exertion and many restrict physical activity. Pulmonary rehabilitation is an effective intervention in COPD, and studies demonstrate that pulmonary rehabilitation can significantly improve dyspnea, exercise capacity, psychological symptoms, and quality of life. Pulmonary rehabilitation is a multidisciplinary intervention that includes education, psychosocial support, optimization of pharmacotherapy, and exercise training. Exercise training is key to improvement in dyspnea and performance. Although it does not alter airflow, by making activity more efficient, less tachypnea, dynamic hyperinflation and dyspnea are noted. Synergies between rehabilitation and pharmacotherapy may be observed and optimal performance achieved by combining both modalities.

(2) Vaccination

Both influenza and pneumonia are important causes of COPD exacerbations and respiratory infections. Influenza vaccination reduces COPD exacerbations and is recommended yearly. Patients with COPD should also be vaccinated against pneumonia. There are two pneumococcal vaccines, a 3-valent pneumococcal conjugate vaccine (PCV13) and a 23-valent pneumococcal polysaccharide vaccine (PPSV23). The CDC recommends that all adults with COPD <65 years of age should receive the PPSV23. All patients ≥65 years old should receive one dose of the PCV13, and this dose should be given at least 1 year after the PPSV23. Additionally, all individuals ≥65 years old should receive a final dose of PPSV23, regardless of whether they have had it before. This dose should be given at least one year after the PCV13, and at least 5 years after the previous PPSV23.

(3) Supplemental Oxygen

Hypoxemia occurs commonly in COPD patients, and is associated with increased mortality. In the 1970s, two trials demonstrated a mortality benefit of supplemental oxygen in patients with hypoxemia, although this has not been replicated in subsequent studies. The GOLD guidelines recommend supplemental oxygen in patients with severe hypoxemia, defined as a resting SpO2 of < 88%, a PaO2 < 55 mm Hg, or in patients with a PaO2 between 55-60 mmHg with evidence of right heart failure. Supplemental oxygen in patients with more moderate hypoxemia or with exercise-induced oxygen desaturation may benefit a select group, but a recent randomized trial showed no benefit of supplemental oxygen in this group.

(4) Non-invasive positive pressure ventilation

Polysomnography should be considered for all patients with COPD. Patients with concomitant COPD and OSA have a worse prognosis than either disease alone. Therapy with CPAP may improve outcomes including mortality and hospitalizations. Additionally, resting hypercapnia (PaCO2>50-55 mmHg) is associated with an increased risk for exacerbations, rehospitalization and mortality. There is some evidence that the use of nocturnal non-invasive positive pressure ventilation may be helpful, especially in patients with a history of COPD hospitalizations or patients with symptoms such as fatigue, dyspnea, or headaches.

(5) Nutrition

Some COPD patients are malnourished, and both malnutrition and a low BMI are associated with poor outcomes in COPD. This was demonstrated by the BODE index (BMI, airflow Obstruction, Dyspnea and Exercise capacity), which is a validated predictor of 4-year survival in COPD. Any patient with a BMI <22 or other evidence of malnutrition may benefit from nutritional supplementation. Additionally, COPD patients have an increased risk for osteoporosis. While there are no guidelines, many advocate for routine screening in any symptomatic individual >50 years old and therapy with calcium and Vitamin D.

(6) Surgical and interventional options

Surgical options should only be considered in patients that have significant respiratory impairment despite maximal pharmacologic therapy and pulmonary rehabilitation. Surgical lung volume reduction surgery should be considered in select patients with upper lobe predominant emphysema, while non-invasivebronchoscopic lung volume reduction surgery is a novel technique that may also be beneficial in select patients with emphysema.

(7) Lung transplantation

Lung transplant, in carefully selected patients with severe COPD, may improve quality of life and functional capacity but is a procedure associated with significant morbidity.

What is the prognosis for patients managed in the recommended ways?

COPD is generally regarded as a progressive disease. The classic study by Fletcher demonstrated that individuals with COPD tended to have more rapid decline in lung function when compared to at-risk individuals without COPD. Recent data suggests that the progressive loss of lung function is most rapid among patients with moderate disease. Additionally, it has been found that rapid decline in lung function exists in approximately half of patients with COPD. If patients are active smokers, smoking cessation can decelerate lung function decline, decrease airway inflammation, and reduce risk of exacerbations although many patients continue to have progressive disease despite smoking cessation. Therefore, while a progressive course is most common, it is impossible to make specific predictions about progression in individual cases.

What other considerations exist for patients with COPD?

None.

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