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  Chronic obstructive pulmonary diseaseHighlightsComplications
Risks
Treatment
Medication
IntroductionChronic obstructive pulmonary disease (COPD) is a condition in which there is limited airflow in the lungs. The disease develops and worsens over time, and although it is not reversible, its progress can be slowed with therapy. Although patients can breathe in normally, changes in the small airways cause the walls to narrow during expiration, making it hard to breathe out. In many patients with COPD, the small sacs where oxygen and carbon dioxide are exchanged are destroyed, gradually starving the body of oxygen. COPD is associated with a set of breathing-related symptoms:
The ability to exhale (breathe out) gets worse over time.  The lungs are located in the chest cavity and are responsible for respiration. The alveoli are small sacs where oxygen is exchanged in the lungs. The two major diseases in this category are emphysema and chronic bronchitis, both covered in this report. The third, less common disease, is obstructive bronchiolitis, an inflammatory condition of the small airways. Asthma shares some of the same symptoms, but is a very different disease. People can have asthma and COPD at the same time. [See In-DepthReport #4: Asthma in adults.] Because smoking is the most common cause of both emphysema and chronic bronchitis, these conditions often develop together and frequently require similar treatments and approaches. When chronic bronchitis occurs together with emphysema, it is often difficult for a physician to distinguish between the two. EmphysemaEmphysema is a disease marked by destruction of the alveoli, grape-like clusters of air sacs at the end of the smallest airways (the bronchioles) in the lung. It generally takes the following course:
 Click the icon to see an image of emphysema. Chronic BronchitisChronic bronchitis is defined as coughing and overproduction of mucus for at least 3 months, during at least 2 consecutive years. In chronic bronchitis, the disease process is generally marked by the following characteristics:
 Click the icon to see an image of bronchitis. The LungsThe lungs are two spongy organs surrounded by a thin, moist membrane called the pleura. Each lung is made up of smooth, shiny lobes. The right lung has three lobes, and the left has two. About 90% of the lung is filled with air; only 10% is solid tissue. When a person inhales, air travels through the following pathways into the lungs:
Capillaries, the smallest of the blood vessels, carry blood throughout the body. Red blood cells carry oxygen throughout the body, and return carbon dioxide to the lungs. White blood cells are the critical infection fighters in the body.  Click the icon to see an image of normal lungs. CausesCigarette smoke accounts for more than 80% of all cases of chronic obstructive lung disease. It contains irritants that inflame the air passages, setting off a cascade of biochemical events that damage cells in the lung, increasing the risk for both COPD and lung cancer. Different effects of smoking can lead to emphysema or chronic bronchitis, but smokers generally have signs of both conditions. The specific diagnosis depends on which disease process predominates. Smoking is the major cause of emphysema. In some rare inherited disorders, emphysema can develop in nonsmokers. Disease ProcessThe key process leading to emphysema is not well understood. It appears that inflammatory cells (T lymphocytes, neutrophils, and alveolar macrophages) release chemicals called enzymes that attack the tissue in the deepest part of the lung where oxygen and carbon dioxide are exchanged. As a result, the bronchioles detach from the alveoli, and holes appear. Airways become narrowed, and exhaling becomes difficult. SmokingThe typical COPD patient is a current or former smoker, over age 50, with a pack-a-day habit of more than 20 years. Lung function continues to get worse as the person ages. Smoking is the major cause of COPD worldwide. In underdeveloped countries, smoke, exposure to industrial pollutants in poorly ventilated work areas, and cooking over wood and coal fires are also major contributors. As smoking has become more widespread among women, the incidence of COPD in women has grown proportionally. What was once considered a man's disease now affects a greater number of women. Moreover, women appear to be more susceptible to the effects of smoking and pollution than men. On the positive side, smoking rates in the U.S. are dropping, and the proportion of adults under 55 with COPD is gradually declining. This indicates the high death rate will eventually level out. In particular, the rate of COPD in young African-Americans is declining significantly. The rate in younger Caucasians is not decreasing as dramatically. Over 80% of people who die from COPD are current or former smokers. The longer a person smokes, the higher the risk for emphysema. Most patients have a history of smoking the equivalent of one pack a year for 20 years, and many have smoked up to the equivalent of 40 years. Once a smoker quits, the rate of lung function loss becomes the same as in a nonsmoker; however, much of the lung damage that occurred during smoking may be irreversible. Emphysema caused by smoking most often occurs in the upper lobes of the lungs. In chronic bronchitis, smoking triggers inflammation that causes damage in the airways. The processes involved include:
GeneticsGenerally, only 15 - 20% of all smokers develop emphysema. Other factors, such as genetic abnormalities, may need to be present to make people more likely to develop airway damage. However, other than alpha-1 antitrypsin deficiency, few genetic factors have been associated with emphysema or COPD in multiple research studies. Alpha 1-Antitrypsin Deficiency. About 1 out of every 5,000 to 7,000 people have an inherited condition called alpha 1-antitrypsin deficiency (A1AD), which can cause emphysema. People with this disorder do not have enough of the protective enzyme AAT. Without enough AAT, early and progressive damage occurs in both the walls of the alveoli and the airways leading to them. Because smoke is a major toxin and deactivates any amounts of AAT that do remain, smokers with AAT deficiency have almost no chance of escaping emphysema. Nonsmokers are also at high risk, however. Emphysema in people with A1AD develops in people as young as 30 years old, who are usually of Northern European descent. Screening tests are now available to detect the genetic defect that causes A1AD. Couples in which one or both partners have a family history of the disease may wish to be tested for the deficiency, so they may take protective measures for themselves and any future children they may have. If the condition is present in the family, testing the children is important. Bacteria and VirusesCertain bacteria, particularly Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis, are common in the lower airways of nearly half of chronic bronchitis patients. However, the role of bacteria, viruses, and other organisms in causing chronic symptoms and inflammation is unclear. Some experts believe that a low-level infection in the lungs may trigger an inflammatory reaction that continues to produce acute attacks. SymptomsThe hallmark symptom of COPD is worsening shortness of breath, often accompanied by a phlegm-producing cough and episodes of wheezing. Symptoms may vary, however, or others may be present, depending on the disease involved. Many patients have symptoms of both chronic bronchitis and emphysema. Symptoms of EmphysemaTypically, the first symptoms of emphysema occur in heavy smokers in their mid-50s:
Symptoms of alpha-1 antitrypsin-related emphysema tend to appear between the ages of 30 and 40. As with standard emphysema, they include:
Symptoms of Chronic BronchitisChronic bronchitis usually causes the following symptoms:
Chronic cough is the hallmark of chronic bronchitis from its early stages onward. Diseases with Similar SymptomsSeveral diseases have similar symptoms and may occur with COPD. Acute BronchitisAcute bronchitis is usually caused by a virus, and in most cases does not require treatment. The cough it causes typically lasts for 7 - 10 days. In about half of patients, however, coughing can last up to 3 weeks, and 25% of patients continue to cough for over 1 month. Acute bronchitis may serve as a marker for future problems in some patients. AsthmaThe classic symptoms of an asthma attack are coughing, wheezing, and shortness of breath (dyspnea). Patients with asthma typically have trouble breathing in and may wheeze when breathing out. Irritation of the nose and throat, thirst, and the need to urinate are common symptoms and may occur before an asthma attack begins. Some people first experience chest tightness or pain or a nonproductive cough that is not associated with wheezing. Chest pain occurs in about 75% of patients; it can be very severe and its intensity is unrelated to the severity of the asthma attack itself. The end of an attack is often marked by a cough that produces a thick, stringy mucus. Lung CancerThere are usually no symptoms of lung cancer until the disease is advanced. Frequent bouts of pneumonia or a lung infection that does not clear up in a seemingly healthy adult may be the first signs of lung cancer. Signs of advanced lung cancer can include:
BronchiectasisBronchiectasis is an irreversible lung disease in which the walls of the airways in the lung are chronically widened (dilated) and are eventually destroyed. The patient may have chronic sinusitis, a chronic cough, and heavy sputum, often containing blood. People with this condition usually have had serious, frequent respiratory infections, often starting in childhood. Other factors associated with bronchiectasis are:
ComplicationsCOPD affects an estimated 9 - 10% of people worldwide in both developed and underdeveloped countries. It is the 4th most common cause of death in the United States, but experts predict that it will be the third leading cause of death in the world by 2020 as the population ages and people continue to smoke. Although COPD has traditionally been considered a man's disease, an increase in women who smoke has caused COPD to skyrocket in women. Women with COPD tend to fare worse than men -- they are more likely to be hospitalized and to die from COPD. They also report more severe symptoms, greater depression, and a worse quality of life than men. Women appear to be more susceptible to the effects of smoking and pollution, possibly because of hormones or other genetic differences. The good news is that women who stop smoking get their lung function back more quickly than men. The leading cause of death from COPD is respiratory failure. However, patients with mild-to-moderate COPD tend to succumb to cardiovascular disease or lung cancer. This likely occurs from chronic low-grade inflammation, which is involved in all three COPD diseases. Traditionally, physicians have measured the severity of COPD by the amount of air that a person can forcibly exhale in one second (FEV1). The amount decreases as COPD worsens. However, COPD affects other systems and body parts, which provide clues about the severity of the disease. Many physicians now use the BODE index to categorize COPD and predict outcome. BODE stands for body-mass index, degree of airflow obstruction, dyspnea (breathlessness), and exercise capacity as measured in a 6-minute walk test.
Acute ExacerbationsAcute exacerbations are episodes that occur when airways suddenly become obstructed and symptoms worsen. Such events are associated with inflammation in the airways and are generally triggered by an infection in the airway or throughout the body. Other factors that can trigger serious lung events:
Acute exacerbations include the following symptoms:
Acute exacerbations occur, on average, between two and three times a year in patients with moderate-to-severe COPD. In about 80% of the cases, they are triggered by infections. Smokers have more episodes than nonsmokers. Acute exacerbations get better on their own, but they are still the most common cause of hospitalization in these patients, and often require different medications to improve. Frequent acute exacerbations of COPD cause lung function to deteriorate quickly, and patients never recover to the condition they were in before the last exacerbation. In COPD patients who are hospitalized, mortality rates are 11%. Survivors of a first hospitalization have a 50% chance of rehospitalization within 6 months. Reduced Quality of Life and MoodNearly half of patients with COPD report a limitation in daily activities. They have trouble walking up stairs or carrying even small packages. Breathing becomes hard work. More than half of patients with COPD have insomnia. Such impairment in quality of life can negatively affect mood. Almost half of patients with COPD have anxiety, depression, or another psychiatric disorder, compared with 31% of people in the general population. Women with COPD are more susceptible to psychological problems than men. If patients with COPD become anxious or depressed, they may have a poorer outlook than those without these emotional problems. COPD patients with moderate-to-severe depression face a greater 3-year mortality rate than those who experience less depression. Low oxygen levels also can impair mental function and short-term memory. Psychological interventions may be particularly helpful for people with COPD. MalnourishmentPeople with COPD often lack good nutrition. Patients with chronic bronchitis tend to be obese. Patients with emphysema tend to be underweight. Loss of weight and muscle mass is associated with a poor outcome in COPD. Good nutrition improves the ability to exercise, which in turn builds muscle strength and lung function. Obese patients with COPD who lose weight sleep better. Heart DiseaseOver time, COPD causes low levels of oxygen (hypoxia) and high levels of carbon dioxide (hypercapnia) in the body. In order to boost oxygen delivery, the body compensates in a number of ways:
Eventually these activities can lead to very serious and even life-threatening conditions:
Other Serious Medical Problems Associated with COPDThe smoking that causes COPD is associated with high risks of pneumonia, lung cancer, stroke, and heart attack. Tobacco smoke contains more than 400 substances, many of which are oxidants, metals (such as lead, cadmium, and aluminum), and carcinogens. Nicotine itself may not damage tissues, but it is the chemical that addicts the smoker to tobacco. Lung Cancer. Patients with a 30-year history of smoking and indications of airflow limitation (in other words, most patients with COPD), are at high risk for lung cancer. Sleep Disturbance. About half of all people with severe COPD experience sleep disorders such as sleep-related hypoxia or insomnia. Nocturnal hypoxia, a lack of oxygen during sleep, occurs when breathing is shallowest during rapid-eye-movement (REM) sleep. It may be due to suppression of the cough reflex and a build-up of mucus. Nocturnal hypoxia is treated with overnight oxygen therapy. As COPD worsens, many patients have trouble falling or staying asleep. COPD patients should not use sleep medications. Nighttime oxygen or a change in COPD medications from beta-agonists to anticholinergics can sometimes help restore restful sleep. Osteoporosis. Osteoporosis is a significant problem in patients with COPD. Many conditions associated with COPD, including smoking, vitamin D deficiency, sedentary lifestyle, and the use of corticosteroid medications put people at risk for bone density loss and osteoporosis. Gastroesophageal Reflux (GERD). More than half of patients with severe COPD have GERD, a condition in which stomach acids back up from the stomach into the esophagus. However, many COPD patients don't report experiencing GERD symptoms such as heartburn. Risk FactorsAbout 12 million adults in the U.S. have been diagnosed with COPD, 3.8 million of them with emphysema. Because emphysema and chronic bronchitis so often occur together, it is difficult to determine the number of emphysema patients versus those with chronic bronchitis. Experts estimate, however, that more than half of people with impaired lung function go undiagnosed. Many patients, even if their symptoms are severe, regard their condition as a natural part of aging, or blame lack of fitness, and fail to seek medical evaluation. The main risk factors for COPD include:
Occupational Risk FactorsWorkers exposed for a long time to toxic chemicals (such as silica or cadmium), industrial smoke, dust, or other air pollutants are at increased risk for COPD. Such workers include:
Allergies and AsthmaAllergens are allergy-causing particles and organisms such as fungi, molds, and house dust. The connection between allergies, asthma, and COPD is the topic of much debate. Some physicians believe allergies and asthma are early stages of COPD. Another school of thought says that COPD produces an airway hyperactivity that manifests as asthma or allergies. While the exact connection is not known, patients with hyperactive airways that appear to be from allergies or asthma are at increased risk for COPD. Patients with COPD whose airway hyperactivity can be controlled with bronchodilators (the medication used in asthma) are less likely to die from COPD. HIVPeople infected with HIV are 50 - 60% more likely to develop COPD than people without HIV. The percentage of HIV patients who smoke is not much larger than those who do not smoke. This suggests that HIV increases susceptibility to COPD or accelerates decline in lung function. Other RisksAbnormal lung development in the womb might increase the risk for COPD later in life. Researchers have found that newborns with poor airway function are more likely to have breathing disorders as adults, and suggest that preventive measures might need to start in infancy. Research also finds that eating bacon, sausage, and other cured meats might reduce lung function and increase the risk for COPD. Cured meats are high in nitrates, which act much like tobacco smoke to damage the lungs, according to researchers. Diagnostic TestsDespite the widespread incidence and seriousness of COPD, studies strongly suggest that it is underdiagnosed, especially in women. Some experts recommend that any adult smoker who complains of a daily cough should be screened for COPD. In one 2002 study, nearly half of patients over 60 who regularly smoked had COPD. Medical and Personal HistoryThe doctor will request a history that evaluates the patient's risk factors. Risk factors include:
Physical ExaminationAppearance. No changes in physical appearance are usually present with mild-to-moderate COPD. In advanced COPD, patients with emphysema may be wasted and thin, with normal-colored pink skin, while those with chronic bronchitis may have bluish lips and fingers, be obese, and may have swollen feet and legs. Breathing may be rapid and shallow, done through pursed lips, with prolonged exhales. The patient will be asked to cough and produce sputum, if possible. Chest Examination. The physician will next perform a simple examination of the chest area with a stethoscope to listen for:
Other findings may include:
Pulmonary Function Tests (Spirometry)The best tests for diagnosing COPD and seeing how well it responds to treatment are pulmonary function tests. The gold-standard test for patients with respiratory symptoms is spirometry. Spirometry measures the volume and force of air as it is exhaled from the lungs. It measures airway obstruction, can identify COPD early, and the results are standardized so they are always consistent. The patient is asked to breathe in and to exhale forcefully into an instrument. This is repeated several times. The force of the air is then measured. From the results, the physician determines two important values: The forced vital capacity (FVC). FVC is the maximum volume of air that can be exhaled (breathed out) with force, and is an indicator of lung size, elasticity, and how well the air passages open and close. The forced expiratory volume in one second (FEV1). FEV1 is the maximum volume of air exhaled in 1 second. Airflow is considered to be limited if the outflow of forced exhalation stays low over the course of 1 second. People with COPD have a decline in FEV1 over time. FEV1 is measured as "percent of predicted:"
 Spirometry is a painless study of air volume and flow rate within the lungs. Spirometry is frequently used to evaluate lung function in people with obstructive or restrictive lung diseases such as asthma or cystic fibrosis. Tests for Measuring the Ability of the Lung to Exchange Oxygen and Carbon DioxideArterial Blood Gas. The physician may request an arterial blood gas test to determine the amount of oxygen and carbon dioxide in the blood (its saturation). Low oxygen (hypoxia) and high carbon dioxide (hypercapnia) levels often indicate chronic bronchitis, but not always emphysema. A blood gas analysis that shows very low oxygen levels is useful for determining which patients would benefit from oxygen therapy (see below). This procedure typically involves drawing blood from an artery in the wrist.  Click the icon to see a depiction of arterial blood gas sampling. Pulse Oximetry Test. A safe and painless test for measuring oxygen in the blood is called pulse oximetry, which involves placing a probe on the finger or ear lobe. The probe emits two different lights, and the amount of each light the blood absorbs is related to how much oxygen the red blood cells carry. This test measures only oxygen in the blood, however, and not carbon dioxide. Results should be taken together with other tests to determine the need for medication or oxygen therapy. Carbon Monoxide Diffusing Capacity. The lung carbon monoxide diffusing capacity (DLCO) test determines how effectively gases are exchanged between the blood and airways in the lungs. Patients should not eat or exercise before the test, and they should not have smoked for 24 hours. The patient inhales a mixture of carbon monoxide, helium, and oxygen and holds his or her breath for about 10 seconds. The gas levels are then analyzed from the exhaled breath. Results can help physicians differentiate emphysema from chronic bronchitis and asthma. Patients with emphysema have lower DLCO results, indicated by a reduced ability to take up oxygen. Such results are also important in helping to determine appropriate candidates for lung reduction surgery. Carbon monoxide levels that are 20% or less than predicted values pose a very high risk for poor survival. Exhaled Breath. The measurement of nitric oxide (NO) in exhaled breath can be a simple method of diagnosing COPD and monitoring the effects of therapy. In most patients with COPD, no levels are below normal. Levels above normal in a patient with COPD indicate that the person also has asthma.  Click the icon to see an image of lung diffusion testing. Imaging TestsChest X-Rays. Chest x-rays are often performed, but they are not very useful for detecting early COPD. By the time an x-ray reveals the disease, the patient is well aware of the condition. Clear signs of COPD include the following:
Chest x-rays are rarely useful for diagnosing chronic bronchitis, although they sometimes show mild scarring and thickened airway walls. Computed Tomography. Computed tomography (CT) scans can accurately assess the severity of COPD and may be used to determine the size of the air pockets (bullae) in the lungs. In one study, 3-dimensional CT was used to visualize the airways in a manner in which their diameter could be measured. In this study, airflow limitation in COPD was seen to be related to the dimensions of the small, rather than the large, airways. Other Tests for COPDNoninvasive Methods for Determining Severity. Questionnaires and short exercise tests are very useful for determining the severity of COPD. Test for alpha-1 antitrypsin deficiency. Physicians will typically test for the protective enzyme alpha-1 antitrypsin in COPD patients who are nonsmokers and who develop emphysema in their 30s. Additional Blood and Sputum Tests. Additional tests may be required if the physician suspects other medical problems. If pneumonia is present, for instance, blood and sputum tests and cultures may be performed to determine the cause of infection. Bronchodilator Challenge. The symptoms of asthma are generally relieved by using a bronchodilator. Patients with COPD typically have a limited response to bronchodilation. A bronchodilator challenge test may help distinguish between the two diseases. Some patients with COPD experience limited and temporary improvement in FEV1 30 - 45 minutes after inhaling medication from a metered dose inhaler. However, their airflow remains poor. TreatmentThe appropriate medications for COPD depend on its stage of severity as determined by symptoms. The Global Initiative for Chronic Obstructive Lung Disease (GOLD) has proposed a strategy that is widely accepted. GOLD categorizes COPD severity as follows:
Gold treatment strategy is additive, meaning that medications are added, but not subtracted, as the disease progresses. Treatment calls for:
The American College of Physicians has issued revised guidelines for COPD treatment, which include:
Treatment Approach for Stable COPDStopping Smoking. Stopping smoking is the first and most important step in treating COPD and slowing its progression. Quitting smoking decreases symptoms of breathlessness and cough, as well as the risk of fatal and nonfatal heart disease, likely due to decreased inflammation. Diet. Good nutrition is always important. Dietary issues become critical in late COPD, when breathing is difficult. Many patients with COPD lose muscle tone and body mass, and appear to waste away. This may be due to the extreme effort it takes to breathe, which rapidly consumes calories. Some patients find it difficult to stop the effort of breathing long enough to chew food. A nutritionist can be tremendously helpful in finding the right foods and designing meal plans to help COPD patients be as healthy as possible. There is not strong evidence to support the use of nutritional supplements in patients with COPD. It may help to avoid cured meats, which research indicates can increase the risk of COPD. Supplemental Oxygen. Supplemental oxygen is an important component of COPD therapy. It can:
All of these factors are affected along with the lungs' ability to exchange carbon dioxide for oxygen. There is some evidence that supplemental oxygen may also reduce heart problems, such as heart-rate variability, in patients with COPD. Long-term oxygen therapy given continuously through the nose has been shown to prolong survival by as much as 30%. Blending oxygen with nitrogen (Heliox) has been shown to be more effective than supplemental oxygen alone in increasing endurance time and exercise ability. Pulmonary Rehabilitation. Pulmonary rehabilitation is a proven method of relieving shortness of breath (dyspnea), reducing hospitalizations and disability resulting from COPD, and improving mental and physical quality of life, although there is no proof that it improves survival. The treatment is recommended for patients with stable chronic lung disease who are significantly affected by respiratory symptoms. Many hospitals offer these programs, which are led by a team of health professionals. Pulmonary rehabilitation is tailored to individual patients, but usually includes:
Programs generally last 6 - 12 weeks, but longer programs appear to provide more sustained benefits. Maintenance programs may slightly improve long-term outcomes. Exercise. Exercise is important for maintaining strength and endurance, both of which are greatly affected by COPD. Weight-bearing exercises are important for maintaining quality of life and the ability to live independently. For the greatest benefit, programs should combine low- and high-intensity exercise with strength and endurance training. The use of noninvasive ventilation (NIPPV) during exercise provides some small, very short-term benefit. Receiving supplemental oxygen during rehabilitative exercise may improve patients' endurance. There is no evidence that inspiratory muscle training is effective during pulmonary rehabilitation. Surgery. When a patient no longer responds to medications, surgery becomes a possible option. Choices include:
General Guidelines for Treating Acute ExacerbationsThe goal of COPD treatment, in addition to providing symptom relief, is to prevent exacerbations. Each exacerbation causes lung function to decline. Bringing lung function back to its pre-exacerbation state can take 6 months. When exacerbations are frequent, lung function may never return to normal, and the patient's condition spirals downhill. Recent studies have found that levels of inflammatory markers in the body rise dramatically during exacerbations and in proportion to the severity of the exacerbation. This may indicate that exacerbations are associated with inflammation throughout the body, not simply in the lungs themselves. Measurement of C-reactive protein (CRP), a marker of inflammation, is being used to confirm exacerbations, predict their severity, and help determine prognosis. Exacerbations are most commonly caused by bacterial or viral infections, or by air pollution. The cause is never identified in about 1/3 of patients. Treatment of exacerbations commonly includes the following measures: Oxygen. Supplemental oxygen with controlled oxygen therapy and noninvasive positive pressure ventilation. Bronchodilation. Inhaled anticholinergics or short-acting beta2-agonists may be used. Theophylline is not recommended, because it provides very little benefit and carries a risk of serious side effects. Corticosteroids. This may be given either through a vein (intravenously) or by mouth (orally), for up to 2 weeks. This treatment is only possible when patients have not received long-term oral corticosteroid therapy. Antibiotics. These may be used if there are signs of infection, such as fever or yellow or green sputum. MedicationsAnticholinergic AgentsAnticholinergic agents relax the bronchial muscles. They are generally inhaled and act as a bronchodilator over time. Although bronchodilation does not have much effect on lung function and does not change the overall course of the disease, the medication helps improve breathlessness, ability to exercise, and quality of life. Brands and Benefits. Anticholinergics used for COPD include short-acting ipratropium (Atrovent) and long-acting tiotropium (Spiriva). They are considered standard maintenance medications for COPD. A single inhaler containing both ipratropium and the common beta2-agonist albuterol (Combivent) may prove to be better than either medication alone. Anticholinergics target the central airways, and beta-agonists target the smaller airways, which explains the possible additive benefits of the combination. Other combinations are being explored. Long-acting anticholinergic medications are being administered along with inhaled corticosteroids and long-acting beta-agonists. While the combination may not reduce the number of exacerbations, it improves lung function and quality of life, and reduces hospitalizations. Side Effects. Anticholinergics have few severe side effects. They are less likely to impair sleep than the other standard inhaled medications. The side effects of respiratory anticholinergic agents include mild cough and dry mouth. Beta2-AgonistsWhen anticholinergics are no longer enough -- and sometimes in place of an anticholinergic -- the doctor will prescribe a beta2-agonist. GOLD guidelines recommend that all patients with COPD stages II - IV take a long-acting beta2-agonist. Short-Acting Beta2-agonists. Short-acting bronchodilators are the primary medications for most COPD patients. Albuterol (Proventil, Ventolin) is the standard short-acting beta2-agonist. Others include:
Newer beta2-agonists, including levalbuterol (Xopenex), have more specific actions than the standard agents. Most are inhaled and are effective for 3 - 6 hours. Long-Acting Beta2-Agonists. Long-acting beta2-agonists salmeterol (Serevent) and formoterol (Foradil) are proving to be particularly effective as long-term maintenance therapy for COPD. Major analyses suggest they reduce exacerbations by 20 - 25%. They may help prevent bacteria from building up on the airways and may offer real improvements in lung function. Unlike short-acting forms, these beta2-agonists may even have anti-inflammatory properties. In 2007, the FDA approved a nebulized formulation of formoterol for the treatment of COPD. Until recently, only short-acting nebulizers were available. Inhalers that combine a long-acting beta2-agonist and a corticosteroid (such as Advair, Seretide, and Symbicort) are more effective than either agent alone -- reducing exacerbations by 35% and improving exercise endurance. Side Effects. Side effects of both long-and short-acting beta2-agonists include anxiety, tremor, restlessness, and headaches. Patients may experience fast and irregular heartbeats. A physician should be notified immediately if such side effects occur, particularly in people with existing heart conditions. Such patients face an increased risk for sudden death from heart-related causes. This risk is higher with oral or nebulized agents, but there have also been reports of heart attacks and angina in some patients using inhaled beta2-agonists. Loss of Effectiveness and Overdose. There has been some concern that short-acting beta2-agonists may become less effective when taken regularly over time, increasing the risk of overuse. The degree to which this affects the airways is uncertain. In some studies, the duration of action has declined with use, but the peak effect appears to be preserved, making these drugs still useful for acute attacks. Regular use of long-acting beta2-agonists may reduce the effect of short-acting forms. A major concern is that patients who perceive beta2-agonists as being less effective may overuse them. Overdose can be serious and, in rare cases, even life threatening, particularly in patients with heart disease or asthma. CorticosteroidsCorticosteroids are powerful anti-inflammatory drugs. Oral Corticosteroids. Oral corticosteroids are reserved for the treatment of COPD exacerbations, and research finds that they are preferable to inhaled corticosteroids for this purpose. They speed the time to recovery and reduce the length of the hospital stay, but appear to have no long-term benefit. They shouldn't be regularly used for stable disease because of the increased risk of side effects. Inhaled Corticosteroids. Inhaled corticosteroids (ICS) are the mainstay of asthma therapy. Their use in COPD is controversial. During the first 6 months of use, ICS may improve lung function. After 6 months, lung function resumes its decline. There is also evidence that ICS increases the risk of dying from pneumonia in patients with COPD. ICS should be reserved for patients with severe COPD and frequent exacerbations. Combining a long-acting bronchodilator (salmeterol) with a corticosteroid (fluticasone) appears to improve survival and reduce exacerbations in patients with severe COPD compared to single-drug treatment. However, further studies are needed to determine whether this combination might increase the number of adverse side effects. Theophylline and Other MethylxanthinesMethylxanthines (primarily slow-release theophylline) are also bronchodilators. These drugs are used in patients with more severe exacerbations when there is an incomplete response to bronchodilators, corticosteroids, oxygen, or antibiotics. These agents do not significantly improve lung function, symptoms, or overall outcomes when used for acute exacerbations. Some experts believe that the modest benefits do not outweigh the risk of toxic effects commonly associated with these agents. These side effects are generally related to the amount of theophylline in the blood, but can include:
Administering Inhaled DrugsMany COPD drugs are inhaled using metered dose inhalers, dry powder inhalers, or nebulizers. Metered-Dose Inhaler. The standard device for COPD medication is the metered-dose inhaler (MDI). This device allows precise doses to be delivered directly to the lungs. A holding chamber, or spacer, improves delivery by giving the patient more time to inhale the medication. Breath-Activated Dry Powder Inhalers. Dry powder inhalers (DPIs) deliver a powdered form of drug directly into the lungs. DPIs are as effective as MDIs and are easier to manage. Humidity or extreme temperatures can affect DPI performance, so these devices should not be stored in humid places (such as bathroom cabinets) or locations subject to high temperatures (such as glove compartments during summer months). Other Hand-Held Inhalers. Respimat delivers a fine-mist spray that is created by forcing the liquid medication through nozzles. It does not use any propellant. Nebulizers. A nebulizer is a device that administers the drug in a fine spray that the patient breathes in. Nebulizers are often used in hospital settings or when the patient cannot use an inhaler.  This metered-dose inhaler is a quick way of administering medicine directly into the bronchial passageways to promote clearer breathing. Medicines That Loosen Lung SecretionsPatients with persistent coughing and sputum often use agents that loosen secretions and help move them out of the lungs. Expectorants. Expectorants, such as guaifenesin (found in common cough remedies), stimulate the flow of fluid in the airways and help move secretions using the motion of cilia (the hair-like structures in the lung) and coughing. Expectorants have not been shown to benefit patients with COPD. Mucolytics. Mucolytics contain ingredients that make sputum more watery and easier to cough up. One of these ingredients, acetylcysteine, also acts as an antioxidant, which could provide additional benefit to people with COPD. The most effective mucolytic is stopping smoking. Anticholinergics appear to decrease the production of mucus. Beta2-agonists and theophylline improve mucus clearance. Other MedicationsSelective Phosphodiesterase-4 Inhibitors. Cilomilast (Ariflo) and roflumilast (Daxas) are selective phosphodiesterase-4 (PDE4) inhibitors. These medications block PDE4, an enzyme overproduced in COPD and asthma that causes inflammation in the airways. The FDA has approved cilomilast for the treatment of COPD and asthma. Approval of roflumilast is pending. One study of cilomilast found that the drug significantly decreased exacerbations and increased quality of life. In other research, rofumilast significantly improved lung function in patients with severe, stable COPD. Statins. Patients with COPD are at an increased risk of death from coronary artery disease. Some studies have found an association between statin use and COPD. The anti-inflammatory properties of statin medications might help slow lung function decline or help in the survival of an exacerbation, especially in longtime smokers and people who have recently quit. These effects have yet to be explained or proven. AntibioticsTreating Acute Bronchitis or Pneumonia in COPD Patients. People with COPD are at heightened risk for pneumonia, but any lung infection can worsen symptoms and speed deterioration of lung function. Antibiotics are usually called for when acute bronchitis or pneumonia occurs, and the patient has signs of bacterial infection, such as green or yellow sputum. The most common organisms causing pneumonia or exacerbations in people with COPD include Streptococcus pneumoniae, Haemophilus influenzae, and Moxarella catarrhalis. The choice of antibiotic depends on the bacteria being treated and the local rate of bacterial resistance to common antibiotics. Preventive antibiotic therapy for patients with frequent exacerbations is discouraged, since this practice contributes to the development of bacterial resistance. Antibiotic OptionsBeta-Lactams Beta-lactam antibiotics include penicillins, cephalosporins, and some newer medications. They share common chemical features, and all interfere with bacterial cell walls. Penicillins. Penicillin was the first antibiotic. Many forms of this still-important drug are available today:
Many people have a history of allergic reaction to penicillin, but some evidence suggests the allergy may not return in a significant number of adults. Skin tests are available to help determine whether someone with a history of penicillin allergies could tolerate these important antibiotics. Cephalosporins. Most of these agents are not very effective against bacteria that have developed resistance to penicillin, and are used for more severe exacerbations. They are classified according to their generation:
Fluoroquinolones (Quinolones) Fluoroquinolones ("quinolones") interfere with the bacteria's genetic material to prevent them from reproducing. These antibiotics are used for more severe exacerbations.
S. pneumoniae strains resistant to the respiratory quinolones are uncommon in the U.S., but resistance is dramatically increasing. Many quinolones cause side effects, including sensitivity to light and neurologic, psychiatric, and heart problems. Pregnant women should not take this class of drugs. Quinolones also enhance the potency of oral anti-clotting drugs. When it comes to treating acute exacerbations of chronic bronchitis, so-called second-line antibiotics [amoxicillin, clavulanate (Augmentin), macrolides, second- or third-generation cephalosporines, and quinolones] appear to be more effective than -- and just as safe as -- first-generation antibiotics (ampicillin, doxycycline, and trimethoprim/sulfamethoxazole). Macrolides, Azalides, and Ketolides Macrolides and azalides also affect the genetics of bacteria. These drugs include:
These antibiotics are effective against atypical bacteria such as mycoplasma and chlamydia. All but erythromycin are effective against H. influenzae. They are also used in some cases for S. pneumoniae and M. catarrhalis, but there is increasing bacterial resistance to these medicines. Macrolide resistance rates doubled between 1995 - 1999, as more and more children were being treated with these antibiotics. Some research suggests these agents may reduce the risk of a first heart attack in some patients by reducing inflammation in the blood vessels. Ketolides. Ketolides are a new class of antibiotics. They are derived from erythromycin and were developed to combat organisms that have become resistant to macrolides. Telithromycin (Ketek), the first antibiotic in the ketolide class, was approved by the FDA in 2004 for the treatment of CAP, acute bacterial exacerbations of chronic bronchitis, and acute sinusitis. However, in February 2007, the FDA withdrew approval of Ketek for acute bacterial sinusitis. The agency decided that the serious risks of Ketek outweighed its benefits for sinusitis treatment. The decision followed several 2006 reports of deaths from severe liver damage. Telithromycin is approved only for the treatment of CAP. The drug carries a strong "black box" warning noting its potentially serious or deadly side effects, including liver failure, vision problems, loss of consciousness, and neuromuscular problems. Tetracyclines Tetracyclines inhibit bacterial growth. They include doxycycline, tetracycline, and minocycline. They can be effective against S. pneumoniae and M. catarrhalis, but bacteria that are resistant to penicillin are also often resistant to doxycycline. The side effects of tetracyclines include skin reactions to sunlight, burning in the throat, and tooth discoloration. Trimethoprim-Sulfamethoxazole Trimethoprim-sulfamethoxazole (such as Bactrim, Cotrim, and Septra) is less expensive than amoxicillin and particularly useful for adults with mild bacterial upper respiratory infections who are allergic to penicillin. The drug is no longer effective against certain streptococcal strains. It should not be used in patients whose infections occur after dental work, or in people who are allergic to sulfa drugs. Allergic reactions can be very serious. Oxygen-Replacement TherapyLung function may eventually worsen to the point that patients may need to rely on supplemental oxygen provided through portable or stationary tanks. Continuous Therapy. Continuous oxygen therapy (more than 15 hours a day) is the only treatment for emphysema that has been proven to prolong survival in certain patients. It also improves alertness, motor speed, and hand strength. Continuous oxygen therapy is usually recommended for patients with:
Ideally, the patient should receive enough oxygen to keep the oxygen level at 65 mm HG, but no less than 60 mm HG, or at an oxygen saturation level of at least 90%. Additional oxygen flow may be needed during sleep or exertion (physical activity). About 40% of patients improve enough in 1 month to stop continuous treatment, although such patients should be observed closely. COPD frequently deteriorates, and patients need to restart oxygen therapy. Some patients worsen in spite of treatment, although at this point it is not possible to predict who is at risk for oxygen therapy failure. The addition of nitric oxide, a gas that dilates blood vessels, may offer additional benefits. Intermittent Oxygen. Patients with less severe COPD who are not on permanent oxygen maintenance may need supplemental oxygen during specific circumstances:
Oxygen During Travel. People on continuous oxygen therapy who are traveling by plane should increase their oxygen by 1 - 2 liters per minute during the trip. Supplemental oxygen may be required during air travel for people on intermittent oxygen therapy if the trip is longer than 2 hours and they develop symptoms, or if they experience a drop in oxygen levels before traveling. People are not allowed to bring their own tanks on board an airplane; many airlines will provide oxygen if notified 48 - 72 hours in advance. It is important to note that aircraft cabins are actually pressurized to the equivalent of 8,000 feet above sea level. Such pressures could be potentially dangerous for people with severe COPD. Oxygen Storage and Delivery SystemsUnless they are bed-bound, patients usually use a combination of stationary and mobile oxygen systems. Stationary Systems. The most common stationary oxygen system is the concentrator, an electrical device that pulls oxygen from the air. It weighs about 35 pounds and cannot be battery operated, so a patient can use only it at home. Portable Units. Portable units containing electronic oxygen-conserving devices weigh only a few pounds and can provide up to 8 hours of oxygen. Some portable units weigh 6.5 lbs, with liquid oxygen supplies lasting 4 hours. Some weigh 9.5 lbs, with an oxygen supply lasting 8 hours when used at a flow rate of 2 liters per minute. Compressed or Liquid Oxygen. Oxygen can be administered from large stationary tanks or small portable ones, either as compressed gas or liquid oxygen. A container of liquid oxygen lasts four times longer than compressed gas of the same weight and is easier to fill. Liquid oxygen is very beneficial for patients who want to maintain an active life, although the tanks require occasional venting to release pressure, and this wastes oxygen. They are also more expensive. In some areas, for example, a stationary liquid oxygen system costs $3,500 and a compressed oxygen tank costs $350. Precautions. Supplemental oxygen is a fire hazard, and some hotels and residences do not allow its use. No one should smoke near an oxygen tank, and tanks should be stored safely, secured to a wall and away from heaters and furnaces. Devices for Administering OxygenOxygen is usually administered in one of three ways: through a nasal canula, transtracheal catheter, or electronic demand device. Nasal Canula. Using a nasal canula, oxygen is delivered through a long, slender plastic tube that runs from the oxygen tank to small plastic prongs that fit in the nostrils. The tube can be very long when attached to a stationary tank in order to accommodate walking throughout a house, or relatively short when attached to a portable unit. A reservoir pouch is a recent innovation added to this device that provides an extra rush of oxygen when a patient starts to inhale. This method is inexpensive and easy to use, but some patients are embarrassed by its appearance under their noses. Transtracheal Oxygen. Transtracheal oxygen is delivered directly into the windpipe (trachea) through a catheter tube implanted by a surgeon. The device is inconspicuous, and patient compliance is excellent. The initial cost is high, but over time expenses are reduced because of more efficient oxygen usage. Long-term complications may include infection, dislodgment, and blockage by mucus, which can be very serious. Complications of the procedure itself occur in 3 - 5% of cases and can include lung spasms and uncontrollable coughing. Electronic Demand Devices. Electronic devices that sense the beginning of a breath and deliver a pulse of oxygen are also available, although they are complicated, expensive, and have a risk for mechanical failure. Newer units have a continuous flow bypass switch that allows delivery of oxygen if the battery runs down. Devices to Assist BreathingIn emergency situations, oxygen may be delivered to the patient in various ways: Noninvasive Positive Pressure Ventilation (NPPV). If the patient is able to breathe naturally, oxygen is delivered through a tube using a tightly fitted oxygen mask to maintain airway pressure during breathing. Some physicians now believe such devices should be first-line treatments (in addition to medications) for managing respiratory failure after an acute exacerbation. They allow the patient to communicate and drink fluids, and are much better tolerated than nose or throat tubes. They cannot be used on patients with rapidly deteriorating COPD, those who are uncooperative, or those with facial structures that do not allow the mask to seal tightly. Intubation. When standard oxygen therapy does not meet a patient's needs, endotracheal intubation may be required to deliver high concentrations of oxygen. With intubation, a tube is inserted down through either the nose or the mouth, and oxygen is administered through the tube. Mechanical Ventilation. In very serious cases such as acute respiratory failure, a mechanical ventilator can be used to take over the function of breathing. The primary goal of ventilation is to eliminate carbon dioxide and restore a balanced exchange of gases. Most patients have a low tolerance for intubation, and the tubes are often removed prematurely due to discomfort. Patients may need painkillers, sedatives, or muscle relaxants. There are also several complications that lead to the removal of breathing tubes:
Lifestyle ChangesQuitting Smoking and Avoiding Other IrritantsQuitting smoking is the first and most essential step in treating COPD and slowing its progress. In many people who quit early, lung function stabilizes and eventually declines to about the rate of nonsmokers in the same age group. In some people, lung function may even improve slightly after quitting. As COPD progresses, quitting can slow the rate of decline; however, lost lung function is never fully recovered. Most patients who smoke try to quit an average of seven times before they are successful. Using a combination of smoking cessation aids improves the likelihood of quitting. These include nicotine replacement products (patches, gum, nasal spray, lozenges), counseling, and prescription medications such as bupropion (Zyban) and varenicline (Chantix). [See In-DepthReport #41: Smoking.] Preventing Upper Respiratory InfectionsGood Hygiene. Hands should be washed with ordinary soap before eating and after going outside the home. Antibacterial soaps add little protection, particularly against viruses. One study suggests that common liquid dish washing soaps are up to 100 times more effective than antibacterial soaps in killing respiratory syncytial virus (RSV), which is known to cause pneumonia. Vaccines. Two important vaccinations are recommended to protect against respiratory infection.
[See In-Depth Report #94:Colds and Flus.] Breathing ExercisesPursed-Lip Breathing. A technique called pursed-lip breathing can help improve lung function before starting activities or doing a strenuous task, such as lifting a heavy box. Pursed-lip breathing helps change pressure in the airways and prevents small airways from collapsing.
Holding Breath and Coughing. A simple technique is to inhale deeply and slowly, hold the breath for 5 -10 seconds, then cough on exhalation. Controlling SecretionsFluids and Humidity. Patients with congestion and heavy sputum can benefit from maintaining good fluid intake and keeping their homes humidified. Chest Therapy. Chest therapy involves rhythmic inhalation for three to four deep breaths followed by coughing to produce sputum. Tapping the chest may also help in loosening and raising sputum in patients with a significant amount of sputum production. Avoid chest therapy during an acute exacerbation of COPD. When coughing to produce mucus, another method is to lean forward and "huff" repeatedly, take relaxed breaths, and huff again. Avoid forceful coughing, if possible. Physical ExerciseBecause COPD is not simply a lung condition, but a systemic disease that causes wasting of the muscles and bones, certain physical exercises may be very helpful. Strengthening Exercises for the Limbs. Exercising and strengthening the muscles in the arms and legs helps some patients improve their endurance and reduce breathlessness. Exercising only one leg at a time (for example, pedaling a stationary bicycle with one leg instead of two) might benefit patients who are usually too out-of-breath to exercise, and help them increase their exercise capacity. Walking. Walking is the best exercise for patients with emphysema. In studies of lung rehabilitation, regular exercise increased walking distance and improved breathing. Patients should try to walk 3 - 4 times daily for 5 - 15 minutes each time. Devices that assist ventilation may reduce breathlessness that occurs during exercise. Yoga and Eastern Practices. Yoga and tai chi, two practices that use deep breathing and meditation techniques, may be particularly beneficial for COPD patients. Research is underway to determine whether yoga is helpful for COPD patients.  Click the icon to see an image depicting yoga practice. Breath TrainingInspiratory Muscle Training and Incentive Spirometer. Inspiratory muscle training involves exercises and devices that make inhaling more difficult in order to strengthen breathing muscles, walking capacity, and quality of life. The use of an incentive spirometer for 15 minutes twice a day may also be helpful. It can help loosen sputum. An incentive spirometer is a small, hand-held device that contains a breathing gauge. The patient exhales and then inhales forcefully through the tube, using the pressure of the inhalation to raise the gauge to the highest level possible. A device called a peak inspiratory flow (PIF) meter measures the patient's ability to draw air into the lungs and assesses the fitness of the breathing muscles. New guidelines released by the American College of Chest Physicians (ACCP) and American Association of Cardiovascular and Pulmonary Rehabilitation (AACVPR) do not recommend the routine use of inspiratory muscle training during pulmonary rehabilitation. Dietary FactorsBecause many patients with chronic bronchitis are obese and many with emphysema are underweight, assessment of nutritional status is an important part of COPD treatment. Lack of vitamins A, C, and E, and a lack of fruits and vegetables, can contribute to the development of COPD. Protein and Fats. Patients with body wasting (cachexia) lack enough protein. Although most healthy diets emphasize proteins from fish, poultry, and lean meat, these people may benefit from foods with a higher-than-average fat content. (People should still prefer healthy fats, however, such as those found in olive oil and oily fish.) Some evidence suggests that high-carbohydrate meals may reduce exercise capacity. Fruits, Vegetables, and Whole Grains. Healthy foods are as important for lung function as they are for health in general. Specific foods that may be important for healthy lungs are those that contain antioxidants (best obtained from fresh, deep green and yellow-orange fruits and vegetables), selenium (fish, nuts, red meat, grains, eggs, chicken, liver, garlic), plant chemicals called flavonoids (apples, onions), and magnesium (green leafy vegetables, nuts, whole grains, milk, and meats). One study found that, compared to a Mediterranean diet, which is high in fruits, vegetables, and whole grains, a Western diet high in red meat and simple carbohydrates increased the risk of COPD fivefold. Dietary Supplements. A meta-analysis of studies in which COPD patients took supplements of N-acetyl-cysteine, an antioxidant, concluded that it was effective in preventing exacerbations, even in patients with COPD who continued to smoke. Use of inhaled steroids seems to lessen its effects, however. Additional studies are needed to confirm these findings. Other antioxidants being studied include L-carnitine and coenzyme Q10. Evidence of benefit is weak for these chemicals, though. Psychological SupportPatients with COPD are at high risk for depression and anxiety, which can impair their outlook on life. The problem worsens along with the disease, which often requires people to limit their activities and social interactions. Psychological counseling and social supports are important for helping people improve their emotional state, cope with daily stresses, and maintain independence and social relationships. Minimizing Airborne ContaminantsAs much as possible, patients should avoid exposure to airborne irritants, including:
To minimize the amount of contaminants in the home:
Surgical ProceduresSurgery -- as a last resort -- may help some patients with COPD. Coverage for such procedures varies among insurance carriers. A major drawback is that patients must be in good enough condition to undergo major surgery. By the time COPD is advanced, however, this is usually not the case. As a result, surgery cannot help the majority of COPD patients. The three available surgical options appropriate for some patients with COPD are lung transplantation, lung-volume reduction surgery, and bullectomy. Lung TransplantationSince 1995, 38% of all lung transplants have been performed for COPD. Three-year survival rates after lung transplantation are about 60% for patients with either emphysema or alpha-1 antitrypsin deficiencies. Transplantation of one lung, both lungs, or the lungs plus the heart may be performed. The increasingly long waiting time for donor organs and the extraordinary expense are both significant problems. Candidates. The best candidates are under 65 and have severe heart and lung disease, with a life expectancy of less than 18 months. However, lung transplantation is becoming more out of favor for patients with end-stage COPD because it is unclear whether transplantation provides a "useful" quality of life. Waiting Time. Up to one-third of patients awaiting lung transplantation die before a suitable donor is available. There were 1,558 lung transplantation operations in North America reported to the International Society of Heart Lung Transplantation in 2006, and as of this writing, 2,127 people are waiting for a new lung. Since 2005, the United Network for Organ Sharing (UNOS) has been assigning lungs for transplants based on an allocation score, rather than time spent on the waiting list. The allocation score takes into account the length of time a patient is likely to survive before and after transplant. This policy applies to transplant candidates age 12 or older. Complications. Transplant patients must take drugs that suppress the immune system to prevent the body from rejecting the transplanted organ. Nevertheless, rejection is the primary cause of late complications and death. The mortality rate from the procedure itself is about 10%. Outcomes. About 38% of lung transplants involve both lungs. Transplanting both lungs as opposed to just one significantly improves survival rates in patients under age 60. Average survival after a bilateral lung transplant in one study was 6.41 years, compared to 4.59 years in patients with a single-lung transplant. Lung Volume-Reduction SurgeryIn lung volume-reduction surgery (LVRS), more than 30% of severely diseased lung tissue is removed, and the remaining parts of the lung are joined together. Improvement in breathing after surgery appears to be largely due to the following factors:
Prognosis. Results of the largest study to date, called the National Emphysema Treatment Trial (NETT), found that patients with upper-lobe disease and poor lung function achieved better 5-year survival rates, improved their exercise ability for 3 years, and had fewer symptoms at 5 years with LVRS than with medical therapy. Those with upper-lobe disease and good ability to exercise did not have a survival advantage with LVRS, but were able to increase their exercise capacity. When the operation is successful, patients report significant improvement in walking distance, weight, and quality of life. Many patients can engage in daily activities, such as golfing or stair-climbing, without oxygen. Even in carefully selected candidates, however, about 15% of patients get little or no benefit from the procedure, and about 4% get worse. Furthermore, even in successful cases, the improvement is most notable within the first 6 months, after which the condition deteriorates again. Beyond 3 years, lung function deteriorates to the same level as it was before the procedure. LVRS is substantially more costly than medical treatment. Possible Candidates. The procedure is used only in people with severe emphysema, and some who have alpha 1-antitrypsin deficiency, but it is not used for those with chronic bronchitis. Appropriate candidates with alpha 1-antitrypsin deficiency, even if they have disease in the lower lobe, may do well, but it is applicable only to a minority of these patients. Candidates must have the following characteristics:
Analysis of patients who underwent LVRS versus lung transplantation found that 1 year after surgery, lung transplant recipients had much better lung function, greater exercise capacity, and less breathlessness than LVRS patients. However, they were less likely to survive, and the transplant was far more expensive than LVRS. Patients may not qualify for LVRS if they have:
Other indicators of a poor outlook include severe lung complications and isolated air pockets in diseased area of the lungs (bullae). Specific Techniques. At this time, the preferred technique is surgery done on both lungs (bilateral lung volume reduction). Surgeons use either an open approach, making a large cut in the chest area, or video-assisted thoracoscopy (VATS), which is less invasive and involves several small cuts. Either method is effective and has similar complication rates. Lines of staples are typically used to reduce lung volume. The alternative technique is surgery done on only one lung (unilateral lung volume reduction). Some centers believe this approach may cause fewer complications and a slower decline in benefits, although not all evidence supports its use over the bilateral method. BullectomyAnother option for COPD is bullectomy, in which giant air pockets and surrounding lung tissue are removed. It is generally limited to patients with giant bullae (not the typical COPD patient) and those with alpha 1-antitrypsin deficiency. Resources
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