Chronic obstructive pulmonary disease

A cardinal symptom of COPD is the chronic and progressive shortness of breath which is most characteristic of the condition. Shortness of breath (breathlessness) is often the most distressing symptom responsible for the associated anxiety and level of disability experienced.[4] Symptoms of wheezing and chest tightness associated with breathlessness can be variable over the course of a day or between days and are not always present. Chest tightness often follows exertion.[4] Many people with more advanced COPD breathe through pursed lips, which can improve shortness of breath.[26] Shortness of breath is often responsible for reduced physical activity and low levels of physical activity are associated with worse outcomes.[27][28] In severe and very severe cases there may be constant tiredness, weight loss, muscle loss and anorexia. People with COPD often have increased breathlessness and frequent colds before seeking treatment.[4]

The most often first symptom of COPD is a chronic cough, which may or may not be productive of mucus as phlegm. Phlegm coughed up as sputum can be intermittent and may be swallowed or spat out depending on social or cultural factors and is therefore not always easy to evaluate. However, an accompanying productive cough is only seen in up to 30% of cases. Sometimes limited airflow may develop in the absence of a cough.[4] Symptoms are usually worse in the morning.[29]

A chronic productive cough is the result of mucus hypersecretion and when it persists for more than three months each year for at least two years, it is defined as chronic bronchitis.[12] Chronic bronchitis can occur before the restricted airflow diagnostic of COPD.[8] Some people with COPD attribute the symptoms to the consequences of smoking. In severe COPD, vigorous coughing may lead to rib fractures or to a brief loss of consciousness.[4]

Many definitions of COPD in the past included chronic bronchitis and emphysema but these have never been included in GOLD report definitions.[8] Emphysema is defined as enlarged airspaces (alveoli) whose walls break down resulting in permanent damage to the lung tissue and is just one of the structural abnormalities that can limit airflow. The condition can exist without airflow limitation but commonly it does.[10] Chronic bronchitis is defined as a productive cough that is present for at least three months each year for two years but does not always result in airflow limitation although the risk of developing COPD is great.[12] These older definitions grouped the two types as type A and type B. Type A were emphysema types known as pink puffers due to their pink complexion, fast breathing rate and pursed lips. Type B were chronic bronchitic types referred to as blue bloaters due to low oxygen levels causing a bluish color to the skin and lips and swollen ankles.[48] These differences were suggested to be due to the presence or not of collateral ventilation, evident in emphysema and lacking in chronic bronchitis.[49] This terminology was no longer accepted as useful, as most people with COPD have a combination of both emphysema and airway disease.[48] These are now recognized as the two major phenotypes of COPD – emphysematous phenotype and chronic bronchitic phenotype.[9]

The primary risk factor for COPD globally is tobacco smoking with an increased rate of developing COPD shown in smokers and ex-smokers.[8][16] Of those who smoke, about 20% will get COPD,[68] increasing to less than 50% in heavy smokers.[8] In the United States and United Kingdom, of those with COPD, 80–95% are either current or previous smokers.[68][69][70] Several studies indicate that women are more susceptible than men to the harmful effects of tobacco smoke.[71] For the same amount of cigarette smoking, women have a higher risk of COPD than men.[72] In non-smokers, exposure to second-hand smoke (passive smoking) is the cause of 1.2 million deaths from the more than 8 million deaths worldwide each year due to tobacco smoke.[73] Women who smoke during pregnancy, and during the early life of the child is a risk factor for the later development of COPD in their child.[74]

Inhaled smoke triggers the release of excessive proteases in lungs, which then degrades elastin, the major component of alveoli.[16] Smoke also impairs the action of cilia, inhibiting mucociliary clearance that clears the bronchi of mucus, cellular debris and unwanted fluid.[16]

Other types of tobacco smoke, such as from cigar, pipe, water-pipe and hookah use, also confer a risk.[12] Water-pipe or hookah smoke appears to be as harmful or even more harmful than smoking cigarettes.[75]

Marijuana is the second most commonly smoked substance, but evidence linking its use to COPD is very limited. Limited evidence shows that marijuana does not accelerate lung function decline.[76] A low use of marijuana gives a bronchodilatory effect rather than the bronchoconstrictive effect from tobacco use, but it is often smoked in combination with tobacco or on its own by tobacco smokers. Higher use however has shown a decline in the FEV1.[77] There is evidence of it causing some respiratory problems and its use in combination may have a cumulative toxic effect suggesting it as a risk factor for spontaneous pneumothorax, bullous emphysema, COPD and lung cancer.[76][78] A noted difference between marijuana use and tobacco was that respiratory problems were resolved with stopping usage unlike the continued decline with stopping tobacco smoking.[76] Respiratory symptoms reported with marijuana use included chronic cough, increased sputum production and wheezing but not shortness of breath. Also these symptoms were typically reported ten years ahead of their affecting tobacco smokers.[76] Another study found that chronic marijuana smokers even with the additional use of tobacco developed similar respiratory problems, but did not seem to develop airflow limitation and COPD.[79]

Access to clean fuel and clean cooking facilities as of 2016.[80]

Exposure to particulates can bring about the development of COPD, or its exacerbations. Those with COPD are more susceptible to the harmful effects of particulate exposure that can cause acute exacerbations brought about by infections.[44] Black carbon also known as soot, is an air pollutant associated with an increased risk of hospitalization due to the exacerbations caused. Long-term exposure is indicated as an increased rate of mortality in COPD.[44] Studies have shown that people who live in large cities have a higher rate of COPD compared to people who live in rural areas.[81] Areas with poor outdoor air quality, including that from exhaust gas, generally have higher rates of COPD.[82] Urban air pollution significantly effects the developing lung and its maturation, and contributes a potential risk factor for the later development of COPD. The overall effect in relation to smoking, is believed to be small.[12]

Poorly ventilated fires used for cooking and heating, are often fueled by coal or biomass such as wood and dry dung, leading to indoor air pollution and are one of the most common causes of COPD in developing countries. Women are affected more as they have a greater exposure.[12] These fuels are used as the main source of energy in 80% of homes in India, China and sub-Saharan Africa.[82]

Intense and prolonged exposure to workplace dusts, chemicals and fumes increases the risk of COPD in smokers, nonsmokers and never-smokers. Substances implicated in occupational exposure and listed in the UK, include organic and inorganic dusts such as cadmium, silica, dust from grains and flour and fumes from cadmium and welding that promote respiratory symptoms.[17][12] Workplace exposure is believed to be the cause in 10–20% of cases and in the United States, it is believed to be related to around 30% of cases among never smokers and probably represents a greater risk in countries without sufficient regulations.[12][83] The negative effects of dust exposure and cigarette smoke exposure appear to be cumulative.[84]

Genetics play a role in the development of COPD. It is more common among relatives of those with COPD who smoke than unrelated smokers.[12] The most well known genetic risk factor is alpha-1 antitrypsin deficiency (AATD) and this is the only genotype (genetic subtype) with a specific treatment.[60] This risk is particularly high if someone deficient in alpha-1 antitrypsin (AAT) also smokes.[85] It is responsible for about 1–5% of cases[85][86] and the condition is present in about three to four in 10,000 people.[87]

Mutations in MMP1 gene that encodes for interstitial collagenase are associated with COPD.[88]

The COPDGene study is an ongoing longitudinal study into the epidemiology of COPD, identifying phenotypes and looking for their likely association with susceptible genes. Genome wide analyses in concert with the International COPD Genetics Consortium has identified more than 80 genome regions associated with COPD and further studies in these regions has been called for. Whole genome sequencing is an ongoing collaboration (2019) with the National Heart, Lung and Blood Institute (NHLBI) to identify rare genetic determinants.[89]

Spirometry measures the amount of airflow obstruction present and is generally carried out after the use of a bronchodilator, a medication to open up the airways.[102] Two main components are measured to make the diagnosis, the forced expiratory volume in one second (FEV1), which is the greatest volume of air that can be breathed out in the first second of a breath and the forced vital capacity (FVC), which is the greatest volume of air that can be breathed out in a single large breath.[103] Normally, 75–80% of the FVC comes out in the first second[103] and a FEV1/FVC ratio less than 70% in someone with symptoms of COPD defines a person as having the disease.[102] Based on these measurements, spirometry would lead to over-diagnosis of COPD in the elderly.[102] The National Institute for Health and Care Excellence criteria additionally require a FEV1 less than 80% of predicted.[104] People with COPD also exhibit a decrease in diffusing capacity of the lung for carbon monoxide due to decreased surface area in the alveoli, as well as damage to the capillary bed.[105] Testing the peak expiratory flow (the maximum speed of expiration), commonly used in asthma diagnosis, is not sufficient for the diagnosis of COPD.[104]

Screening using spirometry in those without symptoms has uncertain effect and is generally not recommended; however, it is recommended for those without symptoms but with a known risk factor.[42]

A number of methods can be used to assess the affects and severity of COPD.[101][42] The MRC breathlessness scale or the COPD assessment test (CAT) are simple questionnaires that may be used.[106][101] GOLD refers to a modified MRC scale that if used, needs to include other tests since it is simply a test of breathlessness experienced.[42][107] Scores on CAT range from 0–40 with the higher the score, the more severe the disease.[108] Spirometry may help to determine the severity of airflow limitation.[4] This is typically based on the FEV1 expressed as a percentage of the predicted "normal" for the person's age, gender, height and weight.[4] Guidelines published in 2011 by American and European medical societies recommend partly basing treatment recommendations on the FEV1.[102] The GOLD guidelines group people into four categories based on symptoms assessment, degree of airflow limitation and history of exacerbations.[107] Weight loss, muscle loss and fatigue are seen in severe and very severe cases.[42]

Use of screening questionnaires, such as COPD diagnostic questionnaire (CDQ), alone or in combination with hand-held flow meters is appropriate for screening of COPD in primary care.[109]

A chest X-ray is not useful to establish a diagnosis of COPD but it is of use in either excluding other conditions or including comorbidities such as pulmonary fibrosis and bronchiectasis. Characteristic signs of COPD on X-ray include hyperinflation (shown by a flattened diaphragm and an increased retrosternal air space) and lung hyperlucency.[5] A saber-sheath trachea may also be shown that is indicative of COPD.[110]

A CT scan is not routinely used except for the exclusion of bronchiectasis.[5] An analysis of arterial blood is used to determine the need for oxygen supplementation and assess for high levels of carbon dioxide in the blood; this is recommended in those with an FEV1 less than 35% predicted, those with a peripheral oxygen saturation less than 92% and those with symptoms of congestive heart failure.[111] WHO recommends that all those diagnosed with COPD be screened for alpha-1 antitrypsin deficiency.[42]

• 
  Chest X-ray demonstrating severe COPD, displaying small heart size in comparison to the lungs.
• 
  A lateral chest X-ray of a person with emphysema, displaying barrel chest and flat diaphragm.
• 
  Lung bulla as seen on chest X-ray in a person with severe COPD
• 
  A severe case of bullous emphysema
• 
  Axial CT image of the lung of a person with end-stage bullous emphysema
• 
  Very severe emphysema with lung cancer on the left (CT scan)

COPD may need to be differentiated from other conditions such as congestive heart failure, asthma, bronchiectasis, tuberculosis, obliterative bronchiolitis and diffuse panbronchiolitis.[5] The distinction between asthma and COPD is made on the basis of the symptoms, smoking history and whether airflow limitation is reversible with bronchodilators at spirometry.[112] Chronic bronchitis with normal airflow is not classified as COPD.[87]

The policies of governments, public health agencies and antismoking organizations can reduce smoking rates by discouraging people from starting and encouraging people to stop smoking.[113] Smoking bans in public areas and places of work are important measures to decrease exposure to secondhand smoke and while many places have instituted bans, more are recommended.[82]

In those who smoke, stopping smoking is the only measure shown to slow down the worsening of COPD.[114][115] Even at a late stage of the disease, it can reduce the rate of worsening lung function and delay the onset of disability and death.[116] Often, several attempts are required before long-term abstinence is achieved.[113] Attempts over 5 years lead to success in nearly 40% of people.[117]

Some smokers can achieve long-term smoking cessation through willpower alone. Smoking, however, is highly addictive and many smokers need further support.[118] The chance of quitting is improved with social support, engagement in a smoking cessation program and the use of medications such as nicotine replacement therapy, bupropion, or varenicline.[113][115][117] Combining smoking-cessation medication with behavioral therapy is more than twice as likely to be effective in helping people with COPD stop smoking, compared with behavioral therapy alone.[119]

A number of measures have been taken to reduce the likelihood that workers in at-risk industries—such as coal mining, construction and stonemasonry—will develop COPD.[82] Examples of these measures include the creation of public policy,[82] education of workers and management about the risks, promoting smoking cessation, checking workers for early signs of COPD, use of respirators and dust control.[120][121] Effective dust control can be achieved by improving ventilation, using water sprays and by using mining techniques that minimize dust generation.[122] If a worker develops COPD, further lung damage can be reduced by avoiding ongoing dust exposure, for example by changing their work role.[123]

Both indoor and outdoor air quality can be improved, which may prevent COPD or slow the worsening of existing disease.[82] This may be achieved by public policy efforts, cultural changes and personal involvement.[124] Many developed countries have successfully improved outdoor air quality through regulations which has resulted in improvements in the lung function of their populations.[82] Individuals are also advised to avoid irritants of indoor and outdoor pollution.[19]

In developing countries one key effort is to reduce exposure to smoke from cooking and heating fuels through improved ventilation of homes and better stoves and chimneys.[124] Proper stoves may improve indoor air quality by 85%. Using alternative energy sources such as solar cooking and electrical heating is also effective. Using fuels such as kerosene or coal might produce less household particulate matter than traditional biomass such as wood or dung, but whether this is better health wise is unclear.[82]

Inhaled short-acting bronchodilators are the primary medications used on an as needed basis; their use on a regular basis is not recommended.[6] The two major types are beta2-adrenergic agonists and anticholinergics; either in long-acting or short-acting forms. Beta2–adrenergic agonists target receptors in the smooth muscle cells in bronchioles causing them to relax and allow improved airflow. They reduce shortness of breath, tend to reduce dynamic hyperinflation and improve exercise tolerance.[6][135] Short-acting bronchodilators have an effect for four hours and for maintenance therapy long acting bronchodilators with an effect of over twelve hours are used. In times of more severe symptoms a short acting agent may be used in combination.[6] An inhaled corticosteroid used with a long-acting beta-2 agonist is more effective than either one on its own.[136]

Which type of long-acting agent, long-acting muscarinic antagonist (LAMA) such as tiotropium or long-acting beta agonist (LABA), is better is unclear and trying each and continuing with the one that works best may be advisable.[137] Both types of agent appear to reduce the risk of acute exacerbations by 15–25%.[132] The combination of LABA/LAMA may reduce COPD exacerbations and improve quality-of-life compared to long-acting bronchodilators alone.[138] The 2018 NICE guideline recommends use of dual long-acting bronchodilators with economic modelling suggesting that this approach is preferable to starting one long acting bronchodilator and adding another later.[139]

Several short-acting β₂ agonists are available, including salbutamol (albuterol) and terbutaline.[124] They provide some relief of symptoms for four to six hours.[124] A long-acting beta agonist (LABA) such as salmeterol, formoterol and indacaterol are often used as maintenance therapy. Some feel the evidence of benefits is limited,[140] while others view the evidence of benefit as established.[141][142][143] Long-term use appears safe in COPD[144] with adverse effects include shakiness and heart palpitations.[132] When used with inhaled steroids they increase the risk of pneumonia.[132] While steroids and LABAs may work better together,[140] it is unclear if this slight benefit outweighs the increased risks.[145] There is some evidence that combined treatment of LABAs with long-acting muscarinic antagonists (LAMA), an anticholinergic, and LABA +ICS (inhaled corticosteroid) may be similar in benefits in terms of fewer exacerbation's and quality of life measures for moderate to severe COPD, but LAMA+LABA offers better improvements in forced expiratory volume (FEV1%) and a lower risk of pneumonia.[146] All three together, LABA, LAMA and ICS, have some evidence of benefits.[147] Indacaterol requires an inhaled dose once a day and is as effective as the other long-acting β₂ agonist drugs that require twice-daily dosing for people with stable COPD.[143]

The two main anticholinergics used in COPD are ipratropium and tiotropium. Ipratropium is a short-acting muscarinic antagonist (SAMA), while tiotropium is long-acting (LAMA). Tiotropium is associated with a decrease in exacerbations and improved quality of life,[148] and tiotropium provides those benefits better than ipratropium.[149] It does not appear to affect mortality or the overall hospitalization rate.[148] Anticholinergics can cause dry mouth and urinary tract symptoms.[132] They are also associated with increased risk of heart disease and stroke.[150] Aclidinium, another long-acting agent, reduces hospitalizations associated with COPD and improves quality of life.[151][152][153] The LAMA umeclidinium bromide is another anticholinergic alternative.[154] When compared to tiotropium, the LAMAs aclidinium, glycopyrronium and umeclidinium appear to have a similar level of efficacy; with all four being more effective than placebo.[155] Further research is needed comparing aclidinium to tiotropium.[153]

Inhaled corticosteroids are anti-inflammatories that are recommended by GOLD as a first-line maintenance treatment in COPD cases with repeated exacerbations.[156][157] Their regular use increases the risk of pneumonia in severe cases.[30] Studies have shown that the risk of pneumonia is associated with all types of corticosteroids; is related to the disease severity and a dose-response relationship has been noted.[156] Oral glucocorticoids can be effective in treating an acute exacerbation.[136] They appear to have fewer side effects than those given intravenously.[158] Five days of steroids work as well as ten or fourteen days.[159]

The use of corticosteroids is associated with a decrease in the number of lymphoid follicles (in the bronchial lymphoid tissue).[96] A triple inhaled therapy of LABA/LAMA/ICS improves lung function, reduces symptoms and exacerbations and is seen to be more effective than mono or dual therapies.[136] NICE guidelines recommend the use of ICSs in people with asthmatic features or features suggesting steroid responsiveness.[139]

Phosphodiesterase-4 inhibitors (PDE4 inhibitors) are anti-inflammatories that improve lung function and reduce exacerbations in moderate to severe illness. Roflumilast is a PDE4 inhibitor used orally once daily to reduce inflammation, it has no direct bronchodilatory effects. It is essentially used in treating those with chronic bronchitis along with systemic corticosteroids.[56] Reported adverse effects of roflumilast appear early in treatment, become less with continued treatment and are reversible. One effect is dramatic weight loss and its use is to be avoided in underweight people. It is also advised to be used with caution in those who have depression.[56]

Long-term preventive use of antibiotics, specifically those from the macrolide class such as erythromycin, reduce the frequency of exacerbations in those who have two or more a year.[160][161] This practice may be cost effective in some areas of the world.[162] Concerns include the potential for antibiotic resistance and side effects including hearing loss, tinnitus and changes to the heart rhythm known as long QT syndrome.[161]

Methylxanthines such as theophylline are widely used. Theophylline is seen to have a mild bronchodilatory effect in stable COPD. Inspiratory muscle function is seen to be improved but the causal effect is unclear. Theophylline is seen to improve breathlessness when used as an add-on to salmeterol. All instances of improvement have been reported using sustained release preparations.[6] Methylxanthines are not recommended for use in exacerbations due to adverse effects.[30]

Mucolytics may help to reduce exacerbations in some people with chronic bronchitis; noticed by less hospitalization and less days of disability in one month.[163] Erdosteine is recommended by NICE.[164] GOLD also supports the use of some mucolytics that are advised against when inhaled corticosteroids are being used and singles out erdosteine as having good effects regardless of corticosteroid use. Erdosteine also has antioxidant properties but there is not enough evidence to support the general use of antioxidants.[56] Erdosteine has been shown to significantly reduce the risk of exacerbations, shorten their duration and hospital stays.[165]

Cough medicines are not recommended.[166] Beta blockers are not contraindicated for those with COPD and should only be used where there is concomitant cardiovascular disease.[56]

Recent studies show that metformin plays a role in reducing systemic inflammation by reducing biomarker levels that are increased during COPD exacerbations.[167]

Supplemental oxygen is recommended for those with low oxygen levels in respiratory failure at rest (a partial pressure of oxygen less than 50–55 mmHg or oxygen saturations of less than 88%).[20] When taking into account complications including cor pulmonale and pulmonary hypertension, the levels involved are 56–59 mmHg.[168] Oxygen therapy is to be used for between 15 and 18 hours per day and is said to decrease the risk of heart failure and death.[168] In those with normal or mildly low oxygen levels, oxygen supplementation (ambulatory) may improve shortness of breath when given during exercise, but may not improve breathlessness during normal daily activities or affect the quality of life.[169] During acute exacerbations, many require oxygen therapy; the use of high concentrations of oxygen without taking into account a person's oxygen saturations may lead to increased levels of carbon dioxide and worsened outcomes.[170][171] In those at high risk of high carbon dioxide levels, oxygen saturations of 88–92% are recommended, while for those without this risk, recommended levels are 94–98%.[171]

Pulmonary rehabilitation is a program of exercise, disease management and counseling, coordinated to benefit the individual.[172] A severe exacerbation leads to hospital admission, high mortality and a decline in the ability to carry out daily activities. Following a hospital admission pulmonary rehabilitation has been shown to significantly reduce future hospital admissions, mortality and improve quality of life.[54]

The optimal exercise routine, use of noninvasive ventilation during exercise and intensity of exercise suggested for people with COPD, is unknown.[173][174] Performing endurance arm exercises improves arm movement for people with COPD and may result in a small improvement in breathlessness.[175] Performing arm exercises alone does not appear to improve quality of life.[175] Pursed-lip breathing exercises may be useful.[26] Tai chi exercises appear to be safe to practice for people with COPD and may be beneficial for pulmonary function and pulmonary capacity when compared to a regular treatment program.[176] Tai Chi was not found to be more effective than other exercise intervention programs.[176] Inspiratory and expiratory muscle training (IMT, EMT) have been suggested and may provide some improvements when compared to no treatment.[177] A combination of IMT and walking exercises at home may help limit breathlessness in cases of severe COPD.[178] Additionally, the use of low amplitude high velocity joint mobilization together with exercise improves lung function and exercise capacity.[179] The goal of spinal manipulation therapy is to improve thoracic mobility in an effort to reduce the work on the lungs during respiration, however, the evidence supporting manual therapy for people with COPD is very weak.[179][180]

Airway clearance techniques (ACTs), such as postural drainage, percussion/vibration, autogenic drainage, hand-held positive expiratory pressure (PEP) devices and other mechanical devices, may reduce the need for increased ventilatory assistance, the duration of ventilatory assistance and the length of hospital stay in people with acute COPD.[181] In people with stable COPD, ACTs may lead to short-term improvements in health-related quality of life and a reduced long-term need for hospitalizations related to respiratory issues.[181]

Being either underweight or overweight can affect the symptoms, degree of disability and prognosis of COPD. People with COPD who are underweight can improve their breathing muscle strength by increasing their calorie intake. When combined with regular exercise or a pulmonary rehabilitation program, this can lead to improvements in COPD symptoms. Supplemental nutrition may be useful in those who are malnourished.[20][182]

People with COPD can experience exacerbations (flare-ups) that are commonly caused by respiratory tract infections. The symptoms that worsen are not specific to COPD and differential diagnoses need to be considered.[30] Acute exacerbations are typically treated by increasing the use of short-acting bronchodilators including a combination of a short-acting inhaled beta agonist and short-acting anticholinergic.[30] These medications can be given either via a metered-dose inhaler with a spacer or via a nebulizer, with both appearing to be equally effective.[124][183] Nebulization may be easier for those who are more unwell.[124] Oxygen supplementation can be useful. Excessive oxygen; however, can result in increased CO₂ levels and a decreased level of consciousness.[184] Corticosteroids given orally can improve lung function and shorten hospital stays but their use is recommended for only five to seven days; longer courses increase the risk of pneumonia and death.[30]

Maintaining room temperatures of at least 21 °C [70 °F] for a minimum of nine hours a day was associated with better health in those with COPD, especially for smokers.[185] The World Health Organization (WHO) recommends indoor temperatures of a slightly higher range between 18 °C and 24 °C [65 °F and 75 °F].[186]

For people with COPD, the ideal indoor humidity levels are 30-50% RH. Maintaining indoor humidity can be difficult in the winter, especially in cold climates where the heating system is constantly running.[187]

Keeping the indoor relative humidity above 40% RH significantly reduces the infectivity of aerosolized viruses.[188]

For severe emphysema that has proved unresponsive to other therapies lung volume reduction surgery (LVRS) may be an option.[189][190] LVRS involves the removal of damaged tissue, which improves lung function by allowing the rest of the lungs to expand.[132][124] It is considered when the emphysema is in the upper lobes and when there are no comorbidities.[191]

Minimally invasive bronchoscopic procedures may be carried out to reduce lung volume. These include the use of valves, coils, or thermal ablation.[20][192] Endobronchial valves are one-way valves that may be used in those with severe hyperinflation resulting from advanced emphysema; a suitable target lobe and no collateral ventilation are required for this procedure. The placement of one or more valves in the lobe induces a partial collapse of the lobe that ensures a reduction in residual volume that improves lung function, the capacity for exercise and quality of life.[193]

The placement of nitinol coils instead of valves is recommended where there is collateral ventilation that would prevent the use of valves.[194] Nitinol is a biocompatible alloy.

Both of these techniques are associated with adverse effects including persistent air leaks and cardiovascular complications. Thermal vapor ablation has an improved profile. Heated water vapor is used to target lobe regions which leads to permanent fibrosis and volume reduction. The procedure is able to target individual lobe segments, can be carried out regardless of collateral ventilation and can be repeated with the natural advance of emphysema.[195]

In very severe cases lung transplantation might be considered.[189] A CT scan may be useful in surgery considerations.[87] Ventilation/perfusion scintigraphy is another imaging method that may be used to evaluate cases for surgical interventions and also to evaluate post-surgery responses.[196] A bullectomy may be carried out when a giant bulla occupies more than a third of a hemithorax.[191]

Globally, as of 2010, COPD is estimated to result in economic costs of $2.1 trillion, half of which occurring in the developing world.[213] Of this total an estimated $1.9 trillion are direct costs such as medical care, while $0.2 trillion are indirect costs such as missed work.[214] This is expected to more than double by 2030.[213] In Europe, COPD represents 3% of healthcare spending.[124] In the United States, costs of the disease are estimated at $50 billion, most of which is due to exacerbation.[111] COPD was among the most expensive conditions seen in U.S. hospitals in 2011, with a total cost of about $5.7 billion.[205]