(Redirected from Chronic obstructive airway disease)
'Chronic obstructive pulmonary disease' ('COPD'), also known as 'chronic obstructive airway disease' ('COAD'), is a group of
diseases characterized by the pathological limitation of airflow in the
airway that is not fully reversible. COPD is the
umbrella term for chronic
bronchitis,
emphysema and a range of other lung disorders. It is most often due to
tobacco smoking,
[1] but can be due to other airborne irritants such as
coal dust,
asbestos or
solvents, as well as
congenital conditions such as
alpha-1-antitrypsin deficiency.
Signs and symptoms
The main
symptoms of COPD include
dyspnea (shortness of breath) lasting for months or perhaps years, possibly accompanied by
wheezing, and a persistent
cough with
sputum production.
[2] It is possible the sputum may contain blood (
hemoptysis), usually due to damage of the blood vessels of the airways. Severe COPD could lead to
cyanosis (bluish decolorization usually in the lips and fingers) caused by a lack of
oxygen in the blood. In extreme cases it could lead to
cor pulmonale due the extra work required by the heart to get blood to flow through the lungs.
[3]
COPD is particularly characterised by the
spirometric measurement of a ratio of forced expiratory volume over 1 second (
FEV1) to forced vital capacity (FVC) being < 0.7 and the
FEV1 < 70% of the predicted value
[4] as measured by a
plethysmograph. Other
signs include a rapid breathing rate (
tachypnea) and a wheezing sound heard through a
stethoscope. Pulmonary emphysema is NOT the same as subcutaneous emphysema, which is a collection of air under the skin that may be detected by the
crepitus sounds produced on
palpation.
[5]
Causes
Cigarette smoking
A primary risk factor of COPD is chronic tobacco smoking. In the
United States, around 90% of cases of COPD are due to smoking.
[6] Not all smokers will develop COPD, but continuous smokers have at least a 25% risk.
[7]
Occupational pollutants
Some occupational pollutants, such as
cadmium and
silica, have shown to be a contributing risk factor for COPD. The people at highest risk for these pollutants include coal workers, construction workers, metal workers and cotton workers, amongst others. However, in most cases these pollutants are combined with cigarette smoking further increasing the chance of developing COPD.
6 These occupations are commonly associated with
other respiratory diseases, particularly
pneumoconiosis (black lung disease).
Asbestosis can appear even with minimal exposure.
Air pollution
Urban
air pollution may be a contributing factor for COPD as it is thought to impair the development of the lung function. In
developing countries indoor air pollution, usually due to
biomass fuel, has been linked to COPD, especially in women.
1
Genetics
Very rarely, there may be a deficiency in an
enzyme known as
alpha 1-antitrypsin which causes a form of COPD.
[8]
Other risk factors
Increasing age, male gender, allergy, repeated airway infection and general impaired lung function are also related to the development of COPD.
Pathophysiology
Chronic bronchitis
Chronic bronchitis is defined in ''clinical'' terms as a cough with sputum production on most days for 3 months of a year, for 2 consecutive years.
[Longmore M, Wilkinson I, Rajagopalan S (2005). ''Oxford Handbook of Clinical Medicine'', 6ed. Oxford University Press. pp 188-189. ISBN 0-19-852558-3.]
Chronic bronchitis is hallmarked by
hyperplasia (increased number) and
hypertrophy (increased size) of the
goblet cells (
mucous gland) of the airway, resulting in an increase in secretion of mucus which contributes to the airway obstruction.
Microscopically there is
infiltration of the airway walls with
inflammatory cells, particularly
neutrophils. Inflammation is followed by scarring and remodeling that thickens the walls resulting in narrowing of the small airway. Further progression leads to
metaplasia (abnormal change in the tissue) and
fibrosis (further thickening and scarring) of the lower airway. The consequence of these changes is a limitation of airflow.
[Kumar P, Clark M (2005). ''Clinical Medicine'', 6ed. Elsevier Saunders. pp 900-901. ISBN 0702027634.].
Emphysema
Main articles: Emphysema
Emphysema is defined ''
histologically'' as the enlargement of the air spaces
distal to the
terminal bronchioles, with destruction of their walls.
The enlarged air sacs (
alveoli) of the lungs reduces the
surface area available for the movement of gases during
respiration. This ultimately leads to dyspnea in severe cases. The exact mechanism for the development of emphysema is not understood, although it is known to be linked with smoking and age.
Diagnosis
The diagnosis of COPD is usually suggested by symptoms; it is a clinical diagnosis and no single test is definitive. A comprehensive history from the patient is very important with regard to smoking and occupation. Physical examination with a
plethysmograph can reveal the true extent of COPD.
The severity of COPD can be classified as follows using spirometry (see above):
| Severity | Post-bronchodilator FEV1 /FVC | FEV1 % predicted |
|---|
| At risk | >0.7 | ≥80 |
| Mild COPD | ≤0.7 | ≥80 |
| Moderate COPD | ≤0.7 | 50-80 |
| Severe COPD | ≤0.7 | 30-50 |
| Very Severe COPD | ≤0.7 | <30 'or' 30-50 with Chronic Respiratory Failure symptoms |
Management
Although COPD is not curable, it can be controlled in a variety of ways.
Smoking cessation
Smoking cessation is one of the most important factors in slowing down the progression of COPD. Even at a late stage of the disease it can reduce the rate of deterioration and prolong the time taken for disability and death.
Occupational change
Workers may be able to transfer to a significantly less contaminated area of the company depending on circumstances. Often however, workers may need complete occupational change.
Pharmacotherapy
Bronchodilators
There are several types of
bronchodilators used clinically with varying efficacy: β
2 agonists, M
3 antimuscarinics, leukotriene antagonists, cromones and xanthines.
[American Thoracic Society / European Respiratory Society Task Force (2005). ''Standards for the Diagnosis and Management of Patients with COPD''. Version 1.2. New York: American Thoracic Society. http://www.thoracic.org/go/copd] These drugs relax the
smooth muscles of the airway allowing for improved airflow. The change in
FEV1 may not be substantial, but changes in the
vital capacity are significant. Many patients feel less breathless after taking bronchodilators.
β2 agonists
There are several highly specific β
2 agonists available.
Salbutamol (Ventolin) is the most widely used short acting β
2 agonist to provide rapid relief and should be prescribed as a front line therapy for all classes of patients. Other β
2 agonists are
Bambuterol,
Clenbuterol, Fenoterol, and
Formoterol. Longer acting β
2 agonists such as
Salmeterol act too slowly to be used as relief for
dypsnea so these drugs should be used as a secondary therapy. An increased risk is associated with long acting β
2 agonists due to decreased sensitivity to inflammation so generally the use of a concomitant
corticosteroid is indicated
[1][2][3].
M3 muscarinic antagonists (anticholinergics)
Derived from the deadly agaric ''
Amanita muscaria'', specific
antimuscarinics were found to provide effective relief to COPD. Inhaled antimuscarinics have the advantage of avoiding
endocrine and
exocrine M
3 receptors. The quaternary M
3 muscarinic antagonist
Ipratropium is widely prescribed with the β
2 agonist
salbutamol.
[4]. Ipratropium is offered combined with salbutamol (Combivent) and with fenoterol (Duovent).
Tiotropium provides improved specificity for M
3 muscarinic receptors.
Cromones
Cromones are
mast cell stabilizers that are thought to act on a
chloride channel found on
mast cells that help reduce the production of
histamine and other inflammatory factors. Chromones are also thought to act on IgE-regulated
calcium channels on mast cells.
Cromoglicate and
Nedocromil, which has a longer half-life, are two chromones available.
[9]
Leukotriene antagonists
More recently
leukotriene antagonists block the signalling molecules used by the immune system.
Montelukast,
Pranlukast,
Zafirlukast are some of the leukotrienes antagonists.
[10]
Xanthines
Theophylline is the prototype of the
xanthine[11] class of drug. Teas are natural sources of methylxanthines, xanthines and
caffeine while
chocolate is a source of
theobromine.
Caffeine is approximately 16% metabolized into theophylline. Nebulized theophylline is used in the EMR for treatment of
dyspnea (Difficulty in breathing). Patients need continual monitoring as theophylline has a narrow
therapeutic range. More aggressive EMR interventions include IV H
1 antihistamines and IV
dexamethasone.
Corticosteroids
Inhaled
corticosteriods (specifically
glucocorticoids) act in the inflammatory cascade and may improve airway function considerably,
however the long term value has not been proven. Corticosteroids are often combined with bronchodilators in a single inhaler. Some of the more common inhaled steroids in use are
beclomethasone,
mometasone, and
fluticasone.
Salmeterol and fluticasone are combined (Advair), however the reduction in death from all causes among patients with COPD in the combination therapy group did not reach the predetermined level of statistical significance.
[12][13]
TNF antagonists
Tumor necrosis factor antagonists (TNF) are the most recent class of medications designed to deal with refractory cases.
Tumor necrosis factor-alpha is a cachexin or cachectin and is considered a so-called biological drug. They are considerered immunosopressive with attendant risks. These rather expensive drugs include
infliximab,
adalimumab and
etanercept.
[14]
Supplemental Oxygen
In general, long-term administration of oxygen is usually reserved for individuals with COPD who have arterial
hypoxemia (
PaO2 less than 55 mm Hg), or a PaO2 between 55 and 60 mm Hg with evidence of
pulmonary hypertension,
cor pulmonale, or secondary
erythrocytosis (hematocrit >55%). In these patients, continuous home oxygen therapy (for >15 h/d) sufficient to correct hypoxemia has been shown to improve survival.
[15]
Vaccination
Patients with COPD should be routinely
vaccinated against
influenza,
pneumococcus and other diseases to prevent illness and the possibility of death.
Pulmonary rehabilitation
Pulmonary rehabilitation is a program of disease management, counseling and exercise coordinated to benefit the individual.
[16] Pulmonary rehabilitation has been shown to relieve difficulties breathing and fatigue. It has also been shown to improve the sense of control a patient has over their disease as well as their emotions.
[17]
Diet
A recent French study conducted over 12 years with almost 43,000 men concluded that eating a
Mediterranean diet "halves the risk of serious lung disease like emphysema and bronchitis".
[5]
Prognosis
A good prognosis of COPD relies on an early diagnosis and prompt treatment. Most patients will have improvement in lung function once treatment is started, however eventually signs and symptoms will worsen as COPD progresses. The median survival is about 10 years if two-thirds of expected lung function was lost by diagnosis.
Bronchitis
Acute bronchitis usually resolves in 7-10 days with no underlying lung disease. Chronic bronchitis however is dependent on early recognition and smoking cessation which improves the outcome significantly.
Emphysema
The outcome is better for patients with less damage to the lung who stop smoking immediately. Still, patients with extensive lung damage may live for many years so predicting prognosis is difficult. Death may occur from respiratory failure,
pneumonia, or other complications.
Asbestosis
The outcome is clouded by the many complications associated with asbestosis.
Malignant mesothelioma is refractory to management affording patients with 6-12 months of life expectancy upon clinical presentation.
Pneumoconiosis
The outcome is good for patients with minimal damage to the lung. However, patients with extensive lung damage may live for many years so predicting prognosis is difficult. Death may occur from
respiratory failure,
pneumonia,
cor pulmonale or other complications.
Pulmonary neoplasms
The stage of the
tumor(s) has a major impact on
neoplasm prognosis. Staging is the process of determining tumor size, growth rate, potential
metastasis, lymph node involvement, treatment options and prognosis. Two-year prognosis for limited small cell pulmonary neoplasms is twenty percent and for extensive disease five percent. The average life expectancy for someone with recurrent small cell pulmonary neoplasms is two to three months.
[6]
The 5-year overall survival rate for pulmonary neoplasms is 14%.
[18]
Epidemiology
According to the
World Health Organization (WHO), 80 million people suffer from moderate to severe COPD and 3 million died due to it in 2005. The WHO predicts that by 2030, it will be the 4th largest cause of mortality worldwide.
[19]
Since COPD is not diagnosed until it becomes clinically apparent, prevalence and mortality data greatly underestimate the
socioeconomic burden of COPD.
In the UK, COPD accounts for about 7% of all days of sickness related absence from work.
Smoking rates in the industrialized world have continued to fall, causing rates of emphysema and pulmonary neoplasms to slowly decline.
References
1. Devereux G. ''ABC of chronic obstructive pulmonary disease. Definition, epidemiology, and risk factors.'' BMJ 2006;332:1142-1144. PMID 16690673
2. U.S. National Heart Lung and Blood Institute - Signs and Symptoms
3. MedicineNet.com - COPD signs & symptoms
4. PatientPlus - Spirometry
5. eMedicine - Barotrauma
6. MedicineNet.com - COPD causes
7. Lokke A, Lange P, Scharling H, Fabricius P, Vestbo J. Developing COPD: a 25 year follow up study of the general population. ''Thorax''. 2006 Nov;61(11):935-9. PMID 17071833
8. MedlinePlus Medical Encyclopedia
9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?holding=npg&cmd=Retrieve&db=PubMed&list_uids=4166895&dopt=Abstract
10. available.http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=13804592&dopt=Citation
11. http://www.chemistry.org/portal/a/c/s/1/acsdisplay.html?DOC=HomeMoleculerchivemotw_xanthine_arch.html
12. http://content.nejm.org/cgi/content/short/356/8/775
13. http://clinicaltrials.gov/show/NCT00268216
14. http://users.rcn.com/jkimball.ma.ultranet/BiologyPages/C/CellSignaling.html
15. http://linkinghub.elsevier.com/retrieve/pii/S014067368191970X.
16. U.S. National Heart Lung and Blood Institute - Treatment
17. Lacasse Y, Goldstein R, Lasserson T J, Martin, S. ''Pulmonary rehabilitation for chronic obstructive pulmonary disease''. Cochrane Database of Systematic Reviews. (4):CD003793, 2006. PMID 12137716
18. John D. Minna, "Neoplasms of the Lung," in ''Harrison's Principles of Internal Medicine'', 16th ed. (2005), p. 506
19. WHO - COPD
External links
★
National Heart, Lung and Blood Institute - COPD U.S. NHLBI Information for Patients and the Public page.
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