Chronic obstructive pulmonary disease

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Chronic obstructive pulmonary disease (COPD), also known as chronic obstructive airway disease (COAD), is an obstructive lung disease that is characterized by the pathological limitation of airflow in the airway that is not fully reversible. This contrasts to asthma which is a obstructive lung disease in which the obstructive is 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 to 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.[9]

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.[10].

Emphysema

For more information, see: Emphysema.

Emphysema is defined histologically as the enlargement of the air spaces distal to the terminal bronchioles, with destruction of their walls.[9]

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 suggested by symptoms; it is a clinical diagnosis and no single test is definitive. A history is taken of smoking and occupation, and a physical examination is done. Measurement of lung function with a spirograph can reveal the loss of lung function.

The severity of COPD can be classified as follows using post-bronchodilator spirometry (see above)[11]:

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

Physical examination

A systematic review by the Rational Clinical Examination concluded that no single medical sign or symptom can adequately exclude the diagnosis of COPD.[12] One study found that the presence of either "a history of smoking more than 30 pack-years, diminished breath sounds, or peak flow less than 350 L/min" has a sensitivity of 98 percent.[13]

Differential diagnosis

25% of patients with "unexplained exacerbation of chronic obstructive pulmonary disease" may have pulmonary embolism.[14]

Management

Although COPD is not curable, it can be controlled in a variety of ways. Clinical practice guidelines by Global Initiative for Chronic Obstructive Lung Disease (GOLD)[11], a collaboration including the American National Heart, Lung, and Blood Institute and the World Health Organization, as well as guidelines by the American College of Physicians[15][16] are available.

Smoking cessation

For more information, see: 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.[10]

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: β2 agonists, M3 antimuscarinics, leukotriene antagonists, cromones and xanthines.[17] 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
For more information, see: Adrenergic beta-agonist.

There is a tendency for long acting β2 agonists to reduce death, especially if they are combined with an inhaled corticosteroid.[18][19] β2 agonists may slow progression of airway obstruction[20].

An increased risk is associated with long acting β2 agonists among patients with asthma due to decreased sensitivity to inflammation so generally the use of a concomitant corticosteroid is indicated [21][22].

There are several highly specific β2 agonists available. Salbutamol (Ventolin) is the most widely used short acting β2 agonist to provide rapid relief and should be prescribed as a front line therapy for all classes of patients. Other β2 agonists are Bambuterol, Clenbuterol, Fenoterol, and Formoterol. Longer acting β2 agonists such as Salmeterol act too slowly to be used as relief for dypsnea so these drugs should be used as a secondary therapy.

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 M3 receptors. The quaternary M3 muscarinic antagonist Ipratropium is widely prescribed with the β2 agonist salbutamol. [3]. Ipratropium is offered combined with salbutamol (Combivent) and with fenoterol (Duovent). Tiotropium provides improved specificity for M3 muscarinic receptors.

Anticholinergics may increase adverse effects.[23][24]

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.[25]

Leukotriene antagonists

More recently leukotriene antagonists block the signaling molecules used by the immune system. Montelukast, Pranlukast, Zafirlukast are some of the leukotrienes antagonists.[26]

Xanthines

Theophylline is the prototype of the xanthine[27] 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 has uncertain value when used in the EMR for treatment of dyspnea (Difficulty in breathing).[28] Patients need continual monitoring as theophylline has a narrow therapeutic range. More aggressive EMR interventions include IV H1 antihistamines and IV dexamethasone.

Corticosteroids

Inhaled corticosteriods (specifically glucocorticoids) act in the inflammatory cascade and may improve airway function considerably,[10] 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".[19]

Inhaled fluticasone may increase the risk of pneumonia.[19]

Oral or intravenous corticosteriods can help treat exacerbations of COPD.[29]

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.[30]

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.[31]

Vaccination

Patients with COPD should be routinely vaccinated against influenza, pneumococcus and other diseases to prevent illness and the possibility of death.[17]

Pulmonary rehabilitation

Pulmonary rehabilitation is a program of disease management, counseling and exercise coordinated to benefit the individual.[32] 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.[33]

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". [4]

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.[5]

The 5-year overall survival rate for pulmonary neoplasms is 14%.[34]

Coronary heart disease

For more information, see: Coronary heart disease.

Chronic airway obstruction may be an independent risk factor for coronary heart disease.[35]

Screening

Chronic obstructive pulmonary disease should not be screened for according to clinical practice guidelines by the American College of Physicians[36] and the Agency for Healthcare Research and Quality[37] This is due to the current lack of treatment for asymptomatic COPD and the inability of spirometric results to motivate smoking cessation.

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.[38]

Since COPD is not diagnosed until it becomes clinically apparent, prevalence and mortality data greatly underestimate the socioeconomic burden of COPD.[17] In the UK, COPD accounts for about 7% of all days of sickness related absence from work.[10]

Smoking rates in the industrialized world have continued to fall, causing rates of emphysema and pulmonary neoplasms to slowly decline.

References

  1. ↑ 1.0 1.1 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. ↑ 6.0 6.1 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. ↑ 9.0 9.1 Longmore M, Wilkinson I, Rajagopalan S (2005). Oxford Handbook of Clinical Medicine, 6ed. Oxford University Press. pp 188-189. ISBN 0-19-852558-3.
  10. ↑ 10.0 10.1 10.2 10.3 Kumar P, Clark M (2005). Clinical Medicine, 6ed. Elsevier Saunders. pp 900-901. ISBN 0702027634.
  11. ↑ 11.0 11.1 Rabe KF, Hurd S, Anzueto A, et al (2007). "Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease: GOLD executive summary". Am. J. Respir. Crit. Care Med. 176 (6): 532–55. DOI:10.1164/rccm.200703-456SO. PMID 17507545. Research Blogging. Cite error: Invalid <ref> tag; name "pmid17507545" defined multiple times with different content
  12. ↑ Holleman DR, Simel DL (1995). "Does the clinical examination predict airflow limitation?". JAMA 273 (4): 313-9. PMID 7815660. [e]
  13. ↑ Badgett RG, Tanaka DJ, Hunt DK, et al (1994). "The clinical evaluation for diagnosing obstructive airways disease in high-risk patients". Chest 106 (5): 1427-31. PMID 7956395. [e]
  14. ↑ Tillie-Leblond I, Marquette CH, Perez T, et al (2006). "Pulmonary embolism in patients with unexplained exacerbation of chronic obstructive pulmonary disease: prevalence and risk factors". Ann. Intern. Med. 144 (6): 390–6. PMID 16549851. [e]
  15. ↑ Qaseem A, Snow V, Shekelle P, et al (2007). "Diagnosis and management of stable chronic obstructive pulmonary disease: a clinical practice guideline from the American College of Physicians". Ann. Intern. Med. 147 (9): 633–8. PMID 17975186. [e]
  16. ↑ Wilt TJ, Niewoehner D, MacDonald R, Kane RL (2007). "Management of stable chronic obstructive pulmonary disease: a systematic review for a clinical practice guideline". Ann. Intern. Med. 147 (9): 639–53. PMID 17975187. [e]
  17. ↑ 17.0 17.1 17.2 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
  18. ↑ Rodrigo GJ, Nannini LJ, Rodríguez-Roisin R (May 2008). "Safety of Long-Acting {beta}-Agonists in Stable COPD: A Systematic Review". Chest 133 (5): 1079–87. DOI:10.1378/chest.07-1167. PMID 18460518. Research Blogging.
  19. ↑ 19.0 19.1 19.2 Calverley PM, Anderson JA, Celli B, et al (February 2007). "Salmeterol and fluticasone propionate and survival in chronic obstructive pulmonary disease". N. Engl. J. Med. 356 (8): 775–89. DOI:10.1056/NEJMoa063070. PMID 17314337. Research Blogging. Cite error: Invalid <ref> tag; name "pmid17314337" defined multiple times with different content Cite error: Invalid <ref> tag; name "pmid17314337" defined multiple times with different content
  20. ↑ Celli BR, Thomas NE, Anderson JA, et al (August 2008). "Effect of pharmacotherapy on rate of decline of lung function in chronic obstructive pulmonary disease: results from the TORCH study". Am. J. Respir. Crit. Care Med. 178 (4): 332–8. DOI:10.1164/rccm.200712-1869OC. PMID 18511702. Research Blogging.
  21. ↑ [1]
  22. ↑ [2]
  23. ↑ Lee TA, Pickard AS, Au DH, Bartle B, Weiss KB (September 2008). "Risk for death associated with medications for recently diagnosed chronic obstructive pulmonary disease". Ann. Intern. Med. 149 (6): 380–90. PMID 18794557. [e]
  24. ↑ Sonal Singh, Yoon K. Loke, and Curt D. Furberg (2008). Inhaled Anticholinergics and Risk of Major Adverse Cardiovascular Events in Patients With Chronic Obstructive Pulmonary Disease: A Systematic Review and Meta-analysis. JAMA: The Journal of the American Medical Association 300 (12), 1439-50 (24 Sep 2008) DOI:10.1001/jama.300.12.1439
  25. ↑ Howell JB, Altounyan RE (1967). "A double-blind trial of disodium cromoglycate in the treatment of allergic bronchial asthma". Lancet 2 (7515): 539–42. PMID 4166895. [e]
  26. ↑ BROCKLEHURST WE (1960). "The release of histamine and formation of a slow-reacting substance (SRS-A) during anaphylactic shock". J. Physiol. (Lond.) 151: 416–35. PMID 13804592. [e]
  27. ↑ http://www.chemistry.org/portal/a/c/s/1/acsdisplay.html?DOC=HomeMolecule\archive\motw_xanthine_arch.html
  28. ↑ Duffy N, Walker P, Diamantea F, Calverley PM, Davies L (September 2005). "Intravenous aminophylline in patients admitted to hospital with non-acidotic exacerbations of chronic obstructive pulmonary disease: a prospective randomised controlled trial". Thorax 60 (9): 713–7. DOI:10.1136/thx.2004.036046. PMID 15939732. PMC 1747521. Research Blogging.
  29. ↑ de Jong YP, Uil SM, Grotjohan HP, Postma DS, Kerstjens HA, van den Berg JW (2007). "Oral or IV Prednisolone in the Treatment of COPD Exacerbations: A Randomized, Controlled, Double-blind Study". Chest 132 (6): 1741–7. DOI:10.1378/chest.07-0208. PMID 17646228. Research Blogging.
  30. ↑ http://users.rcn.com/jkimball.ma.ultranet/BiologyPages/C/CellSignaling.html
  31. ↑ (1981) "Long term domiciliary oxygen therapy in chronic hypoxic cor pulmonale complicating chronic bronchitis and emphysema. Report of the Medical Research Council Working Party". Lancet 1 (8222): 681–6. DOI:10.1016/S0140-6736(81)91970-X. PMID 6110912. Research Blogging.
  32. ↑ U.S. National Heart Lung and Blood Institute - Treatment
  33. ↑ 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
  34. ↑ John D. Minna, "Neoplasms of the Lung," in Harrison's Principles of Internal Medicine, 16th ed. (2005), p. 506
  35. ↑ Ebi-Kryston KL (1988). "Respiratory symptoms and pulmonary function as predictors of 10-year mortality from respiratory disease, cardiovascular disease, and all causes in the Whitehall Study". J Clin Epidemiol 41 (3): 251–60. PMID 3339378. [e]
  36. ↑ Qaseem A et al, “Diagnosis and Management of Stable Chronic Obstructive Pulmonary Disease: A Clinical Practice Guideline from the American College of Physicians,” November 6, 2007, http://www.annals.org/cgi/content/full/147/9/633 (accessed November 2, 2007).
  37. ↑ Agency for Healthcare Research and Quality (2005). “Use of Spirometry for Case Finding, Diagnosis, and Management of Chronic Obstructive Pulmonary Disease (COPD),” August 2005, http://www.ahrq.gov/clinic/tp/spirotp.htm (accessed November 2, 2007).
  38. ↑ WHO - COPD
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