Chronic obstructive pulmonary disease overview: Difference between revisions
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==Diagnosis== | ==Diagnosis== | ||
The diagnosis of COPD requires [[lung function tests]]. | The diagnosis of COPD requires [[lung function tests]]. | ||
===History and Symptoms=== | |||
Chronic obstructive pulmonary disease is a group of diseases that can present with symptoms such as shortness of breath, [[wheezing]], persistent cough and sputum production. Some clinical differences can help distinguish between the types of COPD. While [[chronic bronchitis]] patient present with productive cough with gradual progression to intermittent shortness of breath; recurrent pulmonary infections; and in later stage progressive cardiac/respiratory failure presenting with [[edema]] and weight gain. Classic findings for patients with [[emphysema]] include a long history of progressive shortness of breath with late onset of nonproductive cough; usually mucopurulent; and eventual decrease in appetite and [[respiratory failure]]. | |||
===Physical Examination=== | |||
Chronic obstructive pulmonary disease can be diagnostically evaluated by physical examination through auscultation. Physical examination are quite specific and sensitive for severe disease. The signs are usually difficult to detect in cases of mild to moderate diseases. Findings on general physical examination can be cyanosis, tachypnea, use of accessory respiratory muscles, paradoxical indrawing of lower intercostal spaces is evident (known as the Hoover sign), elevated jugular venous pulse and peripheral edema. Pulmonary examination in can be barrel chest (emphysema), wheezing, hyperresonance, crackles and rhonchi | |||
===Laboratory Findings=== | |||
[[Chronic obstructive pulmonary disease]] has irreversible airflow limitation specially during forced expiration. This is due to the destruction of lung tissue and increase in resistance to flow in the conducting airways. Thus, it doesn't show an improvement in FEV1 post [[bronchodilator]] administration (unlike [[asthma]]). This characteristic feature is used as an diagnostic criteria for COPD, i.e. a COPD is diagnosed by [[spirometry]] if FEV1/FVC < 70% for a matched control. Arterial blood gas may show hypoxemia with or without hypercapnia depending on the disease severity. pH may be normal due to renal compensation. A pH less than 7.3 usually indicate severe respiratory compromise. A blood sample taken from an [[artery]], i.e. [[Arterial Blood Gas]] (ABG), can be tested for blood gas levels which may show low oxygen (hypoxaemia) and/or high carbon dioxide (respiratory acidosis if pH is also decreased). A blood sample taken from a [[vein]] may show a high blood count (reactive polycythemia), a reaction to long-term hypoxemia. | |||
===Electrocardiogram=== | |||
Electrocardiogram can be used in establishing that hypoxia is due to underlying respiratory cause and not cardiac. | |||
===Chest X Ray=== | ===Chest X Ray=== | ||
On [[chest x-ray]], the classic signs of COPD are overexpanded lung ([[Hyperaeration|hyperinflation]]), a flattened diaphragm, increased retrosternal airspace, and bullae.<ref name=Old2007>{{cite journal |author=Torres M, Moayedi S |title=Evaluation of the acutely dyspneic elderly patient |journal=Clin. Geriatr. Med. |volume=23 |issue=2 |pages=307–25, vi |year=2007 |month=May |pmid=17462519 |doi=10.1016/j.cger.2007.01.007 |url=}}</ref> It can be useful to help exclude other lung diseases, such as [[pneumonia]], [[pulmonary edema]] or a [[pneumothorax]].<ref name=Old2007/> | On [[chest x-ray]], the classic signs of COPD are overexpanded lung ([[Hyperaeration|hyperinflation]]), a flattened diaphragm, increased retrosternal airspace, and bullae.<ref name=Old2007>{{cite journal |author=Torres M, Moayedi S |title=Evaluation of the acutely dyspneic elderly patient |journal=Clin. Geriatr. Med. |volume=23 |issue=2 |pages=307–25, vi |year=2007 |month=May |pmid=17462519 |doi=10.1016/j.cger.2007.01.007 |url=}}</ref> It can be useful to help exclude other lung diseases, such as [[pneumonia]], [[pulmonary edema]] or a [[pneumothorax]].<ref name=Old2007/> | ||
Revision as of 21:18, 26 February 2013
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [2]; Associate Editors-In-Chief: Cafer Zorkun, M.D., Ph.D. [3], Priyamvada Singh, MBBS [4]
Overview
Chronic obstructive pulmonary disease is characterized by the pathological limitation of airflow in the airway that is not fully reversible [1]. COPD is the umbrella term for chronic bronchitis, emphysema and a range of other lung disorders. This leads to a limitation of the flow of air to and from the lungs, causing shortness of breath (dyspnea). In clinical practice, COPD is defined by its characteristically low airflow on lung function tests.[2] In contrast to asthma, this limitation is poorly reversible and usually gets progressively worse over time.
Historical Perspective
The terms chronic bronchitis and emphysema were formally defined at the CIBA guest symposium of physicians in 1959. COPD has probably always existed but has been called by different names in the past. Bonet described a condition of “voluminous lungs” in 1679. Matthew Baillie illustrated an emphysematous lung in 1789 and described the destructive character of the condition. The term COPD was first used by William Briscoe in 1965 and has gradually overtaken other terms to become established today as the preferred name for this disease.
Pathophysiology
Pathologic changes in chronic obstructive pulmonary disease (COPD) occur in the large (central) airways, the bronchioles, and the lung parenchyma. Increased numbers of activated polymorphonuclear leukocytes and macrophages release elastases, proteinase-3 and macrophage-derived matrix metalloproteinases (MMPs), cysteine proteinases, and a plasminogen activator resulting in lung destruction. The antiprotease in the body cannot counteract effectively these elastases. Additionally, increased oxidative stress caused by free radicals in cigarette smoke, phagocytes, and polymorphonuclear leukocytes all may lead to apoptosis. In addition to macrophages, T lymphocytes, particularly CD8+, play an important role in the pathogenesis of smoking-induced airflow limitation.
Epidemiology and Demographics
Worldwide, COPD ranked as the sixth leading cause of death in 1990. It is projected to be the fourth leading cause of death worldwide by 2030 due to an increase in smoking rates and demographic changes in many countries.[3] COPD is the third leading cause of death in the U.S. and the economic burden of COPD in the U.S. in 2007 was $42.6 billion in health care costs and lost productivity.[4][5]
Risk Factors
Chronic obstructive pulmonary disease is a group of diseases characterized by the pathological limitation of airflow in the airway that is not fully reversible. A full comprehensive diagnosis is needed to eliminate related conditions and isolate the influence of lifestyle and behavior risk factors on condition outcome. Some common risk factors are cigarette smoking, occupational pollutants, air pollution and genetics. Other risk factors are increasing age, male gender, allergy, repeated airway infection.
Causes
It is most often due to tobacco smoking,[6], [7], [8] but can be due to other airborne irritants such as coal dust, asbestos or solvents, congenital conditions such as alpha-1-antitrypsin deficiency and as well as preserved meats containing nitrites.
Differential Diagnosis
In clinical practice, COPD is defined by its characteristically low airflow on lung function tests.[2] In contrast to asthma, this limitation is poorly reversible and usually gets progressively worse over time. It should be differentiated from certain conditions that have similar presentation for instance congestive heart failure, chronic asthma, bronchiectasis, and bronchiolitis obliterans.
Diagnosis
The diagnosis of COPD requires lung function tests.
History and Symptoms
Chronic obstructive pulmonary disease is a group of diseases that can present with symptoms such as shortness of breath, wheezing, persistent cough and sputum production. Some clinical differences can help distinguish between the types of COPD. While chronic bronchitis patient present with productive cough with gradual progression to intermittent shortness of breath; recurrent pulmonary infections; and in later stage progressive cardiac/respiratory failure presenting with edema and weight gain. Classic findings for patients with emphysema include a long history of progressive shortness of breath with late onset of nonproductive cough; usually mucopurulent; and eventual decrease in appetite and respiratory failure.
Physical Examination
Chronic obstructive pulmonary disease can be diagnostically evaluated by physical examination through auscultation. Physical examination are quite specific and sensitive for severe disease. The signs are usually difficult to detect in cases of mild to moderate diseases. Findings on general physical examination can be cyanosis, tachypnea, use of accessory respiratory muscles, paradoxical indrawing of lower intercostal spaces is evident (known as the Hoover sign), elevated jugular venous pulse and peripheral edema. Pulmonary examination in can be barrel chest (emphysema), wheezing, hyperresonance, crackles and rhonchi
Laboratory Findings
Chronic obstructive pulmonary disease has irreversible airflow limitation specially during forced expiration. This is due to the destruction of lung tissue and increase in resistance to flow in the conducting airways. Thus, it doesn't show an improvement in FEV1 post bronchodilator administration (unlike asthma). This characteristic feature is used as an diagnostic criteria for COPD, i.e. a COPD is diagnosed by spirometry if FEV1/FVC < 70% for a matched control. Arterial blood gas may show hypoxemia with or without hypercapnia depending on the disease severity. pH may be normal due to renal compensation. A pH less than 7.3 usually indicate severe respiratory compromise. A blood sample taken from an artery, i.e. Arterial Blood Gas (ABG), can be tested for blood gas levels which may show low oxygen (hypoxaemia) and/or high carbon dioxide (respiratory acidosis if pH is also decreased). A blood sample taken from a vein may show a high blood count (reactive polycythemia), a reaction to long-term hypoxemia.
Electrocardiogram
Electrocardiogram can be used in establishing that hypoxia is due to underlying respiratory cause and not cardiac.
Chest X Ray
On chest x-ray, the classic signs of COPD are overexpanded lung (hyperinflation), a flattened diaphragm, increased retrosternal airspace, and bullae.[9] It can be useful to help exclude other lung diseases, such as pneumonia, pulmonary edema or a pneumothorax.[9]
CT
A high-resolution computed tomography scan of the chest may show the distribution of emphysema throughout the lungs and can also be useful to exclude other lung diseases.
Echocardiography
Echocardiography helps in a diagnosis of pulmoanry hypertension in the patients with COPD.
Other Diagnostic Studies
The diagnosis of COPD is confirmed by spirometry,[8] a test that measures 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 large breath. Spirometry also measures the forced vital capacity (FVC), which is the greatest volume of air that can be breathed out in a whole large breath. Normally, at least 70% of the FVC comes out in the first second (i.e. the FEV1/FVC ratio is >70%). A ratio less than normal defines the patient as having COPD. Six minute walk tests act as an predictor of mortality in patients with moderate COPD (patients who desaturate have worse mortality compared with those who don't desaturate.)
Treatment
Important management strategies are smoking cessation, vaccinations, rehabilitation, and drug therapy (often using inhalers). Some patients go on to require long-term oxygen therapy or lung transplantation.[8]
Medical Therapy
Treatment of COPD requires a careful and thorough evaluation by a physician. The most important aspect of treatment is avoiding tobacco smoke and removing other air pollutants from the patient’s home or workplace. Symptoms such as coughing or wheezing can be treated with bronchodilator medications like Beta 2 receptor agonist, anticholinergic drugs. The drugs used cause benefit via relaxation of smooth muscle or decreasing inflammatory factors. . Respiratory infections should be treated with antibiotics, if appropriate. Patients who have low blood oxygen levels in their blood are often given supplemental oxygen. Currently, no treatment has been found to be totally curative against COPD except lung transplant. The treatments aim to improve lung function and quality of life. The initial treatment can be done either with Beta 2 agonist or anticholinergic. Both anticholinergics or Beta adrenergic receptor agonists have proved to be equally beneficial but the combination of the two has shown synergistic effects. Long acting bronchodilators are more beneficial than short-acting ones [10], [11].
Surgery
Patients with emphysema may have big bullae ranging from 1-4 cm and may occupy 1/3rd of lung space. These bullae can cause compromise to vetilation and perfusion. Bullaectomy is the surgical removal of these bullae. It is commonly done in patients with FEV1 < 50% of predicted and who are symptomatic. Bullaectomy helps in re-expansion of the lung tissue.
Secondary Prevention
To decrease the number and rate of COPD deaths, public health programs should continue efforts to reduce all personal exposure to 1) tobacco smoke, including passive smoke exposure; 2) occupational dusts and chemicals; and 3) other indoor and outdoor air pollutants linked to COPD. Once COPD is diagnosed, chronic disease management programs should work to prevent further deterioration in lung function and reduce COPD mortality. The numbers of deaths for which COPD was the underlying cause and population estimates for calculation of rates were obtained from the CDC Wonder compressed mortality database† of the National Vital Statistics System.
References
- ↑ Mannino DM, Homa DM, Akinbami LJ, Ford ES, Redd SC (2002). "Chronic obstructive pulmonary disease surveillance--United States, 1971-2000". MMWR. Surveillance Summaries : Morbidity and Mortality Weekly Report. Surveillance Summaries / CDC. 51 (6): 1–16. PMID 12198919. Unknown parameter
|month=ignored (help);|access-date=requires|url=(help) - ↑ 2.0 2.1 Template:Cite doi [1]
- ↑ Mathers CD, Loncar D (2006). "Projections of Global Mortality and Burden of Disease from 2002 to 2030". PLoS Med. 3 (11): e442. doi:10.1371/journal.pmed.0030442. PMC 1664601. PMID 17132052. Unknown parameter
|month=ignored (help) - ↑ COPD (Chronic Obstructive Pulmonary Disease)
- ↑ "2007 NHLBI Morbidity and Mortality Chart Book" (PDF). Retrieved 2008-06-06.
- ↑ Devereux G. ABC of chronic obstructive pulmonary disease. Definition, epidemiology, and risk factors. BMJ 2006;332:1142-1144. PMID 16690673
- ↑ "What is COPD?". National Heart Lung and Blood Institute. U.S. National Institutes of Health. June 01, 2010. Check date values in:
|date=(help) - ↑ 8.0 8.1 8.2 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.
- ↑ 9.0 9.1 Torres M, Moayedi S (2007). "Evaluation of the acutely dyspneic elderly patient". Clin. Geriatr. Med. 23 (2): 307–25, vi. doi:10.1016/j.cger.2007.01.007. PMID 17462519. Unknown parameter
|month=ignored (help) - ↑ Belman MJ, Botnick WC, Shin JW (1996). "Inhaled bronchodilators reduce dynamic hyperinflation during exercise in patients with chronic obstructive pulmonary disease". American Journal of Respiratory and Critical Care Medicine. 153 (3): 967–75. PMID 8630581. Retrieved 2012-03-20. Unknown parameter
|month=ignored (help) - ↑ Maclay JD, Rabinovich RA, MacNee W (2009). "Update in chronic obstructive pulmonary disease 2008". American Journal of Respiratory and Critical Care Medicine. 179 (7): 533–41. doi:10.1164/rccm.200901-0134UP. PMID 19318543. Retrieved 2012-03-20. Unknown parameter
|month=ignored (help)