Chronic obstructive pulmonary disease overview

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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 . 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. 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. 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.

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,, , 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. 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.

Chest X Ray

On chest x-ray, the classic signs of COPD are overexpanded lung (hyperinflation), a flattened diaphragm, increased retrosternal airspace, and bullae. It can be useful to help exclude other lung diseases, such as pneumonia, pulmonary edema or a pneumothorax.

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, 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.

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 , .

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

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